The Animal Parasites of Man (part 5 of 6)

Introduction

The aim of the present volume is to give an account of the animal parasites of man, the number of which is very large. The Protozoa that infest man are very important, and the literature relating to them and to the treatment of the diseases that they produce is very extensive. All that can be done in this Appendix is to give a very brief outline of some of the more recent and approved methods of treatment, for further details of which the reader should refer to standard medical works, among which the following are noteworthy:--

Allbutt and Rolleston (1907): “System of Medicine,” vol. ii, part 2, “Tropical Diseases and Animal Parasites,” London.

Castellani and Chalmers (1913): “Manual of Tropical Medicine” (second edition), London.

Laveran and Mesnil (1912): “Trypanosomes et Trypanosomiases” (second edition), Paris.

Manson (1914): “Tropical Diseases” (fifth edition), London.

Mense (1905): “Handbuch der Tropenkrankheiten,” Leipzig.

Ross (1911): “The Prevention of Malaria,” London.

Scheube (1910): “Die Krankheiten der Warmen Länder,” Jena.

References to the treatments tried in many parasitic diseases can be found in the Sleeping Sickness Bulletin and Kala-azar Bulletin, both now superseded and greatly extended in scope in the Tropical Diseases Bulletin, published by the Tropical Diseases Bureau, Imperial Institute, London, S.W.

The following diseases, due to protozoa and allied forms, are discussed:--

I. Amœbic Dysentery. II. Trypanosomiases. III. Flagellate Diarrhœa and Dysentery. IV. Leishmaniases--Kala-azar and Oriental Sore. V. Spirochætoses--Relapsing Fevers, Yaws, Syphilis and Bronchial. VI. Malaria. VII. Balantidian or Ciliate Dysentery.

I.--AMŒBIC DYSENTERY.

Amœbic dysentery, due to Entamœba histolytica (see pp. 34–41), is present throughout the tropical world and also occurs in temperate zones.

Walker and Sellards[429] (1913) conducted important experiments with amœbæ on prisoners in the Philippine Islands. They showed experimentally that cultural amœbæ are non-pathogenic. As regards experiments with Entamœba coli, after feeding to twenty individuals they concluded that E. coli is a parasite of the human intestine but non-pathogenic and non-culturable. In a third series of experiments, after feeding with motile Entamœba histolytica, tetragena cysts were found in the stools later; when tetragena cysts were administered, motile E. histolytica were present in the subsequent stools. Some of the histolytica cases developed dysentery after a time. They lay stress on the necessity for the frequent examination of stools in order to detect carriers. The incubation period of entamœbic dysentery is usually long.

[429] Philippine Journ. Sc., B, viii, p. 253.

With regard to the symptomatology of amœbic dysentery, Castellani and Chalmers distinguish four types--the acute, chronic, latent, and mixed types.

The acute type has an abrupt onset; pain is felt in the lower part of the abdomen, and the motions, rarely exceeding thirty daily, are accompanied by much griping and straining. Blood and mucus are present in the motions, and occasionally greyish material, consisting of leucocytes, mucus, Charcot-Leyden crystals, amœbæ, and bacteria, sometimes with particles of tissue. Nausea and vomiting may occur. Digestion is usually deranged. The abdomen is sunken, the liver and spleen are normal, but tenderness is felt along the course of the large intestine. The urine may be diminished in quantity.

The chronic type may succeed the acute, or appear like diarrhœa, the motions being fæculent and containing mucus. Between exacerbations, constipation may occur. The number of motions may only be twelve to fourteen per diem. Gangrenous complications may occur at any time, and chronic dysentery may persist for many years.

The latent type is important, as the patients, though free from dysenteric symptoms, harbour amœbæ and act as parasite carriers. The latent condition may lead to acute attacks or to liver abscess.

The mixed type occurs where amœbic and bacillary dysentery are combined. There is much fever, nausea, and vomiting. The motions are numerous and often very offensive.

Treatment.--The most modern method of treatment, due to Leonard Rogers, is by emetine. According to Castellani and Chalmers, it is well to relieve griping and straining by either a hypodermic injection of morphia or by small enemata of 40 minims of laudanum in 1 oz. of mucilage of starch or by using 1/4 gr. morphia or 1/4 gr. codeine suppository. A dose of castor oil (ʒiv to ʒvi) with or without a few minims of liquor opii sedativus or a few doses of saline may be given during the first twenty-four hours. After the castor oil has acted or simultaneously, emetine treatment should be commenced; 1/3 to 1/2 gr. of emetine hydrochloride, dissolved in sterile normal salt solution, is injected hypodermically three times a day for two or three days.

If emetine cannot be obtained, 5 gr. doses of ipecacuanha every three to six hours in the form of membroids, or as pills coated with salol or keratin, can be substituted.

After acute symptoms have disappeared, intestinal irrigations once or twice daily, on alternate days, are useful. A solution of tannic acid (3 to 5 per 1,000) or of quinine bihydrochloride varying in strength from 1 in 5,000 to 1 in 750 is very slowly injected in quantities of 1/2 to 3 pints by means of a long, soft, rectal tube.

For gangrenous dysentery Castellani and Chalmers state that appendicostomy, with irrigation of the whole lower bowel with quinine lotion (1 in 1,000) or collargol (1 in 500), is the only chance.

The use of emetine should be continued in smaller doses after the dysenteric symptoms have ceased, in order to prevent relapses and as a possible safeguard against the development of a liver abscess.

Recently (July, 1914), Dr. W. E. Deeks[430] has given an account of his successful procedure in dealing with the dysenteries in the Ancon Hospital, Panama Canal Zone, of which medical clinic he is the chief. With regard to amœbic dysentery he advocates: (1) Rest, to increase the patient’s resistance; (2) a generous milk diet, which is practically all absorbed before it reaches the large bowel; (3) saline or plain water irrigations, one to three daily; (4) the administration of bismuth sub-nitrate in heroic doses; 180 gr. is given mechanically suspended in about a tumbler of plain or effervescent water every three hours, day and night in severe cases, only lessening the amount when improvement takes place. Mechanical suspension in a large quantity of water is essential. When the stools begin to decrease in number and the tongue becomes clean, the number of doses is reduced to three or four daily. In very chronic cases one or two doses daily for a month after convalescence are recommended.

[430] Annals Trop. Med. and Parasitol., viii, pp. 321, 353.

In exceptional cases of extreme emaciation and exhaustion, showing marked toxic symptoms, surgical treatment is necessary, and at Ancon a wide, open cæcostomy is performed.

The treatment of dysentery with bismuth sub-nitrate has been in use for some years at Ancon. Latterly, a combined treatment by hypodermic injections of emetine and bismuth sub-nitrate by the mouth has been used, and the authorities there consider that it is better to combine the two drugs rather than use each singly. Emetine probably acts as a direct poison to the amœbæ, while the bismuth probably acts by destroying the symbiotic organisms necessary for their growth.

With regard to preventive measures, all drinking water should be filtered and boiled, and uncooked vegetables and salads avoided. Scrupulous care with regard to personal cleanliness, and avoidance of touching the mouth or lips after contact with dysenteric patients, are essential. Isolation of parasite carriers is of great use in combating and controlling outbreaks of amœbic dysentery. The pollution of soil and water must be rigorously prevented.

Liver abscess due to amœbæ must be localized by exploratory punctures, and then opened and drained. Intramuscular injections of emetine hydrochloride, 1/6 gr. to 1/2 gr. every day, will reduce the temperature and afford relief.

Oral endamœbiasis has been recently investigated by Bass and Johns, Smith and Barrett and colleagues (see pp. 43, 733). It responds to treatment with emetine, and 1/2 gr. of emetine hydrochloride administered hypodermically each day is of service. Rinsing the mouth with a solution of fluid extract of ipecacuanha is also useful.

Rogers[431] (1915) recommends a combined treatment of emetine and streptococcal vaccines for pyorrhœa alveolaris.

[431] Ind. Med. Gazette, April, 1915, l, p. 121.

II.--TRYPANOSOMIASES.

The human trypanosomiases are those occurring in Africa, due to Trypanosoma gambiense and T. rhodesiense and spread by Glossinæ, and that due to T. cruzi, occurring in South America and spread by the Reduviid bugs, Triatoma spp. These trypanosomiases present different clinical features and are best dealt with separately.

African Sleeping Sickness.

Sleeping sickness, due to Trypanosoma gambiense or varieties thereof, was first reported from West Africa and is now present, not only along the West Coast and in Nigeria, but throughout the Congo basin into Uganda, north of which it exists in the Bahr-el-Ghazal province of the Sudan. In Nyasaland and Rhodesia a more virulent but less widely distributed disease is produced by Trypanosoma rhodesiense.

There is a general similarity between the two diseases, and the symptoms as described by the leading authorities agree in the main. The malady due to T. rhodesiense has been known only since 1910 and the differences between the malady due to it and to T. gambiense will be indicated.

The course of the disease may be roughly divided into three stages, the incubation, the febrile or glandular, and the cerebral stage.

The exact incubation period is not known with certainty in man. Probably, in most cases, it does not exceed two to three weeks, but disease signs may not appear for months. The bite of the Glossina gives rise to local irritation, which may be overlooked. The irritation usually subsides in the course of a few days.

The febrile, or glandular stage, is marked by attacks of fever of an intermittent type. An erythematous eruption is often found on Europeans. This rash begins as irregularly shaped pinkish patches which clear in the centre until a ring is produced. It may occur on any part of the body but is more frequent on the trunk. A typical symptom is the enlargement of one or more of the lymphatic glands, especially those of the neck. A general, deep hyperæsthesia, known as Kerandel’s sign, may be present, and if the patient strikes a limb against any hard object, a feeling of acute pain is felt, the sensation being slightly delayed. As repeated attacks of fever increase, the patient may become anæmic. The febrile stage may last for years, and cure may be brought about at this phase, but frequently, after the febrile stage has lasted some time, the cerebral stage is reached. Tachycardia is also a symptom. Auto-agglutination of the red blood corpuscles is another useful characteristic, as it is said to occur rarely in other tropical diseases, but some workers doubt its value.

The cerebral, or true sleeping sickness stage is marked by a great change in the habits of the victim, who becomes apathetic and dull, careless and dirty in habits, and begins to experience difficulty in walking. Tremors of varying degrees of severity are common and the gait is peculiar. There is usually fever with rise of temperature from 100° F. to 104° F. in the evening, becoming subnormal in the morning. For some days before death, it often becomes permanently subnormal. Congestion and œdema of the lungs, with patches of pneumonia, are not infrequently observed before death. The torpor gradually deepens, and the patient loses flesh. Frequently the lips swell and saliva dribbles. The patient usually becomes comatose and death ensues. Mania and delusions, and psychical and physical symptoms resembling those found in general paralysis of the insane, sometimes occur, and death may arise from secondary complications such as pneumonia or dysentery.

Pathologically, the disease seems to consist of a chronic inflammation of the lymphatic system. The trypanosomes reach the lymphatic glands which become inflamed, and gradually invade the blood and the cerebrospinal fluid. Sooner or later, as a result of the lymphatic disease, changes occur in the membranes and substances of the brain and spinal cord. There is round-celled perivascular infiltration of the pia-arachnoid of the brain and spinal cord. These changes cause compression of the blood-vessels, and so lessen the supply of blood to the brain and spinal cord. Further changes in the latter organs result in the production of the symptoms that have given the disease the name of “sleeping sickness.”

The disease due to Trypanosoma rhodesiense generally runs a more rapid course than that due to T. gambiense. The torpor and sleepiness may not be obvious or be very slight, and the enlargement of the lymphatic glands of the neck also may not be marked or may appear to be absent. The duration of the disease often appears to be from three to six months.

Treatment is only of use if commenced in the earlier stages of the disease. The substances of most value so far are arsenic in the form of atoxyl (introduced by Wolferstan Thomas in 1905) and antimony in the form of tartar emetic. Castellani and Chalmers and Manson recommend treatment by combining the use of both substances. The combined treatment is recommended not only because both substances have been proved of service independently, but also because certain strains of trypanosomes resistant to arsenic are known, and trypanosomes can develop a resistance to arsenic. Such forms, that would not be affected by the atoxyl, are left open to attack by the antimony salt. Daniels also recommends combined arsenic and antimony treatment, and (1915) uses atoxyl and antiluetin.

Atoxyl is best given intramuscularly in 10 per cent. solution in sterile normal saline solution. Galyl is also said to have given good results.

Castellani and Chalmers recommend: (1) Manson’s method of administration of atoxyl, viz., 2 to 3 gr. of atoxyl are given by intramuscular injection every third day for at least two years; or (2) Broden and Rodhain’s method, 7-1/2 gr. of atoxyl by intramuscular injection every fifth day. For the combined therapy by atoxyl and antimony they recommend the following:--“An atoxyl injection (3 gr.) is given every third day or 7-1/2 gr. every fifth day, and sodiotartrate of antimony (Plimmer’s salt) is administered daily, 2 gr. dissolved in a large quantity of water (2 pints) by the mouth or by the rectum. Tartar emetic, however, is best given by intravenous injections, using solutions of 1 in 100 or 1 in 1,000. The dose of the drug to be given is 5 to 10 cg. per injection. It is important that none of the fluid of the injection should escape into the surrounding tissues, as a violent inflammation may result. These injections should be administered monthly on ten consecutive days for a long period.”

Macfie and Gallagher (1914) injected 6 gr. of atoxyl intramuscularly every week in cases infected with T. nigeriense in the Eket district of Southern Nigeria.

Large doses of atoxyl were often said to cause distressing results such as optic atrophy, and when the onset of such occurred the drug was usually discontinued. However, Daniels[432] (July, 1915) points out that eye troubles, such as iridocyclitis, are symptoms of trypanosomiasis.

[432] Journ. Trop. Med. and Hyg., xviii, p. 157.

Other arsenical preparations such as soamin and arsenophenylglycin have been used, but less successfully than atoxyl. Fowler’s solution, well diluted, has been given by the mouth when treatment by injection was not possible, the doses commencing with 5 minims and increasing to 15 minims.

Salvarsan and neo-salvarsan have also been tried for sleeping sickness. Plimmer recommended powdered antimony suspended in sterile olive oil. Ranken used precipitated metallic antimony in normal saline solution injected intravenously.

Laveran and Thiroux have recommended a combined treatment of atoxyl and an inorganic salt of arsenic such as orpiment. The orpiment is given as pills, in doses of 2 gr. of orpiment two or three times daily. Opium is added to the orpiment to prevent diarrhœa. This treatment is said to have been used in man with good results.

Trypanosoma rhodesiense seems less amenable to treatment than T. gambiense.

The main preventive measures seem to lie in segregation of the sick in areas not infested with Glossinæ, and in measures against these flies, such as bush clearing and destruction, to some extent, of proved reservoirs in big game.

South American Trypanosomiasis.

The chief clinical features of the trypanosomiasis occurring in Brazil have already been indicated (see p. 87). With regard to treatment, according to Castellani and Chalmers the indications are the same as those for African trypanosomiasis, together with treatment for hypothyroidism. Preventive measures are directed against the Reduviid bug, Triatoma megista, that transmits the disease. The bugs occur in numbers in the cracks of the houses of the poor of Minas Geraes, and may be destroyed by sulphur fumigation, lime-washing or whitewashing.

III.--FLAGELLATE DIARRHŒA AND DYSENTERY.

The chief causal agents are Trichomonas hominis (T. intestinalis), Chilomastix (Tetramitus) mesnili and allied organisms (see pp. 54 to 57), and Lamblia intestinalis (see pp. 57 to 60 and Appendix pp. 734 to 736).

These parasites and the associated diarrhœas occur in temperate as well as in warm climates. Probably some of the diarrhœas in India are thus caused. The same, or similar parasites occur in various Muridæ, especially rats and mice, which may act as reservoirs.

(i) Mello-Leitao[433] (1913), writing from Rio de Janeiro, states that there is a primary flagellate dysentery, due to _Trichomonas intestinal_is (Leuckart) and to Lamblia intestinalis (Lambl), either separately or in combination. He considers it a benign disease, and the most frequent form of dysentery in young children. Trichomonas and Lamblia were found to be pathogenic to children under 3 years of age.

[433] Brit. Journ. Children’s Diseases, x, p. 60.

Escomel[434] (1913) collected 152 cases of dysentery in Peru due solely to Trichomonas. Examination of the reservoirs containing the water used for drinking purposes showed the presence of Trichomonas. After the reservoirs were cleaned no more Trichomonas was found and the cases of dysentery ceased.

[434] Bull. Soc. Path. Exot., vi, p. 120.

Brumpt[435] (1912) described a colitis due to Trichomonas intestinalis in a patient returned from Tonkin.

[435] Ibid., v, p. 725.

Cases of infection by Chilomastix (Tetramitus) mesnili, with colitis or dysenteric symptoms, are recorded by Brumpt (1912) from France, and by Nattan-Larrier[436] (1912) from the Ivory Coast respectively.

[436] Ibid., v, p. 495.

Marques da Cunha and Torres[437] (1914) describe five cases of chronic diarrhœa in Brazilian children due to the Chilomastix (Tetramitus).

[437] Brazil Medico, xxviii, p. 269.

Gäbel[438] (1914) described a case of seasonal diarrhœa contracted in Tunis and caused by a Tetramitid parasite which he named Difämus tunensis, as the discoverer considered that it lacked an undulating membrane in its large cytostome.

[438] Arch. f. Protistenkunde, xxxiv, p. 1.

Derrieu and Raynaud[439] (1914) record a case of chronic dysentery in Algeria due to a Trichomonad possessing an undulating membrane and five free flagella. The parasite was named Hexamastix ardindelteili, but the generic name Hexamastix is pre-occupied. Chatterjee’s Pentatrichomonas bengalensis (1915) is possibly the same organism.

[439] Bull. Soc. Path. Exot., vii, p. 571.

Treatment.--Escomel (1913), finding ipecacuanha and calomel useless, recommends turpentine for Trichomonad dysentery. Two to 4 gr of essence of turpentine in an emulsion are given by the mouth, and enemata containing 15 to 20 drops of turpentine emulsified in the yolk of an egg to which is added a little water and tincture of opium. Derrieu and Raynaud found this treatment effective in Algeria. Smithies[440] (1912) reports two cures of cases of severe dyspepsia, in which Trichomonads were found in the stomach contents, after administration of a single dose of 50 to 60 gr. of thymol, given at bed-time, together with 2 gr. of calomel, and followed by an ounce of Carlsbad salts in the morning. The patients came from the Southern United States, and had been in the habit of drinking unfiltered surface water in the localities in which they lived. Mello-Leitao[441] used magnesium sulphate and water or milk diet. Sometimes enemata of collargol (1 per cent.) or electrargol were required. Rosenfeld recommended calomel. Methylene blue has also been tried. Recently, Escomel[442] (1914) recommends enemata of an aqueous solution of iodine (1 per 1,000) and farinaceous diet. Lynch[443] (1915), working in South Carolina, recommends a mouth wash of saturated solution of bicarbonate of soda three times daily in oral infections. A similar solution was used as a douche in vaginal trichomoniasis.

[440] Amer. Journ. Med. Sci., cxliv, p. 82.

[441] Brit. Journ. Children’s Diseases, x, p. 60.

[442] Bull. Soc. Path. Exot., vii, p. 657.

[443] Amer. Journ. Trop. Dis. and Prevent. Med., ii, p. 627.

Stiles (1913) points out that when amœbæ or flagellates are found in a large percentage (10 to 40, or even 60) of the members of a community, means should be taken to improve the methods for the disposal of the dejecta, so that the food supply may be carefully protected against fæcal contamination. Cysts of the parasites may be air-borne or conveyed to food on the bodies of house-flies.

(ii) Lamblia intestinalis in man may cause diarrhœa with dysenteriform stools. The diarrhœa may be of a chronic recurrent character. The flagellate, or a variety of it, is fairly common in the digestive tract of rats and mice.

Mathis[444] (1914) gives an interesting account of cases in Tonkin. In a child, aged 3, the stools were at first glairy and blood-stained, containing many encysted Lamblia. The child’s home was infested with mice. In another case, the house of the patient harboured numerous rats.

[444] Bull. Soc. Med. Chirurg. Indo-Chine, v, p. 55.

According to Mathis, prognosis is favourable, but emetine hydrochloride is without action on Lamblia. Prowazek and Werner[445] (1914), however, state that emetine will act upon the flagellates, but not upon the cysts. They recommend uzara (two tablets, three times daily) and extract of male fern as useful in certain cases. Martin Mayer (1914) found emetine hydrochloride successful in a case in the Hamburg Seamen’s Hospital, but Assmy (1914) points out that a suitable diet and daily doses of magnesium sulphate are sufficient, in his experience, to effect an improvement, and he doubts the specific action of emetine. Escomel (1914) recommends milk diet, then calomel succeeded by castor oil.

[445] Beihefte z. Arch. f. Schiffs- u. Tropen-Hyg., xviii, 5, p. 155.

According to Noc, Lamblia may also be water-borne. Healthy carriers of Lamblia cysts are known. Food should be protected from being soiled by rats and mice.

IV.--LEISHMANIASES.

A. *Kala-azar.*

(i) “Indian” Kala-azar due to Leishmania donovani.

Indian kala-azar due to Leishmania donovani is a very fatal disease with a rate of mortality varying from 70 to 98 per cent. of the cases.

The incubation period is very variable and the early symptoms not well defined. The incubation period seems to range from three weeks to several months after exposure to infection. The onset seems to commence with a rigor and attack of irregular, remittent fever, which may show two remissions per day in a four-hourly temperature chart. Rogers considers the daily double remission almost diagnostic. The duration of this first attack is from two to six weeks. The spleen and liver enlarge, especially the former, and are painful and tender. Towards the end of the time the temperature declines and the first period of the disease ends. After this period an apyrexial interval occurs, which, after some weeks, ends in an attack of fever resembling the first. Periods of pyrexia and apyrexia alternate. Anæmia commences and asthenia appears and deepens steadily. The patient is now thin and wasted, the abdomen much swollen and protuberant, the ribs show clearly, the limbs are wasted and skin and tongue darker than normal. In Europeans the skin is of a remarkable earthy hue, and in natives of India darker than normal, approaching black. Intestinal disturbances, often in the form of very obstinate and intractable diarrhœa or dysenteric attacks, are common. Papular eruptions often appear, particularly on the thighs; hæmorrhages also may occur. The disease lasts for periods varying from seven months to two years, and usually ends fatally.

Treatment, unfortunately, has not been very successful up to 1915. Manson has reported two cases of cure by intramuscular injections of atoxyl daily or every other day in doses of 3 gr. Rogers has advocated large doses of quinine, 60 to 90 gr. daily until the temperature falls and then 20 gr. daily. Castellani and Chalmers consider the best results are obtained by large doses of quinine given intramuscularly, supplemented by a course of quinine cacodylate injections or atoxyl injections. Tartar emetic should be tried (see pp. 627, 629), especially as L. Rogers (July, 1915) has had promising results in ten cases. Castellani (1914) and Mackie (1915), have also had successful results. Leishman states that the administration of red bone-marrow, either raw or in the form of tablets, may be beneficial. Good nursing and careful diet are essential, and diarrhœa or dysentery must receive the appropriate treatment.

With regard to preventive measures, the extermination of bugs and other biting insects seems to be of most service. Domestic and personal cleanliness is of great importance. Patients should be segregated. It would probably be as well if houses in which many cases of kala-azar occurred were destroyed. Dodds Price, in Assam tea gardens, moves the coolie lines 300 to 800 yards from old infected ones, with satisfactory results.

(ii) Infantile Kala-azar due to Leishmania infantum.

This malady is found among children, rarely in adults, along the Mediterranean littoral.

The disease commences insidiously and is often unrecognized until some intestinal disturbance occurs. The spleen is then found to be somewhat enlarged, and the case has often been regarded as one of malaria. The child becomes anæmic, suffers from diarrhœa, alternating with constipation, and has attacks of irregular fever. The spleen continues to enlarge and protrudes from under the cover of the ribs. Hæmorrhages from the nose and gums and into the skin occur. Anæmia and wasting set in. The abdomen then becomes very enlarged. The child becomes much less active both physically and mentally, and looks prematurely old. Death often occurs from exhaustion, though some cases of spontaneous recovery are known.

Treatment up till recently has been unsatisfactory. Some of the remedies tried, as quoted by Castellani and Chalmers, are 15 cg. doses of atoxyl, benzoate of mercury (2 to 4 mg. as a daily injection), thiarsol (5 to 15 mg. by subcutaneous injection), salvarsan, etc. Recently Cristina and Caronia (1915)[446] have given repeated intravenous injections of 1 per cent. aqueous solution of tartar emetic, the dose varying from 2 to 10 cg. The treatment in various cases has lasted from 15 to 40 days.

[446] Bull. Soc. Path. Exot., viii, p. 63.

Prophylactic measures seem to lie in the destruction of infected dogs and diminishing the breeding of fleas (see p. 111).

B. *Oriental Sore, due to Leishmania tropica.*

Oriental sore, known under many other names (see p. 107), is a local infection of the skin due to Leishmania tropica. The incubation period varies from a few days to some weeks, or even months, and then one or several small itching papules appear. Each spot becomes red and shotty, the papules increase slowly in size and the surface becomes covered with papery scales. After a variable time, usually not exceeding three to four months, ulceration occurs and a yellowish secretion is exuded that soon dries into a scab. Under the scab ulceration continues by erosion of the edges, and subsidiary sores arise around the parent ulcer and usually fuse with it. Healing commences after six to twelve months. Granulation begins at the centre and spreads outwards, and when healing is complete, a depressed, whitish or pinkish scar remains.

Many treatments for Oriental sore have been devised but do not seem particularly satisfactory. Castellani and Chalmers state that the scabs should be removed by boracic acid fomentations, and the ulcers thoroughly disinfected once or twice daily with a 1 per 1,000 solution of perchloride of mercury, after which an ordinary antiseptic ointment is applied.

The use of permanganate of potash has been advocated both by French and English doctors. Both large and small sores can be treated. The patient’s skin around the sore is protected by a thick layer of vaseline, and the surface of the ulcer powdered with potassium permanganate, which is kept in position by a pad of gauze and a bandage. The treatment is said to cause great pain for six to eight hours, but at the most, three treatments are necessary before the sore becomes a simple ulcer, well on the way to healing. The permanganate may also be used in ointment. Excision of the ulcer when small is advisable when the site of the ulcer permits of this. According to Manson, reports on treatment by radium, salvarsan and carbon dioxide snow are decidedly promising. Mitchell (1914)[447] reports favourably on the use of carbon dioxide snow in the form of a pencil, in India. In Brazil several workers (1914) record successful results from the intravenous injection of a 1 per cent. solution of tartar emetic in distilled water. Low (1915) has successfully treated a case by direct local application of tartar emetic. Row (1912) has treated cases of Oriental sore by inoculation of killed cultures of the causal organism.

[447] Journ. Roy. Army Med. Corps, xxiii, pp. 440–446 (see _Trop. Dis. Bull._, v, No. 5, p. 276).

As the disease is very contagious, the slightest wound, and any insect bite, should be thoroughly disinfected with 5 per cent. carbolic acid or iodine. Destruction of bugs, lice, and other biting insects should be enforced. As dogs may contract the disease (see p. 108), it is well not to allow them in the house and not to encourage undue contact with them.

Naso-oral Leishmaniasis (Espundia) due to Leishmania tropica.

This form of Leishmaniasis has been reported from South America and recently by Christopherson[448] (1914) from the Sudan. In South America it is often called Espundia, also Buba and Forestal Leishmaniasis. The primary lesion is found usually on the forearms, legs, chest or trunk. This ulcer is of the Oriental sore type, and after some months, or even as long as two years, heals up, leaving a thick scar. While the ulcer is open, or more often after it has healed, lesions appear on the mucosa of the mouth and nose. The hard and soft palate, gums and lips all may be attacked. The mucosa of the nose is usually attacked and the cartilages become destroyed, producing great deformity. In bad cases the pharynx and larynx may become infected.

[448] Annals Trop. Med. and Parasitol., viii, p. 485.

Till recently it was believed that treatment was of little use unless the case could be investigated early. Escomel considered that if the primary cutaneous lesion was excised or destroyed, further progress of the disease was prevented. When lesions have appeared on the mucosa of the mouth or nose, little could be done. The ulcers might be cauterized and mild antiseptic mouth washes used.

In 1913 Vianna, working in Brazil, introduced treatment by tartar emetic, which is now becoming more widely known and proving efficacious. Carini[449] (1914) applies it thus. Tartar emetic (that is, potassium antimonyl tartrate) in 1 per cent. aqueous solution is introduced slowly into a vein, such as the vein at the bend of the elbow, in doses of 5 to 10 c.c. daily or on alternate days according to the tolerance of the patient to the drug. Eighteen to forty injections have been used. In some of the memoirs on the subject, the drug is referred to as antimony tartrate.

[449] Bull. Soc. Path. Exot., vii, p. 277.

The course of the disease is chronic and may last for twenty to thirty years, death usually resulting from some intercurrent disease.

At present the actual transmitter of Espundia is not known with certainty. Various sand-flies (Simulidæ) have been suspected of transmitting the disease, though so far proof is wanting. It has also been suggested that the natural food sources of some Simulidæ known to bite man, namely, certain snakes[450] and lizards,[451] are possible reservoirs of the disease.

[450] Lindsay (1914), Trans. Soc. Trop. Med. and Hyg., vii, p. 259.

[451] Sergent (Ed. and Et.), Lemaire and Senevet (1914), Bull. Soc. Path. Exot., vii, p. 577.

Prophylactic measures would seem to consist in the immediate disinfection of insect bites by tincture of iodine, and by avoidance of areas known to be infested with snakes and lizards, and insects that prey on them and man indifferently. The destruction of the primary lesion as soon as detected is essential, and the isolation of advanced cases of the disease seems advisable.

V.--SPIROCHÆTOSES.

A. *Relapsing Fevers.*

The relapsing fevers of Europe and of America, due to Spirochæta recurrentis and S. novyi (probably a race of S. recurrentis), present much the same symptoms, which differ in some respects from those due to S. duttoni, the excitant of “tick” or “relapsing” fever in Africa (see pp. 116–122).

The incubation period of S. recurrentis varies from two to twelve days, during which time a very slight indisposition may be noticed. The onset is usually sudden, with severe headache, pains in the back, limbs and stomach and a feeling of weakness. There is a rise of temperature to 103° F. or 104° F., and the temperature continues high till about the sixth or seventh day. The skin is yellowish, hot and damp; a rash, disappearing on pressure, may occur on the trunk and legs, nausea is always present and thirst is usual. The liver and spleen both enlarge. The number of respirations and pulse-rate become increased. On the sixth or seventh day a crisis occurs. There is violent perspiration, with a rapid fall of temperature, pulse and respiration become normal and the patient sleeps and awakes better. Improvement continues for some days, and recovery may ensue, but usually about the fourteenth day relapse occurs, lasting usually three or four days. A second relapse is unusual. Numerous complications are known, e.g., bronchitis, pneumonia, diarrhœa and dysentery.

With regard to treatment, the specific appears to be salvarsan. Castellani and Chalmers recommend salvarsan administered intravenously. Intramuscular inoculations (for example, into the buttock) of a suspension of “606” in oil can also be given. The drug is very efficacious, but large doses should not be given. An intravenous injection of 4 or 5 gr. does not give rise to unpleasant symptoms but is sufficient to effect a cure.

The incubation period for the American form of the disease is at least five to seven days, and the first attack lasts about five to six days. The treatment is by salvarsan as detailed previously.

As relapsing fever is spread by body lice and possibly by bugs, preventive measures are directed against these insects. Strict cleanliness of person, clothing, bedding and dwellings is essential. Furniture, e.g., wooden bedsteads, liable to harbour such insects should not be used.

The principal and best-known relapsing fever of Africa is that excited by Spirochæta duttoni, and transmitted to man by ticks, chiefly Ornithodorus moubata. The incubation period is usually about seven days but may be longer. The patient is dull and lethargic, perspires freely and is often constipated. The temperature rises to 103° F. or 105° F., there is headache, pains in the back and limbs, general chilliness and great pain in the region of the spleen, which often enlarges. The symptoms become worse, there is a fall of temperature with improvement in the morning, and a rise, with increase of pain, in the evening. Spirochætes are now found in the blood in greater numbers. The symptoms last three to four days and end in a crisis with profuse sweating and fall of temperature below normal. The day before the crisis there is a pseudo-crisis, when the temperature falls but there is no improvement. The patient is left weak and tired. Recovery may follow, but more usually a relapse occurs. The intermission period varies; five to eight days is common. The symptoms of the relapses are like those of the first attack. The number of relapses varies, five to eleven may occur.

The treatment recommended is by salvarsan, as for the European relapsing fever.

With regard to prophylaxis, localities where ticks abound must be avoided and the parasites themselves destroyed. Native huts should be avoided. Mosquito nets, a bed well off the ground and the use of night lights are advised by Manson to avoid attacks by ticks, which are often nocturnal in their habits.

In North Africa (Algeria, Tunis, Tripoli, Egypt), and sometimes in the Anglo-Egyptian Sudan, a spirochætosis due to S. berbera occurs. According to Castellani and Chalmers, the incubation period varies somewhat. The fever reaches its height during the first twenty-four hours, and afterwards shows a morning remission. Jaundice is often absent, but there may be hepatic tenderness and splenic enlargement. One or two relapses usually occur. The treatment is on the same lines as for the other spirochætal fevers. Sergent and Gillot[452] (1911), working at the Institut Pasteur of Algeria, have had good results by using injections of salvarsan in doses of 0·75 to 1·0 cg. per kilogramme weight of the patient. The prophylactic measures are directed against lice and other biting insects. Personal cleanliness is most necessary.

[452] Bull. Soc. Path. Exot., iv, p. 440.

In Asia, a relapsing fever, due to the spirochæte named S. carteri by Manson in 1907, producing a mortality of about 18 per cent., occurs. The symptoms have a general resemblance to those produced by S. recurrentis, but on the fall of temperature to subnormal on the sixth or seventh day, when profuse perspiration and polyuria occur, instead of improvement following, the patient often becomes collapsed, with a clammy skin and feeble pulse. Improvement is slow. The first relapse occurs about the fourteenth day of the attack, when the temperature may be higher than for the first attack. There are seldom more than four relapses. The treatment is by salvarsan, of which doses of not more than 5 gr. intravenously should be given. Sudden heart failure being common, Castellani and Chalmers state that cardiac stimulants should be given. Prophylaxis is the same as for European relapsing fever.

B. *Yaws or Frambœsia tropica.*

Yaws is essentially a tropical disease, though it is found in the tropical and subtropical zones in all parts of the world, except in the mountains and cold districts. In 1905, Castellani found the causal organism, Treponema pertenue (sometimes called Spirochæta pertennis) (see p. 127). The disease shows three periods: (1) The primary stage, consisting of the development of the primary lesion or papule, which is usually extragenital. The papule dries into a crust beneath which an ulcer lies. (2) The secondary or granulomatous stage, which commences from one to three months after the primary lesion is first seen. It consists of a general eruption of small papules, some of which enlarge and become granulomatous nodules covered with a yellowish crust. They are common on the limbs and face. (3) The tertiary stage, in which deep ulcerations and gummatous nodules appear. Any of the tissues may be involved. Osseous lesions may occur. The disease does not appear to be hereditary; it is usually spread by contact.

The best treatment appears to be by salvarsan or neo-salvarsan. Castellani and Chalmers recommend intramuscular and intravenous injections. For intramuscular injection an alkaline or neutral solution of the drug is preferable, or a suspension of the drug in oil may be used. The dose varies from 0·3 to 0·5 gr according to the age and sex of the patient. For use intravenously, a slightly smaller dose is required. Galyl is also being used.

In countries where frambœsia is endemic, slight skin abrasions should be carefully treated with antiseptics. Yaws patients should be isolated till cured, and their dwellings and personal possessions disinfected.

C. *Syphilis.*

Syphilis, due to Treponema pallidum (sometimes called Spirochæta pallida), is prevalent throughout the tropics as well as in temperate zones. The disease is amenable to treatment by salvarsan and neo-salvarsan, for administration of which see relapsing fever and yaws. Galyl is also being used with favourable results. Lambkin’s mercury cream has been found useful in treating numerous cases in Uganda. The life-history of the parasite is given on p. 124, and further medical details hardly come within the purview of this book.

D. *Bronchial Spirochætosis.*

Bronchial spirochætosis, due to Spirochæta bronchialis (see pp. 122, 739) is probably of wide distribution in the tropics. The spirochætes have been found in cases of chest complaints, especially those with bronchitic symptoms. The disease may be suspected in atypical cases of pneumonia and bronchitis, and may be mistaken for incipient phthisis.

Chalmers and O’Farrell[453] (1913), writing from Khartoum, recommended rest in bed, good food and ventilation, coupled with treatment by arsenic in some form, preferably associated with glycerophosphates. These may be given by the mouth, or intramuscularly as an injection of:--

Sodium cinnamate 0·05 grm. Sodium cacodylate 0·10 " Sodium glycerophosphate 0·10 "

[453] Journ. Trop. Med. and Hyg., xvi, p. 329.

Taylor[454] (1913–14), writing from Entebbe, Uganda, prescribes arsenious acid by the mouth in increasing doses. Creosote has been used in West Africa.

[454] Annual Med. and Sanit. Rept., Uganda, for 1913, p. 80.

VI.--MALARIA.

Malaria, known also under the names of ague, paludism, marsh fever, remittent fever, intermittent fever and climatic fever, among others, is a very widely spread disease. It is most prevalent in the equatorial regions and gradually diminishes north and south of the equator. The various malarial parasites (see pp. 155 to 172) are spread by species of Anophelines, and hence malaria is present in districts favourable to these intermediate hosts, that is, in places where there is a considerable amount of atmospheric moisture and rain, as well as heat.

The principal malarial parasites are: Plasmodium vivax, the agent of simple tertian fever; Plasmodium malariæ, the parasite of quartan malaria, and Laverania malariæ or Plasmodium falciparum, producing malignant tertian or sub-tertian malaria (and quotidian, see p. 167). These various malarial fevers present certain clinical features in common, which will be stated here (see also pp. 155 to 157). For further particulars regarding malaria in all its aspects the reader is referred to the book by Sir Ronald Ross on “The Prevention of Malaria,” to the “Manual of Tropical Medicine,” by Drs. Castellani and Chalmers, and to the “Tropical Diseases” of Sir Patrick Manson.

Typical malarial fevers consist of a series of pyrexial attacks which recur at definite intervals of twenty-four (quotidian), forty-eight or seventy-two hours, according to the parasite present in the patient’s blood. Each attack shows three stages, a stage of rigor, a heat stage and a stage of profuse perspiration. Following on these three stages, there is an interval relatively or actually without pyrexia. Then the fever returns again. A rise of temperature, often accompanied by a general feeling of malaise, may precede the initial stage of rigor. When the latter sets in, the patient feels intensely cold, shivers violently, the skin becomes cold and the features pinched. There may be violent vomiting and convulsive attacks in young children. The temperature, however, is really above the normal, and continues to rise. After about an hour, the shivering abates and the heat stage succeeds it. The temperature rises rapidly, even to 106° F. The patient becomes very flushed, the pulse is rapid, headache may be intense and the skin dry and burning. This stage, that causes acute distress to the patient, may last for one or often three to four hours, and then the patient commences to perspire profusely, the clothing and bedding often being saturated with sweat. After this, the fever rapidly declines, and when the sweating ceases, the patient may feel almost well although somewhat languid. The sweating stage persists from two to four hours, so that the attack lasts as a rule from six to ten hours. After an interval of one, two or three days, a recurrence takes place. During the early part of the attack, especially at the stage of rigor, there is great splenic enlargement. At first the enlargement disappears in the interval, but in the case of repeated attacks the spleen tends to become permanently enlarged. During malarial attacks and during the intermission period, there is a great increase in the amount of nitrogen excreted by the kidneys, while the excretion of iron and bile in the fæces is increased.

Stitt[455] (1914) points out that it is characteristic of malignant tertian paroxysms that they set in with chilly sensations rather than a frank, definite chill, and that the fever is of the remittent type.

[455] “The Diagnostics and Treatment of Tropical Diseases.” London: H. K. Lewis.

Plasmodium malariæ and P. vivax rarely produce marked lesions in the bodies of their hosts, as they sporulate in the circulating blood and so do not accumulate in any one organ. On the other hand, Laverania malariæ (Plasmodium falciparum) multiplies within the internal organs of its host, and consequently aggregates or clusters of the parasites occur therein. The organ in which most sporulation occurs suffers most. The liver is generally enlarged, soft and congested. The capsule of the spleen is tense, but the splenic consistency is less than normal. The bone-marrow is often dark and congested in the spongy bones and brownish-red in long bones. The blood-capillaries of the brain and spinal cord are often filled or blocked with sporulating parasites and large quantities of pigment are found in these organs. Even if the parasites are absent, the pigment is present in the endothelial cells. Pigment is found in most organs of the body.

Atypical forms of malaria may occur in which some or all of the symptoms are much modified. Irregular fevers also may be produced by successive infections by the same parasite, or by the presence of two different malarial parasites.

As regards the diagnosis of malaria, according to Manson the three pathognomonic signs are--periodicity, the effect of quinine, and the presence of the malarial parasite.

Treatment.--The great specific for malaria is quinine. It attacks the merozoites or asexual generation. The drug can be administered by the mouth, by the rectum, by intramuscular injections or by intravenous injections, the two latter methods being adopted in serious infections or where gastric complications are present. When quinine is taken by the mouth, the more soluble acid salts, e.g., quinine bihydrochloride and bisulphate, are better than the sulphate, the form in which quinine is usually sold. Tablets, pills and capsules are convenient means of taking quinine but must not be old or hard, or they may pass unchanged through the body. In the case of mild tertian or quartan malaria, Castellani and Chalmers recommend the administration of a dose of quinine four hours before the sporulation of the parasite is due. Another modification is to give 10 gr. of quinine by the mouth in the morning and a second dose of 10 gr. as above. In many cases they give 5 to 10 gr. of the drug three times a day. Administration of quinine per rectum may be useful but they recommend intramuscular inoculation. The solutions used must be sterile, and the “sterilettes,” small, hermetically sealed vials, containing 1 grm.) or 1/2 grm. (7-1/2 grm.) of quinine in solution, are recommended. A deep injection into the deltoid or gluteus muscle is usual.

For pernicious infections, intravenous inoculation with not less than 1 grm. at a time is recommended.

After the fever has subsided, the administration of quinine in smaller doses must be continued for some time, in order to avoid relapses.

Stitt (1914) writes that “there now seems to be a tendency to use the alkaloid itself instead of its salts, it having been found that the alkaloid and its very insoluble tannate are absorbed from the digestive tract equally as well as the soluble salts.” Euquinine or ethylcarbonate of quinine contains 81 per cent. of quinine, but is expensive.

During malarial attacks, constipation must not be allowed. Headache can be relieved by cold applications, and perspiration must be encouraged in the early stage by hot tea, warm lime drinks, etc. After bad attacks, a change to a cooler climate is desirable, but the quinine treatment must not be discontinued.

Preventive measures take two main forms, directed respectively against the malarial parasites in man, and against the mosquitoes that convey the parasite from man to man.

With regard to man, houses should be built away from low-lying marshy ground, and kept free from vegetation such as grass or brush which furnishes shelter to the mosquitoes. In the tropics, the chief reservoirs of the malarial parasites are the native children, hence European quarters should be away from native dwellings as far as possible. Mosquito nets, having twenty to twenty-four meshes per square inch, should be used invariably, and houses should be screened. Malaria-conveying mosquitoes bite chiefly towards evening. Quinine treatment for preventive purposes is important. A dose of 5 gr. of quinine daily, with a dose of 10 gr. on the seventh day (Castellani), is efficacious. Some workers, however, recommend a large dose (15 gr.) on two consecutive days every eight or ten days for three months, while others recommend 10 gr. twice a week. Celli administered 3 gr. of quinine morning and evening.

The second line of attack is directed against mosquitoes, especially Anophelines, on the lines so well set forth by Sir Ronald Ross.[456] The accumulation of small quantities of water in various vessels, many of them unnecessary, should be prevented, as Stegomyia (Culicines) breed in such receptacles. Anophelines breed in small pools. All drinking water and household vessels, water-butts and cisterns must be effectively screened with wire gauze. Cesspools, etc., must also be screened, and they, and all collections of water, should be oiled with crude petroleum sprays every week or ten days, or fortnight according to some workers. The petroleum is a good larvicide and suffocates the Anopheline larvæ, while its presence renders the site obnoxious to the adult mosquitoes. The amount of crude petroleum or kerosene will vary according to the locality concerned, due regard being paid to its powers of spreading on the surface treated. Different authorities have used different quantities, such as 1 oz. of oil to 1 square yard or to 15 square feet. Others have used 1 pint of the petroleum to a circle of 20 feet in diameter, while 1/2 pint for every 100 square feet of surface has also been recommended. The larvicide used so successfully in Panama consisted of:--

Average mixture Crude carbolic acid (containing 15 per cent. phenol) 300 gallons Caustic soda 30 lb. Resin 200 lb.

[456] “The Prevention of Malaria.” Second Edition (1911). London: John Murray.

One part of this mixture in 5,000 parts of water containing mosquito larvæ destroys them within five minutes; 1 part in 8,000 of water kills larvæ in thirty minutes. Small fish, such as the “millions” fish, that feed on the larvæ, can be introduced into collections of water and are of local service. Ducks may also act as destroyers of larvæ. The growth of water-weeds and rank vegetation, that affords shelter to the larvae, must be prevented as far as possible.

Wherever possible hollows should be filled up, swamps and roads should be well drained. Much good has followed the use of such measures in Panama, Egypt, British Guiana and other places. The ideal conditions for malaria reduction appear to consist in a combination of general quinine prophylaxis with anti-mosquito measures.

VII.--BALANTIDIAN DYSENTERY.

This disease is also known as ciliate or ciliary dysentery. The chief causal agent is Balantidium coli. Others are Balantidium minutum, Nyctotherus faba, etc. (see pp. 200–206).

Balantidiasis is insidious and is marked by alternate attacks of diarrhœa and constipation with vomiting, while mucus is passed in the motions, which are foul smelling. There may be chronic ulceration of the colon. Œdema of the face and limbs and anæmia may occur.

Treatment is at present rather unsatisfactory. Castellani and Chalmers state that “the symptomatic treatment for entamœbic dysentery may be tried.” Various treatments, more or less empirical, by calomel, quinine, carbolic acid in pill form, salicylic acid, extract of male fern, methylene blue, iodine solution, rice water and tannin enemata are mentioned by Prowazek[457] (1913) and by Seifert. E. L. Walker[458] (1913) found, from experimental work, that organic compounds of silver, e.g., protargol, were most effective. Local treatment by large enemata of collargol or protargol seems to be indicated. Behrenroth[459] (1913) successfully treated a Prussian case with thymol, given in 4 grm. doses every two days, followed at the end of a fortnight by de-emetinized ipecacuanha, given in pills containing 6 cg. each, to the number of thirty a day. In about another fortnight the symptoms had subsided. The thymol checked the diarrhœa, but it was necessary to give the de-emetinized ipecacuanha to kill off the balantidia still present. Phillips (1915) also recommends thymol. Ardin-Delteil, Raynaud, Coudray and Derrieu (1914) found neither emetine hydrochloride nor protargol of use.

[457] Beihefte z. Arch. f. Schiffs- u. Tropen-Hyg., xvii, 6, p. 371.

[458] Philippine Jl. Sc., Sect. B, viii, pp. 1–15, 333–349.

[459] Arch. f. Verdauungs Krankheiten, xix, p. 42.

As regards prophylaxis Walker states that pigs “should be confined and not allowed to run in yards and dwellings.” Behrenroth considers that dirty hands, for example, those of farm workers brought into contact with pigs, are probably the medium of infection. The personal cleanliness of such persons is, then, of the greatest importance.

------------------------------------------------------------ |This section, except for minor corrections, is practically a| |translation of the original. | ------------------------------------------------------------

*PLATHELMINTHES* (Flat Worms).

BY

J. W. W. STEPHENS, M.D., B.C., D.P.H.

FASCIOLIASIS.

Fasciola hepatica.

The symptoms of disease evoked by Fasciola hepatica are rarely observed in our part of the world, whereas Kermogant[460] states them to be of frequent occurrence in Tonkin[461]; the parasites are there called “Douves.” In our experience they are only accidentally found post mortem in a certain number of cases, as no changes are manifested during life which would permit of any conclusion being drawn as to the presence of these parasites. In three cases (Bierner,[462] Bostroem[463] and Sagarra[464]) icterus was present; in a fourth case, recorded by Duffek,[465] the parasites had led to a severe and acute distomiasis of the liver, combined with chronic purulent and ulcerative cholecystitis, with purulent cholangitis and dilation of the bile-ducts and numerous small abscesses of the liver. The total number of flukes found in these cases amounted to about fifty. The parasites passed from the duodenum into the bile-ducts, and first obstructed the flow of bile and then set up icterus, followed by cholecystitis and cholangitis.

[460] Kermogant, Soc. méd. des Hôp., February 7, 1905.

[461] [The distomiasis of Tonkin is due to Clonorchis sinensis and not to F. hepatica.--J. W. W. S.]

[462] Bierner, Schweiz. Zeitschr. f. Heilk., 1863.

[463] Bostroem, Deutsch. Arch. f. klin. Med., 1883.

[464] Sagarra, quoted by Duffek.

[465] Duffek, Wien. klin. Wochenschr., 1902, xxx.

As regards localization of the liver fluke in the pharynx, see p. 242.

The treatment must be directed to the principal symptoms; prophylaxis is especially important in districts where distomiasis is of frequent occurrence. As the embryos live in water, only boiled or filtered water should be drunk. The attempts of Tappeiner[466] to discover an effective remedy against liver-fluke disease (liver rot), so prevalent among sheep, were unsuccessful.

[466] Tappeiner, Münch. med. Wochenschr., 1900, l.

Fasciolopsis buski.

This parasite lives in the intestine, not in the liver of man; it produces bloody stools and typical symptoms--high fever and a condition of apathy (Odhner).[467]

[467] Odhner, Centrall l. f. Bakt., 1902, xxxi.

PARAGONIMIASIS.

Paragonimus ringeri.

The disease produced by the lung fluke is specially endemic in Japan, also in isolated parts of China, Formosa and Korea. The fact that the lung-fluke disease is most frequently found in mountainous districts (Katsurada[468]) is worthy of special attention. The onset of pulmonary paragonimiasis is generally insidious (Looss[469]); generally the only symptom is a slight cough, occurring at first at longer, and later at shorter intervals; it is accompanied by the expectoration of discoloured sputum, frequently blood-stained. Though now and then severe hæmorrhages result, up to the present no case has been established in which they have been the direct cause of death.

[468] Katsurada, Ziegler’s Beitr. z. path. Anat., 1900, xxviii.

[469] Looss, “Handb. d. Tropenkrankh.,” von Mense, 1905, i.

Examination of the thorax frequently fails to reveal anything abnormal. Inouye[470] states that the most frequently observed changes consist in retraction of the thorax and in a contraction of its infrascapular portion. Scheube[471] repeatedly observed that the one side, presumably that which harboured the worm, moved less freely than the other. The physical changes are not uniformly spread over the whole lung, but are localized. The disease may come to a standstill for long intervals and then set in again, lasting on the whole from ten to twenty years. In addition to paragonimiasis of the lungs, cysts are frequently found on the eyelids, which occasionally extend deeply into the orbit and hinder the movements of the eyes. Post mortem, cysts the size of hazel nuts containing one, two, or three adult worms are found in the lungs, and in addition, not uncommonly there exist pulmonary emphysema and bronchiectasis. Besides being present in the lungs and in the eyelids, the parasites have also been found in the pleura, the liver, the intestinal wall, the peritoneum, the cervical glands, and in the scrotum, without actually occasioning any actual symptoms in these tracts.

[470] Inouye, quoted by Looss.

[471] Scheube, “Die Krankh. d. warm. Länder,” 1896.

The most dangerous locality is in the brain. Otani,[472] Inouye,[473] Yamagiva,[474] and recently also Taniguchi,[475] have found post mortem the worms and their ova in tumours of the brain, or, in areas of softening in cases of Jacksonian epilepsy; in Taniguchi’s case the eggs were found in masses in the inflammatory areas of softening. In the nineteen cases of paragonimiasis of the brain collected by Inouye, the following symptoms were observed: general convulsions on eight occasions, unilateral convulsions on six occasions, convulsions with paralysis on the same side and hemiplegia, five times each; in Taniguchi’s case, attacks of cortical epilepsy, choreiform twitchings in the right extremities, which gradually become athetotic. The following were symptoms of rarer occurrence: paresis of the right upper extremity, vertigo, dementia, and amnesic aphasia, disturbances of vision. Paragonimiasis of the brain appears to arise by embolism from a primary pulmonary lesion.

[472] Otani, quoted by Looss.

[473] Inouye, quoted by Looss.

[474] Yamagiva, quoted by Looss

[475] Taniguchi, Arch. f. Psych. u. Nervenkrankh., xxxviii.

The diagnosis depends upon the finding of ova in the sputa; if together with ova in the sputa, cerebral disturbances make their appearance, in all probability the cause is the presence of worms or ova in the brain.

The prognosis of pulmonary paragonimiasis is favourable; on the other hand, that of cerebral paragonimiasis is very doubtful.

The treatment of the pulmonary lesion consists only in paying attention to the general condition (good food, rest, cough remedies), as all attempts to destroy the worms in the lungs by means of vermicidal drugs administered internally or by way of inhalation have so far been without result. The treatment of the cerebral lesion is entirely hopeless. Trephining has been proposed for cases the condition of which is more favourable, but it has not reached the stage of performance.

Prophylaxis consists in general management: cleansing and if need be boiling of everything that is eaten or drunk.

Clonorchis sinensis.

According to our present knowledge Clonorchis sinensis is only found in China and Japan; even the post-mortem case reported by Laspeyres[476] was that of an Asiatic sailor who was admitted into the General Hospital St. George, Hamburg, in a moribund condition with the clinical diagnosis of beri-beri. The bile-ducts are the usual site of the parasite, though Katsurada[477] has found them also in the pancreatic ducts. In addition, it is found not uncommonly in the upper portion of the small intestine, especially in the duodenum, also, though decidedly rarely, in the stomach. As these sites, however, do not afford the conditions necessary to life, they are only found here on their way out of the body of the host.

[476] Laspeyres, “Dissert. Kiel,” 1904.

[477] Katsurada, Ziegler’s Beitr. z. path. Anat., 1900, xxviii.

The initial stage of infection with this fluke generally runs a symptomless course; in proportion as the worms multiply the following symptoms are manifested: First there is a morbid sense of hunger and irregularity in defæcation; at the same time the patient experiences a feeling of pressure and pain in the epigastrium and right hypochondrium, or just a dull pain. Pressure increases the pain considerably. The liver appears to be enlarged, sometimes the enlargement is specially perceptible over the left lobe of the liver. The patients maintain a proportionately good general state of health in this state for a long time and may hope to recover. In severe cases there occurs copious and generally bloody diarrhœa, also icterus. The next stages are anæmia, emaciation, epistaxis, ascites, enlarged spleen, and cachexia, to which the patient finally succumbs. In general the course of the disease is very chronic and irregular; in winter and spring there is generally improvement, in the summer and autumn the patient gets worse. At post-mortem the bile-ducts are enlarged and thickened, there is interstitial hepatitis with enlargement of the liver, but not to such an extent as in hypertrophic cirrhosis. After the initial enlargement contraction of the liver sets in, the peritoneal coat and capsule proper of the liver become more or less thickened in places. In the pancreas also dilatation and thickening of the ducts occur, as well as interstitial inflammatory processes. Obstructions in the portal circulation may lead to catarrhal changes in the stomach.

The diagnosis is based on the demonstration of ova in the fæces.

As a radical treatment is still unknown, consequently it can only be purely symptomatic. Prophylaxis consists in the prohibition of drinking unboiled water or eating uncooked molluscs, fish, etc., of canal water. Leaving the epidemic region may bring about gradual recovery.

BILHARZIASIS.

Schistosoma hæmatobium.

The symptoms of bilharziasis are manifested chiefly in the urinary apparatus, and above all as hæmaturia, at the outset without any special troubles. Later, however, it is accompanied by subjective symptoms in the shape of feelings of pain, and of vague pains in the perinæum and lumbar region, and of burning in the urethra during the passing of urine. All the symptoms are usually aggravated after excesses in eating and drinking, and after considerable bodily exertion. Another condition found, but not often mentioned, is lipuria (Stock[478]); the highest amount has been 2 per cent. fat in the urine. Stock found 6 to 20 per cent. of eosinophile cells in ten cases examined by him. They appear to be increased, especially in the early cases; Kautsky[479] also called attention to the excessive degree of eosinophilia, whilst Goebel[480] expresses the opinion that a specific toxic action on the organism generally is not developed in bilharziasis. Kautsky[481] assumes a toxic anæmia as in the case of ancylostomiasis. English authors also have called attention to the eosinophilia and to a considerable amount of leucocytosis (Balfour,[482] Douglas and Hardy[483]). The severe forms occur almost exclusively in men; symptoms of catarrh of the bladder make their appearance, vesical calculi are frequently found, whilst the formation of stone in the kidneys and ureters is rare. Urethral fistula occurs in bilharziasis, often without stricture, and if granulations occur the fistula is distal to them. Goebel[484] regards the bilharzia fistula as a chronic burrowing of pus, caused by the irritation set up by the ova as foreign bodies and consecutive restricted suppuration; and secondly as due to the passage of urine through the defect in the epithelium or the wall of the urethra. The fistulæ, which are generally situated at the neck of the bladder and at the membranous portion, are very tortuous and frequently very numerous; they often lie embedded in well-marked tumours--in fact, in granulation tumours with marked inclination to excessive formation of cicatricial tissue. The opening generally is in the perineal and scrotal regions. In the case of a patient, aged 21, from the Transvaal, Kutner[485] found by cystoscopic examinations the whole summit and walls of the bladder covered with large and small tumours. In addition to smooth glistening tumours, others were more or less disintegrated, and scattered large and small cauliflower-like growths occurred. Like malignant growths, the tumours were inclined to break down, the process extending from within outwards towards the surface. Whether the hydrocele so frequent in Egypt has any connection with bilharzia is not known. A frequent sequela of bilharziasis is complete sexual impotence (Petrie[486]).

[478] Stock, Lancet, September 29, 1906.

[479] Kautsky, Wien. klin. Rundschau, 1903, xxxvi.

[480] Goebel, Arch. f. Schiffs- u. Tropen-Hyg., 1903, vii.

[481] Kautsky, Wien. klin. Rundschau, 1903, xxxv.

[482] Balfour, Lancet, December, 1903.

[483] Douglas and Hardy, ibid., October, 1903.

[484] Goebel, Centralbl. f. d. Krankh. d. Harn u. Sexualorgane, xvii.

[485] Kutner, ibid., xvi.

[486] Petrie, Brit. Med. Journ., July, 1903.

Bilharziasis of the rectum is manifested by symptoms of dysentery; the repeated violent attempts at defæcation lead in time to prolapse of the rectum, which sooner or later induces septic infection and so death. In the mucosa of the rectum, polypoid growths similar to those in the bladder are met with, due to the ova of the parasites in the mucosa and submucosa. In the case of a man, aged 36, who had lived for a long time in South Africa, Burfield[487] found in the excised vermiform appendix ova of Schistosoma hæmatobium; he assumed this to be a gradual secondary infection of the appendix, whilst Kelly[488] mentions a case of primary bilharziasis of the appendix; the eggs lay in the submucosa directly above the muscularis. Tumours containing numerous ova are frequently found in the region of the genitalia, thighs and scrotum. In one case Symmers[489] found numerous male schistosomes in the portal blood and a copulating pair in the left lung. Though schistosome eggs have been found by some observers in the lung tissue, this is nevertheless the first case in which living parasites have been found in the lesser circulation. Perhaps they got there by way of the external iliac vein from the veins of the bladder and rectum.

[487] Burfield, Lancet, February 10, 1906.

[488] Kelly, quoted by Burfield.

[489] Symmers, Lancet, January 7, 1905.

In the female sex bilharziasis is incomparably rarer than in the male and is generally limited to hæmaturia. Bilharziasis of the vagina, which takes the form of an acute vaginitis, is frequent according to Milton.[490] Horwood[491] found in one case a polypoid tumour of the cervix uteri, and in the connective tissue of the tumour Schistosoma ova, both in masses and singly. It could not be established whether the ova reached the vagina and thence the cervix directly, or through the urine from the bladder.

[490] Milton, quoted by Looss, “Handb. d. Tropenkrankh.,” v. Mense, 1905, i, p. 95.

[491] Horwood, Brit. Med. Journ., March 10, 1906.

The course of the disease is chronic, and in slight cases, provided fresh infections do not occur, is not unfavourable; in severe cases the cachexia caused by loss of blood, or intercurrent diseases to which the patients easily succumb--e.g., pyelitis, pyelonephritis, pyæmia, or uræmia--lead to a fatal issue.

In regions in which Schistosoma hæmatobium is endemic, or in patients from such regions, the diagnosis is easy by microscopically finding the eggs in the urine.

As regards the treatment of the affection this much must be said, that so far there is in existence no certain remedy. In countries where bilharziasis is endemic copaiva balsam is considered a specific. Kutner (loc. cit.), however, in the case of his patient who for a long time had taken no inconsiderable amounts of copaiva, had no success worth speaking of to record. Urotropin (three times daily, 1 grm.) has similarly failed, salol (0·75 grm. several times daily) perhaps affords relief in affection of the bladder (Milton). Methylene blue, oil of turpentine with extract of male fern (Brock[492]), or the latter alone and santonin given in small doses for a week at a time, in the morning, are said by Petrie[493] to be of value. Sandwith[494] and Harley[495] were not very successful. By way of experiment Kutner for some time used collargol per rectum, proceeding on the assumption that this preparation, which has proved of such remarkable service in bacterial infection, would perhaps render a continuance of life difficult for the bilharzia worms. But this hope proved illusory. In order so far as possible to limit the loss of blood, Kutner regularly employed stypticin for long periods (three times daily, two tabloids of 0·01 grm.) with undoubted success, in so far that the hæmorrhages became considerably less in amount. As two patients in the course of enteric fever lost their hæmaturia, Stock accordingly recommends subcutaneous injections of Wright’s typhoid vaccine. In the early stages of the rectal lesion suppositories of iodoform, ichthyol, or narcotics might possibly be of use. In the case of urethral fistulæ, division, excision and scraping out of the granulation tissue are recommended; in cystitis with formation of tumours high resection with curetting of the tumours or their destruction with the cautery; in the case of vesical calculi, high resection, curetting the bladder, and then drainage. Tumours of the rectum must also be removed by operation.

[492] Brock, Journ. of Path. and Bact., 1893.

[493] Petrie, loc. cit.

[494] Sandwith, Annal. of Surgery, 1904, xxxix.

[495] Harley, Lancet, 1870.

Prophylaxis is important; it should be extended to all modes of using water, only filtered water being drunk, and only boiled water being used for washing. This advice should be given to tourists who travel through the infected districts, and is also recommended to soldiers and officials who are despatched to the Colonies. The favourable influence of change of climate can only show itself where fresh infections are avoided.

CESTODES.

GENERAL.

It seems advisable to preface the section on the Cestodes with some general observations on the symptoms of disease provoked by tapeworms, especially so far as they relate to the question of toxic effects, and to include the Nematodes in this discussion. After this will follow a brief exposition of the most important intestinal lesions causally connected with intestinal parasites.

It is known to every experienced practitioner that the different intestinal parasites can give rise to a series of nervous symptoms, slight or severe, and produce, above all, blood changes--anæmia of the most varied nature, to the extent of severe progressive anæmia. These symptoms are regarded by many authors as reflex, or, as in the case of ancylostomiasis, the main feature from the loss of blood caused by the habit of life of the intestinal parasites. More frequently, however, they are regarded as toxic conditions produced by the parasites. In view of this divergence of opinion there appears to be some advantage in defining clearly the present position as to the toxic action of parasites. Most interesting in this respect are Dibothriocephalus latus and Ancylostoma duodenale.

We are indebted to the clinic at Helsingfors for our most detailed knowledge of bothriocephalus anæmia. Reyher[496] was the first to demonstrate that this parasite under certain circumstances can produce a severe, progressive and sometimes fatal anæmia, which can be cured, generally in a surprisingly short time, by expulsion of the worm. Among the various hypotheses which have been advanced as to the mode of origin of bothriocephalus anæmia, the greatest importance has been attached to the assumption already mentioned by Reyher, but definitely expressed by von Shapiro,[497] to the effect that Bothriocephalus latus produces a poison which is absorbed by the intestine and exercises a deleterious influence on the composition of the blood, especially on the erythrocytes, perhaps also on the blood-forming organs. This assumption is supported by no slight number of clinical and experimental investigations. Podwissotsky[498] observed severe blood changes in a child, aged 4-1/2, affected with B. latus. In the case reported by Pariser[499] the severe anæmia in a girl disappeared fairly soon after expulsion of the worm. In that reported by Schaumann[500] high fever accompanied the bothriocephalus anæmia; he also proved the hæmolytic properties of the broad tapeworm. The case reported by F. Müller[501] was one of severe anæmia. Also, in the first of the cases described by Kurimoto[502] of Diplogonoporus grandis there were present the same symptoms of anæmia as in the case of B. latus. Meyer[503] observed severe anæmia in two youths caused by B. latus. Rosenquist[504] has discussed the proteid metabolism in anæmia. The presence of B. latus produces in the majority of cases an increased proteid consumption, to which the blood change generally corresponds--toxic anæmia; in a further communication he reports on twenty cases of bothriocephalus anæmia, nineteen of which were cured by expulsion of the worms, while one case proved fatal, and he again emphasizes the toxic properties of the intestinal parasites. In the case reported by Bendix,[505] that of a girl, aged 4-1/2, the anæmia was moderate, whilst in the case of Zinn[506] (a woman, aged 30) the anæmia was so excessive that the patient succumbed five days after expulsion of six bothriocephalus heads. Isaac and van den Velden[507] have established that in the serum of patients who suffer from anæmia due to B. latus, parasitic products are dissolved, as shown by a distinct precipitin reaction. Galli-Valerio[508] considers it likely that toxic substances are secreted by the living helminthes which produce a lowering or raising of the body temperature, nervous disturbances and hæmolysis. Tallqvist[509] succeeded in extracting from B. latus a lipoid-like body which had a strong hæmolytic action. The experimental anæmia thereby produced differed in no respect from the severe chronic bothriocephalus anæmia of man. The question as to under what special conditions severe, and sometimes fatal bothriocephalus anæmia is developed is answered by Leichtenstern[510] and by Lenhartz,[511] by the assumption that among the Bothriocephali some are toxic, that is, manufacture a poison which, when absorbed by the host, produces a severe anæmia.

[496] Reyher, Deutsch. Arch. f. klin. Med., 1886, xxxix.

[497] von Shapiro, Zeitschr. f. klin. Med., 1888.

[498] Podwissotsky, Jahrb. f. Kinderkrankh., 1889.

[499] Pariser, Deutsch. med. Wochenschr., 1892.

[500] Schaumann, Berlin, 1894, and Deutsch. med. Wochenschr., 1898.

[501] Müller, Charité-Annal., xiv.

[502] Kurimoto, Zeitschr. f. klin. Med., xl, and _Kongr. f. inn. Med._, Karlsbad, 1899.

[503] Meyer, Mount Sinai Hosp. Reports, 1903 and 1904, iv.

[504] Rosenquist, Verein f. innere Med. in Berlin, May 6, 1901; and Zeitschr. f. klin. Med. xlix.

[505] Bendix, Deutsch. Aerzte Zeitg., 1904, i.

[506] Zinn, Deutsch. med. Wochenschr., 1903.

[507] Isaac and van den Velden, Deutsch. med. Wochenschr., 1904, xxvii.

[508] Galli-Valerio, Therap. Monatsh., 1905.

[509] Tallqvist, Zeitschr. f. klin. Med., 1907, lxi.

[510] Leichtenstern, “Handb. d. Therap. v. Pentzoldt-Stintzing,” 1898, 2nd edition, iv.

[511] Lenhartz, ibid., 1903, 3rd edition, iv, p. 607.

Certain factors lead him to conclude that an accumulation of poison, dependent on time and place, occurs in the Bothriocephali.

In the case of ancylostome anæmia, experience so far, according to Leichtenstern,[512] by no means supports the hypothesis of a difference in virulence of the worms according to time and locality, ancylostome anæmia being rather, so far as is known at present, in all races of man, everywhere and at all times, simply and solely dependent on the number of ancylostomes, the duration of the disease and--within certain narrow limits--on the individual capability of resisting the loss of blood and the toxic effect of the parasites. As is shown by a short historical résumé of the toxic action that has to be considered in ancylostome anæmia, we must admit that doubtless here, as in the case of bothriocephalus anæmia, the toxins secreted by the parasites exercise a hæmolytic action, even while admitting Leichtenstern’s contention that the significance of the loss of blood due to ancylostomes must not be underrated. The toxic hypothesis acquired a definite standing through a series of experiments of Lussana[513] on rabbits, where he succeeded in producing anæmia by injecting urinary extracts of ancylostome patients. Arslan[514] extracted toxins from the urine of two ancylostome patients and injected them into rabbits, which thereupon sickened and showed the same blood changes as the ancylostome patients. Retinal hæmorrhages, so frequent in ancylostome anæmia, which, according to Fischer[515] and Samelsohn,[516] are not due to direct loss of blood, must also be ascribed to a parasitic toxin. A further argument in favour of the toxic hypothesis is furnished by the blood changes recorded by Zappert,[517] Müller and Rieder,[518] Bücklers,[519] and Neusser,[520] which must be regarded as the expression of toxic action, especially with reference to eosinophilia. The striking increase in proteid destruction in ancylostomiasis observed by Bohland,[521] and which ceased after the parasites had been expelled, also gives additional support to the assumption of toxic action. The observation of Daniels[522] also deserves consideration in this connection, according to which the presence of yellow pigment in the liver and kidney cells is to be attributed to blood destruction by a verminous toxin absorbed from the gut. Looss[523] considers it not at all improbable--in fact, almost certain--that Ancylostoma, in addition to withdrawing blood, exert a kind of toxic action on their host.

[512] Leichtenstern, Deutsch. med. Wochenschr., 1899.

[513] Lussana, Rivista Clin. Arch. ital. di clin. Med., 1890.

[514] Arslan, Rev. mens. des Mal. de l’Enfance, 1892.

[515] Fischer, Versamml. d. ophthal. Gesellsch., 1892.

[516] Samelsohn, ibid.

[517] Zappert, Wien. klin. Wochenschr., 1892.

[518] Müller and Rieder, Deutsch. Arch. f. klin. Med., xcviii.

[519] Bücklers, Münch. med. Wochenschr., 1894.

[520] Neusser, Wien. klin. Wochenschr., 1892.

[521] Bohland, Münch. med. Wochenschr., 1894.

[522] Daniels, Lancet, No. 3,725.

[523] Looss, Centralbl. f. Bakt., 1897.

Scheube[524] attributes almost equal importance to the loss of blood, the digestive disturbances, and the intoxication induced by certain metabolic products of the parasites. According to v. Jaksch[525] ancylostome anæmia is not induced solely by loss of blood, but by the fact that the parasites produce a ferment which has a toxic action and produces stimulation in those organs in which the eosinophile cells arise. The hæmolytic action of ancylostomes has frequently been observed by Galvagno[526] in men employed in sulphur mines. According to Loeb and Smith[527] the anterior half of the body of ancylostomes contains a substance which probably causes anæmia. Bauer[528] found in the urine of ancylostome patients glycuronic acid, which he considers to be a sign of metabolic disturbance due to parasitic toxins. As has been demonstrated by Allessandrini,[529] the secretion of glands in the anterior part of the body has a distinct hæmolytic effect on the erythrocytes. While the worm attaches itself to the mucosa by means of its teeth, these glands discharge their secretion, producing hyperæmia. The extravasated blood is acted on by this secretion, so that it can serve as food for the parasites. Hynek[530] attributes eosinophilia (up to 20 per cent.) to a toxic action. Goldmann[531] expresses a similar opinion, though he assumes that the anæmia is secondary, as the toxin of the cephalic glands, as the parasites bite, penetrates the mucosa and thence into the blood, where it dissolves the red blood corpuscles. Romani[532] discusses the agglutinating hæmolytic action of the serum of ancylostome patients. Whether Ancylostoma produce toxins and what is their nature, or whether the loss of blood causes the anæmia, Liefmann[533] was unable definitely to determine; hæmolytic substances do not appear to take any part in it.

[524] Scheube, “Die Krankh. der warm. Länder,” 1896.

[525] v. Jaksch, Münch. med. Wochenschr., 1902.

[526] Galvagno, Arch. di Patol. e Clin. inf., 1902–1904.

[527] Loeb and Smith, Centralbl. f. Bakt., xxxvii.

[528] Bauer, Wien. klin. Wochenschr., 1904.

[529] Allessandrini, Policlinica, 1904.

[530] Hynek, Klin. Chron., 1904.

[531] Goldmann, Wien. klin. Rundschau, 1905.

[532] Romani, Gaz. d. Osp., 1904.

[533] Liefmann, Zeitschr. f. Hyg., 1905, l.

Berti[534] also is inclined to attribute the anæmia to metabolic products of the ancylostomes; he found, in fact, that a serum obtained from a sheep (after subcutaneous injections of the culture fluid of ancylostome larvæ) was efficacious in the treatment of ancylostome anæmia. Peiper[535] likewise assumes that the parasite secretes a cell toxin. Löbker[536] at the present day still maintains that the cause of the disease must be looked for really, if not perhaps entirely, in the continued withdrawal of blood by the parasites; the secretion of toxins by ancylostomes has not yet, in his opinion, been conclusively proved. Except in the case of Bothriocephalus latus, referred to previously, toxic action appears to be of quite subordinate importance for the other Cestodes occurring in man--especially Tænia solium and T. saginata, which are most frequently found; thus Cao[537] flatly denies the presence of toxins in the body of Tæniæ, while others, such as Messineo and Calmida,[538] Jammes and Mandoul,[539] consider they are justified from their investigations in concluding that Tæniæ contain a specific toxin. Messineo[540] injected, with all bacteriological precautions, extracts of Tænia, dissolved in physiological salt solution. He invariably obtained severe motor disturbances and frequently death. The observation by Pereira[541] of a case of chorea in which rheumatic and cardiac symptoms were absent and which after expulsion of a Tænia was quickly cured, also favours the view of a toxic action. Barnabo,[542] however, was unable to obtain a toxin from Tænia saginata. Gagnoni,[543] on account of a marked eosinophilia which, after expulsion of a Tænia saginata, fell within fourteen days to 1 per cent., assumes the formation of a Tænia toxin. Dirksen’s[544] observation has reference to a sailor affected with serious anæmia, who, after expulsion of twelve pieces of Tænia solium, was rapidly cured. A portion of the worm was already breaking down, the absorption introducing into the body highly toxic hæmolytic products, to which the anæmia must be ascribed. How far the serious disturbances of the nervous system, frequently to be observed in cases of Hymenolepis nana, are to be considered as of purely reflex nature or toxic must remain an open question; the same applies to Dipylidium caninum, in which case Brandt[545] observed serious central nervous symptoms. Caution is necessary in judging as to any connection between worm stimulus and nervous symptoms in cases of Ascaris infection. Peiper[546] is inclined to regard such nervous symptoms not as reflex, but rather as due to a toxin contained in the helminthes, or metabolic in origin.

[534] Berti, Gaz. d. Osp., 1906.

[535] Peiper, Deutsch. med. Wochenschr., 1897.

[536] Löbker and Bruns, Arb. aus dem kaiserl. Reichsgesundheitsamt, 1906, xxiii.

[537] Cao, Riforma Med., 1901.

[538] Messineo and Calmida, Centralbl. f. Bakt., xxx.

[539] Jammes and Mandoul, Acad. des Sciences, 1904.

[540] Messineo, Giorn. med. del regio eserc., 1903.

[541] Pereira, Lancet, September, 1903.

[542] Barnabo, Sperimentale, 1906, v.

[543] Gagnoni, Pediatric., 1903.

[544] Dirksen, Deutsch. med. Wochenschr., 1903.

[545] Brandt, quoted by Pollak in Centralbl. f. Bakt., 1889, v.

[546] Peiper, vide Seifert, “Lehrb. d. Kinderkrankh.,” 1897, p. 243.

In cases of pernicious anæmia when the symptoms disappear after expulsion of Ascaridæ a toxic action must be assumed (Demme[547]). Additional clinical observations do not, indeed, lead to any definite conclusion as to the question whether Ascaridæ produce a toxin which is capable of causing more or less injury either to the nervous system or to the blood, yet it may be worth while to give a brief review of this question. In a case of Kutner’s,[548] that of a girl, aged 12, there was a hæmolysis which was cured after expulsion of twenty-four Ascaridæ. Attacks of opisthotonos in a girl, aged 16, ceased after seventy-eight Ascaridæ had been expelled (Lutz[549]). Unusually serious disturbances were observed in a man, aged 26, who was rapidly cured by Drouillard[550] by the removal of a great number of Ascaridæ. The observations on pseudomeningitis are of especial interest; they are evidently toxic in origin as in the case of Annaratone,[551] of a man who was taken ill with gastro-intestinal symptoms and who died with meningitic symptoms. Post mortem the brain was normal, but the stomach contained a great coil of Ascaridæ. The cases of Delille,[552] Mériel,[553] Papi[554] (the occurrence of Cheyne-Stokes respiration has been ascribed to the action upon the centre in the medulla oblongata of the products of the Ascaridæ), and Taillens[555] related to children in which the meningitic symptoms (meningismus), partly serious, disappeared with the removal of the Ascaridæ. Máreo[556] designates this disease helminthiasis meningitiformis, which exhibits all the symptoms of meningitis, but which is caused by the metabolic products of Ascaridæ.

[547] Demme, vide Seifert, ibid.

[548] Kutner, Berl. klin. Wochenschr., 1865.

[549] Lutz, Centralbl. f. Bakt.

[550] Drouillard, Journ. de Méd., 1900. xi.

[551] Annaratone, Giorn. med. del regio eserc., 1900.

[552] Delille, Journ. de Méd., May 10, 1907.

[553] Mériel, Annal. de Méd. et Chir. inf., 1900.

[554] Papi, Gaz. d. Osp., 1901.

[555] Taillens, Arch. de méd. d’Enf., 1906.

[556] Máreo, Allg. Wien. med. Zeitg., 1902.

Schupfer,[557] Duprey[558] (observations in the West Indies, where such symptoms are said to be of very frequent occurrence), Naab[559] (the flow of water from the mouth at night is mentioned as a remarkable fact), and Hammiss[560] assume the action of an Ascaris toxin in the clinical observations made by them, mostly children with fever and intestinal symptoms. Schupfer assumes in such cases, as he observed it once in a man, aged 23, that the disease termed Lombricoise à forme typhoïde by Chauffard was due to B. coli of marked virulence due to the action of the Ascaridæ. The Widal reaction was negative. Koneff[561] reports a case in which acute attacks of cramp, trismus, and rigidity of the pupil disappeared after expulsion of seven Ascaridæ. Tetanus, as observed by Buchholz[562] in a girl, aged 17, and rapidly cured after expulsion of sixteen Ascaridæ, is manifestly rare, since only Rose[563] mentions this as a cause in his article on Tetanus. Only a few experimental data exist. Cattaneo[564] could detect only a very weak toxin in Ascaris, while Messineo,[565] by injecting into animals extracts in physiological salt solution, invariably succeeded in producing serious motor disturbances and frequently death. Interesting also are the observations of Huber,[566] who, after working with Ascaridæ, suffered from itching of the head and neck, blisters, swelling of the ear, conjunctivitis, ecchymosis and troublesome palpitation in the head. He consequently assumes that Ascaridæ can induce irritation by chemical (toxic) means.

[557] Schupfer, Gaz. d. Osp., 1901.

[558] Duprey, Lancet, 1903.

[559] Naab, Münch. med. Wochenschr., 1902.

[560] Hammiss, Wien. med. Wochenschr., 1904, iii.

[561] Koneff, quoted by Liesen, “Dissert. Bonn,” 1904.

[562] Buchholz, Norsk. Mag. for Läge, 1903.

[563] Rose, Billroth and Pitha, “Chirurgie.”

[564] Cattaneo, Arch. f. Kinderheilk., xliv.

[565] Messineo, Giorn. med. del regio eserc., 1905.

[566] Huber, Deutsch. Arch. f. klin. Med., 1870, vii.

In the case of Trichocephalus dispar no more than in the case of Ascaris lumbricoides can we speak with certainty of a toxic effect, even though a number of observations are available which might justify such an assumption as regards these intestinal parasites. Barth[567] found the brain normal in a man who had died with meningitic symptoms, but the intestines were full of Trichocephalus dispar; Gibson[568] records the rapid cure of serious cerebral symptoms after expulsion of Trichocephalus, so also Pascal,[569] Burchhardt[570] and Rippe.[571] Moosbrugger[572] was the first to draw attention to grave anæmic conditions induced by Trichocephalus, Morsasca[573] and Becker[574] to progressive grave anæmia (trichocephalus anæmia is accompanied by marked reduction of the number of red blood corpuscles, of the specific gravity and of the hæmoglobin, well-marked morphological changes of the red cell, micro-, macro-, and poikilocytosis and nucleated red cells). Sandler,[575] in his case of a boy, aged 11, who died of anæmia, assumes a trichocephalus toxin to be the cause of the disease, and Kahane also reports on anæmic conditions induced by Trichocephalus. Girard,[576] in addition to symptoms in the gastro-intestinal tract, calls attention to those arising in the blood--anæmia and its sequelæ--and also to nervous symptoms: cerebral phenomena, headache, giddiness, aphonia, symptoms of meningitis. In a case of Schiller’s[577] high fever was present, which probably set in when the Trichocephali present in the gut in great numbers commenced their parasitic activity. Hausmann,[578] in order to explain the adaptability of Trichocephalus, assumes that according to the locus minoris resistentiæ, at one time the reflex at another the toxic action is effective, now on one organ, then on another; anæmia being present in most cases, frequently general and local neuroses and cerebral symptoms of various kinds.

[567] Barth, reported by Valleix, Paris, 1845.

[568] Gibson, Lancet, 1862.

[569] Pascal, quoted by Kahane, Korrespondenzbl. f. Schweizer Aerzte, 1907, viii.

[570] Burchhardt, Deutsch. med. Wochenschr., 1880.

[571] Rippe, St. Petersb. med. Wochenschr., 1907, i.

[572] Moosbrugger, Med. Correspondenzbl. f. Württemberg, 1890.

[573] Morsasca, abstract in Centralbl. f. innere Med., 1897.

[574] Becker, Deutsch. med. Wochenschr., 1902.

[575] Sandler, ibid., 1905.

[576] Girard, Annal. de l’Inst. Pasteur, 1901.

[577] Schiller, Beitr. z. klin. Chir., 1902, xxxiv.

[578] Hausmann, St. Petersb. med. Wochenschr., 1900.

With regard to the toxic action of Oxyuris there is only the single record of Hartmann,[579] who noticed the disappearance of epileptic fits and psychic disturbances in a girl, aged 13, after the removal of Oxyuris. Nervous disturbances and blood changes can but rarely be attributed to Strongyloides. Silvester[580] and Valdes[581] report on giddiness, headache and anuria in cases observed by them; whether the eosinophilia recorded by Bücklers[582] and Bruns[583] is due to the toxin of Strongyloides must remain an open question.

[579] Hartmann, Naturforschervers., Köln, 1889.

[580] Silvester, quoted by Schlüter, “Dissert. Kiel,” 1905.

[581] Valdes, quoted by Schlüter, op. cit.

[582] Bücklers, Münch. med. Wochenschr., 1894.

[583] Bruns, Münch. med. Wochenschr., 1907.

Reference has already been made to the possibility that intestinal ciliates (Balantidium coli) can also produce toxins.

The contents of echinococcus cysts appear to contain a substance only moderately toxic, giving rise to urticaria, in a series of cases where the fluid has escaped into the abdominal cavity (during puncture). D. Müller[584] has collected nine such cases out of the literature, to which may be added six cases of Finsen[585] in which the escape of fluid into the peritoneal cavity led to severely itching urticaria, which usually disappeared again after one or two days. On one occasion, indeed, urticaria occurred after rupture into the pleural cavity. In the case recorded by Caffarena[586] of echinococcus of the right lobe of the liver, widespread urticaria developed as the result of the exploratory puncture. In the case of an echinococcus of the liver rupturing into the abdominal cavity La Spada[587] ascribed the symptoms leading to death to toxic influence while the peritoneal symptoms were less marked. Eosinophilia in hydatid disease is slight according to the investigations of Bindi[588] and Santucci,[589] and is, according to Welsh and Barling,[590] no certain sign of echinococcus; it is independent of the age, sex and temperature of the patient, but upon rupture of the cyst eosinophilia invariably sets in.

[584] Müller, D., “Dissert. Würzburg,” 1885.

[585] Finsen, quoted by D. Müller.

[586] Caffarena, Convers. clin. Genova, 1902.

[587] La Spada, Gaz. d. Osp., 1904.

[588] Bindi, ibid., 1907.

[589] Santucci, “Clinica moderna,” 1905.

[590] Welsh and Barling, Scot. Med. and Surg. Journ., 1907.

The question as to the importance of helminthes in relation to certain diseases of the gut requires special discussion, but it concerns only Ascaris lumbricoides, Oxyuris vermicularis, and Trichocephalus dispar, and the question of appendicitis first of all. The entrance of intestinal parasites into the vermiform appendix was already known to medical men in the fifties of last century, as is shown by the works of Merling[591] (1836), Zebert[592] (1859), Platonor[593] (1853), and Schachtinger[594] (1861). Most of these authors have considered intestinal worms, together with other foreign bodies, to be the cause of appendicitis. As regards the part played by these intestinal parasites in the etiology of appendicitis, so much discussion has taken place during the last few years that it is worth while to give a résumé of the later views on this question, even though at the outset it must be admitted that the matter is not cleared up. Bergmann[595] records a case in which an Ascaris perforated the appendix and got into the peritoneal cavity.

[591] quoted by Rostowzeff, Bobritsch. Gaz. Botkina, 1902.

[592] quoted by Rostowzeff, Bobritsch. Gaz. Botkina, 1902.

[593] quoted by Rostowzeff, Bobritsch. Gaz. Botkina, 1902.

[594] quoted by Rostowzeff, Bobritsch. Gaz. Botkina, 1902.

[595] Bergmann, Prag. med. Wochenschr., 1890.

Strümpell[596] reckons among the symptoms of Trichocephalus the possibility of a “typhlitis.” On account of the marked sensitiveness of the ileo-cæcal region, Boas[597] mentions the possibility of confusing it with appendicitis. Still[598] regards Oxyuris as a principal cause of catarrhal affections of the appendix. Arboré-Rally[599] regarded severe symptoms of appendicitis in a boy, aged 10, as due to Ascarides. In all cases of appendicitis Metschnikoff[600] requires a microscopical examination to be made for eggs, and considers treatment for worms carried out otherwise as a cause of the frequency of perityphlitis. Matignon[601] does not agree with this opinion, as in spite of the extraordinary frequency of intestinal worms in China, he has only seen one case of appendicitis in four and a half years, and Des Barres[602] expresses himself in similar fashion. Out of twenty-one cases of appendicitis Kirmisson[603] discovered the ova of Trichocephalus eighteen times and the ova of Ascarides in three of these cases; in twelve cases of enteric fever the examination for eggs was negative nine times. Moty[604] considers Oxyuris to be the sole cause in his three cases of appendicitis. Girard[605] ascribes to Trichocephali the rôle of more or less septic foreign bodies which may bring about the entry of intestinal bacteria into the appendix, and Triboulet[606] describes a case of appendicitis which he considers was due to Ascaris. In Morkowitin’s[607] case numerous Oxyuris had clearly caused the appendicitis. von Genser[608] records the case of a boy, aged 5, who was operated on for appendicitis, and who passed through the operation wound a living Ascaris on the eighteenth day after the operation. In the first case communicated by Schiller[609] the disappearance of the typhlitic swelling after the discharge of the Ascarides pointed to the etiological significance of the parasites, and the same obtained in a further case published at an earlier date by Czerny and Heddäus.[610] In a case abstracted by Kaposi[611] Trichocephali appear to have been a contributory cause in the production of the appendicitis. In a further case reported by Schiller, where the appendix was removed, it was shown that Oxyuris had given rise to a pronounced appendicular colic. In a girl, aged 13, who died from diffuse peritonitis, Schwankhaus[612] found that an Ascaris had perforated the appendix. Ramstedt[613] found in an extirpated appendix a whole “tangle” of Oxyuris, and believes in the possibility of their having provoked the inflammation; he recommends an examination for entozoa before the operation, without, however, after Metschnikoff’s example, substituting worm treatment for the operation. Rostowzeff[614] ascribes only a minimal direct etiological significance to intestinal worms in the origin of appendicitis; in 163 cases he found worms in three instances. Wirsaladze[615] expresses himself in a similar fashion. Oppe[616] observed Oxyuris six times in excised appendices, and emphasizes the opinion that in appendicitis the question of a worm cure ought to be taken into consideration. Ascaris and Oxyuris, if no contra-indication exists, may be expelled, but in the case of Trichocephalus, which frequently defies all expulsive treatment, no attempt should be made, but operation proceeded to forthwith. In a case briefly reported by Hanau[617] Oxyuris was undoubtedly the etiological starting-point; in a case of Galli-Vallerio[618] Oxyuris and Trichocephalus. In the opinion of Ssaweljews[619] in some cases of appendicitis, in addition to other causes, intestinal parasites play a prominent part. The case recorded by Nason[620] is an interesting one; in this an Ascaris in the appendix became twisted with it round a coil of gut, causing obstruction. Spieler[621] argues against the underestimation by many authors as to the part played by intestinal worms in producing appendicitis, although he also does not regard them as a frequent, to say nothing of an exclusive, cause of the disease. In a case recorded by Bégonin[622] fifteen Oxyuris were found in the excised appendix (the mucosa showed some ulceration), and in another recorded by Putnam[623] twenty Oxyuris were present in the appendix, in which there was no evidence of any change. The standpoint Schilling[624] takes is to the effect that entozoa irritate the mucosa and can increase an already existing inflammation, but he considers it very questionable whether they can produce appendicitis. Blanchard[625] assumes the possibility of a secondary infection arising from lesions of the mucosa produced by helminthes (Ascaris and Oxyuris). Moore[626] considers Trichocephalus the excitant of the appendicitis in his case. In a second case of appendicitis recorded by Auley[627] operation became unnecessary owing to the passage of the Ascaridæ. Page’s[628] case is an interesting one; it was that of a man who came up for operation with a diagnosis of appendicitis. On incising the abdominal wall numerous Ascarides were found at the base of the wound, lying in cavities; even after eight days Ascarides escaped from the wound. The author assumes there was a perforation of the gut wall; it is strange that the worms were able to exist a proportionately long time in the muscular tissue. Schoeppler[629] states that there is the danger of an appendicitis even after the death of an Oxyuris that has found its way into the appendix. Oui[630] met with two specimens of Trichocephalus which had become embedded by their thin ends deep in the mucosa. Frangenheim[631] is not in a position to pronounce any opinion as to what part intestinal parasites play in the etiology of appendicitis. In a case recorded by Kahane[632] many Trichocephali were found partly free in the appendix and partly embedded in the mucosa; microscopically appendicitis was diagnosed. At a laparotomy for salpingitis Heekes[633] found the appendix elongated, thickened, and containing about eleven Oxyuris without the mucosa being in any way changed. In one case Andrews[634] claims Ascarides to have been the direct cause of the appendicitis. The literature dealing with this question, so important in our time, has been collected almost without any omissions, but, unfortunately, no decisive opinion as to the significance of parasites in appendicitis can be inferred from it. The vexed question whether intestinal parasites, especially Ascaris, are able to penetrate the intestinal wall is just as little finally decided. Leuckart,[635] Heller,[636] Mosler and Peiper,[637] Henoch,[638] Davaine,[639] Küchenmeister,[640] and Bremser[641] are opposed to the idea that the healthy intestinal wall can be penetrated by intestinal worms, especially Ascarides, whilst a whole series of other authors are of the opinion that even the healthy intestinal mucosa can be perforated. Among these is numbered Mondière,[642] who is of the opinion that Ascaris, by violent pressure against the mucosa, forces it so much apart that it is enabled to escape through the gap thus formed into the peritoneal cavity; this opinion is shared by v. Siebold.[643] Rokitansky[644] considers perforation of the gut by Ascaris as at least a rare occurrence. Gerhardt[645] does not doubt that the worms can actively perforate the intestine. Cases like those of Abrault,[646] Apostolides,[647] Marcus[648] (recorded by Perls as a valid example of “ascaridophagous” gut perforation), Wischnewsky,[649] Galvagno,[650] Salieri[651] certainly show that perforation of the healthy gut wall cannot be denied, but at the same time that this occurrence, compared with the frequency of Ascaridæ, should be regarded as exceedingly rare. It is another matter as to whether it is possible for the worms to penetrate an intestinal wall already diseased, especially when ulcerated; a whole series of observations are in favour of this. In Lini’s[652] case (fifty-six Ascarides escaped from the umbilicus of a girl, aged 7), in Gräffe’s[653] (eighty Ascarides escaped from an inguinal tumour), in Nicolino’s[654] (perforation of the intestinal wall with strangulated hernia), in Liesen’s[655] (a living Ascaris in the peritoneal cavity in a woman suffering from a peritoneal abscess)--in these it is clear that disease processes in the intestine preceded the exit of the worms. In a case described by Boloff[656] the Ascarides appear to have produced, by forming a tight coil, necrosis of the gut with perforative peritonitis. In a case recorded by Lutz[657] the perforative peritonitis was without doubt provoked by Ascaris, and in one by Schiller[658] the Ascaris had clearly gained access to the peritoneal cavity through a gunshot wound opening. In a case observed by Rehn[659] the worm probably entered through a gangrenous portion of the intestine in a hernial sac. Broca[660] is unable to determine whether in his case the intestinal perforation was primary (a worm escaped from the abdominal wound about two months after a laparotomy for suppurative peritonitis). The case reported by Lutz[661] is of special interest: it was that of a young man who had shot himself in the region of the abdomen, and who died after fifteen days. At the post-mortem two Ascarides were found in the pulmonary artery; they had probably escaped from the intestine, and had gained access to the inferior vena cava. Froelich[662] assumes that in his case (a boy, aged 11) the Oxyuris were able to penetrate the whole intestinal wall, but Vuillemin[663] considers this improbable, and is more inclined to think that the Oxyurides penetrated the rectum at small ulcerated points, and thus gained access to the perirectal connective tissue. In females Oxyuris not only have the power of penetrating far into the sexual organs (Marro[664]), and perhaps causing a parasitic endometritis (Simons[665]), but also clearly of gaining access to the peritoneal cavity by way of the tubes, as is to be assumed in the case recorded by Kolb[666] (that of a woman, aged 42, in whom post mortem nodules were found over the peritoneum of Douglas’s pouch, in which the pressure of encapsuled Oxyuris could be demonstrated), in that reported by Chiari[667] (adult Oxyuris in Douglas’s pouch) and by Schneider[668] (an Oxyuris encapsuled in the pelvic peritoneum). Sehrt’s[669] case is worthy of attention; in this an abscess was found in the omentum with numerous Ascaris ova in the pus and a nodular lesion of the peritoneum, with Ascaris ova encapsuled in the nodules. Massive accumulation of Ascarides may give rise to a complete occlusion of the gut. Such an occurrence is not so surprising as might be thought when one reflects that the number of Ascarides in one individual may amount to several hundreds. For instance, one boy evacuated within a single day 600 Ascarides (Fauconneau-Dufresne[670]) and within three years 5,126 worms. In the case recorded by Tschernomikow[671] a boy, aged 2-1/2, evacuated during a day 208 worms, partly through the stomach, partly through the intestine. Coil-formation of such masses of Ascarides renders possible not only constipation, but also complete obstruction with symptoms of ileus, as shown by the five cases quoted by Mosler and Peiper,[672] as well as from observations made by Raie,[673] Schulhof,[674] Rehberg,[675] Rocheblave,[676] Heller,[677] Leichtenstern,[678] Huber,[679] and Wilms.[680] In two cases of Black[681] and Parkinson[682] the intestinal obstruction was caused by a coil of tapeworms.

[596] Strümpell, “Lehrb. d. spez. Path. u. Therap.,” 1894.

[597] Boas, Deutsch. med. Wochenschr., 1895.

[598] Still, Brit. Med. Journ., 1899.

[599] Arboré-Rally, Arch. de Méd. des Enf., 1900.

[600] Metschnikoff, Bull. méd., 1901.

[601] Matignon (abstract), Münch. med. Wochenschr., 1901.

[602] Des Barres, Gaz. des Hôp., 1903.

[603] Kirmisson, Annal. de Méd. et Chir. des Enf., 1901.

[604] Moty (abstract), Münch. med. Wochenschr., 1901, p. 910.

[605] Girard, Annal. de l’Inst. Pasteur, 1901.

[606] Triboulet, Soc. méd. des Hôp. de Paris, 1901.

[607] Morkowitin (abstract), Centralbl. f. d. Grenzgebiete, 1902.

[608] v. Genser, Wien. med. Wochenschr., 1901.

[609] Schiller, Beitr. z. klin. Chir., 1902, xxxiv.

[610] Czerny and Heddäus, ibid., xxi.

[611] Kaposi, ibid., xxviii.

[612] Schwankhaus, Amer. Pract., 1901.

[613] Ramstedt, Deutsch. med. Wochenschr., 1902.

[614] Rostowzeff, Russ. med. Rundschau, 1903.

[615] Wirsaladze, Bobritsch. Gaz. Botkina, 1902.

[616] Oppe, Münch. med. Wochenschr., 1903.

[617] Hanau, ibid., 1903.

[618] Galli-Vallerio, Centralbl. f. Bakt., 1903, p. 1094.

[619] Ssaweljews, Deutsch. med. Zeitg., 1903.

[620] Nason, Journ. Amer. Med. Assoc., 1904.

[621] Spieler, Wien. klin. Wochenschr., 1904.

[622] Bégonin, Journ. de Méd. de Bordeaux, July, 1902.

[623] Putnam, quoted by Spieler.

[624] Schilling, “Würzb. Abhandl.,” 1905. v.

[625] Blanchard, Acad. de Méd., July 3, 1904.

[626] Moore, Brit. Med. Journ., August 18, 1906.

[627] Auley, ibid., 1906.

[628] Page, New York Med. Journ., January 20, 1906.

[629] Schoeppler, Centralbl. f. Bakt., 1906.

[630] Oui, Rev. prat. d’Obstét. et de Paed., 1906.

[631] Frangenheim, Samml. klin. Vortr., 1906, No. 424.

[632] Kahane, Schweiz. Korrespondenzbl., 1907, viii.

[633] Heekes, Brit. Med. Journ., March 16, 1907.

[634] Andrews, ibid., 1906.

[635] Leuckart, “Die Parasiten des Menschen.”

[636] Heller, “Handb. d. spez. Path.,” v. Ziemssen, vii.

[637] Mosler and Peiper, “Spez. Path. u. Ther.,” v. Nothnagel, vi.

[638] Henoch, “Vorlesungen über Kinderkrankheiten.”

[639] Davaine, “Traité des Entozoaires.”

[640] Küchenmeister and Zürn, “Die Parasiten des Menschen.”

[641] Bremser, “Lebende Würmer im lebenden Menschen.”

[642] Mondière, Schmidt’s Jahrb., 1840.

[643] v. Siebold, “Parasiten” in Wagner’s “Handwörterbuch,” 1845.

[644] Rokitansky, “Path. Anat.”

[645] Gerhardt, quoted by Liesen, “Dissert. Bonn.”

[646] Abrault, quoted by Seifert, “Lehrb. d. Kinderkrankh.”

[647] Apostolides, Lancet, 1898.

[648] Marcus, quoted by Seifert, “Lehrb. d. Kinderkrankh.”

[649] Wischnewsky, quoted by Seifert, ibid.

[650] Galvagno, Arch. de Patol. et Clin., inf., 1902.

[651] Salieri, Rif. med., 1902.

[652] Lini, Schmidt’s Jahrb., 1838.

[653] Gräffe, Protokoll d. Ges. f. Natur u. Heilkunde, Dresden, 1853.

[654] Nicolino, Clin. mod., 1902.

[655] Liesen, “Dissert. Bonn.” 1904.

[656] Boloff, quoted by Seifert, “Lehrb. d. Kinderkrankh.”

[657] Lutz, Centralbl. f. Bakt.

[658] Schiller, Beitr. z. klin. Chir., xxxiv, p. 200.

[659] Rehn, see Schiller, loc. cit., p. 201.

[660] Broca, Rev. mens. des Mal. de l’Enf., 1904.

[661] Lutz, Wien. klin. Wochenschr., 1905, xv.

[662] Froelich, Rev. mens. des Mal. de l’Enf., 1897.

[663] Vuillemin, Centralbl. f. Bakt., 1902.

[664] Marro, Arch. per le Sci. med., 1901.

[665] Simons, Centralbl. f. Gynäk., 1899.

[666] Kolb, Centralbl. f. Bakt., 1902.

[667] Chiari, Prag. med. Wochenschr., 1902.

[668] Schneider, Centralbl. f. Bakt., 1904.

[669] Sehrt, Beitr. z. klin. Chir., li.

[670] Fauconneau-Dufresne, quoted by Seifert.

[671] Tschernomikow, quoted by Seifert.

[672] Mosler and Peiper, loc. cit.

[673] Raie, Lancet, 1899.

[674] Schulhof, Münch. med. Wochenschr., 1903.

[675] Rehberg, “Dissert. Königsberg,” 1907.

[676] Rocheblave, Gaz. des Hôp., 1898.

[677] Heller, loc. cit.

[678] Leichtenstern, “Ziemssen’s Handb.,” vii.

[679] Huber, quoted by Rehberg.

[680] Wilms, Deutsch. Zeitschr. f. Chir., xlvi.

[681] Black, Brit. Med. Journ., 1872.

[682] Parkinson, quoted by Rehberg.

In the earlier history of medicine the helminthes played a great part as the excitants of many intestinal diseases and of enteric as well. Even if to-day they no longer be regarded as such, the conception that they represent the predisposing factor in typhoid infection through the injury they inflict on the mucosa (Guiart,[683] Blanchard,[684] Vivaldi and Tonello[685]) must not be summarily rejected. Vivaldi and Tonello found helminthes in 80 per cent. of their typhoid patients, numbering among these Trichocephalus dispar, Oxyuris vermicularis, Ancylostoma duodenale, and Ascaridæ. The report of Leuckart[686] is here worth citing, to the effect that Thiebault never failed to find Trichocephalus in his cholera patients at Naples. Blanchard[687] goes so far as to express the desire that in every febrile affection of the intestine an anthelmintic treatment with thymol should be undertaken as early as possible, even before learning the results of serum diagnosis.

[683] Guiart, Compt. rend. Soc. de Biol., Paris, March 16, 1901.

[684] Blanchard, Arch. d. Par., 1901.

[685] Vivaldi and Tonello, Gaz. d. Osp., October 29, 1905.

[686] Leuckart, quoted by Kahane.

[687] Blanchard, Acad. de Méd., October 18, 1904.

The lesions of the liver and pancreas due to Ascaridæ are briefly discussed in the chapter on Ascariasis (p. 687).

A discussion of the intestinal helminthes from the clinical and therapeutical point of view follows these general considerations.

Dibothriocephalus latus.

From what is known as to the development of Dibothriocephalus latus, the way by which man is infected is self-evident: infection can only take place through the ingestion of insufficiently cooked fresh-water fish (pike, burbot, perch, grayling and vendace); what degree of temperature is necessary to kill the larval forms is still unknown. Dibothriocephalus latus lives in the small intestine of man, alone or in some numbers, frequently also together with Tænia solium. The proglottides are passed always united in large pieces, the ova are deposited through the uterine pore, while the worm is still in the intestine, so that they are easily found in the fæces. The proglottides are so characteristic that they cannot be confused with those of other species. In reference to whether age or sex is spared by D. latus, it is not possible to make any definite statement, especially so far as the endemic area is concerned, whether a person resides in it continuously or visits it, so long as his habit of life is in accordance with those of the country. Bendix[688] certainly emphasizes the fact that early childhood is as a rule immune: his case was that of a child, aged 4-1/2 years.

[688] Bendix, Verein f. innere Med., Berlin, June 16, 1902.

Sparganum mansoni.

According to our present knowledge (Miyake[689]) the disease occurs almost exclusively in China and Japan. On the main island it occurs in all districts, though rarely under observation. It is especially frequent in the neighbourhood of Kioto and Osaka; these places are very near together, and between them there is mutually active intercourse, so that taken together they may be regarded as one district infested by this worm disease. As regards localization in the body, there appears to exist a certain predisposition for definite regions, for instance, the eye and genito-urinary tract. In some cases the parasite manifested the peculiarity of wandering about the body and of appearing at certain favourite points (musc. quadriceps femoris) (Hashimoto[690]). Most patients complain more or less of the onset of attacks of pain and of sensitiveness to pressure. In those cases in which the patients evacuated the worm during micturition, the symptoms were variable; sometimes there was tenesmus of the bladder, sometimes pains in the inguinal region, sometimes hæmaturia. None of these troubles is characteristic of the disease, and does no more than represent the symptoms that follow a mechanical irritation that any kind of foreign body may produce. Besides the onset of attacks of pain, swelling of the regions affected, if superficial, may often be recognized, when a superficial diffuse soft tumour can be felt which often gives pseudo-fluctuation. Sometimes a peculiar crackling can be detected internally, as in the making of a snowball. During the further course an abscess not infrequently forms around the worm. When the situation of the worm is superficial, “an inflammatory tumour with a tendency to migrate” is stated by Omi[691] to be an important diagnostic sign. That, however, is not always the case, as the observation made by Inoye[692] shows. It would be better to add to this sign the onset of paroxysmal pain and the temporary change in volume of the tumour. When once the parasite is removed, the wound heals just as satisfactorily as any other fresh wounds made at operation.

[689] Miyake, Mitteil. aus d. Grenzgebiete, 1904, xiii.

[690] Hashimoto, quoted by Miyake.

[691] Omi, Iji-Shinshi, Tokio, 1898.

[692] Inoye, ibid., 1897.

*Dipylidium caninum* (Tænia cucumerina).

This species belongs to parasites of rare occurrence. Up to the year 1905 Bollinger[693] collected thirty-six cases from the literature, twenty-nine of which were children and seven adults. Since then some further cases have come to light, so that the number now observed amounts to ninety, and among them only eight adults. The youngest child was 6 weeks old (Köhl[694]), in which the first proglottides were passed when the child was 40 days old. This preponderating occurrence in children is clearly connected with the close intercourse between children and dogs, and also cats. Bollinger believes that D. caninum in reality occurs more frequently in adults than has hitherto been supposed. In addition, it must be mentioned that this species is quite unknown to many physicians, and is occasionally confused with Tænia solium. One notices almost daily a large quantity of cucumber-seed-like bodies, reddish or whitish-grey, about 1 cm. long and 2 mm. broad, discharged with the stools. Lindblad[695] remarks that these bodies have lively movements, that they perish rapidly in fresh water, and become white and smooth. These Cestodes, in isolated cases, are parasitic in the intestine in large numbers. Sonnenschein[696] expelled four fragments in the case of a boy, aged 4 months; Asam[697] three fragments in the case of a child, aged 19 months; and Zschokke[698] as many as five or six in that of a boy, aged 4. They do not always produce such striking symptoms as occurred in Pollak’s case.[699] In other cases gastro-intestinal disturbances with or without fever (Krüger[700]), emaciation (Zschokke), or even nervous symptoms of central origin in the form of convulsions (Brandt[701]) have been observed. From the nature and mode of infection children must be kept from close contact with dogs and cats as much as possible to ensure prophylaxis. The appropriate treatment, as it mainly affects children, deserves special mention, whilst the expulsion of the remaining Cestodes may be described in this connection. Among the drugs one may mention flor. kousso 1·0 grm., pulpa tamar. depur. 2 grm., syrup of sugar 50·0 grm., one-third to be taken every hour (Lindblad). Kamala appears to have no effect, although Huber[702] recommends it in small doses according to age from 0·5 to 3·0 grm. He warns against Filix mas preparations, which otherwise, even in early childhood, under careful dosage gives the best results. Young children are given 1·0 to 2·0 grm. extr. fil. maris, with mint syrup or raspberry syrup 30·0 grm., in the morning twice an hour by the mouth, or 1·0 grm. extr. fil. maris is mixed with syrup of mint, and given by means of a stomach tube (Rosenberg[703]). A few hours afterwards a mild laxative may be taken--one to two tablespoonfuls of aqueous tincture of rhubarb (Asam)--or an enema may be given. In a case reported by Sonnenschein decoction of pomegranate root had no effect, as it was vomited up.

[693] Bollinger, Deutsch. Arch. f. klin. Med., 1905, lxxxiv.

[694] Köhl, Münch. med. Wochenschr., 1904.

[695] Lindblad, Hygiea, xlv.

[696] Sonnenschein, Münch. med. Wochenschr., 1903.

[697] Asam, Münch. med. Wochenschr., 1903.

[698] Zschokke, Centralbl. f. Bakt., 1905.

[699] Pollak, Wien. klin. Wochenschr., 1907.

[700] Krüger, St. Petersb. med. Wochenschr., 1887.

[701] Brandt, Centralbl. f. Bakt., 1889.

[702] Huber, suppl. to Asam, Münch. med. Wochenschr., 1903.

[703] Rosenberg, Ges. f. innere Med., February 16, 1904.

Hymenolepis nana.

This species, very rare in Central and Northern Europe, inhabits the small intestine, especially of children; it burrows very deeply into the mucosa. Not uncommonly several thousand have been found in one case (Nicolo,[704] E. Stoerk and Haendel[705]). It is remarkable that these Cestodes have been found so frequently post mortem and after vermifuges given for other reasons. Thus the clinical symptoms must often be very indefinite (Stoerk and Haendel), so that one may assume that only a slight percentage of cases of Hymenolepis nana come under observation and are published as such. On the other hand, it is certainly conceivable that with the large number of parasites that frequently occur in one individual a whole series of symptoms, in part quite severe, are capable of being produced. These are partly symptoms of intestinal catarrh, consisting of abdominal pains, constipation, alternating with attacks of diarrhœa, perverse appetite, and boulimia, abdominal pains of a cramp-like nature, followed by emaciation, headache, sleeplessness, pallor, lassitude, and in part nervous symptoms--epileptiform attacks without loss of consciousness, weakness of memory, melancholia, irregular febrile attacks (Lutz[706]). Possibly, too, Hymenolepis nana infects the urinary organs, producing true chyluria (Predtetschensky[707]). Stoerk and Haendel are inclined to think that this species, unlike other Cestodes parasitic in man and domestic animals, needs no intermediate host for its development, and that the larval forms (cysticercoid) live in the same host as the adults. The diagnosis is based on the demonstration of ova in the stools. As far as expulsion of this Cestode is concerned, santonin, kamala, kousso flowers and thymol appear to have no effect of importance; whilst extract of male fern, recommended by Grassi[708] as a result of his considerable and successful experience, has been given, with the result that the worms really are expelled, and that after the treatment neither worms nor ova are any longer demonstrable in the stools of patients. In his cases of chyluria Predtetschensky prescribed ol. terebinth. 20 drops three times daily for a fortnight, then acid. gallic. 0·5 grm. three times a day for two days, then 1·0 grm. three times a day; the urine became clear, but whether permanent cure resulted remained doubtful.

[704] Nicolo, Gaz. d. Osp., 1904.

[705] Stoerk, E., and Haendel, Wien. klin. Wochenschr., 1907, xxix.

[706] Lutz, Centralbl. f. Bakt., 1894.

[707] Predtetschensky, Zeitschr. f. klin. Med., xl.

[708] Grassi, Centralbl. f. Bakt., 1887.

Hymenolepis diminuta, H. lanceolata, Davainea asiatica, and D. madagascarensis possess no actual clinical interest; with regard to the latter it need only be pointed out that Bordier[709] in studying a case of chyluria found this species in the kidneys of a person in Madagascar.

[709] Bordier, quoted by Predtetschensky, loc. cit., p. 95.

Tænia solium.

Tænia solium inhabits the small intestine of man; single proglottides or whole worms may get into the abdominal cavity and the bladder through fistulæ, and penetrating the abdominal wall escape outwards or become discharged with the urine. Symptoms of intestinal stenosis are certainly very rare, as in the case recorded by Steinhaus[710] of a child, aged 9, the stenosis ceasing after the expulsion of the segments. The usual position of the worm in the small intestine is with the head closely adherent to the mucosa and the proglottides lying along the intestine; from time to time portions are discharged with the fæces per rectum. Its position can also be reversed, and the proglottides in the gut become thus discharged by vomiting.

[710] Steinhaus, Deutsch. med. Wochenschr., 1903.

The diagnosis depends upon the proglottides being generally discharged in pieces in the stools, or eventually an examination for eggs. Larval infection (Cysticercus cellulosæ) occurs also in man through auto-infection or through food.

Cysticercus cellulosæ of the skin and subcutaneous tissue occurs very seldom singly; as a rule they are found in hundreds and thousands in the same individual. They occur in different parts of the body, especially on the flexor surfaces of the extremities (generally symmetrically), small globular swellings, the size of a pea or a hazel nut, smooth, of a tough cartilaginous consistence, fairly movable under the skin, in the muscles less so. They never degenerate or cause the surrounding skin to lose its colour. It is an interesting fact that in the case described by Posselt[711] nodules on the face, namely in the neighbourhood of the left cheek and behind the left ear, reformed. The following are, according to Posselt, characteristic for cutaneous tumours due to cysticerci: (1) the position in the subcutaneous connective tissue (and almost always simultaneously in the muscles); (2) the approximately equal size and regularly rounded oval form; (3) the peculiar density, almost reminding one of cartilage in its hardness and the sensation of tightly distended thick-walled bladders; (4) proportionately slight mobility; (5) with painlessness, absence of any cutaneous reaction (hyperæmia or swelling of the skin or pigmentation). The very gradual appearance generally of the tumours supports the diagnosis, and in addition to this evidence we may emphasize the preponderating liability of the upper part of the body to attack and the symmetrical arrangement of the nodules. Cutaneous and muscular cysticerci cause the most varied symptoms, sensory disturbances, abnormal sensations, depression and a feeling of weariness whenever the diseased parts are moved, weakness in the lower extremities, pains in the course of the sciatic nerve, in addition to those which simulate cramp in the calves, numbness in the hands, pains upon their being moved. In the case of a cysticercus situated in the elbow-joint, painful dragging sensation in the course of the ulnar nerve persisted. In other cases the arm was almost paralysed, or it could not be completely extended; stiffness and bending of the little finger were noticed. Cysticerci of the gluteal muscle cause trouble upon sitting and upon defæcation. Remittent unilateral headaches were present in the case of a cysticercus of the region of the right eyebrow; pains of a neuralgic character radiated from the diseased temporal region. The cysts may be inflamed and may suppurate; this especially happens in the case of solitary cutaneous and muscle cysticerci. The best treatment consists in puncture of the cysts with a Pravaz syringe and subsequent injection of a drop of 1 per cent. sublimate solution. Tincture of iodine has similarly been proposed (Wolff[712]). Frangenheim[713] recommends early extirpation (this, however, only in the case of solitary cysts). Pelagutti[714] believes that in his case diminution in the size of the cysts was obtained by the use of anthelminthic remedies continued over a long period combined with potassium iodide and calcium salts (internally). Cysticercus is very rarely found in the tongue; there the worms generally lie in front of the sulcus terminalis, corresponding to the middle of the tongue, according to Glas.[715] In the case recorded by Gaetano[716] (a boy, aged 10) there was a nodule on the left side of the tongue which grew very rapidly till it reached the size of a nut; it was embedded in the muscle and covered over by normal mucosa. Cysticerci are just as rare in the pleuræ, in the lungs, in the intestinal submucosa, in the submucosa of the small intestine, in the mesenteric glands, in the liver, pancreas, spleen and kidneys, in the mamma, in the heart, in the bones and in the great vessels (Huber[717]). Cysticercus of the eye deserves special mention; in rare cases the cysticercus has been met with in the subcutaneous cellular tissue of the eyelid, once in the muscle bundles of the musculus orbicularis. Subconjunctival cysts are found chiefly in youthful individuals. Their position is most varied, generally in the neighbourhood of the inner angle of the eye. Dilated vessels pass right over the cysts, which are generally movable, together with the base they rest upon, producing a spherical protrusion. The head of the worm can sometimes be seen shining through as a whitish speck. The only symptoms are those of a slight irritation of the connective tissue and some difficulty in closing the lid; larger cysts dislocate the globe. The diagnosis has the rapid growth of the cystic tumour to support it; there is the possibility of its being mistaken for a foreign body (Kaldrovils[718]). After division of the connective tissue capsule extraction is easily performed. It is most rare for the cysticercus to occur in the orbit. Suppuration of the cyst may have serious consequences for the eye. It is only exceptionally that the cysticerci gain access to the anterior chamber of the eye.

[711] Posselt, Wien. klin. Wochenschr., 1899.

[712] Wolff, “Lesser’s Encyclop. d. Haut- u. Geschlechtskrankh.,” 1900.

[713] Frangenheim, Volkm. klin. Vortr., No. 424.

[714] Pelagutti, Giorn. ital. delle mal. vener., 1900.

[715] Glas, Wien. klin. Wochenschr., 1905.

[716] Gaetano, Giorn. int. delle Sci. med., 1904.

[717] Huber, “Bibliographie der klin. Helminthologie,” 1891, pt. 2.

[718] Kaldrovils, Wien. med. Wochenschr., 1902.

Subretinal cysticerci or those localized in the vitreous are more frequent. Upon examination with the ophthalmoscope there is seen in the vitreous a bluish bladder with a smooth surface. The head is seen as a white patch, and the circle of hooks and the suckers also come into view, also the frequent movements which the head and neck make in the vitreous. Operation generally yields good results; in rare instances the globe is atrophied and must be enucleated.

Formerly cysticerci in the brain were met with in fair frequency, but the number of such cases has generally decreased of late years in a remarkable way, in correspondence with the diminution of cysticerci, which is to be attributed to compulsory meat inspection. Whilst, for example, the post-mortem records of the Pathological Institute in Berlin before the year 1875 showed 20 per cent. cysticerci affecting the brain, this number declined later to 16·3 per cent., and of late years has fallen to 1 per cent. (Orth[719]). Nevertheless even now cysticercus still plays no inconsiderable part in the etiology of cerebral diseases. For example, in the clinic of de Amicis at Naples, among seven cases of cysticerci of the skin, they were found four times also in the brain (Sipari[720]). Cysticerci may occur in the dura mater, arachnoid, pia mater, choroid plexus, the surface of the cerebral hemisphere, the medullary substance, the ventricles, the aqueduct, the corpus striatum, corpora quadrigemina, the pineal gland, the pons, the cerebellum, the olfactory trigone, the bulb, the medulla oblongata, and the olive. They are most frequently found in the cortical substance and in the ventricles; the frequency of the latter situation may be explained by the flow of the fluid (Henneberg[721]). The severity of the symptoms is not always in proportion to the number of cysticerci. Cases have been known in which ten, twenty and forty cysticerci have been found (Hagen-Thorn[722]), and yet the clinical symptoms have been remarkably slight. On the other hand, solitary cysts may both run a course completely without symptoms and also cause the severest symptoms when located in specially important parts of the brain (crus, pons, central convolutions). In the case mentioned by Jacobson[723] the invasion of the brain by cysticerci was immense; the largest cyst was found in the cerebral cortex. The chief symptoms of cysticercus of the brain substance consist in the onset of cortical epilepsy, which sometimes runs a very pernicious course, frequently with psychical disturbances, whilst paralyses are absent. Perhaps, too, the localization of pain, spontaneous and on pressure, corresponding with the points observed on the cranium, is of importance. Cysticerci may also change their position in the brain; patients who had earlier suffered from epileptiform convulsions later showed intra-ocular cysticerci after the cerebral symptoms had completely disappeared. Treatment can only be surgical; v. Bergmann[724] operated in two cases with well-marked improvement. Parasites in the ventricles are especially dangerous, more especially so when free in the ventricles, and so capable of giving rise to the danger of sudden closure of the foramen of Majendie (Simmonds,[725] Versé[726]). Stern[727] states the symptoms of cysticercus in the fourth ventricle to be the following: general cerebral pressure symptoms (headache, vertigo, vomiting, somnolence, congested disc caused by internal hydrocephalus); in addition, there are symptoms which point to disease of the hind-brain--pain and stiffness in the neck, vertigo and cerebellar ataxy, violent and persistent vomiting, slowness of pulse; and lastly those rare but certain symptoms of a lesion of the bulb, such as diabetes, respiratory disturbances and paralysis of cerebral nerves, especially of the abducens. These are far less marked than the general symptoms of cerebral pressure. One characteristic is the remarkable alternation between severe general symptoms and periods of complete sense of well-being; in this way a functional nervous affection may be simulated (Jolasse[728]). Brun’s symptom (in the widest sense, sudden onset of violent cerebral symptoms upon change of head-posture) is a specially characteristic sign of free cysticercus in the fourth ventricle; the disease generally terminates with sudden death from cessation of the heart’s action. Defects in motor power, convulsions, implication of other nerves, are rare and unessential complications (Hartmann[729]). Carefully carried out, lumbar puncture may possess some diagnostic and therapeutic value. Treatment is purely symptomatic, or eventually Neisser’s ventricle puncture may be considered.

[719] Orth, Berl. med. Ges., June 29, 1904.

[720] Sipari, “Angelo Trani Neapel,” 1900.

[721] Henneberg, Berl. klin. Wochenschr., 1906, xxxii.

[722] Hagen-Thorn, abstract by Posselt.

[723] Jacobson, Berl. klin. Wochenschr., 1906.

[724] v. Bergmann, quoted by Frangenheim, loc. cit., p. 470.

[725] Simmonds, Münch. med. Wochenschr., 1907, xxvii.

[726] Versé, Münch. med. Wochenschr., 1907, xi.

[727] Stern, Zeitschr. f. klin. Med., lxi.

[728] Jolasse, Münch. med. Wochenschr., 1896.

[729] Hartmann, Wien. klin. Wochenschr., 1902.

At the base of the brain the cysticerci, as a rule, assume that form which is designated as C. racemosus, and consists of rows of delicate grape-like bladders in groups, sometimes also markedly branched, but generally sterile, which develop in the meshes of the soft meninges and may envelop the nerves and vessels of the base of the brain. Such tumours bring about hydrocephalus and chronic leptomeningitis, which must be regarded as the causes of the clinical disturbances (cysticercus meningitis), attacks of loss of consciousness, dementia and apathy, dulness and confusion and headaches. In the case recorded by Meyer[730] symptoms which resembled paralysis agitans were noteworthy, and defects in speech in the case recorded by Durst[731] (C. racemosus in the region of the left Sylvian fossa). According to Markwald[732] C. racemosus of the fourth ventricle is said to represent a characteristic clinical picture: violent headaches, attacks of vertigo followed very soon by deep coma and death in a few days. Treatment in Cysticercus racemosus is ineffectual. In the diagnosis of cerebral cysticerci in general the recognition of multiple cysticerci in the skin and muscle and of the tapeworm is of importance. In cases of cerebral diseases in which cysticerci may be a possible cause, Remmert[733] recommends that the skin of the whole body should be palpated.

[730] Meyer, Deutsch. med. Wochenschr., 1906.

[731] Durst, Lieven. viestnik, 1902.

[732] Markwald, Münch. med. Wochenschr., 1895.

[733] Remmert, “Dissert. Berlin,” 1893.

Cysticercus in the spinal cord and in the vertebral column is occasionally observed; as a rule, other organs, above all the brain and its membranes, are simultaneously affected. Here, too, the cysticercus occurs in two forms--sometimes the cysts are roundish or oval, solitary or multiple, and at other times Cysticercus racemosus occurs.

Tænia saginata.

Occurs in the small intestine of man. It is characteristic of the habit of life of this parasite that once it has become mature its proglottides are dropped off daily in increasing numbers because its growth is extraordinarily rapid. The joints are discharged generally spontaneously during the whole day without a stool. An extraordinarily unpleasant sensation is produced by the damp, cool joints slipping down into one’s lower garments and over one’s legs when walking; women especially, in whom the proglottides slip through their petticoats on to their legs, complain bitterly of this troublesome symptom. Another unpleasant symptom is superadded in the shape of the proglottides tickling the rectum, and this excites irritable people to the last degree. Different species of tapeworms are not mutually exclusive. B. latus and T. solium frequently occur side by side, so also T. solium and T. saginata--for instance, in a butcher’s assistant we once expelled twelve T. solium and one T. saginata at the same time. The greatest number of Tæniæ which have been observed at one time amounted to forty T. solium (Kleefeld[734]). Even though the cysticercus of T. saginata is not, as in the case of T. solium, particularly dangerous to man, a parasite, nevertheless, which requires so much nutrient material during its rapid growth, and thereby sets up manifold disturbances in the general condition of health, ought to be expelled as rapidly and thoroughly as possible.

[734] Kleefeld, see Seifert loc. cit.

Tapeworms are found not uncommonly with other intestinal parasites, such as Ascaris, Oxyuris, Trichocephalus or Ancylostoma. Prunac[735] described a case in which a woman passed a Tænia through the anus while she vomited a Fasciola hepatica.

[735] Prunac, see Eichhorst, “Handb. d. spez. Path. u. Therap.,” ii, p. 281.

The symptomatology of these three large species of Cestodes, Dibothriocephalus latus, Tænia solium, and T. saginata, may very well be summarized together, as, apart from some peculiarities, the clinical symptoms, especially so far as their localization in the intestine is concerned, are practically the same for all three species. In a large number of cases the hosts have no suspicion whatever that they are harbouring a tapeworm; they feel quite well and free from any disquieting symptoms whatever, and only become aware of the fact that they are the carriers of a tapeworm when the discharge of the segments takes place; on the other hand, it is often difficult to rid people of the idea that they are harbouring a Tænia (Küchenmeister calls such Tænia imaginata); usually it is undigested fibrous shreds of beefsteak which are regarded by the patients as proglottides of tæniæ.

In a large number of cases, disturbances of the intestinal tract set in, e.g., sense of pressure in the abdomen, which sometimes becomes constant on one and the same side, or sometimes changes, now at the umbilicus and again at the epigastrium; here and there colicky pains are present. Derangements of appetite and digestion are frequently complained of; the most frequent are the sensations of morbid hunger or irregular appetite, nausea and vomiting. Thus, at the Third Congress of Internal Medicine, Senator recorded a case in which there were symptoms of nervous dyspepsia, cured after a successful vermifuge. There is either constipation or diarrhœa, so that many of such patients are brought for treatment with the diagnosis of “chronic intestinal catarrh” and correspondingly treated. As to the treatment of toxic action of the Tæniæ when such arises, see the special section on the subject (bothriocephalus anæmia, p. 644). The frequent disturbances of the general condition, so-called reflex phenomena, so far as the action of toxic substances is not in question, may be explained by the fact of their occurrence in specially sensitive individuals who are affected by such phenomena. The proof that a diseased condition is produced by a tapeworm will be forthcoming with some degree of certainty if the symptoms cease immediately after the removal of the parasites. As a whole series of troubles, which certainly have nothing to do with them, are erroneously ascribed to the tapeworm, as is frequently assumed, one will do well to be somewhat critical in this respect.

The treatment is of a threefold nature: prophylactic, symptomatic and radical.

Under any circumstances, the best prophylaxis is that which consists in only eating the flesh of those animals in which any of the three larval forms occur (pig, cattle, salmon, pike, burbot, etc.) so prepared that the larval forms have been destroyed and the food thus rendered innocuous. For domestic and public use the rule prescribed by Küchenmeister is under all circumstances most easily understood, namely to roast or boil till the flesh appear greyish-white and sufficiently done by reason of the coagulation of the albumen and decolorization of the blood. The general prophylaxis simply concerns the tapeworm carriers trying to limit as far as possible the further extension of the parasites in the animal world by carefully rendering the expelled segments and worms harmless (pouring sulphuric acid over the fæces and burning the worms) and also by strictly adhering to official regulations. The official system of meat inspection in this respect has been of immense service, and much can still be done by means of thorough official control over cleanliness in abattoirs and butchers’ shops. Galli-Valerio[736] very rightly desires the abolition of the custom of manuring fruit-plants such as strawberries, vegetables and salad with the contents of privies, and would extend the use of privies in the country.

[736] Galli-Valerio, Therap. Monatsh., 1900.

Symptomatic treatment consists, in the case of those Tæniæ which resist radical attempts at expulsion, of repeated use of drugs injurious to the worm as soon as ever new proglottides are formed, or in special cases, as in the case of persons weakened by diseases or operations, or frail old people, or patients with severe heart failure, gastric or intestinal carcinoma, or in pregnancy, in effecting the expulsion of a large chain of proglottides by the mildest measures possible.

Radical treatment of the Tænia is not always equally easy in all three species, even when the means used are the same; the easiest to expel is T. solium, then D. latus, and the most difficult T. saginata. That as yet no certain cure exists for Cestodes is clear from the large number of drugs recommended from time to time, and the increase of bungling treatment in this respect; in addition, there is no department in which there is so much quackery as in vermifuges. The treatment proper should always be preceded by thorough preparatory treatment, the purpose of which is to render the gut as empty as possible once for all, and on the other hand to put the worms themselves into a diseased condition. How far the host himself has been made ill by such preliminary cures (herring, pickle, garlic, onions, preserved strawberries), many a person who has had to do with such things can recount. In the opinion of Fischer[737] strict preparatory treatment appears to favour the development of toxic substances, or else it disposes to vomiting; as a rule it causes the patient far more discomfort than the treatment itself. In recent times far less weight is attached to these preparatory treatments than to carefully prepared and correctly dosed drugs; the preparation is generally limited to relieving the intestine in a simple way, the day before the treatment, of the densest fæcal masses, by a simple aperient or water enema.

[737] Fischer, Stockholm, Nordin and Josephson, 1904.

We recommend the following, which has always proved itself to be the best and simplest remedy against T. saginata. The patient takes early in the evening before the treatment nothing but a plate of soup or a glass of milk, and then takes a laxative (electuar. lenit or infus. sennæ compos. or an enema), so that later in the evening one to two stools are passed. In this connection we fail to agree with Grawitz[738] and Boas,[739] who consider that at least preliminary evacuation of the intestines can be dispensed with. On the following morning the patient should take a cup of black coffee or tea without anything else, and half an hour later the vermifuge.

[738] Grawitz, Münch. med. Wochenschr., 1899.

[739] Boas, Deutsch. med. Wochenschr., 1889.

The best drug is extract. filicis maris æther., which also forms the main constituent of most of the secret remedies recommended for tapeworms. Earlier mishaps with this preparation had their origin principally in insufficient dosage. Also, in addition to correct dosage, extract. filic. maris needs very careful preparation if satisfactory results are to be attained. If preparations with the trade mark “Helfenberg” or “Wohnar” are not used, but the male fern extract has been prepared by a chemist, one must make certain that the roots of the Aspidium filix-mas have been collected in May or October, and only green sappy specimens selected, and that the attached paleæ have been separated, that they have been broken up small and ether poured over them with a little spirits of wine while quite fresh. The whole mass is to be kept in a cool place, but not too closely covered. If at any time a certain quantity is to be used, it is taken out, the ether carefully distilled in a retort till the extract has a suitable fluid consistency. Fischer attaches great importance to the direction in the Pharmacopœia being exactly followed, to the effect that the extract is to be carefully stirred before prescribing, as the active substances undergo partial crystallization if kept for any length of time and sink to the bottom, so that the preparation has a different strength and toxicity in different layers. Of this extract 10 to 12 to 15 grm. are to be taken in gelatine capsules within half an hour. We consider it unjustifiable to give greater doses than 15 grm. to adults, as many cases are known in which to some extent severe toxic symptoms have followed, such as headache, sensation of giddiness, dyspnœa and cyanosis, yellow vision (xanthopsia), delirium, stupor, the most severe cramps in the extremities, rapidly fatal trismus and tetanus. The most serious are defects of vision of various kinds, which may end in amblyopia and amaurosis, with permanent blindness. A complete collection of toxicological literature up to the year 1903 is to be found in Marx’s[740] Dissertation. Since that time further instances of such intoxications have been made known. Nagel[741] observed them only in severe cases. O. Meyer[742] lays special stress on the bad prognosis of the disturbances of vision evoked by poisoning with extract. filicis maris. Studt[742] has seen two cases of optic neuritis, one with circumscribed, the other with diffuse retinal œdema. Uhthoff[743] has only seen one case; in that reported by Noiszewski[744] the toxic retinitis was cured; in Viereck’s[745] case bilateral concentric limitation of the field of vision followed three days after taking 8·0 grm. extract. filicis maris. Stuelp[746] attributes the amaurosis occurring after taking filix mas to a toxic action on the muscularis of the central retinal artery; there followed paralysis of the vessel, vascular engorgement, and thereby nutritional defects of the nervous elements followed. In children one has to diminish the dose correspondingly, as with them, still more so than with adults, severe disturbances arise. Huber[747] claims that this drug should not be given to children indiscriminately. The view is frequently expressed that a combination of extractum filicis maris with fatty oils in which the active constituents are soluble favours intoxication. Marx[748] also argues from this standpoint and assumes that the ideal preparation, free from objection, would be got if from filix-mas extract a preparation free from fatty oils could be made, and he considers it advisable to limit the use of castor oil as an aperient before and after taking the “cure” and to prescribe instead a saline laxative, such as Epsom salts or Glauber’s salts. Sonnenschein[749] also advises against the simultaneous exhibition of extractum filicis maris with oleum ricini, as is the case with Helfenberg’s capsules, and Boas[750] is likewise anxious that ol. ricini should be avoided. Lenhartz[751] appears to consider the warning against the simultaneous combination of the extract with fats or ethereal oils, and especially against the employment of castor oil as an after-treatment, as without justification, and we, too, in the course of our many filix treatments, have never yet witnessed any unfavourable effect from the use of castor oil in the after-treatment. The surest way of obviating the toxic effects of extractum filicis is to give a laxative (ol. ricini) as soon as the extract has left the stomach, say, about half an hour, so that it need not stay longer than necessary in the gut and become absorbed. Perhaps in most cases of poisoning, transgressions against this rule have been the cause of the toxic action. The nausea that sets in the day after taking the drug and the inclination to vomit are best resisted by giving iced coffee, iced tea, iced pills, peppermint tea, cognac, one to two wafer powders of menthol and sacch. lactis āā 0·2 grm. (Apolant[752]) half an hour before the drug is taken. Fischer[753] considers that lying still in the horizontal position is the best remedy. Boas[754] recommends the injection of the drug into the stomachs of patients who tolerate extractum filicis badly, in the form of a thin emulsion (with gi. arab.). In the case of children the extract is prescribed with honey as an electuary. The method recommended by Fowler[755] is without doubt too detailed; he prescribes before the treatment two to three to four days’ rest in bed; special diet, tablets of cascara sagrada three times daily, on the fourth day senna infusion, and then to give the extractum filicis maris in capsules in four doses, to be taken every quarter of an hour.

[740] Marx, “Diss. Würzburg,” 1903.

[741] Nagel, Deutsch. med. Wochenschr., 1903.

[742] Meyer, O., Berl. klin. Wochenschr., 1905.

[743] Studt, ibid., 1905.

[744] Uhthoff, ibid., 1905.

[745] Noiszewski, “Postepokuhst,” 1906.

[746] Viereck, Arch. f. Schiffs- u. Tropen-Hyg., 1906.

[747] Stuelp, Arch. f. Augenheilk., 1906, li.

[748] Huber, M_ünch. med. Wochenschr._, 1903.

[749] Marx, loc. cit.

[750] Sonnenschein, Münch. med. Wochenschr., 1903.

[751] Boas, loc. cit.

[752] Lenhartz, loc. cit.

[753] Apolant, Deutsch. med. Wochenschr., 1905, xliv.

[754] Fischer, loc. cit.

[755] Boas, loc. cit.

[756] Fowler, Brit. Med. Journ., 1906.

Under Jaquet’s[757] direction, Kraft has prepared an amorphous acid from the fern root extract which is designated filmaron. As a vermifuge the drug is prescribed for children of 2 to 5 years of age in doses up to 0·2 to 0·3 grm., for children of from 8 to 12 years in doses up to 0·5 to 0·7 grm., and for adults up to 0·7 to 1·0 grm., so as to expel the parasites. Bodenstein[758] gives the filmaron oil introduced into commerce by the firm of Boehringer (one part filmaron and nine parts castor oil) in still greater dosage, either fasting or, in the case of sensitive patients, one hour after a cup of tea; he gives peppermint tablets against possible nausea. Brieger[759] tested the preparation in twenty-three cases; in twenty-one of these he prescribed it as an ether-castor oil mixture, and in two as capsules. The action always took effect in from two to five hours, and only in three cases were unpleasant after-effects in the shape of colic observed; in sixteen cases the result was positive, in seven negative.

[757] Jaquet, Therap. Monatsh., 1904.

[758] Bodenstein, Wien. med. Presse, 1906.

[759] Brieger, “Therap. d. Gegenwart.,” 1905.

The attempts made by Goldmann[760] to prepare from the bark of Musenna abyssinica, a plant of the order Myrsinaceæ, indigenous to Persia, the active substance, namely sebirol, have shown that when this is given alone it certainly acts as a vermicide, but not as a vermifuge; on the other hand, the results of a combination of sebirol with thymol and salicylates were surprisingly good; this mixture has been introduced into commerce as tæniol, in the shape of pastilles prepared with chocolate for children. The method of giving tæniol is as follows: On the day before the administration a light diet and thorough purging with calomel are ordered; and then on the day of the treatment itself, after a breakfast consisting of a cup of tea, in the case of adults, thirteen to fifteen tæniol pastilles are taken in some red wine at intervals of ten minutes respectively. In the middle of this treatment an interval of some hours is interposed. After the pastilles have been taken a calomel purge is again given. The results obtained by Liermberger[761] are sufficiently encouraging to be put to further test.

[760] Goldmann, Wien. klin. Wochenschr., 1905.

[761] Liermberger, Berl. klin. Wochenschr., 1905.

Fischer[762] has tested in some of his cases extracts of some new species of fern root; he employed the extract from the rhizomes of Aspidium spinulosum and A. dilatatum, two fern roots indigenous to Sweden, and obtained remarkable results (doses of 4 grm.). Laurén[763] had previously recorded similar results, and recently Friedjung,[764] using extr. aspid. spinulos.

[762] Fischer, loc. cit.

[763] Laurén, Therap. Monatsh., 1899.

[764] Friedjung, Ges. f. innere Med., Wien, March 8, 1906.

Cortex radicis granati as fresh bark is a very good drug, and is usually given as a decoction: 180·0 bark to 1,000·0 water, boiled for forty hours to 240·0, and a small cupful to be given every half an hour; colic, vomiting and diarrhœa, are, however, easily induced. The chief constituent of the granate root, pelletierinum, possesses vermicidal properties, and is much recommended, especially in France. Sequelæ easily arise (vertigo, hazy vision, malaise, vomiting, quickened heart’s action, muscular tremors, cramps in the calves), especially in delicate persons and children, so that one should refrain from giving it to the latter especially (Drivon[765]). Sometimes, judging by the experience of Sobotta[766] and Boas,[767] the action is problematical. Where it is desired to employ it in the case of adults, the following is prescribed: pellet. sulfur. 0·3 to 0·4 grm., acid. tannic. 0·5 grm., sir. rub. jd. 30·0 grm., to be taken at one time, and a quarter to half an hour after a purgative (senna infusion). In the case of children it is better to employ semina cucurbitæ maximæ instead of extractum filicis maris. Sixty to 100 pumpkin seeds are pounded up with sugar, which yield a pleasant-tasting electuary, and which are taken all at once; half an hour afterwards a laxative is taken (Storch,[768] Pick[769]), Jungklauss’s preparation is nothing else than a pumpkin extract; its action is favourable; it is, however, too expensive (Ritter[770]). Flores kousso up to 15 to 20 grm. in compressed form or in sugar or honey in the form of electuaries (children 2·0 to 10·0 grm. according to age) is not to be relied upon; kussin, prepared from kousso flowers (Bedall, Munich), is not a pure body; when taken it is divided into four parts up to 1·0 to 2·0 grm. with elæosaccharum menthæ, at half-hourly intervals; it is said to be less unpleasant than treatment with flores kousso (Liebreich and Langgard[771]). Kosinum crystallisatum (dose 1·5 to 2·0 grm.) is prepared by the firm of Merck. Kamala is the least potent of the tapeworm drugs in use, and is principally to be recommended in the treatment of children: 1·5 to 3·0 grm. in electuaries. According to Leichtenstern[772] and White[773] chloroform, even in toxic doses, cannot do any harm to the tapeworm, nevertheless it has been recently recommended by Carratú[774]; chloroform 6·0, sirup. 60·0, one teaspoonful to be taken every hour (fasting). Salol is recommended by Galli-Valerio[775] as an absolutely harmless tapeworm drug; thymotal (a derivative of thymol) by Pool,[776] 3 grm. to be given up to three to four times on four consecutive days.

[765] Drivon, Lyon méd., 1902.

[766] Sobotta, loc. cit.

[767] Boas, loc. cit.

[768] Storch, see Lenhartz, loc. cit.

[769] Pick, Ges. f. innere Med., Wien, March 8, 1906.

[770] Ritter, Prag. med. Wochenschr., 1904, v.

[771] Liebreich and Langgard, “Kompendium der Arzneiverordnung,” 1907.

[772] Leichtenstern, “Therap. der Gegenwart.,” 1899.

[773] White, Scot. Med. and Surg. Journ., 1900.

[774] Carratú, Giorn. med. del regio eserc., 1903.

[775] Galli-Valerio, Therap. Monatsh., 1900.

[776] Pool, Med. Woche, 1901.

The drug well known long ago, cuprum oxyd. nigr., has been recently brought into fresh notice by Dörr.[777] It is also the chief constituent of the tapeworm drug introduced into commerce by the firm of Dehlsen (Itzehoe) (Koch[778]). The coconut is absolutely ineffectual, also naphthalin, croton-chloral, ether, gallanol, strontium lactate, glycerine and bromide of potash.

[777] Dörr, “Therap. der Gegenwart.,” 1901.

[778] Koch, Med. Klinik, 1907.

Where possible one should endeavour to discover the head or the heads of the tapeworm in the stools, so as to make certain whether the treatment has been successful; this search is best carried out by immediately and carefully pouring water over the total quantity of evacuations collected in the night stool, without stirring them up, till only the tapeworm is found lying at the bottom of the vessel.

NEMATODES.

*Strongyloides stercoralis.*

The pathological significance of this intestinal parasite is not yet fully demonstrated. In Seifert’s[779] observation, on what Leichtenstern[780] called the celebrated Würzburg case, the patient had suffered many times from attacks of blood-stained diarrhœa with tenesmus, as in Zinn’s[781] case of a three year old boy who had bloody purulent diarrhœa. Schlüter[782] speaks of a hæmorrhagic enteritis produced by Strongyloides. In other cases besides diarrhœa (either with or without blood) there were noted: pains in the body (Schlüter), tenderness of the abdomen, loss of appetite, gastric troubles of a general kind, headache, giddiness, fainting attacks, anæmia (Silvestri,[783] Valdes,[784] and Trappe[785]), so that even if in isolated cases (Fülleborn[786]) symptoms are absent, some significance cannot be denied these parasites as a matter of course (Bruns,[787] Leichtenstern[788]). According to Kurlow,[789] in Siberia there is a form of sporadic bloody diarrhœa which has its origin in the presence of Strongyloides stercoralis. The parasite does not live only in the intestinal lumen, but also in the intestinal wall, where it causes abscesses, fistulæ and effusions of blood.

[779] Seifert, “Sitzungsberichte der phys.-med. Ges. in Würzburg,” 1883.

[780] Leichtenstern, Arbeiten aus d. kaiserl. Gesundheitsamte, 1905, xxii.

[781] Zinn, Berl. klin. Wochenschr., 1900, xlix.

[782] Schlüter, “Diss. Kiel,” 1905.

[783] Silvestri, see Schlüter loc. cit.

[784] Valdes, ibid.

[785] Trappe, Deutsch. med. Wochenschr., 1907.

[786] Fülleborn, Biol. Abt. d. ärztl.-Vereins in Hamburg, October 14, 1902.

[787] Bruns, Münch. med. Wochenschr., 1907, xix.

[788] Leichtenstern, Deutsch. med. Wochenschr., 1898.

[789] Kurlow, Centralbl. f. Bakt., 1902.

Diagnosis is easily made by the detection of the actively moving larvæ in the stools.

Treatment is rather difficult, as it is not always successful in getting rid of the parasites. Authors differ as to the effectiveness of extr. fil. maris. Goldmann[790] still considers this preparation as the most effective; he recommends preliminary treatment with calomel 0·2 grm. and tuber. jalapæ 0·5 grm. a day before the special treatment, which consists of gelatine capsules of 15·0 grm. extr. fil. maris (to be taken in the course of four hours); afterwards rectified oil of turpentine in gelatine capsules. The thymol treatment (vide Ancylostomiasis, p. 682), thymol alone or in combination with calomel (Schlüter,[791] Valdes,[792] Soussino,[793] Goldmann[794]), has often caused diminution of the number of larvæ, but also often remains resultless. Teissier[795] maintains that by degrees he procured complete cure by the administration of mercury in the form of blue pill. In our case neither thymol nor calomel, santonin, extr. fil. maris, decoct, rad. granat., had any result whatever. Davaine[796] believes he attained decrease and final disappearance of the larvæ by protracted milk-cure. Santonin, tannalbin and other preparations seem ineffectual. Tannin enemata (Mildner[797]), high injections with starch enemata (Schlüter[798]), may alleviate in persistent diarrhœa. Travellers who are visiting regions the native home of Strongyloides must exercise the most extreme care and scrupulous cleanliness, and these are also necessary in patients already suffering from Strongyloides, to prevent auto-reinfection (Trappe[799]).

[790] Goldmann, Deutsch. Aerzte-Zeitg., 1903.

[791] Schlüter, “Diss. Kiel,” 1905.

[792] Valdes, loc. cit.

[793] Soussino, see Schlüter loc. cit.

[794] Goldmann, loc. cit.

[795] Teissier, Arch. d. Méd. exp., 1895.

[796] Davaine, see Seifert, Deutsch. med. Zeitg., 1885.

[797] Mildner, Berl. med. Ges., July 24, 1907.

[798] Schlüter, loc. cit.

[799] Trappe, loc. cit.

*Dracunculus medinensis* (Dracontiasis).

The guinea worm develops in the dermis of human beings without any symptoms; only when it is completely grown does it form boil-like, extremely painful abscesses, in the greater majority of cases in the legs, in the region of the ankle, and is accompanied by general disturbance and a feeling of heaviness, dragging and pricking of the affected part; it occurs more rarely in the arms, certain parts of the back, the head, neck, scrotum and penis; in a superficial position the worm can occasionally be felt through the skin. In most cases there is only one worm and one abscess, but here and there one finds patients with three, four or even up to eight worms, and very exceptionally still more, as in the cases described by Poupée-Desportes[800] (fifty worms) and by Harington[801] (seventeen worms).

[800] Poupée-Desportes, see Looss, “Handb. d. Tropenkrankh.,” 1905, i.

[801] Harington, Brit. Med. Journ., 1906.

Diagnosis offers no difficulty when the worms are presenting or can be felt under the skin.

The inhabitants of the native home of the guinea worm, as a rule, quietly wait till it has got so far out that it can be conveniently grasped; it is then bound round with thread and fastened between the tips of a split piece of wood and slowly wound out. In ten to twelve days it can be wound out in this way. Emily[802] makes injections of a 1 in 1,000 solution of sublimate either in the neighbourhood of the worm or directly into its body. Mense[803] managed to remove the worm in one sitting by laying a wad of cotton wool soaked in chloroform on the exposed portion, thus stupefying it. Our therapeutic observations (Frangenheim[804]) favour the free laying open of the existing abscess and the consequent complete extraction of the worm.

[802] Emily, see Looss loc. cit.

[803] Mense, ibid.

[804] Frangenheim, Volkmann’s Samml. klin. Vorträge, 424.

Prophylaxis depends on care in the use of water in the guinea worm countries, especially dangerous being permanent waters infested by Cyclops sp.

*Filaria bancrofti.*

The parasitism of this filaria leads to the formation of lymphangitis, elephantiasis, chyluria, orchitis, chylocele, abscesses, lymphatic varices, perhaps also to chylous ascites and chylous diarrhœa.

Lymphangitis usually attacks the extremities, beginning generally with a rigor and swelling of the lymphatic vessels with adjoining lymph glands. The lymphatics become hard, knotty and extremely painful, the overlying skin red and swollen in longitudinal lines (Looss), high fever sets in with, to some extent, severe general disturbance. After some days the attack subsides, the swelling then partially disappears, but not completely, and often abscesses develop in consequence of the lymphangitis. Children, as a rule, suffer from such lymphangitic attacks (Finucane[805]).

[805] Finucane, Lancet, 1907.

Diagnosis is not easy, for many other causes frequently produce lymphangitis.

Treatment consists in rest, raising the affected limb, applications of vinegar and alum or liquor plumbi, in some cases incisions into the swollen part under antiseptic precautions.

Elephantiasis (Arabian) is usually situated in the lower extremities, in men in the scrotum and penis, in women in the labium pudendi, mons veneris, and the mammæ; more rarely it attacks the upper extremities or, indeed, the head. The disease develops during repeated attacks, which occur at irregular intervals of weeks, months or years, of fever accompanied by symptoms of lymphangitis and erysipelas (elephantoid fever), and especially as the result of different accidental occurrences such as chills, bodily exertions, external irritation. The extremities become shapeless, heavy cylinders, the scrotum occasionally a colossal tumour, the female genitalia and the mammæ smaller or larger tumours; the penis often shares in the general thickening, the inguinal glands form large hard prominent masses, and enormous deformity is caused. The cause is more often seen in men than women, rarely in children over 10, never in younger children.

Treatment of elephantiasis of the extremities consists in raising the affected part, massage, bandaging, vapour baths; the large elephantoid tumours of the genitalia and mammæ can only be treated by operative removal.

Chyluria (hæmato-chyluria), as a rule, begins by a series of attacks and often ceases for weeks or months, the attacks being accompanied by fever, pain in the back and lumbar region, about the kidneys and in the perinæum. The attacks are separated by intervals of months’ or even years’ duration, a continuous chyluria being quite rare. The disease may last many years without the constitution being markedly weakened, but in other cases anæmia and debility ensue and result in death from marasmus. In chyluria the urine becomes completely opaque like milk; but sometimes, from the presence of blood, is of a peach-like redness: the sediment contains clotted blood, and microscopically one finds fine dust-like fat granules and red cells and leucocytes, and usually, but not always, filaria larvæ. Sclerodermia may possibly be caused by Filaria (Bancroft[806]).

[806] Bancroft, Lancet, 1885.

Treatment, consists in administration of ol. santali, methylene blue (0·12 grm. dose several times daily), ichthyol (in pills from 0·5 to 1·5 grm. per day), ol. terebinthinæ (0·5 to 1·5 gr. per day), thymol (Ziemann[807] had no result from either thymol or methylene blue), together with absolute rest in bed, diminution of all fatty nourishment and administration of light purgatives.

[807] Ziemann, Deutsch. med. Wochenschr., 1905, xi.

Orchitis is in acute attacks a relatively frequent symptom in the East; the chylocele is rarely marked; the fluid usually shows numerous larvæ; in the case of abscesses they are generally caused directly by the adult parasites, as they have often been found in them; varices of the lymphatic vessels are either superficial or deep; lymphorrhagia arises from rupture of the dilated vessels; chylous ascites and chylous diarrhœa may also be produced by Filariæ.

*Loa loa.*

Loa loa, according to modern investigations, is a parasite of the subcutaneous connective tissue of man, and its appearance in the conjunctiva somewhat accidental; in earlier times it seems to have been less common (Ziemann[808]). A number of cases are seen in Europe of patients who have lived in filaria regions, and on return have been found to have this Nematode in the subconjunctival tissue. Pick,[809] in the case of a man who had lived in the Cameroons, found the parasites in active motion under the connective tissue of the eyeball right over the cornea; extraction was easy. Ziemann[810] noted three cases of Loa loa in the eye accompanied by temporary migratory swellings in different parts of the body. In one case, observed by Wurtz and Cleri[811] (a woman from the French Congo), Loa loa was the cause of intermittent elastic swellings in the subcutaneous and subconjunctival tissue (marked eosinophilia). In the case recorded by Pollack[812] (for thirty years police commissioner in the Cameroons) the worm under the connective tissue of the left eye by its snake-like movements caused an unpleasant itching. With cocaine and adrenalin the worm can be made visible, and by means of a strabismus hook can be drawn out of a small wound in the connective tissue. Martens[813] exhibited a Filaria extracted from the eyelid under local anæsthesia.

[808] Ziemann, Deutsch. med. Wochenschr., 1905.

[809] Pick, ibid.

[810] Ziemann, loc. cit.

[811] Wurtz and Cleri, Arch. Méd. expér., 1905, ii.

[812] Pollack, Berl. ophthal. Ges., May 17, 1906.

[813] Martens, Berl. med. Ges., July 24, 1907.

*Trichuris trichiura.*

Whilst many authors consider the whip-worm as a harmless parasite of the large intestine (Leichtenstern,[814] Eichhorst,[815] Askanazy[816]), the number of severe and even fatal cases of diseases caused by it (trichocephaliasis) increase so much that the Trichuris trichiura must be excluded from the group of harmless intestinal parasites. (For disturbances of the nervous system and of the blood [anæmia] from trichocephaliasis, see p. 650). Infection in human beings results from the eggs that have developed outside the body, which probably reach the digestive tract on the hands soiled with dirt or earth, or possibly through drinking water. (Moosbrugger[817] and Kahane[818] mention in their cases that the children had an absolute passion for earth-eating.) Possibly, too, patients reinfect themselves anew, as an intermediate host is not necessary.

[814] Leichtenstern, “Handb. d. Therap. v. Pentzoldt-Stintzing.”

[815] Eichhorst, “Handb. d. Spez. Path. u. Therap.”

[816] Askanazy, Deutsch. Arch. f. klin. Med., 1896.

[817] Moosbrugger, Med. Corresp.-Bl. f. Württemburg, 1890.

[818] Kahane, Korrespondenzbl. f. Schweiz. Aezte, 1907, viii.

The anterior part of the body of the parasite is usually fixed in the mucous membrane, and according to Askanazy feeds on the blood of its host. Moosbrugger,[817] Schulze,[819] Kahane,[818] Vix,[820] Girard[821] and Blanchard[822] all found changes in the mucous membrane of the gut, showing that the parasites had been in the gut for a considerable time. Kahane[818] had an opportunity of seeing at the Pasteur Institute Trichocephali with the anterior part of the body penetrating not only the mucosa but also deep into the muscularis of the gut wall. From this mode of attachment to the wall it is easily understood how Trichocephali, especially when they are numerous in the gut, cause local irritation and inflammatory conditions consisting of frequent attacks of diarrhœa, sometimes twenty times a day, lasting for months, resisting all remedies, and often accompanied by colicky pains and symptoms of peritonitis. The stools often have blood mixed with the fluid, very glassy, jelly-like mucus, more or less abundantly as in the cases of Moesasca, Moosbrugger,[817] Kahane,[818] Girard,[821] Poledne,[823] and Rippe.[824] Nausea and vomiting are rarer symptoms.

[819] Schulze, Deutsch. med. Wochenschr., 1905.

[820] Vix, Zeitschr. f. Psychiat., xvii.

[821] Girard, Annal. d. l’Inst. Pasteur, 1901.

[822] Blanchard, Acad. de Méd., July 3, 1906.

[823] Poledne, Wien. med. Wochenschr., 1906.

[824] Rippe, St. Petersb. med. Wochenschr., 1907.

Diagnosis as a rule can only be made by microscopical examination of the stools; together with the eggs, regular and beautifully formed Charcot-Leyden crystals occur.

The prognosis is unfavourable in severe infections, in slighter cases, where only a few worms are present, the danger of important symptoms is less. Treatment consists in administration per os of vermicides and in local treatment of the large gut. A remedy which was once much used was calomel, which is much lauded by Gibson and given as follows: calomel 0·06 grm., rheum. 0·3 grm., tinct. ferri sesquichlor. 1·2 c.c., aq. dest. 90·0 grm., six dessert-spoonfuls three times daily. Rippe appears to have got no result from the use of this prescription. Thymol, especially in conjunction with local treatment of the large intestine, had unquestionably some effect in certain cases, such as those of Girard, Poledne, Hausmann, Kahane and Schiller. The local treatment of the large bowel is most effectual when high injections of water and benzine are given. Becker[825] obviously used too much benzine (1 dessert-spoonful to 1 litre of water), for severe irritation was set up, whilst Peiper[826] used only a few drops of benzine, 5 drops to 1 litre of water being enough (Schiller). Instead of benzine enemata, garlic, 1 per cent. thymol solution, and physiological saline injections have been used, but the benzine enemata seem to be far and away the most effective. In Schiller’s case 2,000 worms came away on the first day as the result of such a combined treatment (thymol internally and benzine enemata).

[825] Becker, Deutsch. med. Wochenschr., 1902.

[826] Peiper, quoted by Seifert, loc. cit., p. 248.

Trichinella spiralis.

Trichinosis is, happily, becoming so much rarer that many doctors get no opportunity, either in their student days or in private practice, of seeing this severe disease; we ourselves remember having observed one typical case of a peasant, aged 17, from Metz in Med.-Rat Merkel’s clinic in Nuremberg in the year 1879. In the description of the disease we follow Merkel’s[827] observations.

[827] Merkel, “Handb. d. Therap. v. Pentzoldt-Stintzing,” i.

The eating of flesh containing Trichinæ is often followed, if not invariably so, by gastric disturbances of different kinds, especially by vomiting and diarrhœa, with colic, great muscular fatigue, œdema of the eyelids, muscular swellings with hardness and extreme painfulness, disturbance of ocular movements, of deglutition and of breathing, hoarseness, aphonia, intestinal hæmorrhage, bleeding of the nose, ecchymosis of the skin and mucosæ, prurigo, herpes, miliaria, pustules, boils, severe sweating, œdema of the extremities, and, finally, desquamation of the skin; more rarely there is considerable decubitus, bronchial catarrh, hypostatic and catarrhal pneumonia, with dry and purulent pleurisy, and in severe cases symptoms of collapse with delirium close the scene. Slight cases last from three to six weeks, severe ones for several months, and in the latter convalescence is very slow. It is remarkable that in cases of trichinosis of long duration, cancer of the breast was observed at the same time (Klopsch,[828] Langenbeck,[829] Babes[830]). Death during epidemics occurred in 30 per cent. of all cases. The disease begins generally from one to ten days after eating trichinous flesh, yet there have been cases noted in which the disease began several weeks after.

[828] Klopsch, quoted by Babes.

[829] Langenbeck, ibid.

[830] Babes, Centralbl. f. Bakt., 1906, xlii.

Diagnosis in the presence of several cases, or in epidemics, is not difficult, but in isolated cases, on the other hand, it is not easy. If there is a suspicion of trichinosis, from the muscular fatigue and the œdema of the eyelids, the diagnosis can be made by excision of a piece of muscle and by finding the Trichinæ in the tissue, taken with the results of the examination of the previously eaten sausage or meat. In contradistinction to this circumstantial process, there is the examination of the blood, which, according to Schleip[831] (Homburg trichinosis epidemic, August 19 to 26, 1903, 130 cases), is the most valuable method of diagnosing trichinosis when the Trichinæ have not yet penetrated the muscles, for a blood examination shows a large increase in the numbers of the eosinophile cells; Stäubli detected his seven cases in this way, four of the severe ones showing a marked hyperleucocytosis, and a combination of Kernig’s sign with absence of the patellar reflex. On account of the rarity of these two signs in combination in other infective diseases, they have a certain diagnostic value. Stäubli[832] also observed in trichinosis the constant appearance of a remarkably strong positive diazo-reaction of the urine.

[831] Schleip, Deutsch. Arch. f. klin. Med., lxxx.

[832] Stäubli, ibid., lxxxv.

Prophylaxis in trichinosis is fully considered under Trichinella spiralis (p. 429).

Treatment consists in those cases where it is known that trichinous flesh has been swallowed in the first place of washing out the stomach, but still more in a thorough evacuation of the bowels, for which calomel (0·5 grm.), ol. ricini (a dessert-spoonful till the action becomes marked), infusion of senna with sulphate of magnesia and large enemata are employed, and should be repeated at intervals during the first few weeks. Alcohol (cognac up to 250 c.c. a day) is recommended by some, also glycerine (150 grm. at a dose) and large doses of dilute hydrochloric acid. Beside these, a large number of other remedies are recommended, of which, perhaps, benzine and thymol, especially in the form of enemata, are worthy of notice.

When the disease is fully developed the treatment should be symptomatic; a protracted practically continuous luke-warm bath is especially useful.

Eustrongylus gigas.

Eustrongylus gigas is most frequently found in the pelvis of the kidney. Infection in the majority of cases leads to pyelitis. The inflammation extends to the capsule from the pelvis, resulting in a purulent nephritis. In infections of longer duration, the affected kidneys become changed into so-called kidney sacs, while the kidney itself continuously shrinks. Owing to the worm fixing its posterior end in the ureter, and owing to an inflammatory swelling of the mucosa of the ureter, the passage of urine becomes very difficult.

The symptoms resemble those caused by a foreign body, e.g., kidney pain, suppression of urine, dysuria, discharge of blood and pus with the urine. But these symptoms are not sufficient for a diagnosis; this can only be established by finding eggs or the parasite itself in the urine.

Moscato[833] records a case with chyluria, pain in the region of the right kidney, and hysterical symptoms. During an hysterical attack a specimen of Eustrongylus gigas was discharged in the urine, and the chyluria and nervous affections disappeared. In a case described by Stuertz[834] of an Australian with chyluria due to Eustrongylus gigas the chyluria had existed for seven years. In the urine the eggs of Eustrongylus gigas were found. The cystoscopic examination showed that turbid urine was discharging from the left ureter. Nephrectomy was considered.

[833] Moscato, quoted by Predtetschensky, Zeitschr. f. klin. Med., xl.

[834] Stuertz, Ges. d. Charité-Aerzte in Berlin, June 26, 1902.

*Ancylostoma duodenale* (Ancylostomiasis).

Whilst up to quite modern times it has been generally maintained that the great majority of worm diseases cause more or less marked symptoms, the exact investigations of the last few years have made it plain that the great majority of people with worms are not only perfectly healthy, but the most careful clinical observations show no single sign of any ill-effect of the intestinal parasites on the health of the host (Löbker and Bruns[835]). If infection has led to the development of only a few ancylostomes, then injury to the general health is, as a rule, scarcely noticeable. In order to produce severe illness the presence of several hundred worms in the intestine is necessary, and in general the intensity of illness varies in exact proportion to the number of worms. Then the duration of the infection comes into play: the longer the human organism is submitted to the injurious effect of the parasite, the clearer is the effect on the host. Besides, the resistance of the individual has to be considered. Whilst a more robust person can harbour without ill-effect for a longer time a larger number of ancylostomes, the symptoms of the disease become more markedly and much sooner apparent in weakly persons or in those weakened by other diseases.

[835] Löbker and Bruns, Arb. aus. dem. kaiserl. Gesundheitsamte, 1906, xxiii.

The first symptom is disturbance of the digestive system; more often there is a feeling of pain in the epigastrium, more severe upon pressure, heartburn, nausea, vomiting of mucus or food at different times of the day (occasionally ancylostome ova have been found in the vomit). Whether the eggs which reach the frontal sinus with the vomit can develop into larvæ there is questionable, but the records of v. Ziemssen[836] and Huppertz,[837] to the effect that in some instances ancylostomes have been discharged from the frontal sinus, are of interest. The five cases recorded by the latter had a fatal termination from œdematous swellings of the face with severe inflammation of the meninges. The tongue is furred, and extensive catarrhal stomatitis and ptyalism are recorded. The appetite is variable, increasing or diminishing, there is loathing of nourishment or a marked longing for acid food and unripe fruit, whilst ordinary meals are rejected. At first there is often constipation, later diarrhœa with abundant mucus, and often blood in the stools; microscopically eggs and Charcot-Leyden crystals were found.

[836] v. Ziemssen, quoted by Haenisch, “Diss. Strasburg,” 1901.

[837] Huppertz, quoted by Haenisch, “Diss. Strasburg,” 1901.

In the further course of the disease symptoms due to increasing anæmia predominate; the hæmoglobin of the blood diminishes from one-fourth to one-fifth of the normal (Baravalle[838]), the eosinophile cells increase considerably (Boycott,[839] Lohr[840]), yet in regard to diagnosis eosinophilia cannot be regarded as of equal value to a microscopical examination of the fæces (Bruns, Liefmann, and Meckel[841]). The disturbances of the circulatory system take the form of more or less severe palpitation, pain in the region of the heart, quick pulse, œdema of the eyelids, of the face, of the lower limbs, and even of the whole body. Disturbance of the sexual functions (impotence, irregular menstruation, delayed onset of puberty) are not infrequently observed.

[838] Baravalle, Progresso medico, 1903.

[839] Boycott, Journ. of Hygiene, 1904.

[840] Lohr, Zeitschr. f. Heilk., xxvi.

[841] Bruns, Liefmann and Meckel, Münch. med. Wochenschr., 1905.

Infection in human beings takes place by the mouth, if uncleansed vegetables are eaten--in Japan especially, where human fæces are used--and articles of food are not sufficiently carefully cleaned (Inouye[842]), or from putting food into the mouth with dirty hands. Looss[843] does not think that drinking water is dangerous as a rule, for the larvæ sink to the bottom in standing water, and are only brought to the top by shaking. Looss has done most valuable service by discovering that infection can arise also through the skin. During the last few years so many authors have confirmed this at first doubted source of infection, that one must accept this source of infection now, even though it is undecided which mode of infection is the more prevalent, by the mouth or through the skin. Some authors have described the changes induced in the skin by the penetration of the larvæ; for instance, Looss and Schaudinn,[844] itching papules in their own skin, and Dieminger[845] a skin affection in the Graf Schwerin mine which was called the “Schweriner itch,” and a skin affection not unlike scabies in the tea plantations of Assam and South America; pani-ghao (water itch) (Dubreuilh[846]); the penetration of the larvæ through the skin also explains the frequent appearance of boils and itching purulent eczema in miners in infected pits (Goldmann[847]).

[842] Inouye, Arch. f. Verdauungs Krankh., 1905, xi.

[843] Looss, “Handb. f. Tropenkrankh.,” v. Mense, i, p. 129.

[844] Schaudinn, Deutsch. med. Wochenschr., 1904.

[845] Dieminger, Klin. Jahrb., 1905, xiv.

[846] Dubreuilh, La Presse méd., 1905, xxx.

[847] Goldmann, Wien. med. Presse, 1905, ii.

The absolute diagnosis of ancylostomiasis depends on the detection of the ancylostome eggs in the fæces, and presents no difficulties.

Prophylaxis is of the greatest importance, especially to miners. The spread of ancylostomiasis seems to depend only on fæces deposited in damp places, so that on the one hand the deposition of fæces must be prevented, and on the other the fæces must be rendered as far as possible harmless; in addition, there is the individual prophylaxis.

General prophylaxis requires:--

(1) Examination immediately for ancylostomes of miners seeking work and of those newly taken on five to six weeks after.

(2) Indentured workers who are infected with worms are not allowed to work underground until a medical certificate in writing is brought to the effect that they are no more infected with eggs (the same procedure applies to workmen in brick kilns) (Goldmann[848]).

[848] Ibid., “Die Hygiene des Bergmannes.” Halle: W. Knapp, 1903.

(3) Indentured workers infected with worms must submit themselves to the prescribed treatment, and after its completion further submit their stools to three examinations at intervals of about four weeks.`

(4) Special supervision of miners and brick-makers coming from the Italian frontier.

(5) Workmen must be given instructions, both by word of mouth and in writing in their mother tongue, as to the infectivity and danger of ancylostomiasis both to themselves and others.

(6) Orders are to be given as to washing, baths, and changing of clothes at the end of the work.

(7) During the hours of working in the pits, taking of food is strictly forbidden without thorough and entire washing.

(8) All privies must be so arranged that the vessels used for the reception of the excreta must not leak, must be protected by a cover, and easily transportable. The emptying of these vessels must be carried out in specially constructed impenetrable pits.

(9) Defæcation in any other place than a privy is forbidden (alike for miners and brick-makers).

(10) The manure of horses used in the mines is to be regularly removed; possibly infection takes place in this way also. [This is impossible.--J. W. W. S.]

How far it is possible to disinfect a mine already severely infected is a matter of question; Tenholt,[849] Goldmann,[850] and Dieminger[851] recommend washing out with freshly prepared lime water with the addition of caustic soda; Calmette[852] and Manouriez[853] spraying with salt water. Theoretically spraying with hot water or steam should be done every now and again for the destruction of the larvæ (Looss[854]). Personal prophylaxis is partially included in the general prophylaxis in so far as it is a case of oral infection, but something more can be done for the individual to avert the danger of cutaneous infection. According to Manson[855] it is advisable in the tropics to cover the naked hands and feet with green Barbados tar, and the tarred parts thickly with flour; Fabre[856] recommends that miners who might come in contact with infected water should anoint the unprotected parts (hands and feet), as then the larvæ cannot penetrate the skin; this last procedure can easily be carried out on account of its simplicity and cheapness.

[849] Tenholt, Münch. med. Wochenschr., 1905.

[850] Goldmann, Wien. med. Wochenschr., 1905, x.

[851] Dieminger, loc. cit.

[852] Calmette, Acad. de Méd., July 25, 1905.

[853] Manouriez, Bull. de. l’Acad. de Méd., 1905.

[854] Looss, Zeitschr. f. klin. Med., 1905, lviii.

[855] Manson, Brit. Med. Journ., November 5, 1900.

[856] Fabre, Progrès méd., 1905.

Among the usual remedies for the expulsion of ancylostomes thymol certainly comes first, introduced by Bozzolo[857] and since used by many other authors, partly with good and partly with less good results. The day before the beginning of treatment one should endeavour to procure a thorough evacuation of the bowels by means of calomel (Lutz,[858] Grünberger,[859] Smith[860]) or cascara sagrada (Mann[861]), only fluid food should be taken the evening before, and on the day of treatment thymol is given in a quantity of 6, 8, 10 or 15 grm., in single doses of 2 grm. with one or two hours’ interval, and some hours after an aperient. As a rule, one day of this treatment is not enough. (Prowe[862]), but one is compelled to repeat it on two consecutive days, or even oftener, with subsequent intervals of many days. Thymol is either given in wafers, gelatine capsules or mixed with sugar. Caution should be used in giving brandy at the same time or[sic] bodies which dissolve thymol (oil, fat) and thereby considerably favour its absorption. It has been shown in many cases from toxic phenomena that thymol is by no means an indifferent drug; violent burning in the stomach and alimentary canal, lowering of the temperature, shortness of breath and feeble pulse, giddiness, delirium and fainting have all been observed. Sandwith[863] and Thornhill,[864] as well as Leichtenstern,[865] even record cases of death after the use of thymol; 4 grm. thymol caused severe symptoms of poisoning in Grünberger’s[866] case. The black colour of the urine (thymoluria) which so often sets in after the first dose is quite harmless, and is no contra-indication to the continuance of the cure. Now and again there are traces of albumin in the urine, but it is very seldom there is any severe acute inflammation of the kidneys. Thymol is contra-indicated in advanced old age and in debility, also in cases with a tendency to vomiting, in gastritis, dysentery, heart or kidney affections.

[857] Bozzolo, Giorn. del R. Acad. d. Med. di Torino, 1881.

[858] Lutz, Centralbl. f. Bakt.

[859] Grünberger, Wien. med. Wochenschr., 1902, lii.

[860] Smith, Amer. Journ. Med. Sci., 1903.

[861] Mann, Deutsch. Arch. f. klin. Med., lxxiv.

[862] Prowe, Virch. Arch., clviii.

[863] Sandwith, quoted by Looss.

[864] Thornhill, ibid.

[865] Leichtenstern, Deutsch. med. Wochenschr., 1887.

[866] Grünberger, loc. cit.

The combination recommended by Goldmann[867] under the name of taeniol, already mentioned under the treatment of tapeworms, and which consists of thymol, sebirol and salicylate, appears also to render good service in the treatment of ancylostomiasis (Goldmann[868] and Liermberger[869]).

[867] Goldmann, Ges. f. innere Med. in Wien, March 8, 1906.

[868] Goldmann, Wien. med. Wochenschr., 1905, x.

[869] Liermberger, Berl. klin. Wochenschr., 1905.

A carbonate of thymol, thymotal, from which thymol separates off in the intestine, is given three to four times a day, in doses of 3 grm. per diem (children up to 1·0 grm.) on four consecutive days, and at the end of the treatment a purge (Pool,[870] Bauer[871]); Leonardi[872] speaks well of thymol essence (4·0 c.c. per diem) in an emulsion with plenty of water.

[870] Pool, Med. Woche, 1901.

[871] Bauer, Wien. klin. Wochenschr., 1904.

[872] Leonardi, Gaz. d. Osp., 1904.

The next drug for the expulsion of ancylostomes is extractum filicis maris, which is to be employed as in tapeworm treatment, but has not always had the desired result, whilst in such cases as resist the fern extract, thymol attains the desired effect (Mann[873]), whilst the reverse is frequently observed (Grünberger[874]). Nagel[875] prescribes extr. fil. 8 to 10 grm., chloroform 10 to 15 drops, syr. sennæ 16 grm.; before taking, the glass must be placed in hot water, otherwise the contents will not pour freely. Zinn[876] prefers extract. filicis maris (freshly prepared) to all other drugs. Warburg[877] considers the treatment with extr. fil. to be all the more certain the more thoroughly the preliminary treatment is carried out. Filmaron 0·7 grm., thymol 5·0 grm., chloroform 1·5 grm., ol. ricini 20·0 grm. gave good results after being given two to three times (Nagel[878]). Opinions are divided as to the combination of thymol and extractum filicis maris (Hynek,[879] Stockman,[880] Boycott and Haldane,[881] Adams[882]). As regards other remedies, eucalyptus oil is well spoken of by Philips[883] and Hermann[884]: ol. eucalypti 2·0 grm., chloroform 3·0 grm., ol. ricini 30·0 grm., to be taken at one time or in three separate doses in the morning (on the previous evening a saline purgative). Neumann[885] recommends podophyllin, to be taken twice on three consecutive days in doses of 0·035 grm. Podophyllin appears to produce quite a peculiar condition of the intestinal mucosa which is very prejudicial to the Ancylostoma adhering to it. Bentley[886] regards β-naphthol as the best drug; after previous examination of the bowels he gives it two or three times at two-hourly intervals, in doses up to 1·0 grm. (Vide also the Appendix, p. 754, for other drugs.) For the treatment of the anæmia, which often persists very obstinately, good and abundant food, iron and arsenic preparations, Levico water (Goldmann,[887] Liermberger[888]) are suitable.

[873] Mann, loc. cit.

[874] Grünberger, loc. cit.

[875] Nagel, Deutsch. med. Wochenschr., 1903.

[876] Zinn, “Therap. der Gegenwart.,” 1903.

[877] Warburg, Münch. med. Wochenschr., 1904.

[878] Nagel, loc. cit.

[879] Hynek, Sbornik Kliniky, v.

[880] Stockman, Brit. Med. Journ., 1904.

[881] Boycott and Haldane, Journ. of Hyg., ix.

[882] Adams, Arch. of Pediat., 1901.

[883] Philips, Lancet, 1906.

[884] Hermann, La méd. moderne, 1905.

[885] Neumann, Deutsch. med. Wochenschr., 1904.

[886] Bentley, Indian Med. Gaz., 1904.

[887] Goldmann, Deutsch. Aerzte-Zeitg., 1903.

[888] Liermberger, loc. cit.

*Ascaris lumbricoides* (Ascariasis).

Ascaris lumbricoides is one of the most frequent parasites that occur in man, both in adults as well as in children; as a rule, indeed, it most frequently infects children of medium age. The normal situation is the small intestine; this, however, is frequently left, and the Ascarides travel into the stomach, œsophagus, pharynx, bronchi, the nasal cavities and still other regions. It is a peculiarity of the Ascarides that they are prone to glide into narrow canals; for example, Clason[889] records that in the case of an idiot whose custom it was to swallow glass beads, the Ascarides showed a predilection for sticking in the beads and were passed in the fæces. The disturbances which Ascarides occasion in the intestine itself vary; isolated species do not give rise to any symptoms at all, whereas a large number may eventually give rise to severe local symptoms, or those of a toxic or reflex nature which have been discussed in the General Section.

[889] Clason, see Seifert, Deutsch. med. Zeitg., 1885.

Among the local symptoms are the following: loss of appetite, excessive appetite, perverted sense of taste, fœtid breath, sensitiveness to pressure over the abdomen, colicky pains and irregularity of the bowels. The appearance and state of health suffer; the patients, children in especial frequency, become remarkably pale; their complexions undergo rapid change, and rings of grey or bluish-brown are seen about the eyes. Children may become so reduced by this rare condition, enteritis verminosa, due to Ascarides in large numbers, that suspicion of the existence of intestinal tuberculosis arises. Emaciation to a skeleton, excessive meteorism, and evacuations of thin gruel-like stools, sometimes blood-stained, are observed in these cases. Even in the case of adults, chronic uncontrollable vomiting with severe inanition due to the Ascarides has been observed. When the Ascarides escape spontaneously per anum, they frequently cause an exceedingly troublesome irritation in the anal region (pruritus ani).

The most disagreeable symptoms and those most dangerous to life arise from the migrations of Ascarides when they invade the bile-ducts; no inconsiderable number of cases of this kind are recorded in the literature (summarized, up to the year 1901, in Sick’s[890] Dissertation). Penetration post mortem (or shortly before death) of the worms into the bile-ducts cannot be considered as a rarity; the laxity of the muscular orifices easily allows of this invasion also in other directions on the part of the parasite in its escape from the body of its dead host. The occurrence of the worm in the biliary passages in the living is to be regarded as still less frequent, but nevertheless often enough according to the records in literature. Sick[891] was able to collect as many as sixty-one such cases, to which he added two further fresh cases from the Tübingen clinic, that is, from the material provided by his father. In the year 1891 Borger[892] collected fifty-nine cases relating to the invasion by Ascaridæ of the bile-ducts and passages, and Dauernheim’s[893] Dissertation treats of this question as well. A further case of Ascaris in the ductus choledochus (choledochotomy) is recorded by Neugebauer.[894] In the case of Schupper[895] (woman, aged 52), all the biliary passages were distended and filled with fourteen living Ascaridæ (perhaps as they were living they had not led to a septic infection of the biliary passages); in the case communicated by Schiller,[896] an Ascaris had gained access to the biliary passages after an operation for cholelithiasis (with distension of the gall-bladder and formation of a fistula); it had kept itself alive here eighteen days and was extracted from the fistulous opening. Epstein[897] confirms the correctness of the explanation of the mark of strangulation in an Ascaris in Mertens’[898] case (in a woman, aged 30, there was first icterus, later ascites, anasarca, swelling of the liver, then the discharge of two dead Ascaridæ, one of which exhibited a constriction somewhat behind its centre; after that there was rapid improvement in all the symptoms); in his case there was icterus in consequence of closure of the ductus choledochus by an Ascaris. After the discharge of the worm the symptoms persisted; one of the Ascaridæ had a typical strangulation mark. From the observation recorded by Vierordt[899] it follows that, without doubt, mature females can penetrate into the liver and there deposit eggs; in addition, that such eggs appear exceptionally to undergo segmentation. A unique feature in this case consisted in the exclusive discharge of immature worms almost regularly throughout an interval of nine weeks; this cannot be explained from our present knowledge of the biology and pathology of the Ascaridæ. These worms clearly make their way from the intestine outwards, through the opening into the duodenum of the common bile-duct, and unquestionably the fully developed Ascarides, with the aid of their conical head end, are enabled gradually to penetrate the wall of the ductus choledochus (Quincke[900]), and gain access to the gall-bladder, the hepatic duct and its branches.

[890] Sick, “Diss. Tübingen,” 1901.

[891] Sick, ibid., 1901.

[892] Borger, “Diss. München,” 1891.

[893] Dauernheim, “Diss. Giessen,” 1900.

[894] Neugebauer, Arch. f. klin. Chir., 1903, lxx.

[895] Schupper, Gaz. d. Osp., 1904, xxxiii.

[896] Schiller, Beitr. zur klin. Chir., 1902, xxxiv.

[897] Epstein, Deutsch. Arch. f. klin. Med., 1904, lxxxi.

[898] Mertens, Deutsch. med. Wochenschr., 1898, xxiii.

[899] Vierordt, Volkmann’s Samml. klin. Vortr., No. 375.

[900] Quincke, “Nothnagel’s Spez. Path. u. Therap.,” 1899, xviii.

The changes in the biliary passages and the liver are, on the one hand, the mechanical results of a partial or total obstruction to the flow of the bile, and, on the other, of inflammatory processes. The blocking of the common bile-duct and of the trunk of the hepatic duct leads to the well-known symptoms of biliary engorgement; protracted continuance of this condition has, as its sequela, general distension of the whole biliary system and degenerative destruction of the liver-cells. If the Ascaris is situated at some other part of the biliary system, its presence causes a partial arrest of the flow of bile, with the corresponding sequelæ. Many Ascarides perish in the ductus choledochus, and here and in the gall-bladder they may supply the nucleus of a gall-stone; deeper in the liver this does not appear to happen; the dead Ascaridæ here undergo a kind of maceration, disintegrate, and may be completely absorbed; in many cases the worms continue to live for a very long time in the biliary passages. When the worms infect the biliary passages through the invasion of intestinal bacteria, liver abscesses arise (Dauernheim,[901] Saltykow[902]). Leer[903] goes so far as to maintain that Ascaridæ may be the second most frequent cause of liver abscesses. That Ascaris in the pancreas may simulate liver abscess in a remarkable fashion is shown by Vierordt’s[904] observation, which is quite unique, while Ascaridæ have been found to occur in isolated instances in the excretory ducts of the pancreas and in its branches, where they have remained living for a long time.

[901] Dauernheim, loc. cit.

[902] Saltykow, Prag. Zeitschr. f. Heilk., 1900.

[903] Leer, Brit. Med. Journ., 1906.

[904] Vierordt, loc. cit.

It is no rare occurrence for Ascaridæ, in consequence of their migration into the stomach, to be ejected by the act of vomiting, and in such way to gain access into the upper air passages, or to find their way during sleep into the nose or accessory sinuses (Mosler and Peiper[905]) without giving rise to special symptoms. For example, Troja[906] found in the frontal sinus of a cadaver a large coiled-up Ascaris which occupied the whole cavity. Wrisberg[907] made the same observation in the cadaver of a boy. Deschamps[908] and Fortessin[909] mention an Ascaris being met with in the antrum of Highmore. Observations of the discharge of living or dead Ascarides from the nose are frequently recorded. To this class belongs the case mentioned by Albrecht,[910] in which an Ascaris was removed from the nose of a girl, aged 7; also the case recorded by Benievini,[911] from the nose of one of whose friends a worm escaped; he had suffered from the most violent headaches, fainting fits, dimness of vision and vomiting; after the escape those untoward symptoms disappeared. Similar records have been made by Forest,[912] Lanzoni,[913] Langelott,[914] Tulpe,[915] Reisel,[916] Fehr,[917] Bruckmann,[918] Bahr,[919] Slabber,[920] Lange,[921] and Chiari.[922] A rarer case is that recorded by Haffner,[923] that of a child, aged 4, in whom an Ascaris reached the nasal cavity through the act of vomiting, and from there it gained access through the naso-lachrymal duct and the inferior lachrymal sac into the lower punctum lachrymale, from which half of it protruded.

[905] Mosler and Peiper, “Nothnagel’s Handb.,” 1894, vi.

[906] Troja, Napoli, 1771.

[907] Wrisberg, see Blumenbach, Göttingen, 1907.

[908] Deschamps, see Blass, “Diss. Strasburg,” 1902.

[909] Fortessin, see Bardeleben, “Lehrb. d. Chirurgie,” 1875.

[910] Albrecht, Commer. Noricum. T. I. Annal., 1739.

[911] Benievini, “Prol. Anat. d. Sin. front.,” Göttingen, 1779.

[912] Forest, see Tiedemann, Mannheim, 1844.

[913] Lanzoni, idem.

[914] Langelott, idem.

[915] Tulpe, idem.

[916] Reisel, idem.

[917] Fehr, idem.

[918] Bruckmann, Commer. Noric., 1739.

[919] Bahr, idem.

[920] Slabber, idem.

[921] Lange, “Blumenbach’s Med. Bibl.,” Göttingen, 1788.

[922] Chiari, “Krankh. d. Nase,” 1902.

[923] Haffner, Berl. klin. Wochenschr., 1880.

Among the rarer causes of the occurrence of strange bodies in the pharynx and naso-pharyngeal cavity, Jurasz[924] mentions in the first place vomiting, which may afford opportunity for the more solid bodies of the stomach contents, and even parasites of the digestive tract, especially Ascaridæ, to become firmly lodged in the pharyngeal or naso-pharyngeal cavity. Ascaridæ may obtain access from the naso-pharyngeal cavity to the middle ear by way of the Eustachian tube, as has been observed by Reynolds[925] and Wagenhäuser[926]; in the case recorded by Turnbull[927] (girl, aged 8, with pains in her ear) the Ascaris apparently reached the external auditory meatus by the same route.

[924] Jurasz, Heymann’s “Handb. d. Laryngol. u. Rhinol.,” iii.

[925] Reynolds, Lancet, 1880.

[926] Wagenhäuser, Arch. f. Ohrenheilk., 1889, xxvii.

[927] Turnbull, Virchow-Hirsch Jahresbericht, 1880.

The irritation of the larynx and air passages by Ascaridæ is far more dangerous than their penetration into the nose and naso-pharyngeal cavity, because not only are attacks of suffocation, but sudden suffocation thereby induced. Oesterlein[928] records a fatal attack of choking from Ascaridæ in the trachea. In a case recorded by Smyly[929] of a boy, aged 3-1/2, tracheotomy for extreme asphyxia was performed without relief. At the post-mortem the cause of the asphyxia was found to be an Ascaris in the trachea. Fürst[930] collected twenty-five observations of invasion of the larynx and trachea by Ascaris. Mosler[931] reports the case of a patient with aphonia and dyspnœa from whose larynx an Ascaris was removed. Donati[932] reports a case of four Ascarides in the larynx, and Cerchez[933] of asphyxia from Ascarides in the larynx or trachea. Wagner[934] records the case of a boy, aged 8, in whom a coil of worms was ejected from the stomach by vomiting; the mass blocked the entrance to the larynx and led to death from suffocation. A case similar to that recorded by Smyly is communicated by Rabot[935]; it was that of a child who underwent tracheotomy for diphtheria, and who was not relieved by the operation; when, however, an Ascaris appeared in the cannula and the parasite was removed the child breathed well. In Negresco’s[936] case, that of a boy, aged 3, an Ascaris gained access to the larynx and from there into the trachea, and a fatal issue from asphyxia resulted.

[928] Oesterlein, Deutsch. Klin. 1851.

[929] Smyly, Dubl. Journ., 1867.

[930] Fürst, Wien. med. Wochenschr., 1879.

[931] Mosler, quoted by Liesen.

[932] Donati, Ann. Univ. de Méd. et Chir., Milano, 1875.

[933] Cerchez, Clinica, 1891, iv.

[934] Wagner, Deutsch. med. Wochenschr., 1902.

[935] Rabot, Soc. de Sci. méd. de Lyon, September 9, 1904.

[936] Negresco, Soc. de Méd. légale, November 9, 1903.

The route by which Ascaridæ obtain access to the urinary passages must remain undecided. Schlüter[937] treated a woman, aged 60, with retention of urine. Upon catheterization the hinder end of an Ascaris hung out from the catheter opening; the anterior end was fixed in the tube and the lumen was obstructed. Perhaps in the female sex Ascaridæ travel from the gut into the vulva and from there into the bladder, as they have already been observed in the vagina, where they cause troublesome symptoms (pruritus pudendi).

[937] Schlüter, Münch. med. Wochenschr., 1902.

The diagnosis of ascariasis is not in general difficult; now and then the worms are discharged spontaneously; if not, the ova, which cannot be mistaken, can easily be detected in the fæces upon microscopical examination. Epstein’s[938] method--namely, on every occasion to obtain fresh material for examination--is much to be recommended. This consists in introducing a Nelaton’s catheter into the rectum with a rotatory motion and then drawing it out. A small portion of fæces forced into the catheter opening is more than sufficient to demonstrate the presence of ova of the parasites upon microscopical examination of a preparation.

[938] Epstein, see Seifert, “Lehrb. d. Kinderkrankh.,” p. 273.

In spite of all pressure on the part of relatives, treatment directly against Ascaridæ should not be carried out until the diagnosis is certain.

As regards prophylaxis, much can be done by not throwing the worms, when expelled, on to the dung-hill or into the privy, but straightway into the fire. Metschnikoff[939] has issued a warning against the consumption of unboiled or badly washed vegetables, salad, strawberries, etc., and also against drinking polluted water.

[939] Metschnikoff, Gaz. hebd. de Méd. et Chir., 1901.

For the expulsion of the worms flores cinæ were formerly considered the most useful means; now, however, santonic lactone--santonin--which is prepared from them, is almost universally preferred. By many, especially in practising among children, flores cinæ are still recommended in the form of Störk’s worm electuary (consisting of flores cinæ, rad. jalapæ, valerian and oxymel simplex). Guermonprez[940] recommends them because he thinks that santonin only excites the worms and consequently causes unpleasant symptoms. Besides, in the form of the above-mentioned electuary, flores cinæ can also be given several times daily with raspberry jelly up to 0·5 grm. to 2 grm. (children and adults).

[940] Guermonprez, see Seifert, Deutsch. med. Zeitg., 1885.

Santonin is prescribed either in single doses from 0·03 to 0·05 to 0·1 grm. with sugar in the form of powder, or else in oily solution. When given in the latter form the absorption of the santonin in the stomach is excluded and the whole quantity introduced is thus enabled to reach the worms in the intestinal canal. Küchenmeister[941] has already recommended combination of santonin with ol. ricini. Lewin,[942] however, states that ol. morrhuæ, ol. olivarum, ol. cocos and ol. cinæ can also be taken. In prescribing santonin in oily solution Henoch[943] also prefers the combination with ol. ricini. According to Lewin’s direction the prescription would run as follows:--

℞ Santonin 0·2 grm. Ol. ricini. 20·0 grm. Ol. cinæ æth. gtt. iv.

M., d.s. S., one tablespoonful to be taken two to three times.

[941] Küchenmeister, loc. cit.

[942] Lewin, see Seifert, Deutsch. med. Zeitg., 1885.

[943] Henoch, idem.

If the patients should manifest a repugnance to castor oil, Starke’s ricinus paste may be selected:--

℞ Santonin 0·2 grm. Ol. ricini 20·0 grm. Ol. cinæ æth. gtt. iv. Sacch. albi. q.s.

Pasta moliis. S., to be used for two days.

If necessary the first-mentioned mixture might be given in gelatine capsules. Small children should be given 0·025 grm. santonin in warm olive oil slightly sweetened with sugar (a teaspoonful) in the morning; if in the course of the forenoon specimens of Ascaris escape, a second dose should follow in the afternoon about two hours after the meal. Older children should be given santonin in combination with castor oil or calomel:--

℞ Santonini 0·01 to 0·02 to 0·03 grm. Calomelan 0·025 grm. Sacch. albi. 0·5 grm.

M.f.p. D. tal. dos. x. S., one powder about six, seven, and eight o’clock on three consecutive days.

As santonin causes slight toxic symptoms such as urticaria, vomiting, retention of urine, headache, vertigo, yellow vision (xanthopsia), it is in every case advisable to follow with a laxative to expel the drug from the body as speedily as possible. The urine is coloured yellow from one to two days and assumes a scarlet red colour upon the addition of alkalis; this, however, soon disappears, while it persists in the case of rhubarb and senna.

In the place of santonin iodoform in the form of a powder mixed with bicarbonate of soda is given by Schidlowsky[944] in doses up to 0·01 to 0·06 grm. three times daily, and a dose of castor oil on the day after the iodoform is given. Thymol in addition to thymol enemas may be tried, in doses up to 0·5 to 2·0 grm. per diem (Calderone,[945] Hausmann[946]), also β-naphthol up to 0·45 grm. three times daily (Du Bois[947]), and--

℞ Benzo-naphthol 2·0 grm. Semin cinæ 1·0 grm. Sacch. albi. 0·5 grm.

M., f.p. Divide in part. æq. xxii. S., three to five powders daily.

[944] Schidlowsky, see Seifert.

[945] Calderone, idem.

[946] Hausmann, St. Petersb. med. Wochenschr., 1900.

[947] Du Bois, see Lenhartz in “Penzoldt-Stintzing’s Handbuch,” p. 619.

(Ferran[948]), filmaron oil 1·0 to 2·0 to 3·0 grm. in gelatine capsules, according to age (Bodenstein[949]). Brüning[950],[951] recommends the so-called American worm-seed oil, derived from a plant native to the United States, Chenopodium anthelminticum, Gray. It is given in emulsion (ol. chenopodii anthelm. 10·0 grm., vitelli ovi unius, ol. amygd., gi. arab. pulver. āā 10·0 grm., aq. destill. 200 grm.; f. emulsio) up to 0·25 to 0·5 grm. three times daily at one to two-hourly intervals, or as a pure oil from 8 to 15 drops in sugar and water; to be followed an hour after the last dose by oleum ricini or pulvis curellæ. If no action takes place by the afternoon, a laxative should again be given. The treatment frequently must be repeated the next day. Thelen[952] appears to have had good results from this drug.

[948] Ferran, idem.

[949] Bodenstein, Wien. med. Presse, 1906.

[950] Brüning, Med. Klin., 1906.

[951] Idem, Deutsch. med. Wochenschr., 1907.

[952] Thelen, “Diss. Rostock,” 1907.

Corsican moss (mousse de Corse), kamala, Artemisia absinthium, valerian, semen sabadillæ, have all been supplanted by santonin and at most are used as adjuvants for the latter.

*Oxyuris vermicularis* (Oxyuriasis).

Oxyuridæ do not remain at rest in the gut, but leave it, generally at night time, to migrate around the anus, into the gluteal folds, and in females into the vulva and vagina and still higher up, giving rise in these different sites to a whole series of irritative symptoms. In the rectum, also, Oxyuridæ give rise to such symptoms, which are manifested in the form of catarrhal inflammation; numerous chronic intestinal catarrhs are thus explained. The frequent coincidence of hæmorrhoidal troubles with Oxyuridæ may be attributed to the fact that the veins of the rectum participate in those changes which have been described as occurring in the intestinal mucosa. Oxyuridæ may also give rise to prolapse of the anus, either by the tenesmus they bring about having such a prolapse as its direct sequel, or the proctitis that supervenes constituting a further etiological factor for its occurrence (Ungar[953]). Anal fistulæ which still further increase the trouble, and even rectal fistulæ, appear to be capable of onset in consequence of the irritation of the mucosa brought about by Oxyuridæ (Trendelenburg[954]). The conditions recorded by von Wagener[955] and Ruffer[956] appear to be of interest. At the post-mortem on a child, aged 5, the former found fifteen to twenty quite minute nodules on some Peyer’s patches, and in several of these Oxyuridæ were found upon microscopical examination between the calcareous concretions within the patches. He presumes that the parasites penetrated the follicular ulcers, and after healing of the latter that they died and became calcified. In the case of a man who died from cirrhosis of the liver, Ruffer found in the rectum, at a distance of about 6 in. from the anal orifice, several tumours covered by the intestinal mucosa, the smallest of which was the size of a pin’s head and the largest that of a walnut. The tumours looked like calculi overgrown by connective tissue; under the microscope, countless Oxyuridæ ova were found in their interior.

[953] Ungar, see Seifert, “Lehrbuch der Kinderkrankh.,” p. 246.

[954] Trendelenburg, see Seifert, idem.

[955] von Wagener, Deutsch. Arch. f. klin. Med., lxxxi.

[956] Ruffer, Brit. Med. Journ., 1901.

The symptoms of irritation set up by these migrations from the intestine are troublesome to the last degree; the pruritus thereby induced is often unendurable; as this irritation from itching comes on with especial severity during the night, the night’s rest is grievously interfered with; many attacks of night terrors appear to be occasioned by these worms. But the general condition suffers as well; the children become pallid and affected with nervous excitability. Through the act of scratching the irritated parts the ova of the parasites may be conveyed by contaminated fingers directly into the oral or nasal cavities, certainly also into the oral cavity by the contamination of food (auto-infection). In the case of boys the sexual organs may be excited sympathetically through irritation of the sacral nerves of the rectum; girls may be induced to practise onanism in consequence of the entrance of the worms into the vulva.

As a result of the itching irritation which the scratching gives rise to, and of the irritation due to the parasites migrating to the area surrounding the anus, congestion and inflammatory symptoms may arise in the peri-anal and perineal regions (weeping eczema, Seifert),[957] and these do not abate till after the removal of the oxyuriasis. Some authors speak of an oxyuriasis cutanea (Majochi[958]), in the more limited sense of a dermatitis intertriginoides. So far five such cases have been recorded, one each by Szerlecky,[959] Michelson,[960] Majochi,[961] Barbagallo[962] and Vignolo-Lutati.[963] Szerlecky’s case was that of a young woman with intertrigo over the thighs (the skin was covered as if with leather); Michelson’s case was that of a boy, aged 13, with intertrigo on the skin of the genito-crural fold, of the scrotum and of the thigh; Majochi’s was that of a man, aged 38, with the same localization; Barbagallo’s case was that of a boy, aged 14, in whom the dermatitis extended to the hypogastrium (rhagades on the scrotum); and Vignolo-Lutati’s case was that of a man, aged 24, with intertrigo of the peri-anal and perineal region, of the scrotum and the inner side of the thigh.

[957] Seifert, “Lehrb. d. Kinderkrankh.,” and Lesser’s “Encyklop. d. Haut-u. Geschlechtskrankh.,” p. 373.

[958] Majochi, Boll. d. Sci. med. d. Bologna, 1893.

[959] Szerlecky, Journ. Ann. Med. prat., Paris, 1874.

[960] Michelson, Berl. klin. Wochenschr., 1877, xxxiii.

[961] Majochi, loc. cit.

[962] Barbagallo, Gaz. d. Osp., November 16, 1900.

[963] Vignolo-Lutati, Arch. f. Derm., lxxxvii, pt. 1.

On leaving the gut, Oxyuridæ frequently migrate to the stomach, to the œsophagus, to the mouth, to the nasopharyngeal cavity, and into the nose (Zarniko[964]) (the localization in the nose has been referred to as associated with the possibility of auto-infection--see p. 695 as to the development of embryos from the ova in the moist nasal mucosa). Still the occurrence of Oxyuridæ in the nose is among the greatest of rarities. Chiari[965] records the case of a girl, aged 14, who suffered from pains at the root of the nose and in the left side of the forehead; female specimens of Oxyuris vermicularis were evacuated from her nose on several occasions. A similar case is recorded by Hartmann[966]; it was that of a girl, aged 13, with epileptiform convulsions and psychic disturbances; numerous Oxyurides frequently escaped from her nose. With their departure the symptoms of irritation of the central nervous system also disappeared. Rheins[967] records a case, that of a woman, in which a specimen of Oxyuris vermicularis was discharged from the right nostril during the act of sneezing. Proskauer[968] found in the nose of a woman, aged 30, a conglomerate of from fifteen to twenty very small worms which proved to be Oxyuris embryos.

[964] Zarniko, “Die Krankh. d. Nase, u.s.w,” S. Karger, Berlin, 1905.

[965] Chiari, “Erfahr. auf d. Gebiete der Hals- u. Nasenkrankh.,” Wien, 1887.

[966] Hartmann, Naturforscherversamml., Köln, 1889.

[967] Rheins, “Der prakt. Arzt.,” 1893.

[968] Proskauer, Zeitschr. f. Ohrenheilk., 1891.

The diagnosis of oxyuriasis is not difficult to make, as the troublesome sensations in the anus and about the genitals necessarily suggest the presence of Oxyuridæ. As a rule the small white worms are seen crawling about over recently evacuated fæces, or the ova are found upon microscopical examination of soiled matter adhering to the anus, or in scrapings removed with the spatula from the surface of the skin (in the case of oxyuriasis cutanea).

Prophylaxis has to be directed to infection with Oxyurides generally, on the one hand, and, on the other, to the possibility of auto-infection. With reference to the first-mentioned point, Metschnikoff’s[969] directions should be borne in mind, to the effect that badly washed vegetables, salad, etc., ought not to be eaten (vegetables to be rinsed with boiling water), and also that the members of the family of the diseased individual should be examined for Oxyuridæ and eventually be treated (Heller[970]). With regard to the second point, one has to observe strict cleanliness in general (Barbagallo[971] found ova of the parasites in the layer of dirt under the finger-nails).

[969] Metschnikoff, Med. Klin., 1907, xlii, p. 1284.

[970] Heller, Deutsch. Arch. f. klin. Med., lxxvii.

[971] Barbagallo, loc. cit.

Treatment of oxyuriasis must be of a twofold nature; first, medicinal, the administration per os of vermicidal drugs in combination with purgatives; and secondly, local treatment of the gut by means of enemata, suppositories and high injections. Following the method prescribed by Ungar,[972] pulv. glycyrrhizæ co. is first given in the case of smaller children, castor oil or calomel in that of those older, in order to evacuate the intestine, and four times daily on two days following one another a dose of naphthalin, not directly after meal-time, but as far as possible in the interval between two meals, and at the same time the ingestion of fatty or oily nutriment is as far as possible to be avoided. After eight days this treatment should be repeated, and under certain circumstances once again after a further interval of a fortnight. The dose varies between 0·05 and 0·1 grm. (children of 1 year old), 0·1 to 0·2 grm. (children of 2 to 3 years old) and 0·2 to 0·4 grm. (children of 4 to 10 years old). Dornblüth[973] employs the same medicament in a form only slightly modified from Ungar’s method, Barbagallo[974] gives internally only a purgative (decoct. sennæ cum natr. sulfur). Thymol, santonin, kousso, kamala or valerian may be tried instead of naphthalin. For enemata the following are employed: naphthalin in a solution of 1 in 50, ol. olivar. or thymol 0·1 in 200 aq. destill., diluted solutions of lysol, menthol in 1/2 per cent. oily solution, salicylate of soda in watery solution, decoctum tannaceti with santonin, with the addition of some drops of ol. terebinth. (Barbagallo). Decoctions of garlic, infusion of valerian, sulphur water (sublimate is to be avoided), aq. calcariæ, ol. olivarum camphoratum (Vignolo-Lutati). Santonin 0·1 grm. is the best to employ for suppositories.

[972] Ungar, see Seifert, “Lehrb. d. Kinderkrankh.”

[973] Dornblüth, Arztl. Zentral-Anzeiger, 1903.

[974] Barbagallo, loc. cit.

For high injections, large quantities of plain water are employed (2 to 4 litres), or soapy water (0·2 to 0·5 per cent. solution of sapo medicatus, Heller,[975] Still[976]), 1/2 per cent. salicylic acid solution or liq. alum. acet. (one tablespoonful to a litre of water, Dornblüth[977]), or gujanosol (2 to 3 to 4 to 5 per cent. solution, Rahn[978]). The employment of benzine for such high injections is not advisable according to the experience of Senger,[979] owing to the symptoms of poisoning after the external application of benzine, at least not in the case of young children.

[975] Heller, loc. cit.

[976] Still, Brit. Med. Journ., 1899.

[977] Dornblüth, loc. cit.

[978] Rahn, Münch. med. Wochenschr., 1905.

[979] Senger, Berl. klin. Wochenschr., 1907, xxxviii.

That diseases of the intestine which are accompanied by frequent thin fluid evacuations may lead to recovery from oxyuriasis has frequently been observed by us in the case of young children who have suffered from dysentery (Seifert[980]). Inunctions of cod-liver oil appear to be very valuable in the treatment of oxyuriasis (Szerlecky, Vignolo-Lutati), whilst those with mercurial ointment may easily increase the inflammatory symptoms. The luxury recommended by Esser,[981] that patients every evening before going to sleep should have the female Oxyuridæ picked from the anal fold in the knee-elbow position is one which is certainly only in the power of a few people to carry into execution.

[980] Seifert, Deutsch. med. Zeitg., 1885.

[981] Esser, Schweiz. Korrespondenzbl., 1893.

An essay has been published by Hippius and Lewinson (Deutsch. med. Wochenschr., 1907, xliii.) in which the relationship of Oxyuridæ to appendicitis is considered and the treatment of oxyuriasis is discussed. The instructive case recorded appears to show that germs through Oxyuridæ gain access to the tissue of the appendix, and, indeed, are carried in by them. In view of this more recent communication as to the part which intestinal parasites play in the etiology of appendicitis, it seemed to me [O. S.] to be worth while to interrogate my surgical colleagues as to this point. About 2,000 appendicectomies have been jointly performed by Drs. Burkhardt, Enderlen, Pretzfelder, Riedinger, Rosenberger and Siber, and in not one of these cases could entozoa be found to be a possible cause of the appendicitis. Such figures without doubt speak in favour of the fact that even if in individual cases entozoa might come into reckoning as a possible cause, such an etiological factor must be classed among the greatest of rarities. My colleague, Dr. Ries, who practised for ten years in Mexico, informed me that there practically speaking every Indian without exception harboured parasites of the most varied kind, and that in spite of the very extensive professional standing he enjoyed among these people he never had under observation among them a single case of appendicitis. As far as the observation of the authors in question as to the treatment of oxyuriasis is concerned, it must be energetically directed to the employment of local measures for the intestine; they maintain that the use of enemata would be irrational, and that it is astonishing that this method has been able to maintain its standing down to the present day.

*HIRUDINEI* (Leeches).

The only one of the leeches that comes under consideration from the clinical point of view is Limnatis nilotica (Hæmopsis sanguisuga), which obtains access to the mouth with drinking water, and becomes lodged, even in the case of man, in the pharynx, larynx, trachea, œsophagus and nose.

Amongst the causes of severe hæmorrhage from the pharynx Jurasz[982] mentions the occurrence of leeches in that region: in Northern Europe this must be accounted one of the greatest of rarities, whilst at all times in southern countries, such as South Italy, Spain, Greece, Algiers, Tunis and Egypt, it appears to have been more frequent. Even the physicians of antiquity had much to say about it. Upon the occurrence of blood-stained expectoration, Hippocrates recommends the oral cavity to be examined to see whether a leech is not present in it. Galen speaks of hæmatemesis due to the presence of leeches in the pharynx and stomach. Similar mention is found in the writings of Celsus, Asclepiades, Scribonius Largus, Dioscorides, Aëtius, Oribasius, Paulus Aegineta and others. In recent times, Cortial[983] has published observations relating to this subject which he had the opportunity of making in Constantine. Palazzolo[984] also in Sicily found leeches in two cases in the pharynx, in one case on the posterior wall, in the other in the crypt over the left tonsil. According to Roset,[985] leeches adhere by preference behind the uvula, simulating hæmatemesis and hæmoptysis, and the persistent hæmorrhages they give rise to may lead to severe anæmia. Leeches are found in still greater frequency in the larynx than in the pharyngeal cavity. Huber[986] records several observations of this kind in his historical and therapeutical study. In the case of a man, aged 64, Ramon de la Sota y Lastra[987] observed a leech on the nodulus epiglottidis; this was removed with the forceps. In the case recorded by Photiades,[988] a leech had remained adherent to the vocal cord for more than twenty-two days. Maissurianz[989] records two such cases: in one the leech had remained in the sinus morgagni for three weeks, in the other in the same place for ten days. The case recorded by Schmolitschew[990] is an interesting one; it was that of a woman who for four days had suffered from violent hæmoptysis, the cause of which was a leech that was fixed on the laryngeal wall of the epiglottis close above the vocal cords. In his case (that of a soldier), Godet[991] was forced to perform thyrotomy to remove the leech from the larynx. Ficano[992] removed a live leech with the forceps from the lower laryngeal cavity in a man, aged 30. Massei[993] reports a similar case. The case reported by Winternitz and Karbinski[994] was that of a peasant girl, aged 16, who suffered from coughing, hoarseness, and blood-stained expectoration; a leech had lodged on the root of the epiglottis. Aubert[995] removed a leech from the larynx of a woman after the performance of tracheotomy. Seifert[996] reports three cases: in the first the leech had become fixed to the left vocal cord, in the second it was found in the lower laryngeal cavity, and in the third on the border of the left ligamentum aryepiglotticum. Leone[997] has published the case of a leech in the larynx, Martin[998] two cases with the leech lodged in the lower laryngeal cavity, Berthoud[999] a similar case, Palazzolo[1000] two such cases, Panzat[1001] one case (lower laryngeal cavity). Moucharinski[1002] reports a case in which the leech had stayed more than twenty days in the larynx. Martin[1003] easily removed a leech from the posterior portion of the vocal cord with the forceps. Vieus and Nepeon[1004] record a case of a leech in the larynx. It is quite exceptional for leeches to gain access to the trachea; cases of this kind have been recorded by Aubert,[1005] Vicano,[1006] Ridola[1007] and Tapin[1008] (the leech was firmly fixed to the bifurcation and caused coughing, hæmoptysis and attacks of asphyxia; it was easily removed by the aid of a tracheal tube). Now and then leeches are found in the nose.

[982] Jurasz, Heymann’s “Handb. d. Laryng. u. Rhinol.,” 1899, ii.

[983] Cortial, Union méd., 1886.

[984] Palazzolo, Bull. del. mal. dell’ orecchio, etc., 1895.

[985] Roset, Rev. d. Cienc. méd. de Barcelona, 1907, ii.

[986] Huber, Deutsch: Arch. f. klin. Med., xlvii.

[987] Ramon de la Sota y Lastra, Rev. méd. de Sevilla, 1883.

[988] Photiades, Int. Zentralbl. f. Laryng., 1884.

[989] Maissurianz, St. Petersb. med. Wochenschr., 1883.

[990] Schmolitschew, Wratsch, 1884.

[991] Godet, Arch. de Méd. et Pharm. milit., 1887.

[992] Ficano, Rev. de Laryng., 1890.

[993] Massei, Int. Journ. of Laryng., 1890.

[994] Winternitz and Karbinski, Prag. med. Wochenschr., 1890.

[995] Aubert, Echo méd., 1891.

[996] Seifert, Rev. de Laryng., 1893.

[997] Leone, Boll. del. mal. dell’ orecchio, etc., 1892.

[998] Martin, Arch. de Méd. et Pharm. milit., 1891.

[999] Berthoud, ibid., 1893.

[1000] Palazzolo, Boll. del. mal. dell’ orecchio, 1895.

[1001] Panzat, Arch. de Méd. et Pharm. milit., 1896.

[1002] Moucharinski, Wratsch, 1896.

[1003] Martin, Rev. barcelon de enf. de oido, 1906.

[1004] Vieus and Nepeon, Monatsschr. f. Ohrenheilk., 1884.

[1005] Aubert, Echo méd., October 12, 1891.

[1006] Vicano, Boll. del. mal. dell’ orecchio, etc., 1892, ix.

[1007] Ridola, Arch. ital. di Laryng., 1894, ii.

[1008] Tapin, Siglo med., March 16, 1907.

Lusitanus[1009] relates the case of a man who suffered from severe headaches. A medical man ordered the application of a leech to the anterior portion of the nostril. Owing to the carelessness of the surgeon the leech crawled right into the nose; it was impossible to extract the leech or to kill it, and it produced a severe hæmorrhage which led to the death of the patient within two days. In a case recorded by Sinclair,[1010] a leech, Hæmopsis sanguisuga, gained access to the nose of a boy, aged 3; it remained there a fortnight; it caused frequent attacks of epistaxis and in the end it was removed by means of forceps. Condorelli-Francaviglia[1011] records a case in which severe epistaxis was caused by a leech which had probably entered the anterior portion of the left nostril by way of the pharynx and become tightly fixed there. It was seen by posterior rhinoscopy, and was removed from in front by means of slightly curved forceps. Sota y Lastra[1012] mentions the occurrence of leeches in the nose, and Keng[1013] reports the case of nasal obstruction from a leech. The removal of leeches is effected by means of injections or by the direct sprinkling of salt or acid solutions on their bodies, which brings about their detachment. When possible a previous attempt should be made to seize them with forceps so as to make their immediate extraction possible. The species of Hæmadipsa (Looss[1014]) live in tropical regions in moist places on the ground or in the jungle. They climb bushes and even trees with astonishing rapidity upon the approach of larger animals and also of man (whom they clearly recognize from the vibration of the ground caused by footsteps). From thence they let themselves fall on their victims to suck their blood. Their bites are generally painless, and of themselves not dangerous, but if they are unusually numerous they rapidly accumulate on the body in large numbers and give rise to marked debility and, if the wound become infected, to severe complications and even death. On the other hand, under careful treatment the wounds heal easily and fairly rapidly.

[1009] Lusitanus, see Seifert in Heymann’s “Handb.,” p. 599.

[1010] Sinclair, Brit. Med. Journ., June 20, 1885, i.

[1011] Condorelli-Francaviglia, Spallangini, 1892.

[1012] Sota y Lastra, Rév. méd. de Sevilla, 1887.

[1013] Keng, Scot. Med. and Surg. Journ., October, 1899.

[1014] Looss, “Handb. d. Tropenkrankh.,” v. Mense, i, p. 194.

Firm leather and firmly adhering clothes afford no certain protection against the attacks of these leeches, as they know how to force themselves with extraordinary rapidity through the narrowest interstices between the clothes and thus gain access to the skin. When they have sucked their fill--and this may take several hours to accomplish--they fall off of themselves. To effect an earlier removal drops of irritative or corrosive fluids are employed (salt solutions, acids, etc.). Tearing away the leech by force should be avoided, as in this way portions of the leech’s body may be left behind in the wound and inflammation be set up.

ARTHROPODA.

*Leptus autumnalis* (Grass, Harvest, or Gooseberry Mite[1015]).

In the hot season of the year, that is, during the months of July and August, it is noticed that those people who stray amongst syringa bushes or who pick gooseberries or kidney beans are attacked by the Leptus autumnalis. On the uncovered parts of the body there appear numerous red spots and papules, which itch and burn smartly. The itching does not commence diffusely, as in the case of scabies (MacLennars[1016]), but is limited to the particular points where the parasite is situated. There are especial outbreaks of itching in the morning, arising perhaps from the hatching of ova in the host after lying in the warmth of the bed.[1017] Leptus frequently provokes general erythema, eczematization or severe feverish urticaria, which in France is known by the name of fièvre de grain (Mégnieu, Besnier[1018]). If the individual efflorescences be carefully examined, there will be noticed almost without exception a minute boss towards the centre, noticeable by its yellowish-red colour. If an attempt is made to remove it with the point of a needle or to scrape it off the surface, one can often perceive, even with the naked eye, a small reddish creature moving actively about. The treatment of these very troublesome symptoms consists in warm baths with soapy lavages, also lavages with alcohol, spirit salmiac (G. P.), 5 per cent. carbol or creolin solution, diluted vinegar, benzine, emulsions of balsam of Peru, rubbing in sulphur ointment (Sandwith[1019]); ointments of creosote or eucalyptus are recommended. Other grass and grain mites also occasionally penetrate the skin of man and produce transitory but sometimes very severe eruptions, urticaria and eczema papulosum, as Geber[1020] and subsequent to him Josai[1021] have reported of the barley mite. In sensitive individuals the skin becomes bright red, to a greater or less extent their temperature is raised and frequently slight febrile affections are present. If the inflammatory skin symptoms have reached their culminating point after three or four days and no fresh complications arise, they only remain for a short while, the effects of scratching and pigment spots being left.

[1015] There is no reason for calling this the gooseberry mite. It is rarely found on this fruit. The gooseberry mite is Bryolia pretiosa.

[1016] MacLennars, Lancet, 1905.

[1017] [This cannot be the case, as Leptus autumnalis is the larval form of Trombidium holosericeum.--F. V. T.]

[1018] Sack, “Handb. d. Hautkrankh.,” v. Mraček, 1907.

[1019] Sandwith, Lancet, 1905.

[1020] Geber, “Handbuch d. Hautkrankh.,” in v. Ziemssen’s “Handbuch d. spez. Pathol. u. Therap.,” 1884, xiv.

[1021] Josai.

*Kedani, Akaneesch* (The Japanese River or Inundation Disease).

This disease is only known in Japan, and is limited to the neighbourhood of some great rivers on the west coast. The people mostly attacked are those who cut the hemp harvest in the infected localities, occasionally those who transport it or come into contact with it (Looss[1022]). The disease is frequently manifested in the form of indefinite disturbances of the general condition; it commences generally on the sixth day after the presumed infection with rigors, headaches, feeling of weakness, swelling of the lymphatic glands in the loin or in the arm-pits; in the periphery a black dry scab is formed. In addition there is an intense conjunctivitis, and added to symptoms of fever an exanthema resembling measles that lasts from four to seven days. There is frequent delirium and difficulty of hearing which persist for a long while. Obstinate constipation is a striking symptom. At the end of a fortnight, earlier in slighter cases, the fever commences to abate and a rapid convalescence sets in. In pregnant women abortion with fatal issue is frequent. With regard to prophylaxis, Baelz[1023] recommends as rapid a cultivation of the soil as possible, which has led to a speedy disappearance of the disease in districts where it was once dreaded. Treatment is symptomatic. Japanese do not tolerate antipyretic drugs as well as Europeans.

[1022] Looss, “Handbuch d. Tropenkrankh.,” v. Mense, p. 195.

[1023] Baelz, Virchow’s Archiv, lxxviii.

Dermanyssus gallinæ (avium).

During the day the resort of bird mites is in the droppings and in the woodwork, etc., of cages in which canaries, crossbills and parrots are kept; in the crevices of doors, in the chinks between the board planks of bedsteads, so that at night they may seek some domestic animal to suck the blood and so satisfy their hunger. It is by no means rare for young animals, chickens and unfledged pigeons, etc., to perish in consequence of the great loss of blood. This nocturnal habit of life explains why no mites can be found during the day in spite of the most careful examination of the human body, to which they may be transmitted. On the uncovered parts of the body they not only cause severe irritation, but also severe diffuse itching erythema and eczema. Thorough disinfection of the cages by hot solution of caustic potash, in addition, sprinkling over with tar, red carbolic acid or petroleum, thoroughly powdering over the birds with flores pyrethræ, washing with water containing oleum anisi, washing the walls, doors and bedsteads with soap, disinfection of the mattresses, linen and clothes, will protect against further infection. In the case of man the disease needs no special treatment, as the eruptions generally disappear after some days. Heinecke[1024] recommends lavages with 1 per cent. carbolic acid solution. [Vide also p. 492 in body of this work.--F. V. T.]

[1024] Heinecke, Münch. med. Wochenschr., 1901.

[Dermanyssus hirundinis, Hermann, is identical with this species. By far the best treatment is with paraffin or kerosene oil applied to the places where they pass the day.--F. V. T.]

Ixodes reduvius (ricinus).

The female is occasionally transmitted to the human skin, and bores its proboscis deep into it and sucks itself full of blood. At sensitive points of the cutaneous surface--for example over the skin of the penis--a feeling of severe pain is produced. Buy’s[1025] observations as to the geographical distribution of the Ixodinæ show that in all lands in which cattle, horses, sheep and dogs exist, Ixodinæ are to be found. Recent observations show that the Ixodinæ play an important part in the transmission of Hæmosporidia (vide body of work, pp. 493, 494). Sprinkling with oil, vaseline, benzine, ether, petroleum, naphtha, turpentine (Jelgenum[1026]), will easily lead to the removal of the parasite; if the body is torn away with violence and the proboscis is left sticking in the skin, the presence of the latter will give rise to inflammation and suppuration.

[1025] Buy, “Histoire naturelle et médicale des Ixodes,” “Thèse de Lyon,” 1906.

[1026] Jelgenum, Med. Weekblad v. Noord- en Zuid-Nederland, 1901, i, No. 24.

*Sarcoptes scabiei* (Scabies).

The disease produced by Sarcoptes scabiei shows itself in polymorphous areas, such as accompany eczema, and are produced on the one hand by the Sarcoptes alone and on the other hand by the scratching with the nails. The localization of both kinds of efflorescences is different from those which are produced by the Sarcoptes; they occur as papules, vesicles, pustules and mite-tracks, and their usual situation is between the fingers, on the ulnar border of the hand, on the wrist, on the palm of the hand, on the anterior border of the axilla, on the penis and at the base of the thorax. The excoriations are situated on the forearm, over the thigh, over the abdomen, and may be distributed in greater or less degree over the whole body; the back and the face only remain free. The symptoms consist in violent itching, the onset of which specially takes place at night.

The mite-tracks are fine curving lines, curved like *a*, *u*, *c*, or *s*, which appear as if they had been scratched with a fine needle. Upon closer examination with the magnifying glass one sees in their course small openings. These openings, in persons who keep themselves clean, are scarcely coloured; but in patients whose occupations necessitate their being associated with coloured or dirty substances, they are dark. The length of the tracks varies from some millimetres to 1-1/2 to 2 cm. They are at the one end, where the Sarcoptes is embedded in the epidermis, widened like a funnel and slightly exfoliated. The track at this point is sharply defined; the mite shows through the epidermis as a yellowish round point. In the course of the track there develop papulæ, vesicles or pustules, which raise the level of the track. The intensity of these inflammatory appearances depends upon the susceptibility of the human individual and upon the capability of the reaction of the skin. There are people in whom scarcely any inflammatory symptoms make their appearance; on the other hand there are some, especially children and lymphatic individuals, in whom severe impetiginous ecthymatous pustules, together with their sequelæ, are set up.

The results produced by scratching consist in papules, which usually bear a small scab of blood, and are arranged in the form of striæ, in eczematous surfaces, weeping or sanguineous scabs, vesicles, pustules, etc. The complications that set in are frequently urticaria and even furuncles, lymphangitis and inflammation of the glands, which now and then is followed by the formation of abscesses in the glands.

The duration of the disease is unlimited; when untreated it leads to a form of rare occurrence, that of scabies norvegica[1027]; in this the collection of crusts and scales, in which a quantity of dead mites, larvæ and ova are present, may become colossal.

[1027] [This is produced by a distinct species, vide pp. 519–20.--F. V. T.]

The symptoms of scabies abate in the presence of intercurrent acute diseases and reappear after the malady is over. The fact has for long contributed to the idea of scabies being regarded as a disease capable of being “driven in” upon the internal organs and forming metastases.

The diagnosis is rendered certain upon the discovery of a track. Traces of scratching on the extremities and on the abdomen, papular or pustular efflorescences between the fingers, toes, in the neighbourhood of the wrist, of the elbow, on the anterior border of the arm-pit, on the tuber ischii, in the girdle region, and especially the presence of disintegrated tracts over the penis (prepuce and glans), will allow of the diagnosis being made. Certain occupational eczemas (grocers, lime-workers, maltsters, bakers and others), also prurigo, must be borne in mind when diagnosing this disease.

The prognosis is always a favourable one. Even after such a long duration and after such severe symptoms the disease may completely clear up. There are, however, frequently left behind post-scabious inflammatous and pruriginous conditions which only yield after protracted treatment. Scabiophilia, which persists in certain patients for a long time after the scabies has been cured, must here be mentioned.

In the treatment of scabies four points must be kept in view. (1) The mites and the ova must be killed by the treatment; (2) the treatment must have regard to the intensity of the inflammatory symptoms; (3) the clothes (body-linen) of the patients must be disinfected; the bed-linen, the beds and the bedsteads must be cleansed; (4) when a person suffers from scabies his entourage must be examined, and all diseased conditions treated in the same way as under (3).

The treatment (1) should be preceded by a bath with thorough soap ablution, and when the inflammatory symptoms are not too severe, with green soap. After the bath the skin is dried and the scabies remedy proper applied in warmth. Sulphur preparations receive first consideration; among such Vlemingkz’s mixture occupies a prominent position; this is rubbed in for half an hour by means of a strong camel-hair brush, to be followed by another bath and powder applications after drying. Repeat this method for three days one after the other, or for two days, and a third time eight days later. The latter method is worthy of recommendation as the ova, which perhaps resist the parasiticide action, have by this time developed into larvæ, and the latter can then be destroyed with certainty. The remaining sulphur preparations, which are specially employed in the form of ointments, are more complex, as the ointment should remain on the skin. Helmerisch’s and Wilkinson’s ointments are the kinds specially employed. Nagelschmidt[1028] recommends thiopinol as a very suitable sulphur preparation in the form of baths or as a 10 or 5 per cent. ointment in the following way: Upon his reception the patient is given a thiopinol bath, in which he remains for thirty minutes. Immediately afterwards 30 to 40 grm. 10 per cent. thiopinol vaseline is carefully rubbed in. The rubbing is repeated daily, and the treatment is concluded on the second to fourth day with a second thiopinol bath. Thiopinol produces no more irritation than the ordinary sulphur ointments; it is, however, much more penetrative and more capable of absorption.

[1028] Nagelschmidt, Med. Klin., 1907, xxxv.

We frequently make use of Kaposi’s naphthol ointment, as it renders the skin supple, causes proportionately little irritation, and has but little smell. Treatment with balsam of Peru is certainly expensive, but in the slighter attacks it is relatively the simplest. We give the patient a bath, have him thoroughly dried and rub in 30 to 40 to 50 grm. balsam of Peru carefully and evenly all over, wrap him in a covering of wool, and make him rest in bed for twelve to fifteen hours, to be followed by a bath with careful cleansing with soap; this treatment need rarely be repeated. The balsam of Peru can be applied undiluted for the rubbings or mixed with ung. glycerini, or resorbin or glycerine in equal parts. [Norman Walker uses balsam of Peru 1/2 oz. dissolved in rectified spirit; to be painted on with a brush.]--J. P. S. The manufacturers name the undiluted product of the active constituent of balsam of Peru, benzoic acid benzyl-ester, Peruscabin. For the treatment of scabies it is recommended by Sachs[1029] that it should only be administered when mixed with ricinus oil, under the name of Peru oil, in applications repeated three times within thirty-six hours.

[1029] Sachs, Deutsch. med. Wochenschr., 1900.

Sack[1030] also considers Peru oil a non-irritant, effectual, pleasant, inodorous and non-staining drug. But he only allows the applications to be used every twelve hours for three to four consecutive days (altogether 200 to 300 grm. of Peru oil are requisite), and after the sixth or seventh rubbing a bath should be taken with the use of Dutch soap. Juliusberg[1031] considers this treatment specially suited for private practice. Another modern drug is epicarin ([Beta]-oxy-naphthyl-ortho-oxy-meta-tolyol acid); this is applied in 10 to 20 per cent. ointments (Pfeiffenberger[1032]), epicarin 7·0 grm., cretæ alb. 2·0 grm., vasel. flavi 30·0 grm., lanolin 15·0 grm., axungia poric. 45·0 grm. (Rille[1033]); epicarin 15·0 grm., sapon. virid. 5·0 grm., axung. poric. 100·0 grm., cretæ alb. 10·0 grm. (Kraus[1034]); for children, epicarin 5·0 grm., lanolin 90·0 grm., ol. olivar. 10·0 grm. (Kaposi[1035]). Siebert[1036] lays stress upon the odourlessness and colourlessness of epicarin ointment as a strong reason for its use, and points out that it is a harmless drug, the action of which is certain. Endermol (salicylic acid ointment) has a destructive action on the mites even in a 0·1 per cent. ointment (Wolters,[1037] Demitsch[1038]); it is, however, very expensive and not wholly free from danger; and the same applies to nicotiana soap (Taenzer,[1039] Schumann[1040]).

[1030] Sack, “Handb. d. Hautkrankh.,” v. Mraček.

[1031] Juliusberg, Therap. Monatsh., 1901.

[1032] Pfeiffenberger, Klin. therap. Wochenschr., 1900.

[1033] Rille, “Die Heilkunde,” 1900.

[1034] Kraus, Allg. wien. med. Zeit., 1900.

[1035] Kaposi, Wien. med. Wochenschr., 1900.

[1036] Siebert, Münch. med. Wochenschr., 1900.

[1037] Wolters, Therap. Monatsh., 1898.

[1038] Demitsch, Wratsch, 1905, iv.

[1039] Taenzer, Monatsh. f. prakt. Derm., xxi.

[1040] Schumann, Allg. med. Central-Zeitg., 1901.

To give an account in detail of the drugs and methods--old and new--used in the treatment of scabies would far outrun the limits of this work.

Demodex folliculorum.

It is not yet certain whether the Demodex folliculorum is capable of developing pathological conditions in man. Veiel[1041] assumes that the hair follicle mite has no connection either with the formation of comedones or even with sebaceous gland disease. Kaposi[1042] considers that they cause no disease in man and cannot be regarded as a cause of acne. Saalfeld[1043] clearly adheres to the same standpoint, similarly so Jessner,[1044] who, when discussing comedones, makes no mention of acne of hair follicle mites. Weyl[1045] and Geber[1046] adhere to the opinion that the presence of a Demodex in man in contradistinction to its presence in animals possesses absolutely no pathogenic influence. On the other hand de Amicis,[1047] Majochi,[1048] and Dubreuilh[1049] report single cases of pronounced circumscribed clear brown pigmentations which they attribute to Demodex folliculorum. In all these cases, moreover, as regards localization the affection had a certain resemblance to pityriasis versicolor; nevertheless, in the scales separated off with the scalpel no fungi were found, but on the other hand Demodices in moderate quantity. In his earlier cases Majochi has seen the Demodex in the secretion from meibomian glands and had claimed it to be the excitant of chalazion and, as Mibelli[1050] did, considered it to be the cause of some diseases of the eyelids. Ivers[1051] found the parasite in 69 per cent. of normal borders of the eyelids, and attributes a pathological signification to it. Hünsche[1052] and Mulder[1053] arrive at the same conclusions; in the light of their investigations the Demodex is found as a constant accessory--certainly not in the meibomian glands, as it is limited only to the internal part of the hair follicle. Lewandowsky[1054] considers that it can hardly be demonstrated at present that the same parasite which in individual specimens causes no symptoms is capable of producing pathological conditions when markedly increased in numbers.

[1041] Veiel, v. Ziemssen’s “Handb. d. spez. Path. u. Therap.,” 1884, xiv.

[1042] Kaposi, “Path. u. Therap. d. Hautkrankh.,” 1899.

[1043] Saalfeld, Lesser’s “Encyclop. d. Haut- u. Geschlechtskrankh.,” 1900.

[1044] Jessner, “Kompend. d. Hautkrankh.,” 1906, 3rd ed.

[1045] Weyl and Geber, v. Ziemssen’s “Handb. d. spez. Path. u. Therap.,” 1884, xiv.

[1046] Weyl and Geber, v. Ziemssen’s “Handb. d. spez. Path. u. Therap.,” 1884, xiv.

[1047] de Amicis, quoted by Lewandowsky.

[1048] Majochi, Centralbl. f. Bakt., xxv.

[1049] Dubreuilh, La Prat. Derm., Paris, 1901.

[1050] Mibelli, quoted by Lewandowsky.

[1051] Ivers, ibid.

[1052] Hünsche, Münch. med. Wochenschr., 1900, xlv.

[1053] Mulder, Weekbl. v. het Nederl. Tijdschr. v. Geneesk., 1889.

[1054] Lewandowsky, Deutsch. med. Wochenschr., 1907, xx.

Treatment is by the removal of the comedones, above all, by their mechanical removal by pressure with a watch-key and with the various comedo-compressors, and by subsequent cleansing of the skin with ether, benzine or spirit. If the eyelids should be affected with blepharitis due to the presence of Demodex in large numbers, epilation and administration of a parasiticide is recommended.

Demodex folliculorum canis.

Transmission from dog to man is in any case very rare, and by many its occurrence is generally doubted. Nevertheless Gruby[1055] and Remak[1056] claim that it is transmissible--an opinion which has also been shared by Neumann[1057] and Zürn.[1058] The latter saw in the case of a married couple who had the care of mangy dogs the onset of diseased areas on their hands and feet, which were like those on the dogs and contained the same parasites.

[1055] Gruby, quoted by Lewandowsky.

[1056] Remak, ibid.

[1057] Neumann, ibid.

[1058] Zürn, ibid.

A. Babes[1059] also reports several observations which go to show that persons who, to some extent, have been shown to have been in contact with mange-stricken dogs have been attacked by a scabies-like eruption localized over the thorax, abdomen, back and extremities; large numbers of Demodices were found in the follicular pustules. Lewandowsky[1060] reports one case--that of an Italian workman, who suffered from an outbreak on the face, like impetigo; there was crust formation and at the edge of the crusts the epidermis appeared like a narrow row or border of vesicles. A small portion of the covering of the row of vesicles was lifted off, and after slight warming examined in 40 per cent. liquor potassæ. In this a large number of animal parasites of the Demodex group were found, and without doubt Demodex folliculorum canis alone. Hünsche[1061] assumes that Demodex folliculorum penetrates into the tissues and produces abscesses.

[1059] Babes, ibid.

[1060] Lewandowsky, Deutsch. med. Wochenschr., 1907, xx.

[1061] Hünsche, Münch. med. Wochenschr., 1900, xlv.

Treatment first consisted in dusting with zinc amyl powder, but after four days there was no change. After the regular use of xeroform as a powder application, the affection cleared up within fourteen days.

INSECTA.

*Pediculus capitis* (Pediculus capitis) (Head Louse).

We find Pediculus capitis in very young children and in others more grown up to be the incessant and frequent cause of impetiginous crust-forming eczemas. It is more frequent in girls than in boys. In families it is endemic, in schools epidemic, but it also occurs in fair frequency in female adults (servant maids, waitresses) who may pay little attention to bodily cleanliness. The puncture of the parasites sets up a severe irritation, which leads to violent scratching. The consequences of this are the formation of nodules and pustules, crusts and “weeping” patches; the hairs become felted and the final clinical picture is that of plica polonica. The conditions of irritation which are produced by these parasites and then by the scratchings of the impetiginous, and frequently the very severe suppurative processes of the hair-bed, lead to swellings in the neck and sometimes even to glandular suppurations. The eczematous processes not infrequently extend over the face, the neck and the thorax. Blepharitis and conjunctivitis may be due to Pediculus capitis.

The means of infection are often very remarkable. Transmission from one individual to another certainly often occurs, but infection may take place in railway carriages and in other ways. A case under the observation of a colleague in Frankfort is a most remarkable one: he diagnosed pediculosis as the cause of a head eczema occurring among the children of one of the best families there. The infection took place through dolls adorned with human hair, in which the presence of nits could be demonstrated.

The diagnosis of Pediculus capitis is not difficult to make when the hairs and hairy scalp are carefully examined for nits and living parasites. In better families it is a good plan to point out the corpora delicti to their possessors and to make them aware of the possible sources of infection.

As regards treatment, lotions of sabadill vinegar are recommended; in slighter cases these are quite sufficient. In severe cases cure will not result unless dressings of petroleum, naphthol ointment (5 to 10 per cent.) and balsam of Peru be applied. In the case of plica polonica, the hair must be cut quite short (even in adults) so as to control matting of the hair. To get rid of nits from hair that is not matted, careful combing and washing with strongly alkaline fluids or with hot vinegar is suitable.

*Pediculus vestimenti* (Clothes Louse).

The clothes louse attacks adults by preference, and with especial frequency old and emaciated persons. It lives in the clothes, but derives its nourishment from the body. At the moment at which the clothes louse inserts its proboscis into the skin the person experiences a slight sting, which, however, at once ceases to hurt. If the body of the louse is sucked full of blood it falls off and the individual has rest from it for a time. A wheal develops around the hæmorrhagic area of the bitten spot and itches severely. The itching goes on until the eruption is scratched all over. This is followed by crust formation. When many parasites are present the itching reflexes become more severe, and the patients scratch themselves considerably and make long marks at those places where the Pediculi have been. The localization of the scratching effects is characteristic, corresponding with folds between portions of clothing (regions between the shoulder-blades, wrist and neck). If the condition lasts for a month, the scratching effects extend over the whole body, and secondary efflorescences become associated with it, such as pustules, ulcers and eczemas. Intermediate between this we find cicatrices and pigmentation, the latter under certain circumstances extending over the whole body. Sulla, Herod, Cardinal Dupet, Philip II, and others are said to have died from louse disease. That even at present many human beings are exposed to the danger of being devoured by lice is a fact that we have had the opportunity of observing on several occasions. Only to record one instance, a man, aged 65, was received into our clinic some time ago in an absolutely neglected condition (he had been staying for some weeks in a stable, lying on a wretched bed). The whole of the surface of his body was covered with countless furuncles, of greater and less size, which had partly become changed into undermined ulcers. Over the ulcers and beneath their undermined edges Pediculi were swarming.

*Phthirius inguinalis* (Pediculus pubis) (Crab Louse).

The transmission of these parasites generally takes place during coitus, and therefore they especially occur in the pubes. It is possible also that transmission is effected through dirty clothes and bed-linen and privy seats.[1062] Starting from the pubes the animals crawl out over the other parts of the body provided with hairs to the abdominal wall and the thorax (so far as these parts are furnished with thick hair) to the arm-pits, the beard, the eyebrows; not, however, to the hair of the head, or rarely so; among our numerous cases we have never met with an example of the crab louse attacking the hair of the head.

[1062] [A case of infection through a dirty station privy in Switzerland came to my knowledge in 1899, and numbers of pediculi were found there.--F. V. T.]

The irritation produced by the crab louse is extraordinarily severe, especially during the night, as the warmth of the bed incites the lice to active sucking. In consequence of the violent scratching indulged in, eczemas are set up at the points attacked, and these often spread to the neighbouring parts not covered with hair.

Of special interest is the onset of maculæ cæruleæ (tâches bleues) in some persons affected with crab lice (people disposed to sweating seem to be peculiarly liable to these). They consist in pale blue patches of various size and shape, varying from that of a hemp-seed to that of a lentil, and again to that of a nail in size and form. These are found over the cutaneous surface of the abdomen, thorax and thigh, and are often only seen by a good lateral illumination. Duguet[1063] considers that the condition is a toxic erythema, that it is set up, on the occasion of the bite of the parasite penetrating the skin, by the poisonous substance derived from it. Oppenheim[1064] considers that it is a colouring substance that is formed in the salivary glands of the parasites, and which penetrates the skin when the insects bite, and thus forms the maculæ cæruleæ. We have on several occasions emulated the experiment of Duguet (trituration in a mortar of crab lice freshly taken from the human body and inoculating the mass thus obtained beneath the skin), and have similarly been enabled to produce the maculæ cæruleæ experimentally, but we have certainly been unable to determine which of the hypotheses is the correct one, the toxic erythema or the colouring substance inhibition theory.

[1063] Duguet, Annal. de Derm., II Sér., i.

[1064] Oppenheim, “Handb. d. Hautkrankh.,” v. Mraček, 1907.

The diagnosis of phthirasis is very easy, for either the sexually mature parasites or the nits are found on the hairs.

As regards treatment, grey ointment is regarded as a generally useful application; it gives rise, however, to a slight eczema of the genitals, especially in males, when injudiciously used. Geber[1065] recommends petroleum or balsam of Peru, Oppenheim[1066] a 1 per cent. sublimate solution for lotions, or a mixture of equal parts of petroleum and benzine when the sublimate cannot be borne. The use of a 5 per cent. ointment with hydrarg. oxid. flavum is worth considering in treatment of pediculosis of the eyebrows and eyelashes. The simplest method of treatment, and one with a radical effect, is that by sulphuric ether recommended by Thomer.[1067] It certainly produces a sharp burning sensation, but the living parasites and nits are destroyed in one sitting. We prefer ether lotions as a rule, and we thoroughly rub the affected parts with a pad of wadding well soaked with the ether. The dead parasites and the nits fall on to what lies beneath when the rubbing is done thoroughly, and the burning sensation caused by the ether only lasts a few minutes.

[1065] Geber, see Seifert, Lesser’s “Encyclop.,” p. 387.

[1066] Oppenheim, loc. cit.

[1067] Thomer, see Seifert, Lesser’s “Encyclop.,” p. 387.

*Cimex (Acanthia) lectularia*[1068] (Cimex lectularius) (Bed Bug).

[1068] Vide genus Cimex, p. 534.

The puncture in the skin made by the bed bug gives rise to an extraordinary amount of severe itching and a burning sensation, and when the skin is sensitive wheals of remarkable size (urticaria ex cimicibus). These eruptions that cause such severe itching are scratched by those attacked, till very soon blood begins to flow, and this generally leads to the formation of a dried crust of blood at the point of eruption.

The diagnosis is not always easy, as urticaria arising in other ways frequently leads to similar vigorous scratching and formation of crusts of dried blood. Men who have some experience in this matter (for example, commercial travellers), when they are attacked by severe itching at night, are in the habit of striking a light and searching in their bed and body-linen for the bugs, in order to be able to hand over the corpora delicti to the landlord if need be. The assumption that the bugs in the East play an actual part in the propagation of tuberculosis and bubonic plague has been proved by investigations made by Nuttall[1069] to be at least very exaggerated if not wholly without foundation. Further investigations may decide how far the bugs participate in the transmission of kala-azar, as is believed by Rogers to take place.

[1069] Nuttall, see Sack “Handb.,” v. Mraček, p. 290.

The bed bugs must be exterminated by spraying the chinks and joints in the boards with petroleum and benzine, pulling up the carpets and cleansing the bedsteads. For the treatment of the bite itself the methods recommended as an antidote against insects’ stings in general are suitable: 2 per cent. carbol vaseline (Rosenbach[1070]), thymol dissolved in spirit (1 in 50[1071]), æthrol or deci-æthrol, form-æthrol (manufactured by Dr. Nordlinger, Flörsheim a. /M.), formol[1072] (formol 15 parts, xylol 5 parts, acetone 44 parts, Canada balsam 1 part), with the aid of a pad of wadding placed over the part bitten, lavages with vinegar, citron juice and spirit of salmiac.

[1070] Rosenbach, Therap. Monatsh., 1903.

[1071] Leipzig. med. Monatsh., 1907, vi.

[1072] Chemist and Druggist, August 25, 1906.

*Pulex irritans* (Human Flea).

The bite of the flea produces a slight discharge of blood about the size of a pin’s head, which rapidly becomes surrounded with a circular area similar to a patch of roseola. The redness fades away after a longer or shorter while (several hours), whilst the discharge of blood is to be seen for one or two days longer. In dirty people the whole body may be covered with such discharges of blood. Individuals with very delicate, sensitive skin, especially small children, show true wheal formation at the site of the bite. In certain cases there develops from one such single bite an urticaria that extends over a large part of the body. The manner by which an irritating substance is introduced into the skin upon biting by the bed bug and also by the flea is clear. The bite is followed by a feeling of itching, which is liable to rob nervous persons of their sleep. Sensitive individuals are upset even by the fleas moving over the surface of the skin during their rest at night.

Treatment consists in extreme cleanliness, capture of the parasites, sprinkling the body and bed-linen with insect powders. The fleas are difficult to remove from barracks, schools and hospitals.

*Dermatophilus* (*Sarcopsylla*) *penetrans* (Sand Flea).

The fertilized females penetrate into the skin with their heads, and here they swell, in consequence of the numerous and growing eggs and larvæ, to a white ball the size of a small pea, on which the head is recognizable only as a small brown point.

In this way a small brown tumour arises, over which, at the commencement, the skin is not reddened; after some days, however, it becomes inflamed; in the centre of it a small opening is seen. If the parasite is not extracted the skin that lies over it becomes destroyed by suppuration, and thus becomes removed. At the commencement the part affected itches, with increasing inflammation; the symptoms of irritation become more severe and may amount to actual pain. If the small suppurative processes be neglected, inflammation and gangrenous and septic processes may arise. The region of the body sought out by preference by the sand flea is the sole of the foot, the toes, under the free ends of the nails and the digito-plantoid folds--more rarely the scrotum, thigh and other parts are attacked (Scheube[1073]). The number of parasites found on one person may amount to several hundreds.

[1073] Scheube, “Die Krankh. d. warmer Länder,” 1896.

Treatment consists in the removal of the parasites from the skin with a needle or a small sharp knife and the application of a bandage. Rubbing the feet with copaiba or Peru balsam, sprinkling them with insect powder, or washing them with bay rum (Berger[1074]) acts as a prophylactic or removes the irritation of the skin produced by the parasites.

[1074] Berger, Therap. Monatsh., April, 1907.

Myiasis.

Under the name of myiasis we designate the complex symptoms which parasitic dipterous larvæ give rise to in man (Braun), and we conceive under the term myiasis externa (dermatosa s. cutanea) all lesions of the human integument caused by fly larvæ and of the cavities covered with mucosa therewith connected, such as the external auditory meatus, the oro-nasal cavity, the urethra and vagina. The occurrence of dipterous larvæ in the digestive tract is named myiasis intestinalia or interna.

Myiasis externa.

The larvæ of a species of fly belonging to the Muscidæ, Lucilia macellaria,[1075] are found in relative frequency in the nose, especially in America and India.[1076] Riley[1077] has stated that the screw-worm of Central America and of the United States is nothing else than the larva of Lucilia macellaria, and also that the Brazilian fly named “berna” may be no other than Lucilia macellaria. Their offspring may set up inflammatory disturbances in the soft tissues of man. This fly has a wide distribution, from the Argentine Republic to Canada, also in the British portions of the East Indies, where the disease is named “peenash.” This word is derived from the Sanskrit, and is said to be a collective name for all diseases of the nose. Lahory[1078] states that within a period of nine years ninety-one cases of “peenash” occurred in Allyghar, two of these ending fatally. Lucilia macellaria is not at all timid but bold, like the house-flies and blue-bottles, its relatives. It not only lives at no great distance from human dwellings, and forces its way into villas and country houses, but even attacks its victims without awaking them from their sleep. Although this species shows a certain preference for nasal cavities affected with catarrh or pus (v. Frantzius[1079]), and also the external auditory meatus, as well as ulcerated or wounded parts of the body, and even badly ulcerated skin carcinoma (Lutz[1080]), it is not a rare thing for it to penetrate into one of the above-mentioned cavities rapidly to deposit its eggs, without these parts having been previously affected. The report also of Conil,[1081] in which these flies bear the name of Calliphora anthropophaga[1082] is an interesting one. Probably it was the same species of Muscid in the cases of myiasis nasi observed by von Tengemann, Delasiauve,[1083] Weber,[1084] Mankiewicz,[1085] and Kirschmann.[1086] In the case recorded by Prima,[1087] and in that recorded by Britton,[1088] the issue was a fatal one; in the latter the larvæ escaped through the pharynx and nose; the hyoid bone and the soft parts of the palate were destroyed, the speech and power of swallowing were hindered. At the post-mortem extensive destruction of the internal nose was found, so that the nasal bones could only be kept in their position by the aid of the external skin. Even during life 227 larvæ escaped. Similar destructive processes were found in the case communicated by Richardson.[1089] In two cases reported by Schmidt[1090] 300 and 350 larvæ were respectively removed from the nose, and the patients recovered. Wolinz[1091] found his patient had lost consciousness, and that in the pus filling up the entrances to the nose numerous larvæ were moving; recovery followed. In the case communicated by Adler,[1092] more than 150 larvæ escaped from the nose of an old man. Curran[1093] states that people suffering from “peenash” frequently die from meningitis. The cases reported by Pierre[1094] related to the forms of severe myiasis frequently to be observed in Guiana. In a patient who was suffering from typhus (? typhoid), Douglas[1095] found the conjunctival sacs full of larvæ; in two other individuals the nasal cavities were attacked.

[1075] [Chrysomyia macellaria, p. 587.--F. V. T.]

[1076] [C. macellaria, Fabricius, the screw-worm fly, is found in tropical America and the West Indies. The genus is restricted to America. The species from India is a Pycnosoma.--F. V. T.]

[1077] Riley, American Naturalist, 1883, xvii.

[1078] Lahory, Edin. Med. Journ., 1856.

[1079] v. Frantzius, Virchow’s Archiv, 1868, xliii.

[1080] Lutz, see Joseph, Deutsch. med. Zeitg., 1885.

[1081] Conil, Annal. de Science nat. zool., 1878.

[1082] [This fly belongs to the genus Cordylobia, and is peculiar to Africa. C. anthropophaga, or the tumbri fly, is, when a larva, a subcutaneous parasite of man and animals.--F. V. T.]

[1083] Delasiauve, Gerhardt’s “Handb. d. Kinderkrankh.,” 1878, iii.

[1084] Weber, Mexique Rec. d. Mém. de Méd. milit., 1867.

[1085] Mankiewicz, Virchow’s Archiv, 1868, xliv.

[1086] Kirschmann, Wien. med. Wochenschr., 1881.

[1087] Prima, “Thèse de Paris,” 1881.

[1088] Britton, Cambridge, Massachusetts, 1883.

[1089] Richardson, Medical Monthly, 1883.

[1090] Schmidt, Texas Med. Journ., 1887.

[1091] Wolinz, Wratsch, 1884.

[1092] Adler, Med. Record, 1885.

[1093] Curran, Med. Press and Circ., 1887.

[1094] Pierre, “Thèse de Paris,” 1888.

[1095] Douglas, Kansas City Med. Index, 1890.

The case observed by Summa[1096] was that of a man, aged 28, who suffered from nasal obstruction, fœtor, epistaxis and pain in the nose. Out of seven of the cases occurring at Fort Clark, U.S.A., and in its neighbourhood, six ended fatally; in all these cases Kimball[1097] diagnosed ozæna; attracted by the strong odour the flies forced their way into the noses of the patients when asleep and there deposited their ova. In a case reported by Carrière[1098] an abscess of the nasal septum was produced by the larvæ of flies; Chiodi[1099] reports seven cases of myiasis due to Lucilia macellaria; among these was a case of rhinitis myiatica, in which a cerebral abscess leading to a fatal termination developed, being produced by the migration of a larva into the brain. Among the three cases of Lesbini[1100] was that of a girl, aged 16, with 250 larvæ in the diseased nasal cavity. Quintano[1101] observed larvæ beneath the eyelids in one case. It is possible that the cases of Cesare[1102] and Calamida[1103] were those of myiasis nasi due to Lucilia macellaria. The larvæ are also found in the nasal accessory sinuses, as is seen from the cases reported by De Saulle[1104] (frontal sinus), Delasiauve[1105] (frontal sinus), MacGregor[1106] (antrum of Highmore), and Bordenave[1107] (antrum of Highmore).

[1096] Summa, St. Louis, 1889.

[1097] Kimball, New York Med. Journ., 1893.

[1098] Carrière, Gaz. hebd. de Méd. et de Chir., 1898, xciv.

[1099] Chiodi, La Argent. Med., March 1, 1905.

[1100] Lesbini, ibid.

[1101] Quintano, “Cronic oftalm. de Cadiz,” 1878.

[1102] Cesare, Arch. ital. di Otol., April, 1903.

[1103] Calamida, Giorn. d. R. Accad. de Med. di Torino, September, 1903.

[1104] De Saulle, Gaz. des Hôp., Paris, 1857.

[1105] Delasiauve, Gaz. hebd. de Méd., Paris, 1885.

[1106] MacGregor, Arch. gén. de Med., No. 1,031.

[1107] Bordenave, “Deuxième Mém. présenté à l’Acad. de Chir.,” v, p. 387.

If a survey is made of the literature of the cases described of myiasis nasi produced by Lucilia macellaria[1108] the following information is forthcoming: In Europe this form of the disease is of very rare occurrence, whilst in America and India[1109] it is frequent. Persons suffering from ozæna are rendered the most liable to danger as the penetrating odour entices the flies in tropical countries with intense frequency, so much so that v. Frantzius does not consider this myiasis as an independent disease, but as a complication of ozæna of frequent occurrence in warm countries. The infection is so far of interest in its nature, in that it only takes place during the day. The fly is on the wing only by day when the sun is shining, and consequently only deposits its eggs at this time. Therefore persons suffering from ozæna are principally exposed to the danger of being pursued by the flies when they succumb to sleep during the mid-day hours in the open or in dwellings that are not closed up.

[1108] [And the other species, of course, must be included here.--F. V. T.]

[1109] [Concerning Europe and India, macellaria does not occur.--F. V. T.]

Headache is the symptom which most troubles the patients. It extends over the whole cranium and persists uninterruptedly, with more or less severe periods. Violent headaches in the frontal and buccal regions are almost always present in this complaint; they are experienced either only on one side or on both simultaneously; sometimes the pain is extended to the lower jaw and region of the neck, following the whole extent of the trigeminal nerve. The inflammation of the nasal mucosa produced by the penetration into it of the larvæ extends right into the frontal sinus and antrum. Simultaneously the patients, at the height of their trouble, suffer from persistent sleeplessness and severe vertigo, so that they reel and cannot walk straight; excessive sneezing always sets in at the commencement. The larvæ immediately spread over the nasal mucosa to seek a place suitable to feed, and irritate the nasal mucous membrane by the tickling sensation they produce. Later the patients frequently sneeze when the maggots move to and fro.

One very characteristic symptom consists in the peculiar swelling of the face, which is extended either over the whole or only one half of it, and may alternate with attacks of erysipelas (Brokaw[1110]).

[1110] Brokaw, see Seifert, in Heymann’s “Handb.,” p. 595.

The discharge from the nose is of special diagnostic value. It consists of a blood-stained serous matter or blood-stained fluid, which is perpetually trickling from one or both nostrils. The larvæ especially choose the anterior portions of the nasal cavity, where they can be seen lying in groups together at the base of the choanæ. The consequence of this is that the soft palate becomes intensely swollen, and this in turn makes swallowing very difficult; speech is impeded, and the voice acquires a nasal intonation. Symptoms of fever become more or less pronounced according to the number of larvæ present, and according to the nature and constitution of the individual. The appetite is in abeyance throughout the whole duration of the illness, and sometimes there is the onset of slight attacks of diarrhœa.

If the larvæ are not removed in good time there follows excessive destruction of the interior of the nose and of the turbinals; and the whole nasal framework undergoes disintegration, frequently, too, the velum palati, so that the larvæ come into sight in the oral cavity. Individuals thus severely attacked succumb through exhaustion, symptoms of meningitis (cerebral abscess) or septicæmia (Prima[1111]). Twenty-one out of thirty-eight cases recorded (collected) by Maillard[1112] died.

[1111] Prima, “Thèse de Paris,” 1881.

[1112] Maillard, “Thèse de Montpellier,” 1870.

The method of prophylaxis is self-evident from what has been stated. On bright summer days neither the healthy nor those suffering from diseases of the nose should sleep during the day-time in the open or in public habitations; sufferers from nasal diseases should pay special attention to this.

Treatment consists in the removal of the larvæ; this, however, is not always easy.

With regard to the methods which have proved to be effectual in the destruction of living larvæ and their expulsion from the nose, strongly smelling and easily diluted fluids come first, such as alcohol, eau-de-Cologne, and ether, which should kill the creatures when injected into the nostrils. The earlier physicians, such as Salzmann,[1113] Honold,[1114] and Henkel,[1115] have seen good results from the use of these methods, whilst Mankiewicz[1116] and Goldstein[1117] obtained no results whatever. Kimball’s[1118] careful investigations have shown that a decoction of bitter herbs recommended by Behrends[1119] (tansy, wormwood) have just as little effect as the tobacco decoction employed by Boerhave[1120] and Kilgour.[1121] The sternutatories employed by the older physicians are entirely neglected. Delasiauve[1122] experienced good results from the inhalation of the smoke of paper cigarettes, which were soaked with a solution of 2·0 pot. arsenic in 30·0 distilled water. Whilst, according to Kimball, balsam of Peru had no effect on the larvæ, Mankiewicz succeeded in removing the larvæ from the nose with the help of that drug. Turpentine steam or mixtures of turpentine employed by Indian physicians have not been very effectual according to Moore,[1123] Kimball and Goldstein. Success has been attained in some cases by the use of insufflations of calomel (Roura,[1124] Cerna,[1125] Schmidt[1126]) or of iodoform (Pascal[1127]). Joseph[1128] recommends concentrated alum solution being sniffed up into the nose as very effectual. Sublimate and carbol solutions do not appear to be very successful (Kimball, Moore, Goldstein), whilst benzine inhalations (Pierre[1129]) have shown better results. Scheppegrell[1130] strongly recommends injections of oil which kill the larvæ, while it is perfectly harmless to the nasal mucosa. Cesare[1131] employed nasal lavages with solutions of salicylate of soda with good results, and Calamida[1132] lavages with physiological saline solution. Bresgen[1133] recommends the nose being cocainized and the larvæ being removed with a pincette. Roorda-Smit[1134] cocainized the nose, then insufflated calomel and plugged the nose with a gauze tampon dusted with calomel. After two hours fifty-six larvæ crawled out along the plug. Continuation of the treatment resulted in a complete cure.

[1113] Salzmann, see Tiedemann, Mannheim, 1844.

[1114] Honold, ibid.

[1115] Henkel, ibid.

[1116] Mankiewicz, Virchow’s Archiv, 1868, xliv.

[1117] Goldstein, New York Med. Journ., 1892.

[1118] Kimball, ibid., 1893.

[1119] Behrends, see Tiedemann.

[1120] Boerhave, ibid.

[1121] Kilgour, ibid.

[1122] Delasiauve, loc. cit.

[1123] Moore, Chicago Med. Times, 1893.

[1124] Roura, Gaz. di San. milit., 1884.

[1125] Cerna, New York Med. Journ., 1893.

[1126] Schmidt, Texas Courier, 1884.

[1127] Pascal, Arch. d. Méd. milit., 1895.

[1128] Joseph, Deutsch. med. Zeitg., 1885.

[1129] Pierre, “Thèse de Paris,” 1888.

[1130] Scheppegrell, New York Med. Journ., 1898.

[1131] Cesare, loc. cit.

[1132] Calamida, loc. cit.

[1133] Bresgen, Eulenburg’s “Real. Encyclopädie,” third edition.

[1134] Roorda-Smit, Deutsch. med. Wochenschr., 1906.

Injections of chloroform water (Jourdran[1135]) or chloroform inhalations, or injections of pure chloroform into the nose, have proved the most effectual (Goldstein,[1136] Osborn,[1137] Jourdran, Durham,[1138] Jennings,[1139] Kimball,[1140] Mackenzie,[1141] Oatmann,[1142] Zarniko,[1143] Antony,[1144] Folkes[1145]). Camphorated carbolic solutions are very well spoken of: Grayson[1146] states that these kill the larvæ immediately. Some authors have removed the larvæ with forceps (Goldstein[1147]), others with pincettes; thus Brokaw extracted 200 fragments with the forceps, Pascal eighty fragments with the pincettes, and Wolinz[1148] also appears to have removed the larvæ with forceps.

[1135] Jourdran, Arch. de Méd. nav., 1895.

[1136] Goldstein, New York Med. Journ., 1892.

[1137] Osborn, Daniel’s Med. Journ., 1891.

[1138] Durham, Chicago Med. Times, 1893.

[1139] Jennings, Kansas City Med. Index, 1890.

[1140] Kimball, New York Med. Journ., 1893.

[1141] Mackenzie, “Diseases of the Nose and Throat.”

[1142] Oatmann, Med. Mirror, February, 1894.

[1143] Zarniko, “Lehrb. d. Krankh. d. Nase.”

[1144] Antony, Bull. Soc. méd. des Hôp. de Paris, 1903.

[1145] Folkes, New York Med. Record, 1907.

[1146] Grayson, St. Louis Med. and Surg. Journ., 1891.

[1147] Goldstein, New York Med. Journ., 1892.

[1148] Wolinz, Wratsch, 1884.

Greater operative measures than these do not appear to have been undertaken in latter days; yet Morgagni[1149] states that the army surgeon, Cæsar Mogatus, at Bologna, first trephined the frontal sinus and then extracted a “worm” from it.

[1149] Morgagni, see Tiedemann.

Larvæ of other Muscidæ have come under observation much more rarely (Cheval[1150] [larvæ of Galleria mellonella[1151]], Bond,[1152] Dumesnil[1153] [larvæ of Piophila casei]). Species of the genus Scolopendra (Myriapoda), which all shun the light and seek their food during the night--which consists of animal and vegetable substances--frequently make their way into the nasal cavities of people when asleep. They are found not only in the nose, but in the accessory cavities. In the chapter on the “Parasites of the Nose”[1154] we have collected striking instances, but we have omitted to mention the observation made by Bertrand[1155] (Scolopendra in sinus maxillaris) and that made by Bergmann[1156] (Scolopendra in sinus frontalis). In the same chapter some remarks are made as to the occurrence in the nose of earwigs, caterpillars, scorpions and termites, as well as of animals which have not been identified.

[1150] Cheval, Journ. de Méd. et de Chir., 1893.

[1151] [This is the larva of a moth.--F. V. T.]

[1152] Bond, Int. Zentralbl. f. Laryng., 1896.

[1153] Dumesnil, see Friedreich, “Die Krankh. d. Nase,” 1858.

[1154] Seifert, see Heymann’s “Handb.”

[1155] Bertrand, Soc. méd. de Bologne, 1839.

[1156] Bergmann, Korrespondenzbl. d. deutsch. Ges. f. Psych., Neuwied, 1859.

The larvæ that develop in the auditory meatus penetrate the membrana tympani, destroy the middle ear and may produce meningitis and intracranial suppurations. In one case Vesescu[1157] extracted seven living larvæ from the ear with the aid of a thin pair of pincettes. Köhler[1158] recommends the infusion of drops of ol. terebinth. to destroy the larvæ, Quintano[1159] the insufflation of the following powder: Oxid. hydrarg. rubr., sulfur., āā 1·0 grm., pulv. gi. arab. 8·0 grm.; Lesbini[1160] recommends tincture of iodine. In the case reported by Henneberg[1161] the larvæ were those of Lucilia cæsar.

[1157] Vesescu, Riv. stiintelor med., February, 1906.

[1158] Köhler, Monatsschr. f. Ohrenheilk., 1885.

[1159] Quintano, see Seifert, loc. cit.

[1160] Lesbini, La Argent. Med., 1905.

[1161] Henneberg, Berl. med. Ges., February 18, 1903.

Eye affections due to Lucilia macellaria are very uncommon; the literature relating to the lesions of the eye produced by the larvæ of flies has been collected in Kayser’s[1162] work. In the cases under the observation of Schultz-Zeyden[1163] both the eyes of a female tramp were destroyed, and quantities of larvæ were also found in the nasal fossæ and in the ears.

[1162] Kayser, Klin. Monatsbl. f. Augenheilk., 1905.

[1163] Schultz-Zeyden, Berl. klin. Wochenschr., 1906.

The Lucilia is found relatively seldom on the cutaneous surface. Henneberg’s[1164] case was that of a neglected girl, aged 20, in whom countless larvæ (L. cæsar) were found in a plica polonica; after the plica polonica had been removed the scalp was found to be covered with a large quantity of ulcers which swarmed with larvæ, large and small. The skin of the trunk was also much macerated and covered with larvæ. Death resulted from sepsis; Westenhöffer[1165] remarks on this case that a lesion of the head from which the patient had suffered previously and the perpetual state of intoxication in which she was had probably given rise to the lodgment of the fly larvæ. Whether the communications made by Munk[1166] of maggots in the mouth relate to Lucilia I do not know. Vesescu,[1167] in one case with extensive ulceration and deep fistulæ in the skin, removed 176 larvæ with the pincette. In Roorda-Smit’s[1168] case there were two ulcers in the neck of a girl, aged 17, and larvæ appeared at their base. After dusting with calomel and the application of a bandage the next day fifty-two dead or half-dead larvæ came to light. Recovery took place. Lesbini,[1169] in the case of an old lady, saw numerous larvæ in an ulcer of the leg she was suffering from. Hector’s[1170] case appears to have been one of myiasis cutanea provoked by Lucilia.

[1164] Henneberg, Berl. med. Ges., February 18, 1903.

[1165] Westenhöffer, Verein f. innere Med., Berlin, May 7, 1906.

[1166] Munk, Wien. med. Presse, xxi.

[1167] Vesescu, loc. cit.

[1168] Roorda-Smit, Deutsch. med. Wochenschr., 1906.

[1169] Lesbini, loc. cit.

[1170] Hector, Lancet, 1902.

The first exact observations of myiasis cutanea from Sarcophaga magnifica are due to Wohlfahrt,[1171] in whose honour Portschinsky[1172] named this species of fly S. wohlfahrti. Portschinsky ascertained that S. wohlfahrti was not confined to man as its sole host, but that several of our domestic animals, such as cattle, horses, pigs, dogs and geese, were visited. In these animals small wounds serve to entice the flies and to supply them with a suitable site for the deposition of their eggs. The oral armature of the young larvæ renders it easy for them to penetrate not only the mucosa and cutaneous surface but also intact places in the submucous connective tissue. In many localities more than half the herds have proved to be infected by the flies. The fly only frequents open spaces and never enters human dwellings, and is so timid that it approaches man only during sleep; infection, therefore, takes place only out of doors, in summer, in clear, warm weather, and only in such individuals as sleep in the open air. Individuals are most exposed to risk who suffer from catarrhs or inflammations, combined with purulent secretions of the nasal cavity (ozæna), or otorrhœa, or ulcers in any parts of the body accessible to the female fly.

[1171] Wohlfahrt, “De vermibus per nares excretis,” Norimbergae, 1770.

[1172] Portschinsky, “Norae Soc. entomolog. Rossicae,” 1875.

The frequency and intensity of the infection will be in inverse proportion to the advance in civilization of the inhabitants, their idea of cleanliness, their having timely medical aid and the chances of their being rapidly attended to. On that account the majority of cases of myiasis (Sarcophaga) are reported from Russia. The literature of this kind of myiasis nasalis is not very extensive; in addition to Wohlfahrt, Portschinsky and Joseph,[1173] there is a communication by Gerstäcker,[1174] who found fifteen adult larvæ of S. wohlfahrti in the nasal cavity of one man. The larvæ transmitted from Ordruf by Dr. Thomas to Löw,[1175] in Vienna, which were discharged from the nose of a woman, aged 71, suffering from ozæna, were recognized by the well-known dipterologist Braun as belonging to S. wohlfahrti. Among the cases reported by Joseph, one only affected the nose; it was that of a peasant girl, aged 11, who had suffered from ozæna; she had travelled on the open road and had there gone to sleep. Severe symptoms set in and death followed under delirium. In making the post-mortem it was found that the interior of the nose was extensively destroyed by larvæ of S. wohlfahrti. Powell found Sarcophaga larvæ in two persons who had slept in the open air; the larvæ were killed by injections of chloroform and sublimate. Destruction of the eyes by S. wohlfahrti has only been observed in a few cases; it is reported by Cloquet[1176] that, in the case of a ragman who had lain some time in the fields, both eyes were pierced by larvæ. On the outer skin the larvæ of S. wohlfahrti have been found more than once in inflammatory or festering areas. Freund[1177] demonstrated that from a five year old child, which had suffered for some time from an impetiginous eczema of the skin of the head, from two suppurating abscess cavities which extended to the periosteum, which was already affected, twenty-one living larvæ were taken; rapid healing took place under antiseptic bandaging.

[1173] Joseph, Deutsch. med. Zeitg., 1885.

[1174] Gerstäcker, “Sitzungsberichte d. Ges. f. naturf. Freunde in Berlin,” 1875.

[1175] Löw, Wien. med. Wochenschr., 1883, xxxi.

[1176] Cloquet, see Schultz-Zehden, loc. cit.

[1177] Freund, Ges. f. innere Med. in Wien, December 5, 1901; and Wien. med. Wochenschr., 1910, li.

The small treatise by Balzer and Schimpff[1178] contains two new observations on myiasis externa; in the one case an ulcer on a man’s foot was full of larvæ, in the other case the head of a woman showed numerous larvæ without the skin of the head being destroyed. Brandt’s[1179] observation is interesting, for he found such larvæ in the gums of a sick person.

[1178] Balzer and Schimpff, Annal. de Derm. et de Syph., 1902.

[1179] Brandt, Wratsch, 1888.

The impression which one obtains of the active movement of larvæ on wounds is a strange and at the same time uncanny one. One finds that the larvæ to obtain protection against the drying of the surface of the abscess almost incessantly burrow with their heads, first contracting and then expanding the body, which rises and falls, and keeping the tail upwards. Owing to these movements producing irritation, increase of inflammation may ultimately arise, causing erysipelas and cellulitis.

The treatment of myiasis nasalis caused by Sarcophaga is the same as in myiasis caused by Lucilia, and in the other places where found it is merely a question of the removal of the larvæ and the subsequent proper treatment of the surface of the abscess. In Northern Nigeria Lelean[1180] found Auchmeromyia depressa to be the cause of myiasis externa.[1181]

[1180] Lelean, Brit. Med. Journ., 1904.

[1181] [Numerous instances of attacks by Auchmeromyia are known and referred to under that genus, pp. 593–4. The species referred to here is not depressa, Walker.--F. V. T.]

The occurrence of Oestrid larvæ in a human being is very rare, at least up till now myiasis oestrosa has been very seldom observed in man in Europe. Whilst the hosts of the Muscidæ comprise a considerable number of warm-blooded animals, on which the larvæ develop, each species of the Oestridæ appears, on the other hand, to have a definite host or some definite hosts of the class Mammalia. No species of Oestrid is peculiar to man. Although in America, as well as in Europe, Oestrus hominis was spoken of up to the middle of the last century, no such species exists.

But in both hemispheres, in America much more often than in Europe, Oestrid larvæ have been found in man. In Florida, Mexico, New Granada, Argentina, Brazil, Costa Rica and other districts, and especially where large herds of cattle are kept, myiasis oestrosa has been observed in shepherds, huntsmen and amongst the rural population. The larvæ of Hypoderma bovis, according to the observations of Goudot,[1182] occur as a parasite in man. Poilroux[1183] found larvæ of cavicolous Oestridæ in the nose of a man, aged 55. Amongst the species of warble flies, whose larvæ are parasites in domestic animals and game in Europe, reliable observers have found larvæ of two kinds, Hypoderma bovis and Hypoderma diana, also in man.[1184]

[1182] Goudot, Annal. d. Sci. nat., 1845.

[1183] Poilroux, Journ de Méd., Chir., etc., 1809.

[1184] [Hypoderma linearis is frequently confused with H. bovis.--F. V. T.]

The larvæ of H. bovis have very seldom been observed in the nose. The case quoted by Kirschmann,[1185] which was that of a peasant woman, aged 50, who was suffering from ozæna, and in which violent attacks of sneezing, epistaxis, pain in the forehead, and swelling of the face were observed, is, according to Löw[1186] and Joseph,[1187] not an Oestrid; Muscid larvæ were evidently the cause. By the injection of diluted iron chloride solution seventy-nine larvæ were removed from the nose. In the case reported by Razoux[1188] the species of larva is not definitely known--at least, v. Frantzius[1189] did not consider them Oestrid larvæ. Joseph does not definitely say that Oestrid larvæ were the cause of a case which he quotes. He was sent a number of uninjured larvæ of Oestrus ovis ready to pupate, which were said to have been expelled, during violent sneezing, from the nose of a peasant woman who had suffered for six months from continuous frontal headache and chronic nasal catarrh.

[1185] Kirschmann, Wien. med. Wochenschr., 1881.

[1186] Löw, Wien. med. Wochenschr., 1882.

[1187] Joseph, Deutsch. med. Zeitg., 1885.

[1188] Razoux, Journ. de Méd., Chir., etc., 1758.

[1189] v. Frantzius, Virchow’s Archiv, 1868, xliii.

The Oestrides prefer to use the surfaces of wounds on the skin of man to lay their eggs, which develop into larvæ; but they often use their ovipositors[1190] to make a fresh wound. In this case there arise in the skin, and particularly in the subcutaneous connective tissue of the neck, in the region of the shoulder, as well as in other parts of the body painful, furuncle-like inflammations which are known under the name of gad-fly boils. These boils may become the size of pigeons’ eggs; if several are together, they appear to form a connected tumour. Each tumour is elastic and somewhat movable, and has an orifice through which the larva breathes and discharges its excreta. At times these turn to festers and gangrenous disintegrations, which may even cause the loss of a limb. Wilms[1191] had the opportunity a few years ago of observing a case of myiasis dermatosa oestrosa in Leipzig. The fistula which led to the larva was slit open and the larva extracted. As a notable characteristic of myiasis oestrosa Joseph states that the larvæ grow very slowly. The flight time of the Oestridæ is the hot summer months.

[1190] [The Oestrides appear to lay their ova on the hair of animals. They do not puncture the skin.--F. V. T.]

[1191] Wilms, Deutsch. med. Wochenschr., 1897.

Adams[1192] observed on the Isthmus of Panama a number of cases of a skin disease which is caused by the larvæ of Dermatobia noxialis (Gusano-peludo-Muche). The larvæ penetrate not only the skin but also the mucous membrane of the pharynx and larynx, and from there proceed through the tissue to the subcutaneous cellular tissue. The infection seems to result from bathing.

[1192] Adams, Journ. Amer. Med. Assoc., 1904.

The study of “thimni,” a human myiasis caused by Oestrus ovis, by Ed. and Et. Sergent,[1193] deals more with the zoology and with the geographical distribution of this insect in North Africa than with the clinical appearances of myiasis. [This paper deals with matters of great interest, with important facts.--F. V. T.]

[1193] Ed. and Et. Sergent, Annal. de l’Inst. Pasteur, 1907.

The treatment consists in the removal of the larvæ (from the nose); in Brazil it is the custom to drop tobacco juice into the boil in order to kill the larvæ (Strauch[1194]).

[1194] Strauch, Journ. of Cut. Dis., 1906.

One is only justified in speaking of myiasis intestinalis when there is no doubt that living fly maggots or flies themselves can be proved to have been found in the fresh contents of the stomach or intestine (Schlesinger and Weichselbaum[1195]). In the discussion of myiasis intestinalis we give the evidence of Schlesinger and Weichselbaum, as well as that of Wirsing,[1196] to which must be added a number of other investigations.

[1195] Schlesinger and Weichselbaum, Wien. klin. Wochenschr., 1902, i.

[1196] Wirsing, Zeitschr. f. klin. Med., 1906, lx.

In a great number of acute cases apparently only the stomach was affected, there being no signs in the intestine. In these cases sudden illness is noticed, colic, sometimes unbearable pains in the region of the stomach, pyrosis, vomiting or continuous intense inclination to vomit, occasionally even with the mixture of blood. Frequently a general feeling of malaise, twinges of pain in the muscles, and attacks of giddiness were notified, very rarely fever. Generally all the symptoms disappeared in a short time when the larvæ had been removed by an act of vomiting or by washing out the stomach.

It is well to note that in the history of many cases the pains preceding the expulsion of the larvæ are stated to be extremely violent.

Acute myiasis of the intestinal canal frequently runs a course without special symptoms and is only an accidental condition; one has, however, in such cases to guard against errors. The fæces may be deposited in vessels or places where fly larvæ are in great numbers, or a subsequent infection of the fæces with the eggs or larvæ of flies may have taken place. Only when the inspection of the excrement immediately following defæcation proves the presence of living larvæ, and when there were certainly no fly larvæ in the vessel previously, can one speak of the passing of fly larvæ from the intestine. More frequent than the cases showing no special symptoms are those with pronounced disturbances in the intestinal passage, obstruction or diarrhœa (also constipation and diarrhœa alternately), violent and sometimes agonizing abdominal pains (Pottiez[1197]), which preceded the evacuation of the larvæ and subsided after their removal. General symptoms, like weakness, languor, transitory vague pains, loss of appetite, sickness, rarely fever, giddiness, attacks of faintness, epileptic attacks (Krause[1198]) are observed. In a few cases blood and pus have been noticed in the evacuation of the bowels.

[1197] Pottiez, Bull. de l’Acad. royale de Méd. de Belgique, xv.

[1198] Krause, Deutsch. med. Wochenschr., 1886, xvii.

In the cases of chronic myiasis of the intestine the aspect of the disease is dominated by the complex symptom of colitis mucosa.

The following features are noticeable, namely, the intermittent passing of blood, the influence over the expulsion of the larvæ of mechanical procedure (massaging of the abdomen), the duration of the process for several years, the sometimes enormous number of insects contained in the dejecta. Another clinically important factor is the passing of the larvæ in batches. While for some time no larvæ may appear in the stools, they may suddenly be ejected in great numbers, either because the conditions of feeding are not suitable, or because medicaments remove them from the intestine. The hæmorrhage is ascribed by Schlesinger and Weichselbaum directly to lesions of the mucous membrane caused by the larvæ; in the case reported by these writers there were found shreds of tissue as well as pus in the stool. The pains occurring spontaneously in the abdomen are at times influenced by position and attitude of the body, often they were more violent after rest and after evacuation of the bowels; often they were continuous, but in that case less intense; pressure on the abdomen is generally little felt. The condition of the blood was in two cases (Pasquale[1199] and Schlesinger and Weichselbaum) a marked chlorotic one. The state of nutrition seems almost always to suffer with prolongation of the disease, but in Peiper’s[1200] cases this was not so. The condition of the appetite was in some instances good, in others very bad. A frequent symptom is headache of a migraine-like character and neuralgic pains in different parts.

[1199] Pasquale, Centralbl. f. Bakt., 1891.

[1200] Peiper, “Fliegenlarv. als gelegentl. Parasiten d. Menschen,” Berlin, 1900.

Schlesinger and Weichselbaum’s case shows that there are forms of myiasis intestinalis which, after prolonged sickness, lead to death, and that in consequence of the formation of intestinal abscesses stricture of the intestine may arise from the subsequent formation of a scar.

The question of the mode of infection is interesting; in this mouth, nose and anus must be considered. The most frequent way is certainly by means of food on which flies have laid their eggs, or which is permeated with young maggots. This may be raw (especially grated) meat, cheese, fruit, salad, milk, cabbage, cold farinaceous foods, raspberries. When the stomach is affected, when the gastric juice has lost acidity and power of digestion, the larvæ will be able to stay and develop more easily. According to Csokor,[1201] if the eggs get into the gastro-intestinal canal of man with the food, the delicate stages of the young larvæ would certainly not survive the action of the gastric juice. Salzmann[1202] assumed that the invasion occasionally occurred through the rectum, the larvæ creeping into the anus while the person is asleep. Wirsing accepts this method of infection for two of his cases, where it was a question of the infection of an infant. Salzmann[1202] reports a case where the maggots of Anthomyia[1203] scalaris were passed in great numbers from the urethra of an old man. The patient had been catheterized on account of urethral stricture and was probably infected with eggs or larvæ at the same time.

[1201] Csokor, Wien. klin. Wochenschr., 1901, p. 129.

[1202] Salzmann, Württemberg. med. Korrespondenzbl. 1883, liii.

[1203] [This is presumably Homalomyia (Fannia) scalaris.--F. V. T.]

The diagnosis of the affection is easy and sure, if living larvæ are found in the contents of the stomach or in the stools, and if contamination is out of the question.

The number of different species of flies whose larvæ are found in myiasis intestinalis is considerable. The larvæ of species of Anthomyia (A. canicularis,[1204] A. scalaris, etc.), of Sarcophaga carnaria and S. magnifica and of Musca vomitoria[1205] are especially observed.

[1204] [This fly, common in houses, is known as Homalomyia canicularis, and the next belongs to the same genus.--F. V. T.]

[1205] [This fly belongs to the genus Calliphora, not Musca.--F. V. T.]

The prognosis is certainly generally favourable, but must be made with some reserve in chronic cases, in view of the observations of Schlesinger and Weichselbaum (intestinal stenosis).

The treatment must aim at removing the larvæ as soon as possible from the digestive canal.

In cases of myiasis of the stomach, a thorough washing out of the stomach (Joseph,[1206] Staniek[1207]) is to be preferred to emetics used with success in individual instances; perhaps it would be advisable to add menthol or thymol to the mixture.

[1206] Joseph, Deutsch. med. Zeitg., 1885 and 1887.

[1207] Staniek, see Schlesinger and Weichselbaum, p. 47.

In myiasis of the intestine internal remedies and local treatment of the intestine must be considered.

So far santonin seems to have proved to be the best remedy. In some cases extract. filicis maris, calomel, semina cucurbitæ, naphthalene 0·1 to 0·5 (Peiper[1208]), infus. of Persian insect powder (5 in 200), mineral waters, Carlsbad water, seem to have had good results.

[1208] Peiper, “Fliegenlarv. als gelegentl. Parasiten d. Menschen,” Berlin, 1900.

For irrigation of the rectum, weak solutions of argentum nitricum, tannin, thymol, gelatine, ol. ricini, naphthalene may be used. Wirsing administered an aperient (Rurella compound liquorice powder) and a soap enema after the passing of the first larvæ.

The principal thing is the prophylaxis, which must include the careful protection of articles of food, on which flies may lay their eggs (protection by glass dishes, tulle or fine wire nets). Fruit should not be eaten before being washed or rubbed with a cloth.

*Gastricolous Oestridæ* (Creeping Disease).

Syn.: Creeping eruption; Larva migrans; Hautmaulwurf; Dermatomyiasis linearis migrans oestrosa; Hyponomoderma; Dermatitis linearis migrans; Linea migrans; Epidermiditis linearis migrans Wolossatik; Kriechkrankheit; Hautkratzschorf; Myiase hypodermique.

Under the name “creeping disease,” R. J. Lee[1209] has recorded a peculiar affection of the skin in a three year old girl, which appeared first in the form of pale red, thread-like irregular protuberances, which seemed partly to become entwined on the right malleolus and had spread without causing special disturbances to the abdomen. Dickinson, Fox and Duckworth[1210] reported, in connection with this, that they observed a growth of this red line of about 1 in. per diem. Since then a number of similar cases have been reported which, without doubt, were cases of larvæ creeping under the skin. Crocker[1211] saw such a case in a two year old girl, the progress of the red line varying in one night between 4 and 7-1/2 in. In Europe the first case was observed in Vienna, by v. Neumann and Rille,[1212] also in a two year old girl.

[1209] R. J. Lee, Journ. Clin. Soc. Lond., November 27, 1874.

[1210] Dickinson, Fox and Duckworth, ibid., 1875.

[1211] Crocker, “Diseases of the Skin,” 1893; “Atlas of the Diseases of the Skin.”

[1212] v. Neumann and Rille, Wien. klin. Wochenschr., 1895; Dermatologenkongr., Graz, 1895.

v. Samson-Himmelstjerna,[1213] Sokoloff,[1214] Rawnitzky[1215] found larvæ at the end of the tract, which had been recorded as larvæ of Gastrophilus by Cholodowsky.[1216] According to Blanchard (Arch. f. Par., 1901) the larvæ were those of Hypoderma bovis.

[1213] v. Samson-Himmelstjerna, Wratsch, 1895; Arch. f. Derm. u. Syph., 1897.

[1214] Sokoloff, Wratsch, 1896.

[1215] Rawnitzky, Derm. Zeitschr., v, p. 704.

[1216] Cholodowsky, Wratsch, 1896.

How these larvæ get into the skin has not yet been definitely ascertained; v. Samson is of the opinion that they usually obtain access to man as larvæ, Stelwagon[1217] believes that the infection generally occurs in a seaside watering place; a patient of Ehrmann’s[1218] fell ill when he returned from the manœuvres, where he had lain for some time on the ground. Here and there it is reported that the eruption was preceded for a longer or shorter time by lesions of the skin (incised wounds, furuncles, slight excoriations, v. Harlingen[1219]).

[1217] Stelwagon, Journ. Cut. Dis., xxii, 8.

[1218] Ehrmann, Wien. derm. Ges., November 17, 1897.

[1219] v. Harlingen, Amer. Journ. of Med. Sci., 1902.

Twice it has been suggested that perhaps the parasites might come from vineyard snails (Crocker, Lenglet and Delaunay[1220]), and it is pointed out by v. Samson that in Russia the infection of peasants who work in the fields was specially frequent. It is noticeable how frequently the affection begins on uncovered parts of the body (face, hands, arms); but that fact, on the whole, is not in conflict with the statement (Kengsep[1221]) that the disease makes its first appearance over the nates, because children often sit on the ground and play with that part of their body uncovered. A case observed by us was that of an elderly lady who did not do this and was properly clothed, yet showed the typical lines of creeping disease on the nates, and asserted again and again that she had the feeling as if a worm were creeping under her skin.

[1220] Lenglet and Delaunay, Annal. de Derm. et de Syph., 1904.

[1221] Kengsep, Derm. Centralbl., 1906, vii.

The disease occurs in children as well as adults, so that age, sex and calling offer no determining point etiologically.

The clinical symptoms of the disease consist in the sudden appearance of itching and burning; if the cause is looked for one perceives a red line, raised but little above the surface of the skin, with irregular curves, never branched, but often entwined, broadening more or less rapidly at one end (1 to 15 cm. in twenty-four hours). The larva can be seen sometimes with a lens under pressure of the skin as a dark spot; formations of pus, such as other larvæ produce, are not noticed; now and again there is a formation of little vesicles (Hamburger,[1222] v. Harlingen,[1223] Bruno,[1224] Ehrmann,[1225] Brodier and Fouquet,[1226] Rawnitzky[1227]). It may happen that the parasite burrows through a small region of the skin with many close curves for some time; on the other hand, observations exist where it covered large tracts in a short time. The itching and smarting cease in the place left by the larva, so that the patients even in the shortest tract can point out at which end the larva is, even if they have not watched the lengthening of the tract. Very rarely the larva invades the mucous membrane of the mouth, the nose, and the conjunctiva, proceeding from thence to the external cutaneous area.

[1222] Hamburger, Journ. of Cut. Dis., 1904.

[1223] v. Harlingen, loc. cit.

[1224] Bruno, v. Rille and Riecke, “Handb. d. Hautkrankh. v. Mraček.”

[1225] Ehrmann, loc. cit.

[1226] Brodier and Fouquet, Bull. de la Soc. franç. d. Derm., 1904.

[1227] Rawnitzky, loc. cit.

The localization of the affection is very varied; the primary seat has been observed on the glutei muscles (Lee, Kengsep, Morris,[1228] Rille, Seifert) and their surroundings (Stelwagon, Hamburger, Bruno), on the lower extremities (Stelwagon, Lenglet and Delaunay, Hutchins, Moorhead, Lee, Crocker, Schmid,[1229] v. Harlingen), on the upper extremities (Samson, Meade and Freeman, Hutchins, Sokoloff, v. Harlingen, Brodier and Fouquet, Shelmire,[1230] Stelwagon), on the face (Sokoloff, Moorhead, Kumberg,[1231] Rawnitzky, Crocker, Boas[1232]), on the neck (Sokoloff), and on the body (Ehrmann, Brodier and Fouquet, Kaposi,[1233] Topsent[1234]).

[1228] Morris, Brit. Journ. Derm., 1896.

[1229] Schmid, Verein der Aerzte in Steiermark, February 12, 1900.

[1230] Shelmire, Journ. Cut. Dis., 1905.

[1231] Kumberg, St. Petersb. med. Wochenschr., 1898.

[1232] Boas, Monatsh. f. prakt. Derm., 1907, xliv.

[1233] Kaposi, Wien. klin. Wochenschr., 1898.

[1234] Topsent, Arch. de Par., 1901.

The duration of the affection varies very much; it varies between a few hours and some years[1235]; several times a spontaneous recovery has been reported.

[1235] [This is extremely unlikely, as the bots of Hypoderma only live for nine or ten months at the most!--F. V. T.]

The diagnosis of the disease is not at all difficult owing to its peculiar appearance.

The treatment can only consist in the removal or killing of the larvæ, since one cannot rely on spontaneous recovery, even if it has occurred in some cases. If one should succeed in locating the larva as a black spot at the end of the tract, its removal by means of a needle is the simplest method (Quortrup and Boas[1236]). In some instances a cure has been successfully accomplished by excision of the active end of the tract (v. Neumann and Rille, Schmid). In opposition to this method, which not all patients will allow, the method practised by Arab women (Rille and Riecke[1237]) of killing the worm with red hot needles is quite rational. Shelmire[1238] used the electrolytic needle for the destruction of the maggots, Stelwagon[1239] made use of cataphoresis, by means of which he applied a sublimate solution, afterwards cauterizing with a drop of nitric acid, as excision was refused. Crocker[1240] and v. Harlingen[1241] injected small quantities of carbolic acid; Moorhead[1242] by a single freezing of the skin with ethyl chloride, attained a definite cessation of the attack at the active end. Hutchins[1243] in one case made use of hypodermic injection of a few drops of solution of cocaine and afterwards of 1 to 2 drops of chloroform; in a second case of repeated applications of tincture of iodide, as Lenglet and Delaunay[1244] did. v. Harlingen[1245] allayed the affection in his first case by rubbing in sapo viridis and tar, in Kensep’s[1246] case the cure seems to have been accomplished by an ointment containing resorcin, in Meade and Freeman’s[1247] case by a 20 per cent. ichthyol paste. In our case we made exclusive use of Lassar’s paste; within four weeks a cure resulted, probably spontaneously, since one cannot ascribe any essential effect to this paste.

[1236] Quortrup and Boas, Hospitalstid., 1907.

[1237] Rille and Riecke, “Handb. d. Hautkrankh.,” v. Mraček, 1907, iv.

[1238] Shelmire, loc. cit.

[1239] Stelwagon, loc. cit.

[1240] Crocker, loc. cit.

[1241] v. Harlingen, loc. cit.

[1242] Moorhead, Texas Med. News, 1906.

[1243] Hutchins, Journ. Cut. Dis., 1906.

[1244] Lenglet and Delaunay, loc. cit.

[1245] v. Harlingen, loc. cit.

[1246] Kensep, loc. cit.

[1247] Meade and Freeman, Brit. Journ. Derm., October, 1906.

APPENDIX ON PROTOZOOLOGY,

Comprising Notes on Recent Researches, Formulæ of some Culture Media, and Brief Notes on General Protozoological Technique.

BY

H. B. FANTHAM, M.A., D.Sc.

I.--NOTES ON RECENT RESEARCHES.

Since the foregoing section on Protozoology was sent to press, certain interesting observations and results have been published. Brief notes on such, and some references thereto, are now added.

It is necessary, however, to remark that sometimes it is impossible to give a precise or rigid definition to a genus of Protozoa, owing to differences of opinion, to differences regarding nomenclature or to incompleteness of knowledge. Such a lack of definition, while inconvenient for the time being, is not unhopeful, as it directs attention to the necessity for further work, which is inevitable in such a relatively new and wide subject as protozoology. Thus, it may be noted in illustration that Minchin, in 1912, in his text-book regarding the genus Entamœba writes: “The entozoic amœbæ are commonly placed in a distinct genus, Entamœba, distinguished from the free-living forms by little, however, except their habitat and the general (but not invariable) absence of a contractile vacuole.”

*Differences between Entamœba histolytica and E. coli.*--In continuation of the remarks on pp. 34 and 40, it may be added that Lugol’s solution (iodine in aqueous potassium iodide solution) in fresh specimens shows by brownish staining the presence of glycogen in the vacuoles of Entamœba coli. Such a reaction is rarely or never given by E. histolytica.

*Phagedænic Amœbæ.*--Carini and others record cases in which the skin around an operation wound in connection with liver abscess became gangrenous. Amœbæ, possibly Entamœba histolytica, were found therein and may have been responsible for the gangreno-phagedænic action.

*Endamœba gingivalis* (see pp. 43, 44).--Smith and Barrett,[1248] after analysing the early literature, state (June, 1915) that Endamœba gingivalis, Gros, 1849, is the correct name for the following organisms: E. buccalis, Prowazek, 1904 (see p. 43); Amœba gingivalis, Gros, 1849; Amœba buccalis, Steinberg, 1862, and Amœba dentalis, Grassi, 1879. They conclude that E. gingivalis is the causal agent of pyorrhœa alveolaris, and that this disease responds to treatment with emetine.

[1248] Journ. of Parasitol., i, p. 159.

*Entamœba kartulisi* (see p. 44), synonym E. maxillaris, Kartulis, is considered to be E. gingivalis.

Smith and Barrett adopt the generic name Endamœba, Leidy, 1879 (see footnote on p. 31, also p. 34). Leidy worked on Endamœba blattæ.

*Craigia and Craigiasis* (see p. 45).--Barlow[1249] (May, 1915) found Craigia (Paramœba) hominis in cases of chronic diarrhœa and mild dysentery in Honduras. He also described a new species of Craigia under the name of C. migrans. Fifty-six cases were studied, five of which were due to Craigia hominis, the remainder to C. migrans. In C. migrans, each flagellate, on attaining full development, becomes an amœba without dividing. Each amœba encysts and produces a number of flagellates which are somewhat like cercomonads. On the other hand, in C. hominis the flagellate form produces, by longitudinal fission, several generations of flagellates before entering upon the amœbic stage. The cysts of C. migrans contain fewer “swarmers” (flagellulæ) than those of C. hominis, but the “swarmers” are somewhat larger, namely, 5 µ instead of 3 µ in diameter. Further, there is no accessory nuclear body in C. migrans, but its flagellum stains more deeply than that of C. hominis and has a peculiar banded appearance.

[1249] Amer. Journ. Trop. Dis. and Prevent. Med., ii, p. 680.

*Human Trichomoniasis* (see pp. 52–56).--Lynch[1250] (April and May, 1915), working in Charleston, seems to favour the view that the trichomonads found in the vagina, urethra, mouth, lungs and alimentary tract are one and the same organism, and that these flagellates may further excite already existing inflammatory conditions. He gives detailed histories of cases of (a) infection of the vagina and gums, and (b) intestinal infection manifested as intermittent attacks of diarrhœa. The flagellates were found in catarrhal vaginal discharge, in blood-stained scrapings from the gums (together with Endamœba buccalis), and in stools after a purge of magnesium sulphate. The parasites were tetratrichomonads (see footnote, p. 53), that is, each possessed four flagella anteriorly as well as an undulating membrane. Lynch successfully infected rabbits from the cases and from cultures of the parasite. Encysted trichomonads were seen in a patient’s stools, in rabbits infected therefrom and in cultures. The culture medium used was bouillon acidified with about 0·05 per cent. acetic acid and the cultures were maintained at 30° C.

[1250] Ibid., p. 627; New York Med. Journ., May 1, 1915, ci, p. 886.

Trichomonads occur in the digestive tracts, for example, the cæca of rats and mice (fig. 422). In man allied flagellates can occur in similar situations, as well as in other parts of the intestine.

Other trichomonad-like organisms have been recently described from the fæces of man, more particularly from cases of chronic dysentery in the tropics. Derrieu and Raynaud[1251] (July, 1914), working in Algeria, found a flagellate possessing five free flagella anteriorly and an undulating membrane apparently lateral. They named the parasite Hexamastix ardin-delteili, but the generic name Hexamastix is pre-occupied. Chatterjee[1252] (January, 1915), working in India, found probably the same flagellate and called it Pentatrichomonas bengalensis.

[1251] Bull. Soc. Path. Exot., vii, p. 571.

[1252] Ind. Med. Gaz., l, p. 5.

*Chilomastix* (*Tetramitus*) *mesnili* (see p. 57).--Alexeieff[1253] (1914) now places the parasite originally called Macrostoma mesnili, by Wenyon (1910), in the genus Chilomastix, Alexeieff. The differential characters of the genera Tetramitus and Chilomastix are not especially well marked. According to Alexeieff, Tetramitus is characterized by four unequal flagella (which he figures anteriorly), a ventral cytostome in the form of a linear cleft and a pulsatile vacuole in front of the anterior nucleus. Chilomastix, according to the same author, has three forwardly directed flagella and a fourth backwardly directed one in the cytostome, which is well developed (fig. 423). Some authors consider that the fourth flagellum forms the edge of an undulating membrane in the cytostome.

[1253] Zool. Anzeiger, xliv, pp. 203, 206; and ibid., xxxix, p. 678.

Diagrams of Chilomastix mesnili are given in fig. 423.

*Giardia* (*Lamblia*) *intestinalis* (see p. 57).--Alexeieff[1254] (1914) considers that Lamblia intestinalis, Lambl, should be placed in the genus Giardia, Kunstler, 1882. Bipartition occurs in the encysted state. The axostyles persist in the quadrinucleate cyst.

[1254] Zool. Anzeiger, xliv, p. 210.

*Cercomonas hominis* (see p. 61).--This parasite is considered by some authors to be of a doubtful nature, as it is thought to have been mistaken for deformed or incompletely observed Trichomonas or Chilomastix or even Lamblia.

Wenyon[1255] (1910) described Cercomonas longicauda from cultures of human fæces. It is considered that the genus is very confused, and the author points out that the tail flagellum has been overlooked. He considers that the genus Cercomonas should include flagellates with an anterior blunt end from which arises a single long flagellum, and a posterior tapering end also with a flagellum, which can be traced over the surface of the body towards the insertion of the anterior flagellum.

[1255] Quart. Journ. Micros. Sci., lv, p. 241.

Another species, Cercomonas parva, has been found in cultures of human fæces by Hartmann and Chagas[1256] (1910). It has a somewhat different structure.

[1256] Mem. Inst. Oswaldo Cruz, ii, p. 67.

Further researches are necessary on the organisms variously referred to the genus Cercomonas.

*Transmissive Phase of Trypanosomes in Vertebrates.*--In addition to the general remarks on the morphology of trypanosomes set forth on pp. 70 to 72, it may be noted that Woodcock[1257] (November, 1914) states that, in certain cases, there is a definite transmissive phase of a trypanosome in its vertebrate host. He quotes the work of Minchin and himself on T. noctuæ of the little owl, in which the transmissive form is spindle-shaped and occurs in the bird’s peripheral blood during the early summer months (see p. 69). A similar phase occurs in T. fringillarum, and Robertson[1258] has found that the short, stumpy form of T. gambiense is its transmissive phase in vertebrates.

[1257] Arch. f. Protistenk., xxxv, p. 197.

[1258] Proc. Roy. Soc., B, lxxxv, p. 527.

*Trypanosoma lewisi* (see p. 88).--Brown (1914–15) has published some interesting results on the potential pathogenicity of T. lewisi.

*Blepharoplastless Trypanosomes* (see p. 101).--Laveran[1259] (April, 1915) suggested a practical use of strains of blepharoplastless trypanosomes produced by the action of drugs. He finds that tryposafrol will also produce such strains, and remarks on blepharoplastless strains of T. evansi and T. brucei, which in the former case can undergo 450 passages without reversion, and in the latter 273 passages. He states that if it is desired to inoculate surra or nagana to Capridæ or Bovidæ in order to produce immunity, use should be made of the blepharoplastless races of the respective trypanosomes, which races are a little less virulent than the corresponding normal ones. Also, the immunity which follows from an infection due to blepharoplastless T. evansi or T. brucei is only a little less complete than that following infections from either of the respective normal strains.

[1259] C. R. Acad. Sci., clx, p. 543.

*The Experimental Introduction of certain Insect Flagellates into various Vertebrates, and its bearing on the Evolution of Leishmaniasis.*--In continuation of the remarks on pp. 103, 104, and 112, further researches have been conducted on the introduction into vertebrates of flagellates normally parasitic in insects. The vertebrates became infected by inoculation with the flagellates or by being fed on insects containing the protozoa. Fantham and Porter[1260] (June, 1915) published the following results. Flagellates from sanguivorous and non-sanguivorous insects were used, and cold-blooded as well as warm-blooded vertebrates as hosts. The introduced protozoa were pathogenic to the mammals, but not markedly so to the cold-blooded vertebrates. Herpetomonas jaculum, H. stratiomyiæ, H. pediculi, and Crithidia gerridis (parasitic in certain waterbugs) proved pathogenic to mice. A puppy was infected by way of the digestive tract with H. ctenocephali. Frogs became infected with H. jaculum and with C. gerridis, toads and grass snakes with H. jaculum, lizards with C. gerridis, and sticklebacks with H. jaculum. Second and third passages of some of the parasites were obtained. The protozoa, whether Herpetomonas or Crithidia, were present in the vertebrate hosts in either the non-flagellate or the flagellate form, or usually both. They were more abundant in the internal organs of the hosts, more particularly in the liver, spleen and bone-marrow. In all experiments in which C. gerridis was used the parasite invariably retained the crithidial facies in the vertebrate host. No transition to a trypanosome was ever seen. Infections in adult animals were not so heavy as in the young ones, and the parasites were more virulent in young hosts, as is the case with Mediterranean kala-azar in children.

[1260] Proc. Camb. Philosoph. Soc., xviii, p. 137; and Annals Trop. Med. and Parasitol., ix, p. 335.

The mode of infection of the vertebrate in Nature seems to be contaminative, either by its food or through an already existing abrasion or puncture on the surface of its body. Cases in which the flagellate-infected insects have been allowed to suck the blood of vertebrates have proved negative up to the present. In areas where leishmaniases are endemic, an examination should be made of all insects and other invertebrates likely to come into contact with men or dogs, or rats and mice (see below), in order to ascertain if these invertebrates harbour herpetomonads. Preventive measures should be directed against such invertebrates, especially arthropods. Further, it is likely that certain vertebrates, such as reptiles and amphibia (especially those that are insectivorous), may serve as reservoirs of leishmaniases, or, as they should preferably be termed, herpetomoniases. From such reservoirs the herpetomonads may reach man by the agency of ectoparasites or flies, especially such as are sanguivorous.

That vertebrates in Nature can harbour herpetomonads in their blood has been shown by the work of Dutton and Todd (1903) on the herpetomonads of Gambian mice, while the recently published investigations of Fantham and Porter[1261] (June, 1915) on natural herpetomonads in the blood of mice in England have shown that these rodents may be a natural reservoir of herpetomoniasis. The origin of the infection of mice is to be sought in a flagellate of an ectoparasite of the mouse, very probably Herpetomonas pattoni parasitic in various fleas, which protozoön can adapt itself to life in the blood of mice. Herpetomonads were also found naturally in the blood of birds by Sergent (1907). Recently, Fantham and Porter have successfully infected birds with herpetomonads experimentally.

[1261] Parasitology, viii, p. 128.

The significance of insect flagellates in relation to the evolution of disease has recently been set forth by Fantham[1262] (June, 1915). The deductions to be made from the occurrence of a herpetomonad stage in Leishmania, especially in L. tropica, in man himself, and of flagellate stages of the so-called Histoplasma capsulatum in man are fully discussed and correlated. It is pointed out that flagellosis of plants (see p. 104) may possibly be connected with leishmaniasis. The evolution of Leishmania from flagellates of invertebrates is thus traced and the way again indicated for preventive measures against leishmaniasis, as first set forth by Dodds Price and Rogers.

[1262] Annals Trop. Med. and Parasitol., ix, p. 335.

Franchini and Mantovani (March, 1915) have successfully infected rats and mice by inoculation or by feeding with Herpetomonas muscæ domesticæ obtained from flies and from cultures.

It is of great interest to note that the recent observations of Ed. and Et. Sergent, Lemaire and Senevet[1263] (1914) have demonstrated the presence of a herpetomonad flagellate in cultures of the blood and organs of geckos obtained from areas in Algeria in which Oriental sore, due to L. tropica, is prevalent. Phlebotomus flies, which may harbour a natural herpetomonad, feed on the geckos and on men. Hence animals like geckos may possibly act as reservoirs of leishmaniasis. Lindsay[1264] (1914) writes that the parasite of dermo-mucosal leishmaniasis in Paraguay is believed by native sufferers to be conserved in rattlesnakes, and spread by ticks or flies (Simulium) feeding on the reptiles and transferring the parasite to man.

[1263] Bull. Soc. Path. Exot., vii, p. 577.

[1264] Trans. Soc. Trop. Med. and Hyg., vii, p. 259.

*The Transmission of Spirochæta duttoni* (see p. 116).--It is probable that Ornithodorus savignyi acts as the transmitting agent of S. duttoni in places like Somaliland (Drake-Brockman, 1915).[1265]

[1265] Ibid., viii, p. 201.

*Spirochæta bronchialis* (see p. 122).--The morphology and life-history of S. bronchialis have been investigated by Fantham[1266] (July, 1915). From researches conducted in the Anglo-Egyptian Sudan, he found that S. bronchialis is an organism presenting marked polymorphism, a feature that has only been determined by the examination of numerous preparations from the deeper bronchial regions of various patients.

[1266] Annals Trop. Med. and Parasitol., ix, p. 391.

S. bronchialis varies in length from 5 µ to 27 µ, and its breadth is about 0·2 µ to 0·6 µ. These variations are due to the processes of growth and division. Many of the parasites measure either 14 µ to 16 µ long, or 7 µ, to 9 µ, the latter resulting from transverse division of the former. The ends show much variation in form, but approach the acuminate type on the whole. The discrepancies in dimensions given by the very few previous workers on the subject are probably the result of the measurement of a limited number of parasites. All such sizes can be found on some occasion during the progress of the disease, when a larger number of spirochætes is examined.

The movements of S. bronchialis are active, but of relatively short duration, when it is removed from the body. The number of coils of the spirochæte is rather an index of its rapidity of motion than a fixed characteristic of the species.

The motile phase of S. bronchialis is succeeded by one of granule formation, the granules or coccoid bodies serving as a resting stage from which new spirochætes are produced. The formation of coccoid bodies and reproduction of spirochætes from them can be observed in life.

S. bronchialis is a species distinct from the spirochætes occurring in the mouth. It differs from them in morphology, pathogenicity and in staining reactions. It is not a developmental form of any bacterium, and is an entity in itself.

The passage from man to man is effected most probably by means of spirochætes, and especially coccoid bodies, that leave the body in the spray with expired air and by way of the nasal secretions. Owing to the fragility and short life of S. bronchialis extracorporeally, the resistant coccoid bodies in air, in dried sputum and dust, and possibly also on the bodies of flies and other insects, are probably instrumental in inducing attacks of bronchial spirochætosis in human beings, especially those having a lowered bodily resistance, such as occurs after a chill. Lurie (December, 1915), has described a case from Serbia.

*The Spirochætes of the Human Mouth* (see p. 122).--Two species of spirochætes were recorded as occurring in the human mouth about forty or fifty years ago. These are Spirochæta buccalis, Steinberg (often ascribed to Cohn, 1875), and S. dentium, Miller (often attributed to Koch, 1877).

The most recent work on S. dentium and S. buccalis is that of Fantham[1267] (July, 1915), who observed the parasites ascribed to Cohn and to Koch, these being the two common spirochætes seen in the mouths of natives of the Sudan and of Europeans in England, as well as the forms described and cultivated by recent investigators. Some of the mouth spirochætes are not very active, but there is marked corkscrew and boring movement, and they are flexible. Tangles or tomenta of these mouth spirochætes are common. Internal structure is seen with some difficulty, but in some specimens it can be determined, and chromatin granules are then seen. Mühlens (1907) figured stained specimens of S. buccalis and S. dentium, in which chromatin-coloured granules were distributed along the bodies of the organisms.

[1267] Annals Trop. Med. and Parasitol., ix, p. 402.

S. dentium has tapering ends, and varies in length from 4 µ to 10 µ. S. dentium is rather like Treponema pallidum, and has been placed by some workers--for example, Dobell--in the genus Treponema. It has already been mentioned, on p. 128, that Noguchi cultivated three species of Treponema from the human mouth--namely, T. macrodentium, T. microdentium, and T. mucosum, but they cannot be easily distinguished morphologically, and so may appear to be biological varieties of S. dentium.

S. buccalis has somewhat rounded or bluntly acuminate ends and varies in length from 9 µ to 22 µ. A slight membrane or crest may sometimes be observed. S. buccalis was found to be the predominant spirochæte in the mouths of eight natives examined by Fantham in the Anglo-Egyptian Sudan.

S. buccalis and S. dentium take up stains well and with relative ease. Intracellular stages of the parasites are uncommon. Multiplication by binary fission has also been observed. Coccoid bodies or granule stages of the mouth spirochætes are formed, but appear to be relatively few in number.

J. G. and D. Thomson[1268] (1914) have written an interesting paper on various spirochætes occurring in the alimentary tract of man and of some of the lower animals. They have also given a useful list of references, and the work of some of the earlier authors is discussed in the paper.

[1268] Proc. Roy. Soc. Med., vii, pt. 1, p. 47.

With regard to the general morphology of spirochætes, it may be noted that the so-called axial fibre of Zuelzer is acknowledged to be homologous with the membrane or crista of molluscan spirochætes.

*Coccidia in Cattle.*--Regarding the remarks on coccidiosis or “red dysentery” in cattle on p. 147, it may be added that Schultz[1269] (July, 1915) has found the malady among cattle in the Philippine Islands. He states that some irregular or atypical cases of apparent rinderpest are really due to coccidia. As has been pointed out by Montgomery, rinderpest can be transmitted by blood inoculation, while coccidiosis cannot be so transmitted, but may be diagnosed by the microscope. These differences should be remembered as the two diseases are often found to be associated and are difficult to separate clinically. Coccidia have also been found in Australian cattle.

[1269] Journ. Infect. Dis., xvii, p. 95.

*The Hæmosporidia.*--It is likely that this order (see p. 151) may be soon abolished. Mesnil[1270] (April, 1915) considers that the grouping of the three families, Plasmodiidæ (or Hæmamœbidæ), Hæmogregarinidæ and Piroplasmidæ in the order Hæmosporidia is no longer possible, because of the coccidian nature of the Hæmogregarines (see p. 154). The Coccidia are divisible into the Adeleidea and the Eimeridea (see p. 141). The Hæmogregarinidæ are allied to the former, and the Plasmodiidæ to the latter. The Piroplasmidæ, until more is known of their life-cycle in the invertebrate host, cannot be more definitely placed.

[1270] Bull. Soc. Path. Exot., viii, p. 241.

*The Leucocytozoa of Birds.*--Regarding the statement, on p. 153, that Laveran and França consider that avian leucocytozoa may inhabit red blood cells, it may be added that França[1271] (April, 1915) remarks that the action of the parasites on the red cells is very rapid and very intense. The host cells become so altered that it is difficult to recognize their true nature. He used very young birds in his researches. Two shapes of host cell are considered, namely, those with fusiform prolongations, and those which are rounded and without such prolongations (see p. 153). The movements and form of the Leucocytozoa determine the shape of the host cell, as was pointed out by Fantham[1272] in 1910.

[1271] Ibid., p. 229.

[1272] Proc. Zool. Soc. Lond., 1910, p. 694.

Schizogony of these parasites has been seen by França (1915) and by Coles (1914), in addition to Fantham (1910), and to Moldovan (1913), mentioned on p. 153. Schizogony may also take place in the lungs of the host. The genus Leucocytozoön, established by Ziemann in 1898, belongs to the family Hæmamœbidæ.

II.--FORMULÆ OF SOME CULTURE MEDIA.

(1) *Culture Media for growing Amœbæ.*--There has been much discussion as to whether the true parasitic Entamœbæ or Endamœbæ can be grown on culture media (see p. 42). Undoubtedly certain free-living amœbæ can be so grown, and it is considered that some of the earlier researches on the so-called artificial growth of the dysenteric amœbæ were really due to contaminations with free-living forms. The following media are worthy of note:--

Musgrave and Clegg in 1904 devised a culture medium for amœbæ. The organisms grown by them were probably not dysenteric amœbæ, as was thought, but free-living forms. Phillips[1273] (1915) gives a slightly modified formula of Musgrave and Clegg’s medium, thus:--

Agar-agar 2·5 grm. Sodium chloride 0·05 " Liebig’s beef extract 0·05 " Normal sodium hydroxide 2·0 c.c. Distilled water 100·0 "

[1273] “Amœbiasis and the Dysenteries,” p. 8.

Without clarifying, sterilize at 7 kilograms pressure per square centimetre for about three-quarters of an hour. It should be neutral to phenolphthalein.

Anna W. Williams[1274] (1911) described a medium consisting of fresh tissue spread on agar plates for the culture of amœbæ. There are three stages in the procedure: (1) obtaining living amœbæ free from other living organisms; (2) obtaining sterile tissue; and (3) making successive transplants of amœbæ and tissue, and showing that every transplant is free from other living organisms. Each step requires many controls. The essentials of the method may now be given. Remove aseptically and rapidly the tissue required, such as brain, liver, kidney, or spleen, from a freshly killed animal (guinea-pig, rabbit, or dog). Put each tissue on a separate agar plate. Cut the selected tissue into tiny pieces, and spread them over freshly made agar plates. Place these plates in a thermostat at 36° C. for twenty-four hours to insure sterility. Add the broken up tissue to the amœbæ, free from bacteria, and maintain the cultures in thermostats, some at 36° C., and some at 20° C. to 24° C. Emulsions of liver and brain in sterile neutral glycerine may also be used. The freshly removed tissue serves as food for the amœbæ.

[1274] Journ. Med. Research, xxv, p. 263; and _Proc. Soc. Exper. Biol. and Med._, viii, p. 56.

The cultural amœbæ mentioned on p. 42 were grown on such media or modifications thereof. One modified medium actually used was brain tissue, to which blood was added from day to day, and an easily assimilable bacterium (one of the influenza group of bacilli) was present, which did not overgrow the medium at a temperature of 38° C. Different conditions of food and of temperature produced morphological variations in the cultural amœbæ.

Couret and J. Walker[1275] (1913) state that they have cultivated five varieties of intestinal amœbæ, the associated bacteria having been previously separated. They used a medium consisting of agar to which sterile autolysed tissue had been added. The sterile tissue, such as brain or liver, was kept in a sterile thermostat at a temperature of 40° C. for ten to twenty days. The surface of the agar should be broken up before use, and the medium must not be too acid (not over 1·5 per cent.). They consider that autolysed tissue is necessary for the growth of Entamœbæ, and that naturally associated bacteria aid growth by autolysing the tissues.

[1275] Journ. Exper. Med., xviii, p. 252.

(2) *Culture Media for the growth of Protozoa parasitic in the Blood.*--MacNeal and Novy,[1276] in 1903, used a mixture of blood and agar for the cultivation of trypanosomes such as T. lewisi and T. brucei. They employed varying proportions of the blood and agar, a medium consisting of two parts of defibrinated rabbit’s blood mixed with one part of agar being useful. The trypanosomes grew in the water of condensation. Some of the authors’ earlier formulæ contained different proportions of blood and agar with a little peptone, while one of these media contained meat extract, agar, peptone, salt and sodium carbonate. The temperature, like the proportion of blood and agar, varied with the trypanosome investigated, but the optimum was 25° C.

[1276] See Sleeping Sickness Bulletin (1909), i, No. 8, p. 287.

Mathis[1277] (1906) somewhat simplified the technique of Novy and MacNeal. He collected the blood of a suitable animal, such as rabbit, cow or dog, strict asepsis not being essential. The blood was defibrinated in the ordinary way. One part of blood was added to two parts of agar at 50° C. The mixture was sterilized several times by heating to 75° C. or 100 ° C. Slopes were made and the water of condensation was inoculated with a little blood containing the trypanosomes. Blood may be obtained from a superficial vein or from the heart.

[1277] C. R. Soc. Biol., lxi, p. 550.

Novy-MacNeal-Nicolle or N. N. N. Medium.--In 1908 C. Nicolle[1278] brought forward a modification of the Novy-MacNeal (N.N.) medium. The formula is as follows:--

Agar 14 grm. Sea salt 6 " Water 900 "

[1278] C. R. Acad. Sci., cxlvi, p. 842.

Apparently pure sodium chloride can be substituted equally well for sea salt. The mixture is placed in tubes and sterilized in an autoclave. To each tube one-third of its volume of rabbit blood, taken by aseptic puncture of the heart, is added. The salt agar is kept liquid at 45° C. to 50° C. and the blood is added to the mixture. The culture medium so prepared is maintained for five days at 37° C., and then for a few days at room temperature. This medium was devised for the cultivation of Leishmania (see p. 106), but trypanosomes may also be grown thereon. Subsequently, Nicolle recommended the use of citrated rat’s blood heated to 45° C. for half an hour, instead of defibrinated rabbit’s blood. On such a medium, J. G. Thomson and Sinton[1279] (1912) succeeded in growing Trypanosoma gambiense and T. rhodesiense (see pp. 76, 83).

[1279] Annals Trop. Med. and Parasitol., vi, p. 331.

Noguchi’s media for the cultivation of Spirochætes and Treponemata are described on pp. 123, 125. Hata’s modification is discussed on p. 126.

Bass’s glucose-blood medium for the cultivation of malarial parasites is described on pp. 170–172. It has also been used successfully for the cultivation of Piroplasma or Babesia (see p. 172).

III.--BRIEF NOTES ON GENERAL PROTOZOOLOGICAL TECHNIQUE.

The object of this book is to give accounts of the structure and life-histories of the numerous parasitic organisms that affect man more particularly. It is, therefore, inappropriate to devote much space to a consideration of technique, regarding which many volumes have already been written. Methods of procedure are largely matters of opinion, and the technique that gives brilliant results when used by one investigator may be a complete failure in the hands of another. In the present appendix, brief notes regarding certain relatively simple methods only can be given, because the number of fixatives in use is very great; there are also large numbers of stains as well as many modifications of them, while the methods of applying both fixatives and stains are, perhaps, still more numerous. There are so many, in fact, that confusion frequently arises from the multiplicity of choice presented to the worker. Those desiring more information on the subject of technique are advised to consult the treatises of Bolles Lee[1280] and of Langeron.[1281]

[1280] “The Microtomist’s Vade Mecum” (7th edition, 1913). London: J. and A. Churchill.

[1281] “Précis de Microscopie” (1913). Paris: Masson et Cie.

Fresh Material.

(a) Simple Examination.

Fluid Substances, such as Blood and Sputum.--A small quantity of the substance to be examined is taken on a sterile platinum loop and transferred to a perfectly clean glass slide. A clean cover-slip is gently lowered on to the drop, air bubbles being avoided. The preparation is luted with vaseline or paraffin and examined first with a low power and then with a high power objective. The light is cut down by partly closing the diaphragm of the substage of the microscope.

Skin Ulcers and Similar Sores.--Scrapings are made from the edge of the sore, mixed with sterile physiological salt solution, and prepared and examined as above.

Fæces.--A small portion of fæces, or flakes of mucus (which may be blood-stained) from the same, is removed on a sterile platinum loop, spread out thinly after dilution, if necessary, with physiological salt solution on a slide, covered and examined as before.

Alternatively, hanging drop preparations of blood, ulcerative tissue, or fæces, appropriately diluted if necessary with sodium citrate or physiological salt solution, may be made on a cover-slip, which is inverted over a slide with a well in it. The cover-slip is then luted and examined.

For the elucidation of the developmental processes of such organisms as trypanosomes, spirochætes and piroplasms, fresh preparations may be often kept under observation longer by the use of a thermostat, maintained at or near blood heat, in which the microscope is inserted.

(b) Intra vitam Staining of fresh Preparations.

Intra vitam staining is of service on some occasions, more particularly for the study of the nucleus and other chromatoid substances of the living organism. Two methods are in common use. In the first case, the stain, employed usually in very dilute solution, is mixed with the medium containing the organism. The latter takes up some of the stain, the amount of coloration depending on the organism concerned and on the stain employed.

The commoner intra vitam stains are pure, medicinal (zinc-free) methylene blue and neutral red, used in aqueous solutions. A solution of methylene blue of 1 per 1,000 of water may be tried, while neutral red in the proportion of 1 per 3,000 parts of water has proved of service.

The second method of vital colouring consists in placing a drop of 1 per cent. solution of methylene blue on a slide or cover-slip, slightly spreading it, and allowing it to dry. The living organism is then placed in a drop of saline on the prepared slide or cover-slip, which is then mounted and examined under the microscope. Progressive staining of the organism occurs and its internal structure can be seen. A similar procedure may be followed for neutral red. Intra vitam staining is useful for relatively large and easily deformed protozoa such as ciliates, as well as for amœbæ and flagellata of the gut.

When examining very actively motile organisms, it is sometimes useful to endeavour to restrict their movements by adding a little gum or gelatine to the medium.

(c) Examination by aid of the Paraboloid Condenser.

The use of one of the dark-ground illuminators (so-called ultra-microscopes) is of service for the detection of minute living organisms or of organisms present in small numbers only. The forms of paraboloid condenser manufactured by the firms of Zeiss and Leitz can be recommended. For details of their methods of employment, reference should be made to the leaflets of the firms supplying the said instruments. By the use of the paraboloid condenser, the finer details of certain stages of life-cycles, such as the formation of granules in spirochætes and treponemata, can be observed more readily than by using the ordinary substage of the microscope. The use of the paraboloid condenser for the detection of small numbers of living organisms renders it of value for rapid diagnostic purposes.

Stained Material.

Fuller accounts of the technique of fixed and stained material will be found in Bolles Lee and in Langeron, already mentioned.

Thin Films.--For the examination of blood-inhabiting Protozoa, it is necessary to make first thin films or smears of blood. There are many ways of doing this, and opinions differ as to their respective merits. A simple method is to take a straight surgical needle about 2 in. long, the eye of which has been removed, and a clean glass slide. The patient’s skin is pricked, and when the bead of blood reaches the size of a small pin’s head, the slide is applied to the surface of the blood, about 1/3 in. from the far (left-hand) end of the slide. The shaft of the needle is laid across the drop of blood, which spreads between the slide and the needle. The latter is drawn evenly along the slide towards the right. The film is dried by waving it in the air. The film should possess a straight edge parallel with that of the slide and should be as uniform and thin as possible. Another glass slide may be used as a spreader, or a cover-slip or thin glass rod may be employed.

Thick Films.--These are of service in detecting malarial parasites or trypanosomes, especially when the parasites are few. The method of Ross, or a modification thereof, has been much used. A small drop of fresh blood is spread evenly and quickly with a needle-point over a square area somewhat less than that of an ordinary square cover-glass. The blood is allowed to dry. The film is then carefully dehæmoglobinized in water in which there is a trace of acetic acid. The dehæmoglobinizing fluid is then carefully drained off and the film again dried. It is fixed in absolute alcohol and stained with Romanowsky’s solution. A cubic millimetre of blood divided into quarters may be thus dehæmoglobinized and stained. The parasites in such a cubic millimetre of blood may be counted. Such a procedure was followed by R. Ross and D. Thomson,[1282] in determining the periodic variation of the numbers of trypanosomes in the blood of a patient, as mentioned and figured on pp. 78 and 79.

[1282] Proc. Roy. Soc., B, lxxxii, p. 411.

* * * * *

For cytological details of various Protozoa, thin film preparations on cover-slips or slides are often useful. Cover-slip preparations are preferable, unless the organisms under investigation are extremely scanty. The medium containing the organisms, such as blood, lymph, intestinal contents, sputum, scrapings of ulcers, and urine, is spread thinly, either alone or diluted with a little physiological salt solution, on the cover-slip. Fixation while still wet is necessary. Various methods are employed.

*Fixatives.*--A useful procedure is to fix the wet film by exposure to 4 per cent. osmic acid vapour for ten to thirty seconds, then place in absolute alcohol for five minutes to harden. Grade down from absolute alcohol through 90 per cent., 70 per cent., 50 per cent., and 30 per cent. alcohols to water. Stain wet with a suitable stain such as hæmatoxylin, and gradually dehydrate by grading through the necessary strengths of alcohol, clear in xylol or other oily clearing medium and mount in Canada balsam.

Other fixatives may be employed, such as are also useful for fixing pieces of tissue for sectioning. Films or smears on cover-slips while still wet are floated on the surface of the fixative in a watch glass. Some good fixatives of wide application are:--

Schaudinn’s Fluid.--This consists of a mixture of

Saturated aqueous solution of corrosive sublimate 2 volumes Absolute alcohol 1 volume

Two modifications of Schaudinn’s formula may be found useful. A saturated solution of corrosive sublimate in physiological salt solution may be substituted for the aqueous one, and the addition of a few drops of glacial acetic acid to either of the preceding mixtures may be made.

Some workers prefer to use hot fixatives, raised to a temperature of about 50° C.

Fixation by corrosive sublimate solutions must be followed by thorough removal of the mercury salt by washing repeatedly in 30 per cent. alcohol or with iodine-alcohol.

Bouin’s Fluid, or modifications thereof, is also very useful for wet fixation. Bouin’s picro-formol solution consists of:--

Saturated aqueous solution of picric acid 30 volumes Formalin, 40 per cent. 10 " Acetic acid, glacial 2 "

The best-known modification is one due to Duboscq and Brasil, and often known as Bouin-Duboscq Fluid. Its formula is as follows:--

Alcohol, 80 per cent. 150 c.c. Formalin, 40 per cent. 60 " Acetic acid, glacial 15 " Picric acid 1 grm.

Thorough washing of the smear or cover-slip preparation with 70 per cent. alcohol until the yellow colour disappears is necessary to remove excess of fixative.

Other fixatives, which may be of use, more especially for fixing small pieces of tissue for sectioning, are the solutions of Flemming (chromo-aceto-osmic acids) and of Zenker (sublimate-bichromate-acetic, with sodium sulphate).

Regarding the time of fixation, there is much difference of opinion. Usually, exposure to or contact with the fixative for five minutes is sufficient in the case of films or smears. Material for sections should be cut into small cubic pieces, of a thickness of about 5 mm. (1/5 in.). One or two hours should be sufficient time for the fixation of such pieces of tissue, though some, as Langeron, prefer a longer time of fixation. On the other hand, Gustav Mann[1283] recommends a short fixation period. The excess of fixative should be thoroughly washed out of the tissue in the manner appropriate to the particular fixative used. If it is desired to keep the tissue for some time before sectioning and staining, it should be transferred to 70 per cent. alcohol.

[1283] “Physiological Histology,” 1902, Clarendon Press, Oxford.

When fluid fixatives are employed, large quantities of the fixing media are necessary. The volume of the fixative should be at least ten to twenty times that of the object, and the latter should be suspended in the middle of the fixative. The tissue should be fixed as soon as possible after the death of the host.

For sectioning tissue parasitized by Protozoa, embedding in paraffin is generally recommended. Microtome sections should not, if possible, exceed 5 µ in thickness. Details of special procedures must be sought in larger works.

*Staining.*--Here, as with fixatives, much choice is presented. The various modifications of the Romanowsky stain have aided greatly in the detection of various Protozoa parasitic in the blood. Such stains, however, leave something to be desired in the revealing of finer cytological details. Other stains, more especially the hæmatoxylins, must be employed for cytological purposes.

Formulæ of some of the principal Romanowsky and hæmatoxylin stains may now be given.

The underlying principle of the Romanowsky Stain is the reaction between alkaline methylene blue and eosin, forming the so-called eosinate of methylene blue which stains chromatin purplish-red. A solution of medicinal methylene blue after having been subjected to the action of an alkali, such as sodium carbonate, becomes partly converted into certain derivatives, the chief of which are methylene azure and methylene violet. These substances are also present in matured polychrome methylene blue.

The formula of a slightly modified Romanowsky Stain which gives excellent results is given below:--

Two stock solutions are required--

Solution A.--Methylene blue, pure medicinal 1·0 grm. Sodium carbonate 0·5 " Water 100·0 c.c.

Keep in a warm incubator for two or three days, until the solution is distinctly purple in colour. It improves with age.

Solution B.--Eosin, water soluble, extra B.A. 1·0 grm. Water 1,000·0 c.c.

This solution must be kept in the dark, in dark-tinted (amber-coloured) bottles, as unfortunately it is decolorized by light.

Before use each stock solution must be diluted. Thus, make up 5 c.c. of each stock solution to 100 c.c. by adding distilled water. For staining, 1 volume of solution A is added to 2 or 3 volumes of solution B. Mix thoroughly by shaking, pour the mixture over the film, previously fixed in absolute alcohol, and stain for ten to fifteen minutes. Wash carefully in running water, then dry. The cytoplasm of a protozoan parasite will be stained blue, the chromatin purplish-red and vacuoles or very tenuous protoplasm will remain colourless.

The exact proportions of solutions A and B, which must be mixed together, should be determined by experiment. Freshly mixed stain must be used on each occasion.

Leishman’s Stain is the precipitate resulting from the interaction of alkaline methylene blue and eosin. The washed and dried precipitate is collected and dissolved in pure methyl alcohol, which acts as a fixative; 0·015 grm. of Leishman powder may be dissolved in 10 c.c. of methyl alcohol for staining films. The film is covered with the solution for one minute, twice the volume of water is then added and mixed with the stain on the slide. The staining is then continued for five to ten minutes, and the film is finally washed with water.

Giemsa’s Stain.--This should be procured ready made. Azure II is a mixture of methylene azure and methylene blue. (Methylene azure is sometimes known as Giemsa’s Azure I.) The formula given by Giemsa himself in 1912 is:--

Azure II-eosin 3·0 grm. Azure II 0·8 " Glycerine, pure 125·0 " Methyl alcohol, pure 375·0 "

The film is first fixed in absolute alcohol. The proportion of stain usually used is one drop of stain to 1 c.c. of water. Stain for about ten minutes and then wash in water.

The details of the application of the Giemsa stain to films fixed wet and to sections must be sought in larger works on technique. These works should also be consulted for information regarding the use of Pappenheim’s Panchrome mixture.

* * * * *

There are numerous formulae of stains containing ripened Hæmatoxylin or its essential principle, Hæmatein. A mordant is necessary, one of the alums being usually employed. The mordant may be included as an ingredient in the staining mixture, or it may be used separately as in the case of the so-called iron-hæmatoxylins, wherein ferric ammonium alum is used separately and is followed by staining with hæmatoxylin or hæmatein. A few of these stains of general application may now be mentioned.

Delafield’s (or Grenachier’s) Hæmatoxylin.

Hæmatoxylin crystals 4 grm. Absolute alcohol 25 c.c. Saturated aqueous solution of ammonia-alum 400 "

Mix these ingredients, and leave exposed to light and air for three to four days. Filter and add--

Glycerine 100 c.c. Methyl alcohol 100 "

Allow the mixture to stand until the colour is sufficiently deep, then filter and place in a stoppered bottle. The solution should be allowed to ripen for at least two months before use. Dilute aqueous solutions of the stain are of service for films and for sections. A trace of acetic acid may be added at the moment of use, for sharp differentiation.

Ehrlich’s acid hæmatoxylin, Mayer’s hæmalum, and Mayer’s glychæmalum are also useful. Their formulæ will be found in larger works.

The chief Iron-Hæmatoxylin Stain is that devised by Heidenhain. Unfortunately the procedure involved is a long one, and various modifications have been made to obviate this disadvantage. Hæmatein may be used instead of ripened hæmatoxylin.

One efficacious modification of Heidenhain’s stain is that of Rosenbusch. The smear or tissue, after fixation, must be graded downwards through the alcohols to water. Mordant for one and a half hours in a 3-1/2 per cent. aqueous solution of ferric ammonium sulphate. Stain for about three minutes in 1 per cent. solution of ripe hæmatoxylin or hæmatein in absolute or 96 per cent. alcohol, to which a drop of saturated aqueous solution of lithium carbonate, sufficient to produce a wine-red colour, has been added. Differentiate under the microscope with a very dilute solution of the ferric ammonium sulphate. Wash, gradually dehydrate, clear and mount in balsam. It must be remarked that iron-hæmatoxylin is a regressive stain, hence great care must be exercised in differentiating with the iron alum.

Gentian Violet.--A 1 per cent. alcoholic solution of gentian violet, or of methyl violet, or of crystal violet, will be found useful for staining spirochætes.

Methyl Green.--This substance is considered to be a chromatin stain, for either fresh or perhaps recently fixed tissues. A concentrated aqueous solution contains about 1 per cent. of the stain. This should be added to a 1 per cent. solution of acetic acid. It may be used for demonstrating the nuclei of ciliates.

* * * * *

In conclusion it is essential to remember that the actual magnification of figures of Protozoa should be given, and not merely the combination of objective and ocular that has been used, for unless the tube-length and distance of the drawing board from the ocular be also given, it is not possible to compute the magnification from such information. Drawings should always be made with the aid of a camera lucida, drawing prism or other form of projection apparatus.

APPENDIX ON TREMATODA AND NEMATODA.

BY

J. W. W. STEPHENS, M.D., B.C., D.P.H.

TREMATODA.

*Artyfechinostomum sufrartyfex*, Clayton Lane, 1915.--Leiper thinks this may be the same as Echinostoma malayanum, Leiper, 1911, which species Odhner assigns to the genus Euparyphium.

*Metagonimus* (Yokogawa) *yokogawai* occurs in dogs in Shanghai. Encysted cercariæ probably in the perch.

*Opisthorchis sp.*--Skin covered with spines. Gut forks almost reach end of body. Œsophagus two to three times length of pharynx. Ovary multilobed. Ovary and testes in posterior fourth of body. Vitellaria end opposite the ovary. Distinguished from O. felineus by presence of spines and lobed ovary; from O. pseudofelineus and O. noverca by the lobed ovary, and by the fact that the yolk glands do not extend as far as the anterior testis. It agrees with Poirier’s description of O. viverrini in the Indian civet cat, but whether this species has spines on the cuticle is not known.

Habitat.--Man in Chiengmai (Malay States). Fifteen per cent. of prisoners in the jail showed the ova of this species in their fæces.

Schistosome cercariæ.

*Schistosome cercariæ* belong to the furcocercous division of the Distomata cercariæ.

Distomata cercariæ.

Body without a floating membrane. Tail absent, or if present not cleft to the base. Mouth anterior, gut forked. Oral sucker present. Ventral sucker near middle of body. Eyes generally absent.

Group *Fercocercous cercariæ*.

Cercariæ single (not in colonies). Tail forked at its end.

Family. *Schistosomidæ.*

Pharynx absent.

*Cercaria bilharzia*, Leiper, 1915.

Pigment spots (eyes) anterior to ventral sucker absent, cuticular keel on forks of tail absent.

In Bullinus sp. and Planorbis boissyi in Egypt, (?) in Physopsis africana, South Africa. Adult form, Schistosoma hæmatobium.

*Cercaria bilharziella*, Leiper, 1915.

Cuticular keel on tail forks present. Pigment spots (eyes) in front of ventral sucker present.

In Planorbis boissyi and P. mareoticus, and in Melania sp. Adult form (?).

For characters of numerous other cercariæ which occur in fresh water molluscs see “Die Susswasserfauna Deutschlands,” Max Lühe, H. 17 (Gustav Fischer, Jena, 1909).

The characters of Cercaria japonica of S. japonicum in the mollusc Katayama nosophora and of C. mansoni have still to be defined.

*Schistosoma mansoni*, Sambon, 1907.

The evidence appears to be strong that terminal-spined eggs are not found in the West Indies, and that therefore the lateral-spined eggs found in fæces there belong probably to S. mansoni. If this be true, then the egg described by Stephens and Christophers in man in India probably also belongs to another species of Schistosome.

NEMATODA.

*Ancylostomiasis.*--Treatment: (1) Oleum chenopodii (U.S.P.), dose ♏ x to ♏ xv on a lump of sugar, three doses at two-hourly intervals, preceded and followed by a purge. It is cheap, not unpleasant to take, and non-toxic. Effective also against Ascaris lumbricoides.

(2) Milk of the higueron Ficus laurifolia. A spoonful in milk, three times daily for three days followed by a purge. Described as a harmless but very successful form of treatment.

*Ground-itch.*--Completely cured in a few days by a 3 per cent. solution of salicylic acid in ethyl alcohol. Apply for five minutes twice daily.

*Ascaris lumbricoides* can be kept alive for twelve days in Kronecker’s solution; NaOH 0·069 grammes, normal saline 1,000 c.c.

Eggs are laid and develop in about a fortnight at ordinary room temperature. At 70° C. they are readily killed.

*Filariasis.*--Dutcher and Whitmarsh have cultivated from the blood and from the exudation fluids of cases of filariasis (elephantiasis, lymphangitis, etc.), in about sixteen cases, a bacillus resembling B. subtilis. Controls were negative. They propose the name Bacillus lymphangiticus for this organism, and they believe it to be the cause of the diseases grouped under the designation “filariasis.”

*Oncocerca volvulus.*--Unsheathed embryos (indistinguishable from those taken from the uterus of this worm) have been found in lymphatic glands and in the blood (if considerable pressure is used so as to squeeze out lymph at the time of taking the finger blood, otherwise none occurs in the specimens). The measurements in dried films are: Nerve ring 23·7 per cent. of length; G1 cell 69·6 per cent.; end of last tail cell 96·3 per cent; total length 274·3 µ.

*Strongyloides stercoralis.*--Pathology: They occur in the wall of the intestine and may be associated with ulceration. They also occur in lymphatics and blood-vessels.

BIBLIOGRAPHY.

[In the following pages the letters C. f. B., P. u. Inf. are used to indicate the Centralblatt für Bakteriologie, Pathologie und Infektions-Krankheiten.]

*(A) PROTOZOA* (pp. 25 to 210, 617 to 637, and 733 to 742).

[This list applies to the earlier literature only. More recent references are given as footnotes in the text.]

(a) GENERAL.

BÜTSCHLI, O. Protozoa in Bronn’s Klass. u. Ordn. d. Tierreichs, Leipz., 1880–1889.

CALKINS, G. N. The Protozoa, Columbia Univ. Biol. Ser., vi, New York, 1901.

DELAGE, Y., and E. HÉROUARD. Traité de Zool. Concr., i, La cellule et les protozoaires, Paris, 1896.

FARMER, J. B., J. J. LISTER, E. A. MINCHIN and S. J. HICKSON. Protozoa, in A Treatise on Zoology, edited by E. Ray Lankester, London, 1903, i, 2.

LANG, A. Lehrb. d. vergl. Anatomie d. wirbellos. Tiere, 2. Aufl., 2. Lief, Protozoa, Jena, 1901.

(b) PATHOGENIC PROTOZOA IN GENERAL.

DOFLEIN, F. Die Protozoen als Parasiten u. Krankheitserreger, Jena, 1901; Lehrbuch der Protozoenkunde, 1912.

DOFLEIN, F., and S. V. PROWAZEK. Die pathog. Protoz. mit Ausnahme d. Hämospor., in Handb. d. path. Mikroorganism.; issued by W. Kolle and A. Wassermann, 11. and 12. Lief, Jena, 1903.

KÄSTNER, P. Die tierpathogenen Protozoen, Berlin, 1906.

KISSKALT, K., and M. HARTMANN. Praktikum der Bakteriologie und Protozoologie, Jena, 1907.

LÜHE, M. Die im Blute schmarotzenden Protozoen und ihre nächsten Verwandten, in Handb. d. Tropenkrankh., issued by C. Mense, Leipz., 1906, iii.

PFEIFFER, L. Die Protozoen als Krankheitserreger, 2. Aufl., Jena, 1891; Supplement, Jena, 1895.

ROOS, E. Die im menschl. Darm vork. Protozoen u. ihre Bedeutg., Med. Klinik, 1905, i, p. 1328.

SCHNEIDEMÜHL, G. Die Protozoen als Krankheitserreger der Menschen und der Haustiere, Leipz., 1898.

SIEVERS, R. Zur Kenntn. d. Verbreitg. d. Darmparas. d. Mensch, Helsingfors, 1905, Festschrift f. Palmèn.

WARD, H. B. Protozoa, Wood’s Ref. Handbook of the Med Sci., 1904, viii.

*Class I.--Sarcodina* (pp. 29 to 50).

ORDER. Amœbina (p. 29).

Entamœba coli; Entamœba histolytica (pp. 32 to 41, 618 to 620, and 733).

BLANCHARD, R. Traité de Zool. médic., 1885, i, Paris, p. 15.--Maladies paras., 1895, p. 658.

BOWMANN, M. H. Dysentery in the Philippines, Journ. Trop. Med., 1901, iv, p. 420.

BUNTING, C. H. Hæmatogenous Amœbic Abscess of the Lung, Arch. f. Schiffs- u. Tropenhyg., 1906, x, p. 73.

CALANDRUCCIO. Anim. par. dell’ uomo in Sicilia, Atti Accad. Gioen., iv, 1890, ii, p. 95.

CASAGRANDI, O., and P. BARBAGALLO. Sull’ amœba coli, Boll. Accad. Gioen. sci. nat., Catania, 1895.

-- -- Entamœba hominis s. Amœba coli Lösch, Annal. d’Igiene sperim., 1897, vii, 1.

CELLI, A., and R. FIOCCA. Beitr. z. Amoebenforsch., ii, C. f. B. u. Par., 1894, xvi, p. 329; Ric. int. alla biol. d. Amœbe, Bull. Accad. med. Roma, 1894–95, xxi, p. 285; abstracted in C. f. B., P. u. Inf., 1897, i, xxi, p. 290.

COUNCILMAN, W. P., and H. A. LAFLEUR. Amœbic Dysentery, Johns Hopkins Hosp. Rep., 1891, ii, p. 395.

CRAIG, C. F. Etiology and Pathology of Amœbic Infection of the Intestines and Liver, Intern. Clin., Philad., 1905 (14), iv, p. 242.

CUNNINGHAM, D. Seventh Ann. Rep. San. Comm. of India, Calcutta, 1871.

-- Unters. üb. d. Verh. mikrosk. Organ. z. Cholera in Indien, Zeitschr. f. Biol., 1872, viii, p. 251; Quart. Journ. Micros. Sci., 1881 (2), xxi, p. 234.

GRASSI, B. Dei protozoi par. e spec. di quelli che sono nell’ uomo, Gazz. med. ital.-lomb., 1879 (8), i, p. 445; Int. ad alc. prot. endop., Atti soc. ital. sci. nat., 1882, xxiv, p. 1; Morf. e sist. di alc. prot. par., Atti Acc. Lincei. Rendic. (4), iv, 1, p. 5; Signif. patol. d. prot. par. dell’ uomo, ibid., p. 83.

GROSS, A. Beobacht. üb. Amoebenenteritis, Arch. f. klin. Med., 1903, lxxvi, p. 429.

HARRIS, H. F. Amœbic Dysentery, Amer. Journ. of Med. Sci., April, 1898.

-- Experimentell bei Hunden erzeugte Dysent., Arch. f. path. Anat., 1901, clxvi, p. 66; On the Alterations Produced in the Large Intestine of Dogs by the Amœba coli, Philadelphia, 1901.

HOPPE-SEYLER, G. Üb. Erkrankung des Wurmfortsatzes bei chron. Amoebenenteritis, Münch. med. Wochenschr., 1904, No. 15.

JAEGER, H. Die in Ostpreuss. heim. Ruhr eine Amoebendysent., C. f. B., P. u. Inf., 1902, i Abt. Orig., xxxi, p. 551.

-- Erwiderg. a. d. Bemerk. Shigas, ibid., 1902, xxxii, p. 865.

JANOWSKI, W. Zur Ätiol. d. Dys., C. f. B., P. u. Inf., 1897, i, xxi, pp. 88, 151, 194, 234.

JÜRGENS. Zur Kenntn. d. Darm-Amoeb. u. d. Amoeben-Enteritis, Veröff. a. d. Geb. d. Milit.-Sanitätswes., Berl., 1902, Heft 20, p. 111.

KARTULIS. Über Riesenamoeben (?) bei chron. Darmentdg. d. Ägypt, Virch. Arch. f. Path., 1885, xcix, p. 145; Zur Ätiol. d. Dysent. in Ägypt, C. f. B. u. Par., 1887, v, p. 745; Üb. trop. Leberabsc. u. ihr Verh. z. Dysent., Virch. Arch. f. Path., 1889, cxviii, p. 97; Einiges üb. d. Path. d. Dysenterie-Amœb., C. f. B. u. Par., 1891, ix, p. 365; Article: Dysenterie in Spec. Path. u. Ther. v. H. Nothnagel, Wien, 1896, v, 3.

-- Gehirnabscesse nach dysent. Leberabsc., C. f. B., P. u. Inf., 1904, i Orig., xxxvii, p. 527.

KOCH, R., and G. GAFFKY. Bericht üb. d. Tätigkeit d. z. Erforschg. d. Cholera ents. Kommiss., Arb. a. d. kais. Gesundheitsamt, 1887, iii.

KOVACS, F. Beob. u. Vers. üb. d. sog. Amoeben-Dys., Zeitschr. f. Heilkde., 1892, xiii, p. 509.

KRUSE, W., and PASQUALE. Eine Exped. nach Ägypt, Deutsch. med. Wochenschr., 1893, No. 15, p. 354; No. 16, p. 368.

-- -- Untersuch. üb. Dys. u. Leberabsc., Zeitschr. f. Hyg., 1894, xvi, p. 1.

LAMBL. Aus d. Franz-Joseph-Kinderspit. in Prag, 1860, i, p. 362.

LESAGE, A. Culture de l’amibe de la dysenterie des pays chauds, Ann. Inst. Pasteur, 1905, xviii, p. 9; 1905, xix, p. 8.

LEWIS. Sixth Ann. Rep. San. Comm. of India, Calcutta, 1870.

LÖSCH, F. Massenh. Entw. v. Amoeben im Dickd., Virch. Arch. f. Path., 1875, lxv, p. 196.

MARCHOUX. Note sur la dysentérie d. pays chauds, C. R. Soc. Biol., Paris, 1899 (11), i, p. 870.

MUSGRAVE, W. E., and M. T. CLEGG. Amœbæ, their Cultivation and Etiological Significance. “Treatment of Intestinal Amœbiasis,” in the Trop. Manila, 1904, Bur. of Govern. Lab., Biol. Lab., No. 18.

NORMAND. Note sur deux cas de colite parasit., Arch. méd. nav., 1879, xxxii, p. 211.

QUINCKE and ROOS. Über Amoebenenteritis, Berl. klin. Wochenschr., 1893, xxx, No. 45, p. 1089.

ROOS, E. Zur Kenntn. d. Amoebenenteritis, Arch. f. exper. Path. u. Pharm., 1894, xxxiii, p. 389.

RUGE, A. Amoebenruhr., Handb. d. Tropenkrankh., issued by C. Mense, 1906, iii, p. 1.

SCHAUDINN, FR. Unters. üb. d. Fortpflanz. einig. Rhizopod, Arb. a. d. kais. Gesundheitsamt, 1903, xix, 3, p. 547.

SCHUBERG, A. Die paras. Amoeb. d. menschl. Darms, C. f. B. u. Par., 1893, xiii, pp. 598, 654, 701.

SHIGA, K. Bemerk. zu Jaegers Die in Ostpreuss. einh. Ruhr eine Amoebendys., C. f. B., P. u. Inf., 1902, i Abt. Orig., xxxii, p. 352.

STRONG, R. P., and W. E. MUSGRAVE. Report on the Etiology of the Dysentery of Manila, Rept. Surg.-Gen. of the Army to the Secretary of War, Washington, 1900, p. 251.

VERDUN. Sur quelq. caract. spécif. de l’amibe de la dysenterie et des abscès trop. du foie, C. R. Soc. Biol., 1904, lvi, p. 183.

WOOLLEY, P. G., and W. E. MUSGRAVE. The Pathology of Intestinal Amœbiasis, Dept. of the Int. Bureau of Government Lab., No. 32, Manila, 1905, Journ. Amer. Med. Assoc., Chicago, 1905, xlv, p. 1371.

Entamœba buccalis (pp. 43 and 620).

LEYDEN E. V., and W. LOEWENTHAL. Entam. bucc. Prow, bei einem Fall von Carcinom d. Mundbod, Charité-Ann., Berl., 1905, xxix; Berl. klin. Wochenschr., 1905, xlii, No. 7, p. 187.

PROWAZEK, S. Entamœba buccalis n. sp., Arb. a. d. kais. Gesundheitsamt, Berl., 1904, xxi, 1, p. 42.

TIETZE, AL. Ein Protozoenbef. i. ein. erkrankt. Parotis., Mitt. Grenzgeb. Med. u. Chirurg., 1905, xiv, p. 302.

Entamœba undulans (p. 43).

CASTELLANI, A. Dysentery in Ceylon, Journ. of the Ceylon Branch of the Brit. Med. Assoc., 1904.

-- Observations on some Protozoa found in Human Fæces, C. f. B., P. u. Inf., 1905, i Abt. Orig., xxxviii, p. 67.

Entamœba kartulisi (pp. 44 and 734).

DOFLEIN, F. Die Protoz. als Paras. u. Krankheitserreg., Jena, 1901, p. 30.

FLEXNER. Amœbæ in an Abscess of the Jaw, Johns Hopkins Hosp. Bull., 1892, No. xxv; abstracted in C. f. B., P. u. Inf., 1893, xiv, p. 288.

KARTULIS. Üb. pathog. Protoz. b. Mensch., Zeitschr. f. Hyg., 1893, xiii, p. 9. -- Über Amoebenosteomyelitis d. Unterkief, C. f. B., P. u. Inf., 1903, i Abt., Ref. xxxiii, p. 471.

Amœba gingivalis, A. buccalis and A. dentalis (pp. 44 and 733).

GRASSI, B. Gazz. med. ital.-lomb., 1879 (8), i, No. 45, p. 445.

GROS, G. Fragm. d’helm. et de phys. micros., Bull. soc. Imp. d. natur. de Moscou, 1849, i, 2, P. 555.

STEINBERG. In Zeitschr. f. neuere Med. (Russ.), issued by Walter in Kiew, 1862, Nos. 21–24.

Craigia (Paramœba) hominis (pp. 45 and 734).

CRAIG, CH. F. A new Intestinal Parasite of Man: Paramœba hominis, Amer. Journ. Med. Sci., 1906, N.S. cxxxii, Philad. and New York, p. 214.

SCHAUDINN, FR. Über den Zeugungskreis von Paramœba eilhardi n. g. n. sp., Sitzgsber. Kgl. Pr. Akad. d. Wiss., Berlin, Phys.-math. Cl., 1896, No. 2.

Entamœba pulmonalis (p. 45).

ARTAULT, ST. Flore et faune d. cav. pulm., Arch. de paras., 1898, i, p. 275.

BLANC, L. Sur une Amibe viv. accid. dans le poumon du mouton, Ann. Soc. Linn. Lyon, 1899 (2), xlv, p. 529.

Amœba urogenitalis (pp. 45, 46).

BAELZ, E. Üb. einige neue Paras, d. Mensch., Berl. klin. Wochenschr., 1883, p. 237.

JEFFRIES. Present. of a Specimen of Urine containing Amœbæ. Med. Rec., New York, 1904, xlvi, p. 356.

JÜRGENS. In Deutsche med. Wochenschr., 1892, p. 454.

KARTULIS. Pathog. Prot. b. Mensch, Zeitschr. f. Hyg., 1893, xiii, p. 2, Anm. 2.

POSNER, C. Üb. Amoeben im Harn, Berl. klin. Wochenschr., 1893, xxx, No. 28, p. 674.

WIJNHOFF, J. A. Over amoeburie, Nederl. Tijdschr. v. Geneeskde., 1895, p. 107.

Amœba miurai (p. 46).

IJIMA, J. On a New Rhizopod Parasite of Man, Ann. zool. japon., 1898, ii, 3, p. 85; abstracted in C. f. B., P. u. Inf., 1899 (i), xxv, p. 885.

MIURA, K. Amoebenfund i. d. Punktionsflüss. bei Tumoren d. Peritonealh., Mitt. med. Facult. d. kais. Jap. Univ., Tokyo, 1901, v, p. 1.

Chlamydophrys and Leydenia (pp. 47 to 50).

CIENKOWSKI, L. Üb. einige Rhizop. u. verwandte Organismen, Arch. f. mikr. Anat., 1876, xii, p. 39.

LAUENSTEIN, C. Üb. ein. Fund von Leyd. gemmip., Deutsche med. Wochenschr., 1897, xxiii, p. 733.

LEYDEN, E. V., and F. SCHAUDINN. Leyd. gemmip., ein neuer i. d. Ascites-Flüssigk. d. leb. Mensch. gefund. amoebenähnl. Rhizop., Sitzgsb. kgl. Preuss. Akad. d. Wiss., Berlin, 1896, xxxix, p. 951.

LEYDEN, E. V. Zur Ätiol. d. Carcin., Zeitschr. f. klin. Med., 1901, xliii, p. 4.

SCHAUDINN, FR. Untersuch. üb. d. Fortpflanz. einig. Rhizopod., Arb. a. d. kais. Gesundheitsamt, 1903, xix, 3, p. 560.

SCHNEIDER, A. Beitr. z. Naturgesch. d. Infus., Müllers Arch. f. Anat., Phys. u. wiss. Med., Jahrg. 1854, p. 191.

*Class II.--Mastigophora* (pp. 50 to 128, 620 to 633, and 734 to 741).

BILAND, J. Beitr. z. Frage d. Pathog. d. Flagellat., Deutsch. Arch. f. klin. Med., 1905, lxxxvi, p. 274.

BLOCHMANN, F. Mikrosk. Tierw. d. Süsswassers, 2. Aufl., 1895.

KENT, W. S. Manual of the Infusoria, London, 1880–81.

PROWAZEK, S. Flagellatenstudien, Arch. f. Protistenkde., 1903, ii, p. 195.

SENN, G. Flagellata in Engler und Prantl, Die natürlich. Pflanzenfam., Lief 202, 203, Leipzig, 1900.

STEIN, F. V. Der Organismus der Infus., iii, Der Org. d. Flagellaten, Leipzig, 1878.

Trichomonas vaginalis (pp. 52, 53, and 734).

BAATZ, P. Trich. vag. in der weibl. Harnblase, Monatsber. f. Urol., 1902, vii, 8.

BLOCHMANN, F. Bemerk. über einige Flagell., Z. f. wiss. Zool., 1884, xl, p. 42.

DOCK, G. Flagellate Protozoa in the freshly passed Urine of a Man, Med. News, 1894, lxv, p. 640.

-- Trichomonas as a Parasite of Man, Amer. Journ. Med. Sci., 1896, p. 1.

DONNÉ, A. Rech. sur la nature du mucus, Paris, 1837.

HAUSMANN. Die Paras, der weibl. Geschlechtsorg., Berlin, 1870.

KUNSTLER, J. Trichom. vag. D., Journ. de Micrographie, 1884, viii, p. 317.

LAVERAN, A., and F. MESNIL. Sur la morph. et la syst. d. Flag. à membr. ondul., C. R. Acad. Sci., Paris, 1904, cxxxiii, p. 131.

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-- Remarks [in the paper by K. Miura], ibid., 1894, xvi, p. 74.

MIURA, K. Trichom. vag. im frischgelass. Urin eines Mannes, ibid., 1894, xvi, p. 67.

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Trichomonas intestinalis (pp. 54 to 56, 623, and 734).

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-- Zur klinisch-mikrosk. Diagnose der nicht-pylor. Magencarcinome, Festschr. f. Jul. Lazarus, Berlin, 1899, p. 65.

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-- Unters. über einige paras. Flagell., Arbeit. aus dem kais. Gesundheitsamt, 1904, xxi, 1, p. 1.

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-- Rem. sur le Megast. ent., Bull. Soc. Zool. France, 1888, xiii, p. 18.

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-- Intorno ad alc. prot. endop., Atti soc. ital. sci. nat., 1882, xxiv, and Arch. ital. de biol., 1882, ii, p. 421.

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LAMBL. Unters. der Darmexkrete, Vierteljahrsschr. f. prakt. Heilkunde, 1859, lxi, Prag, p. 51.

-- Aus dem Franz-Josef-Kinderspit. in Prag, 1860, i, Prag, p. 360.

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-- Flagellaten im Magen, Wiener klin. Wochenschr., 1904, xvii, 38, p. 1007.

Cercomonas hominis (pp. 61, 62, and 736).

ARTAULT, ST. Flore et faune d. cav. plum., Arch. de Paras., 1898, i, p. 278.

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FENOGLIO. Entérocolite par Amœba coli, Arch. ital. de méd., 1890, xiv, p. 62.

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LAMBL. Cercomonas et Echinococcus in hepate hominis, Med. Wjestnik, 1875, No. 33.

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Monas pyophila (p. 62).

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Prowazekia urinaria (pp. 63 to 65).

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Trypanosomes (pp. 67 to 102, 620 to 623, and 737).

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BRODEN, A. Trypanosomiasis et maladies du sommeil, Bruxelles, 1904, Publ. Soc. d’étud. colon. de Belg.

-- La Trypanosomiase chez l’Européen, Bruxelles, 1905, ibid.

BRUCE, D. Preliminary Report on the Tsetse-fly Disease or Nagana in Zululand, Durban, 1895, C. f. B., P. u. Inf., 1896, i Abt., xix, p. 955.

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DUTTON, J. E., and J. L. TODD, in Brit. Med. Journ., 1903, i, ii; First Report of the Trypanosome Expedition to Senegambia, Liverpool School of Trop. Med., Memoir XI, 1903; Memoir XVI, 1905.

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Leishmania (pp. 104 to 112 and 626 to 629).

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DONOVAN, C. Human Piroplasmosis, Lancet, 1904, ii, p. 744; Brit. Med. Journ., 1904, ii, p. 651.

FIRTH, R. H. Note on the Appearance of Certain Sporozoon Bodies in the Protoplasma of the Oriental Sore, Brit. Med. Journ., 1891.

LAVERAN, A., and F. MESNIL. Sur un protozoaire nouveau (Piroplasma donovani), paras. d’une fièvre de l’Inde, C. R. Acad. Sci., Paris, 1903, cxxxvii, p. 957; 1904, cxxxviii, p. 187.

LEISHMAN, W. B. On the Possibility of the Occurrence of Trypanosomiasis in India, Brit. Med. Journ., 1903, i, p. 1253.

-- The Nature of the Leishman-Donovan Body, ibid., 1904, ii, pp. 29, 642.

LEISHMAN, W. B., and J. C. B. STATHAM. The Development of the Leishman Body in Cultivation, Journ. Roy. Army Med. Corps, March, 1905.

MANSON, P., and G. C. LOW. The Leishman-Donovan Body and Tropical Splenomegaly, Brit. Med. Journ., 1904, i, p. 183.

MARCHAND, F., and J. C. G. LEDINGHAM. Über die Infektion mit Leishmanschen Körperchen (Kala-Azar?) und ihr Verhältnis zur Trypanosomenkrankheit, Zeitschr. f. Hyg. u. Infkrankh., 1904, xlvii, i, p. 1.

MARZINOWSKI, J. E., and S. L. BOGROW. Zur Ätiologie der Orientbeule, Arch. f. path. Anat., 1904, clxxviii, 1, p. 112.

RIEHL, G. Zur Anatomie und Ätiologie der Orientbeule, Vierteljahrsschr. f. Dermat. u. Syph., 1886, p. 805.

ROGERS, L. On the Development of Flagellated Organisms from the Spleen; Protozoic Parasites of Cachexial Fevers and Kala-Azar, Quart. Journ. Micros. Sci., 1904, xlviii, p. 367.

-- Further Work on the Development of the Hepatomonas [Herpetomonas] of Kala-azar and Cachexial Fever from Leishman-Donovan Bodies, Proc. Roy. Soc., London, 1906, lxxvii, B, p. 284.

WRIGHT, J. H. Protozoa in a Case of Tropical Ulcer, Journ. Med. Research, 1903, x, 3, p. 472.

Spirochætes (pp. 114 to 128, 629 to 633, and 739 to 741).

SCHAUDINN, FR., and E. HOFFMANN. Vorl. Ber. über das Vork. von Spirochaeten in syph. Krankheitsprod. und bei Papillomen, Arb. a. d. kais. Gesundheitsamt, 1905, xxii, p. 527.

*Class III.*--*Sporozoa* (pp. 128 to 197).

BALBIANI, G. Leçons sur les Sporozoaires, Paris, 1884.

HAGENMÜLLER, P. Bibliographie générale et spéciale des travaux concernant les Sporozoaires parus antérieurement au 1er janvier, 1899, Ann. Mus. d. ’Hist. nat., Marseille, 2 sér., 1899, i.

LABBÉ, A. Sporozoa, Berlin, 1899, Das Tierreich, 5. Lief.

LÜHE, M. Ergebnisse der neueren Sporozoenforschung, Jena, 1900. Reprinted from C. f. B., P. u. Inf., 1900, xxvii and xxviii.

WASILIEWSKI, TH. V. Sporozoenkunde, Jena, 1896.

TELOSPORIDIA.

ORDER. Gregarinida (pp. 129 to 135).

BENEDEN, E. VAN. Sur une nouvelle espèce de Grégarine désignée sous le nom de Gregarina gigantea, Bull. Acad, roy., Belg., 2e sér., 1869, xxviii, p. 444.

-- Recherches sur l’évolution des Grégarines, ibid., 1871, xxxi, p. 325.

BERNDT, A. Beitrag zur Kenntnis der im Darme der Larve von Tenebrio molitor lebenden Gregarinen, Arch. f. Protistenkde., 1902, i, p. 375.

BRASIL, L. Recherches sur la reproduction des Grégarines monocystidies, Arch. Zool. exp., 4e sér., 1905, iii, p. 17; 1905, iv, p. 69.

BÜTSCHLI, O. Kleine Beiträge zur Kenntnis der Gregarinen, Zeitschr. f. wiss. Zool., 1881, xxxv, p. 384.

-- Bemerkungen über einen dem Glycogen verwandten Körper in den Gregarinen, Zeitschr. f. Biol., 1885, xxi, p. 603.

CAULLERY, M., and MESNIL, F. Sur une Grégarine coelomique présentant dans son cycle évolutif une phase de multiplication asporulée, C. R. Soc. Biol., Paris, 10e sér., 1908, v, p. 65; C. R. Acad. Sci., Paris, 1898, cxxvi, p. 262.

-- -- Le parasitisme intracellulaire et la multiplication asexué des grégarines, C. R. Soc. Biol., Paris, 1901, liii, p. 84.

CAVOLINI, F. Memoria sulla generazione dei pesci e dei granchi, Napoli, 1787, p. 169. Translation into the German by E. A. W. v. Zimmermann, Berlin, 1792, p. 169.

CRAWLEY, H. The Progressive Movement of Gregarines, Proc. Acad. Nat. Sci., Philadelphia, 1902, p. 4.

CUÉNOT, L. Recherches sur l’évolution et la conjugaison des grégarines, Arch. de Biol., 1901, xvii, p. 581.

DRZEWECKI, W. Über vegetative Vorgänge im Kern und Plasma der Gregarinen des Regenwurmhodens, Arch. f. Protistenkde., 1904, iii, p. 107.

DUFOUR, L. Note sur la Grégarine, nouveau genre de ver qui vit en troupeau dans les intestins de divers insects, Ann. Sci. nat., 1e sér., 1828, xiii, p. 366.

DUJARDIN, F. Recherches sur les organismes inférieures, II, Sur les Infusoires appelées Protées, Ann. Sci. nat., 2e sér., Zool., 1835, iv, p. 352.

GIARD, A. Contributions à l’histoire naturelle des Synascidies, IV, Sur une Grégarine parasite d’un Amaraecium, Arch. Zool. expér., 1873, ii, p. 495.

GREEFF, R. Über die pelagische Fauna an den Küsten der Guinea-Inseln, Zeitschr. f. wiss. Zool., 1885, xlii, p. 452.

HENLE, J. Über die Gattung Gregarina, Müllers Arch. f. Anat. u. Phys., 1845, p. 369.

KÖLLIKER, A. Beiträge zur Kenntnis niederer Tiere, I, Über die Gattung Gregarina, Zeitschr. f. wiss. Zool., 1848, i, p. 1.

LÉGER, L. Recherches sur les Grégarines, Tabl. zool., 1892, iii, p. 1.

-- Nouvelles recherches sur les Polycystidées parasites des Arthropodes terrestres, Ann. Fac. Sci., Marseille, 1896, vi, p. 3.

-- Sur un nouveau Sporozoaire des larves de Diptères, C. R. Acad. Sci., Paris, 1900, cxxxi, p. 722.

-- La réproduction sexuée chez les Stylorhynchus, Arch. f. Protistenkde., 1904, iii, p. 303.

LÉGER, L. Etude sur Taeniocystis mira, Grégarine métamérique, Arch. f. Protistenkde., 1906, vii, p. 307.

LÉGER, L., and O. DUBOSCQ. Les Grégarines et l’épithélium intestinal chez les Trachéates, Arch. de Parasitologie, 1902, vi, p. 377.

-- -- Nouvelles recherches sur les Grégarines et l’épithélium intestinal chez les Trachéates, Arch. f. Protistenkde., 1904, iv, p. 335.

-- -- La reproduction sexuée chez Pterocephalus, Arch. Zool. exper., 4e sér., 1903, i; Notes et revue p. cxli.

LIEBERKÜHN, N. Evolution des Grégarines, Mém. Cour. et Mém. d. Sav. étrang., Acad. Belg., 1855, xxvi.

LÜHE, M. Bau und Entwicklung der Gregarinen, I, Arch. f. Protistenkde., 1904, iv, p. 88.

MAUPAS, E. Sur les granules amylacés du cytosome des Grégarines, C. R. Acad. Sci., Paris, 1886, cii, p. 120.

NUSBAUM, J. Über die geschlechtliche heterogame Fortpflanzung einer im Darmkanale von Henlea leptodora schmarotzenden Gregarine (Schaudinella henleae), Zeitschr. f. wiss. Zool., 1903, lxxv, p. 280.

PAEHLER, FR. Über die Morphologie, Fortpflanzung und Entwickelung von Gregarina ovata, Arch. f. Protistenkde., 1904, iv, p. 64.

PROWAZEK, S. Zur Entwickelung der Gregarinen, Arch. f. Protistenkunde, 1902, i, p. 297.

REDI, FR. De animalculis vivis, quae in corporibus animalium viventium reperiuntur, Amstelod., 1708, p. 270. [An earlier account was published in 1684.]

SCHEWIAKOFF, W. Über die Ursache der fortschreitenden Bewegung der Gregarinen, Zeitschr. f. wiss. Zool., 1894, lviii, p. 340.

SCHNEIDER, AI. Sur quelques points de l’histoire du genre Gregarina, Arch. Zool. exper., 1873, ii, p. 515.

-- Contributions à l’histoire des Grégarines des Invertébrés de Paris et de Roscoff, ibid., 1875, iv, p. 493; also Thèse de Paris, 1876.

-- Second contribution à l’étude des Grégarines, ibid., 1882, x, p. 432.

-- Sur le développement du Stylorhynchus longicollis, ibid., 2e sér., 1884, ii, p. 1.

-- Etudes sur le développement des Grégarines, Tabl. zool., 1885, i, pp. 10, 81.

-- Grégarines nouvelles ou peu connues, ibid., pp. 25, 90; 1887, ii, p. 67.

SCHNITZLER, H. Über die Fortpflanzung von Clepsidrina ovata, Arch. f. Protistenkunde, 1905, vi, p. 309.

SIEBOLD, TH. V. Beiträge zur Naturgeschichte der wirbellosen Tiere, Über die zur Gattung Gregarina gehörenden Helminthen, Neueste Schrift d. naturforsch. Ges., Danzig, 1839, iii, p. 56.

SIEDLECKI, M. Über die geschlechtliche Vermehrung der Monocystis ascidiae, R. Lank., Anz. Akad. d. Wiss., Cracow, 1899, p. 515.

-- Contributions à l’étude des changements cellulaires provoqués par les Grégarines, Arch. d’anat. micros., 1901, iv, p. 87.

STEIN, FR. Über die Natur der Gregarinen, Müllers Arch. f. Anat. u. Phys., 1848, p. 182.

-- Neue Beiträge zur Kenntnis der Entwickelungsgeschichte und des feineren Baues der Infusionstiere: I, Die Entwickelungsgeschichte der Vorticella microstoma Ehrb., nebst vergleichenden Bemerkungen über die Entwickelungsweise der Gregarinen, Zeitschr. f. wiss. Zool., 1852, iii, p. 474.

WOLTERS, M. Die Conjugation u. Sporenbildung bei Gregarinen, Arch. f. mikr. Anat., 1891, xxxvii, p. 99.

Schizogregarinea (p. 135).

LÉGER, L. La reproduction sexuée chez les Ophryocystis, C. R. Soc. Biol., Paris, 1900, lii, p. 927.

-- Les Schizogrégarines des Trachéates: I, Le genre Ophryocystis, Arch. f. Protistenkunde, 1907, viii, p. 160.

LÉGER, L., and HAGENMÜLLER. Morphologie et évolution de l’Ophryocystis schneideri, Arch. Zool. exp., 3e sér., 1900, viii; Notes et revue p. xl.

SCHNEIDER, AI. Ophryocystis bütschlii, sporozoaire d’un nouveau type, Arch. Zool. expér., 2e sér., 1884, ii, p. 111.

-- Ophryocystis francisci, Tabl. zool., 1885, i, p. 1.

ORDER. Coccidiidea (pp. 135 to 150, 741 and 742).

BALBIANI, G. Leçons sur les Sporozoaires, Paris, 1884, p. 104.

BLANCHARD, R. Les coccidies et leur rôle path., Causeries scientif. Soc. Zool. France, No. 5, Paris, 1900.

EIMER, TH. Über die ei- und kugelförmigen Psorospermien der Wirbelthiere, Würzburg, 1870.

HAKE, A. A Treatise on Varicose Capillaries as constituting the Structure of Carcinoma of the Hepatic Ducts, with an account of a New Form of the Pus Globule, London, 1839.

KAUFFMANN, W. Anal. ad tubercul. et entoz. cognitionem, Diss. inaug., Berol, 1847.

KLOSS, H. Über die Parasiten der Niere von Helix, Abh. Senckenb. nat. Ges. Frankf. a. M., 1855, i, p. 189.

LABBÉ, A. Recherches zoologiques, cytol. et biol. sur les Coccidies, Arch. Zool. exp. 1896 (3), iv, p. 516.

LAVERAN, A., and F. MESNIL. Sur la coccidie trouvée dans le rein de la Rana esculenta et sur l’infection générale qu’elle produit, C. R. Acad. Sci., Paris, 1902, cxxxv, p. 82.

LÉGER, L. Le cycle evol. d. Coccidies chez les Arthrop., C. R. Soc. Biol., Paris, 1897 (10), iv, p. 382.

-- Coccidies nouv. du tube digest. d. Myriap., C. R. Acad. Sci., Paris, 1897, cxxiv, p. 901.

LEUCKART, R. Die Parasiten des Menschen, 2. Aufl., 1879, i, p. 248.

LIEBERKÜHN, N. Über die Psorospermien, Müllers Arch. f. Anat. u. Phys., 1854, p. 1.

-- Evolution des grégarines, Mem. cour. et Mém. d. say. étrang., Acad. roy. de Belg., 1855, xxvi.

MILIAN, G. Les sporozooses humaines, Thèse, Paris, 1899.

MOUSSU, G., and G. MAROTEL. La coccidiose du mouton et son paras., Arch. de Paras., 1902, vi, p. 82.

NASSE, H. Üb. d. eiförmigen Zellen der tuberkelähnlichen Ablagerungen in den Gallengängen der Kaninchen, Müllers Arch. f. Anat. u. Phys., 1843, p. 209.

PFEIFFER, L. Beiträge z. Kenntnis d. pathogenen Gregarinen: II, Über Gregarinose, ansteckendes Epitheliom und Flagellaten-Diphtherie der Vögel, Zeitschr. f. Hyg. u. Inf., 1889, v, p. 363.

-- Die Protozoen als Krankheitserreger: 1. Aufl., Jena, 1890; 2. Aufl., 1892.

PFEIFFER, R. Beiträge zur Protozoenforschung: I, Die Coccidienkrankheit der Kaninchen, Berlin, 1892.

REINCKE. Nonnulla quaedam de psorosp. cuniculi, Diss. inaug., Kiliae, 1866.

REMAK, H. Diagnost. und pathog. Untersuchungen, Berlin, 1845.

RIVOLTA, G. Psorospermi i psorospermosi negli anim. dom., Med. veter., 1869 (3), iv.

SCHAUDINN, F. Unters. über d. Generationswechsel d. Coccidien, Zool. Jahrb. Anat., 1900, Abt. xiii, p. 197.

-- Studien über krankheitserr. Protozoen: I, Cyclospora caryolytica, der Erreger der perniciösen Enteritis des Maulwurfes, Arb. kais. Gesundheitsamt, 1902, xviii, p. 378.

SCHAUDINN, F., and M. SIEDLECKI. Beitr. z. Kenntnis d. Coccidien, Verh. d. D. zool. Ges., 1897, vii, p. 192.

SCHNEIDER, AI., and M. L. PFEIFFER. Le cycle évolutif des Coccidies, Tabl. zool., ii, p. 105.

SCHUBERG, A. Die Coccidien aus dem Darm der Maus, Verh. nat.-med. Ver. Heidelberg, N. F. V., 1895, p. 369.

SIMOND, P. L. L’évolution d. sporoz. du genre Coccidium, Ann. Inst. Pasteur, 1897, xi, p. 545.

-- Note sur une Coccidie nouv. (Cocc. kermorganti) paras. de Gavialis gangeticus, C. R. Soc. Biol., Paris, 1901, liii, p. 483.

SMITH, TH., and H. P. JOHNSON. On a Coccidium (Klossiella muris) parasitic in the Renal Epithelium of the Mouse, Journ. Exp. Med., 1902, vi, p. 303.

STIEDA, L. Über die Psorospermien der Kaninchenleber, Virchows Arch. f. pathol. Anat., 1865, xxxii, p. 132.

WALDENBURG, L. De struct. et origine cystidum verminos, Diss. inaug., Berol, 1860; Virchows Arch. f. path. Anat., 1862, xxiv, p. 149.

-- Zur Entwickelung der Psorospermien, ibid., 1867, xl, p. 435.

Eimeria stiedae (pp. 145 to 148).

FELSENTHAL and STAMM. Veränder. i. Leber und Darm bei d. Coccidienkrankh. d. Kaninchen, Virchows Arch. f. path. Anat., 1893, cxxxii, p. 36.

LINDEMANN, KR. Weiteres über Gregarinen, Bull. soc. Imp. Nat., Moscow, 1865, xxxviii, 2, p. 385.

LÜHE, M. Über Geltung und Bedeutung. d. Gattungsnamen Eimeria und Coccidium, C. f. B., P. u. Inf., 1902, i Abt. Orig., xxxi, p. 771.

METZNER. Untersuchungen an Coccidium cuniculi I, Arch. f. Protistenkde., 1903, ii, p. 13.

PIANESE, G. Le fasi di sviluppo del coccidio oviforme e le lesioni istologiche che induce, Arch. d. Paras., 1899, ii, p. 387.

PODWYSSOTZKI, W. Zur Entwickel. d. Coccidium oviforme als Zellschmarotzer, Bibl. med., 1895, Abt. D., ii, p. 4, Cassel.

RIECK, M. Sporozoen als Krankheitserreger bei Haustieren, Deutsche Zeitschr. f. Tiermedizin u. vergl. Path., 1889, xiv, p. 52.

STILES, CH. W. Eimeria stiedae. Correct Name of the Hepatic Coccidia of Rabbits, Eleven Miscellaneous Papers on Animal Parasites, U.S. Dept. Agric., Bur. An. Ind., Bull. No. 35, Washington, 1902.

WASILIEWSKI, TH. V. Studien u. Microphot. z. Kenntn. d. pathog. Protozoen: I, Bau Entw. u. pathog. Bedeutung d. Coccidien, Leipzig, 1904.

Isospora bigemina (pp. 149, 150).

FINCK. Sur la physiol. de l’épith. intest., Thèse, Strasb., 1854, p. 17.

GRASSI, B. Intorno ad alc. prot. endopar., Atti Soc. Ital. Sci. Nat. Milano, 1882, xxiv.

GRUNOW. Ein Fall von Protozoen- (Coccidien?) Erkrankung des Darmes, Arch. f. exp. Path. u. Pharm., 1901, xlv, p. 262.

RAILLIET, A., and A. LUCET. Notes s. quelq. esp d. Cocc. encore peu conn., Bull. Soc. Zool. France, 1891, xvi, p. 249.

STILES, CH. W. Notes on Parasitology, No. 11, Journ. Comp. Med. and Vet. Arch., 1892, xiii, p. 517; Bull. Soc. Zool. France, 1891, xvi, p. 163.

VIRCHOW, R. Helminth. Notiz. 3, Virchows Arch. f. path. Anat., 1860, xviii, pp. 342 and 527.

WASILIEWSKI, TH. V. Studien u. Mikrophot. zur Kenntnis d. path. Prot., I, Leipzig, 1904, pp. 88 ff.

Doubtful Species (p. 150).

BLANCHARD, R. Les cocc. et leur rôle path., Caus. scient. Soc. Zool. France, 1900, No. 5.

BORINI, A. Assoc. paras. ed il nuovo prot. di Perroncito, Giorn. R. Accad. Med., Torino, 1899, No. 7.

KUNSTLER, J., and A. PITRES. Sur une psorospermie trouv. dans une humeur pleurét., Journ. Microgr., 1884, viii, p. 469.

MONIEZ, R. Traité de parasit., Paris, 1896, p. 52.

PERRONCITO, E. Di un nuovo protoz. dell’ uomo e di talune specie, Giorn. R. Accad. Med., Torino, 1899, No. 1; Cinquantenn. de la Soc. Biol., Paris, 1899, p. 184.

-- Il coccidio jalino ed il microspor. poliedrico nell’ uomo, ibid., ann. 65, 1902, p. 378.

SEVERI, A. Gregarinosi polmonale in infante natomorto, Rif. med., 1892, ii, p. 54; Boll. Accad. med., Genova, 1892, vii, No. 2.

ORDER. Hæmosporidia (pp. 151 to 155, and 742).

BALFOUR, A. A Hæmogregarine of Mammals, Journ. Trop. Med., 1905, viii, p. 241.

BÖRNER, C. Unters. über Haemosporidien, I, Zeitschr. f. wiss. Zool., 1901, lxix, p. 398.

BÜTSCHLI, O. Einige Bemerk. über d. rot. Blutk. d. Frosches, Abh. Senckenb. nat., Ges., Frankf. a. M., 1876, p. 49.

CASTELLANI, A., and A. WILLEY. Hæmatozoa of Vertebrates in Ceylon, Spolia zeylanica, Colombo, 1904, ii, p. 2.

CELLI, A., and F. SANFELICE. Paras, d. rot. Blutk. d. Mensch. u. d. Thiere, Fortschr. d. Med., 1891, Nos. 11–15; Ann. ist. d’igien. esp., Roma, N.S.I., 1891.

CHAUSSAT. Des hématozoaires, Thèse, Paris, 1850.

DANILEWSKY, B. Die Haematozoen der Kaltblüter, Arch. f. mikr. Anat., 1885, xxiv, p. 588.

-- Matér. pour servir à la paras. du sang, Arch. slav. de biol., 1886, i, pp. 89, 364; 1887, ii, pp. 33, 157, 370; Biol. Centralb., 1885, v, p. 529.

DURHAM, H. E. Drepanidium in the Toad, Liverpool School of Trop. Med. Memoir VII, Liverpool, 1902, p. 78.

GAULE, J. Über Würmchen, welche a. d. Froschblutkörp. auswandern, Arch. f. Anat. u. Phys., Phys. Abt., 1880, p. 57.

-- Die Beziehungen der Cytozoen zu den Zellkernen, ibid., 1881, p. 297.

GRASSI, B., and R. FELETTI. Malariaparas. in den Vögeln, C. f. B. u. Par., 1891, ix, p. 403; 1891, x, p. 449.

HINTZE, R. Lebensweise u. Entw. v. Lankesterella minima (Chauss)., Zool. Jahrb., Anat. Abt., 1902, xv, p. 693.

KRUSE, W. Über Blutparasiten, Arch. f. path. Anat., 1890, cxx, p. 541, and cxxi, p. 359.

LABBÉ, A. Rech. zool. et biol. sur les paras. endoglob. du sang. d. vertébrés, Arch. Zool. exp., 3 sér., 1894, ii, p. 55.

LANKESTER, E. RAY. On Undulina, the Type of a New Group of Infusoria, Quart. Journ. Micros. Sci., 1871, xi, p. 387.

-- On Dreipanidium ranarum, ibid., 1882, xxii, p. 53.

LEBAILLY, CH. Rech. sur les hémat. par. des téléastéens marins, Arch. de Paras., 1906, x, 3, p. 370.

OSLER, W. An Account of Certain Organisms occurring in the Liquor Sanguinis, Proc. Roy. Soc. Lond., 1874, xxii, p. 391.

RUGE, R. Unters. über d. deutsche Proteosoma, C. f. B., P. u. Inf., 1901 (1), xxix, p. 398.

SIEGEL. Die geschlechtliche Entw. v. Haemogregarina stepanovi im Rüsselegel Placobdella catenigera, Archiv für Protistenkunde, 1903, ii, p. 339, with additions by F. Schaudinn.

SIMOND, P. L. Contrib. à l’étude des hématoz. endoglob. d. reptiles, Ann. Inst. Pasteur, 1901, xv, p. 319.

WALLERSTEIN. Über Drepanidium ranarum, Inaug.-Diss., Bonn, 1882.

MALARIAL PARASITES OF MAN (pp. 155 to 172).

(a) Comprehensive Works.

CELLI, A. La malaria sec. le nuove ricerche, Roma, 1900.

KERSCHBAUMER, FR. Malaria, ihr Wesen, ihre Entstehung und ihre Verhütung, Wien, 1901.

LAVERAN, A. Traité des fièvres palustres, Paris, 1884.

LÜHE, M. Cf. p. 765, Die im Blute schmar. Prot., 1906.

MANNABERG, J. Die Malariaparasiten, Wien, 1893.

NEVEU-LEMAIRE, M. Les hématozoaires du paludisme, Paris, 1901.

REINHARDT, LUDW. Die Malaria und deren Bekämpfung nach den Ergebn. d. neuesten Forschg., Würzb., 1905.

RUGE, R. Einführung in das Studium der Malariakrankh. mit bes. Berücksicht. d. Technik, Jena, 1901.

STEPHENS, J. W. W., and S. R. Christophers. The Practical Study of Malaria and other Blood Parasites, 3rd edition, London, 1908.

ZIEMANN, H. Über Malaria- und andere Blutparasiten, Jena, 1898.

-- Malaria, Handb. d. Tropenkrankh., Lpzg., 1906, iii, p. 269.

(b) Special Studies.

ARGUTINSKY, P. Malariastudien, Arch. f. mikros. Anat., 1901, lix, p. 315; 1902, lxi, p. 331.

-- Zur Kenntn. d. Tropica-Paras., C. f. B., P. u. Inf., i Abt. Orig., xxxiv, p. 144.

ATTI della società per gli studi della malaria, Roma, 1899–1906, i-vii.

BIGNAMI, A. Das Tropenfieber u. die Sommer-Herbstfieber d. gemäss. Klimate, C. f. B., P. u. Inf., 1898, (1), xxiv, p. 650.

BIGNAMI and BASTANIELLI. Osserv. nelle febbre malar. estivo-autunn., Rif. med., 1890, p. i334.

-- -- Studi sull’ inf. mal., Bull. R. Accad. med., Roma, 1893–94, xx.

-- -- Sulla strutt. dei par. mal. e in specie dei gameti d. par. est.-aut., Atti Soc. stud. d. mal., 1899, i.

CELLI, A., and F. SANFELICE. Über d. Paras. d. roth. Blutk. im Menschen u. in Thieren, Fortschr. d. Med., 1891, pp. 499, 541; Ann. istit. d’igiene sperim., Roma, 1891, N.S. i.

DANILEWSKI, B. Zur Parasit. d. Blutes, Biol. Centralbl., 1885–86, v, p. 529.

-- La parasitologie comp. du sang, Charkow, 1889.

-- Sur les microb. d’ infect. malar. aiguë et chron. chez les oiseaux et chez l’homme, Ann. Inst. Pasteur, 1890, p. 753; 1891, p. 758.

-- Über den Polymitus malariae, C. f. B. u. Par., 1891, ix, p. 397.

DIONISI, A. La malaria di alcune pipistrelli, Ann. d’igiene sperim., 1899, ix, 4; Atti soc. ital. p. stud. d. malaria, 1899, i.

GERHARDT. Über Intermittensimpfungen, Arch. f. klin. Med., 1884, vii.

GOLGI, C. Sull’ infezione malarica, Arch. p. le sci. med., 1886, x; Arch. ital. de biol., 1887, viii; Fortschr. d. Med., 1889, 3.

-- Sul ciclo evolutivo dei paras. mal. nella feb. terz., Arch. p. le sci. med., 1889, xiii.

GRASSI, B. Preliminary Communication in: Rend. R. Accad. d. Lincei, Roma, 1898, ser. 5, vii, pp. 163, 234, 314; 1899, viii, p. 165.

-- Studi di un zoologo sulla malaria, Atti R. Accad. dei Lincei, Mem. cl. fis., 1900, ser. 5, iii; Roma, 1900; Die Malaria, Studien eines Zoologen, 2. Aufl., Jena, 1901; also in Italian, Roma, 1901.

-- Documenti rig. la storia della scop. del modo di trasmiss. della malaria umana, Milano, 1903.

GRASSI, B., and A. DIONISI. Il ciclo. evol. degli emosporidi, Rend. R. Accad. d. Lincei, Roma, 1898, ser. 5, vii, 2 sem., p. 308.

GRASSI, B., and R. FELETTI. Über d. Paras, d. Malaria, C. f. B. u. P., 1890, vii, pp. 396, 340; Malariapares. in d. Vögeln, ibid., 1891, iv, pp. 403, 429, 461; Weiteres zur Malariafrage, ibid., 1891, x, pp. 449, 481, 517.

JANCSÓ, N. Zur Frage d. Inf. d. Anopheles claviger mit Mal.-Paras. b. nied. Temp., C. f. B., P. u. Inf., 1904, i Abt. Orig., xxxvi, p. 624; Der Einfl. d. Temp. a. d. geschl. Generationsentw. der Mal.-Paras. u. auf d. exper. Mal.-Erkr., ibid., 1905, xxxviii, p. 650.

KOCH, R., and R. PFEIFFER. Beiträge z. Protozoenforsch.: I, Die Coccidienkrankh. d. Kaninchen, Berlin, 1892.

-- -- Ärztl. Beob. i. d. Tropen, Verhandl. d. D. Kol.-Ges. Abt. Charlottenburg-Berlin, 1897–98, Heft 7, p. 280.

-- -- Die Malaria in Deutsch-Ostafrika, Arb. kais. Gesundheitsamt, 1898, xiv, p. 292.

-- -- Reiseberichte über Rinderpest ... trop. Malaria ... Berlin, 1898.

-- -- Ergebn. d. wiss. Exped. nach Italien z. Erf. d. Malaria, Deutsche med. Wochensch., 1899, p. 69.

-- -- [Zwei] Berichte üb. d. Tätigkeit d. Malaria-Exp., ibid., p. 601; 1900, p. 88.

-- -- Über die Entwickelung d. Mal.-Paras., Zeitschr. f. Hyg. u. Inf., 1899, xxxii, p. 1.

KOSSEL, H. Über einen malariaähnl. Blutparas. b. Affen, Zeitschr. f. Hyg., 1899, xxxii, p. 25.

KRUSE, W. Über Blutparasiten, Virchows Arch. f. path. Anat., 1890, cxx, p. 451; 1891, cxxi, p. 1395.

LABBÉ, A. Rech. zool. et biol. sur les par. endoglob. du sang d. vertébr., Arch. Zool. exp., 1894 (3), ii, p. 55.

LAVERAN, A. Note sur un nouveau paras. trouvée dans le sang de plus. malad. att. de fièvre palustre, Bull. Acad. de Méd., Paris, 1880, November 23 and December 28.

-- Communication sur la nat. paras. des accid. de l’impalud., C. R. Acad. Sci., Paris, 1881, xciii, p. 627; 1882, xcv, p. 737.

-- Nature parasitaire des accidents de l’impaludisme, Paris, 1881, 8vo.

MCCALLUM, W. G. On the Hæmatozoan Infection of Birds, Journ. Exper. Med., Baltimore, 1898, iii, p. 117.

MARCHIAFAVA, E., and A. CELLI. Les altér. des glob. roug. dans l’infect. par malaria, Arch. ital. de biol., 1884, v.

-- -- Nuove ricerche sulla infez. malarica, Annali di agric., 1885, 1886; Fortschr. d. Med., 1885, Nos. 11 and 24; Arch. p. le sci. med., 1886, ix; 1888, xii; 1889–90, xiv; Arch. ital. de. biol., 1887, viii, p. 131; 1888, ix.

MAURER, G. Die Tüpfelung der Wirtszelle des Tertianparasiten, C. f. B., P. u. Inf., 1900, i Abt., xxviii, p. 114.

-- Die Malaria perniciosa, C. f. B., P. u. Inf., 1902, i Abt. Orig., xxxii, p. 695.

NUTTALL, G. H. F. Die Mosquito-Malariatheorie, C. f. B., P. u. Inf., 1899, xxv, pp. 161, 209, 245, 285, 337.

-- Neuere Forsch. üb. d. Rolle d. Mosqu. bei d. Verbreit. d. Mal., ibid., pp. 877, 903; xxvi, p. 140; 1900, xxvii, pp. 193, 218, 260, 328.

PANICHI, M. Sulla sede del par. mal. nell’ eritrocito dell’ uomo, Arch. Farmacol. sper. e scienze aff., 1902, i, pp. 418, 450.

PEZOPOULO, N., and J. P. CARDAMATIS. Die Malaria in Athen, eine biolog. u. histol. Studie üb. d. Malariaplasmodien, C. f. B., P. u. Inf., 1906, i Orig., xl, p. 344.

PLEHN, F. Beitr. z. Lehre d. Malariainf., Zeitschr. f. Hyg., 1890, p. 78.

Reports to the Malaria Committee, Roy. Soc. Lond., 1900–1903, i-viii.

ROMANOWSKY, D. Zur Frage d. Paras.... d. Malaria, St. Petersb. med. Wochenschr., 1891, Nos. 34, 35.

ROSS, R. Untersuchungen über Malaria (translated by Schilling), Jena, 1905.

RUGE, R. Über d. Plasmod. bei Malariaerkr., Deutsche mil.-ärztl. Zeitschr., 1892, xxi, pp. 49, 109.

-- Ein Beitr. z. Chromatinfärb. d. Mal.-Par., Zeitschr. f. Hyg., 1900, xxxiii, p. 178.

-- Zur Tüpfelung der rot. Blutscheib. bei Febr. interm. tert., Arch. f. klin. Med., 1902, lxxii, p. 208.

SCHAUDINN, F. Über d. Generationswechsel d. Coccid. u. die neueren Mal.-Forsch., Sitzungsb. Ges. nat. Frde., Berlin, 1899, p. 159.

-- Stud. üb. Krankheitserreg. Prot.: II, Plasmodium vivax, d. Erreger d. Tertianfieb. b. Mensch., Arb. Reichsges.-Amt., 1902, xix, p. 169.

SCHOO, H. J. M. Over Malaria: I, Welke Temperatur ist noodig voor de Amphigonie von Plasmodium vivax? Nederl. Tijdschr. v. Geneeskde., 1901, ii, p. 1338.

SCHÜFFNER, W. Beitr. zur Kenntn. der Malaria, Deutsch. Arch. f. kl. Med., 1899, lxiv, p. 428; Zur Tüpfelung der r. Blutsch. bei Febr. int. tert., ibid., 1901, lxxi.

SERRA. Contrib. allo stud. d. posiz. del par. mal. in rapp. glob. rossi, Giorn. Accad. di med., Torino, 1905, Nos. 5 and 6.

THAYER, W. S. Recent Investigations upon Malaria, Med. News, 1899, lxxiv, p. 617.

VASSALL, J. J. Sur un hématoz. endoglob. nouv. d’un mammifère, Annal. Inst. Pasteur, 1905, xxi, p. 224.

ZIEMANN, H. Blutparas. bei heim. und trop. Malaria, C. f. B., P. u. Inf., 1896, i Abt., xx, p. 653; Z. Morph. d. Malariaparas., ibid., 1897, xxi, pp. 641, 805.

Babesia (pp. 174 to 178).

BABES, V. Die Ätiologie der seuchenhaften Hämoglobinurie des Rindes, Virch. Arch. f. path. Anat., 1889, cxv.

-- Bemerk. über d. Paras. des “Carceag.” der Schafe und die paras. Ictero-Hämaturie der Schafe, ibid., 1895, cxxxix.

-- Bemerk. über d. Entdeckung der seuchenhaften Hämoglobinurie des Rindes und des Carceag. des Schafes, C. f. B., Par. u. Inf., 1903, i Abt., xxxiii, p. 449.

BONOME. Über paras. Ictero-Hämaturie der Schafe, Virch. Arch. f. path. An., 1895, Bd. cxxxix, p. 1.

CELLI, A., and F. G. SANTORI. Die Rindermalaria in der Campagna von Rom, C. f. B., P. u. Inf., 1897, xix, p. 561.

CHAUVELOT, E. Les babésioses, Paris, 1904.

DSCHUNKOWSKI, E., and J. LUHS. Die Piroplasmosen der Rinder, C. f. B., P. u. Inf., 1904, i Abt. Orig., xxxv, p. 486, 3 Taf.

FANTHAM, H. B. Piroplasma muris from the Blood of the White Rat, Quart. Journ. Micros. Sci., 1906, 1, p. 483, 1 pl.

KINOSHITA, K. Untersuchungen üb. Babesia canis, Arch. f. Protistenkde., 1907, viii, p. 294.

KLEINE, F. K. Kultivierungsversuche d. Hundepiroplasmen, Zeitschr. f. Hyg. u. Inf., 1906, liv, p. 10.

KOCH, R. Reiseberichte, über Rinderpest ... Texas-Fieber, Berlin, 1898.

-- Vorl. Mitt. über die Ergebn. einer Forschungsreise nach Ostafrika, Deutsche med. Wochenschr., 1905, No. 45.

-- Beitr. z. Entwicklungsgesch. der Piroplasmen, Zeitschr. f. Hyg. u. Inf., 1906, liv, p. 1.

KOSSEL, H., WEBER, SCHÜTZ and MIESSNER. Über die Hämoglobinurie der Rinder in Deutschland, Arb. a. d. Kais. Gesundheitsamt, 1903, xx, 1, 3 Taf.

LAVERAN, A. Contrib. à l’étude de Piroplasma equi, C. R. Soc. Biol., Paris, 1901, liii (14), p. 385.

LEBLANC, P. Piroplasma canis, C. R. Soc. Biol., Paris, 1900, lii, p. 168.

LINGARD, A. Can the Piroplasma bigeminum find a Habitat in the Human Subject? C. f. B., P. u. Inf., 1904, i Abt. Orig., xxxvi, p. 214.

LINGARD, A., and E. JENNINGS. A Preliminary Note on a Piroplasmosis found in Man and in Some of the Lower Animals, Ind. Med. Gaz., 1904, xxxix, p. 161.

LÜHE, M. Zur Kenntnis von Bau und Entw. d. Babesien, Zool. Anz., 1906, xxx, p. 45.

MIYAJIMA and SHIBAYAMA. Über das in Japan beobachtete Rinderpiroplasma, Zeitschrift f. Hyg., 1906, lii, p. 189.

NOCARD and MOTAS. Contrib. à l’étude de la piropl. canine, Ann. Inst. Pasteur, 1902, xvi, 1, p. 257, 2 pl.

NUTTALL, G. H. F., and G. S. GRAHAM-SMITH, Canine Piroplasmosis V, Journ. of Hyg., 1906, vi, p. 586.

SCHMIDT, A. Die Zeckenkrankh. der Rinder, Arch. f. wiss. u. prakt. Tierheilkunde, 1904, xxx, p. 42.

SMITH, T., and F. KILBORNE. Investigations into the Nature, Causation, and Prevention of Texas or Southern Cattle Fever, Eighth and Ninth Annual Reports, Bureau of Animal Industry, Washington, U.S.A., 1893, pp. 177–304, 10 pl.

THEILER, A. Die Piroplasmose des Maultieres und des Esels, Zeitschr. f. Tiermed., 1904, viii, p. 383.

WILSON, L. B., and W. M. CHOWNING. Studies in Piroplasmosis hominis, Journ. Infect. Dis., 1904, p. 31, 2 pl.

NEOSPORIDIA.

ORDER. Myxosporidia (pp. 181 to 184).

BALBIANI, G. Sur l’organis. et la nature d. psorosp., C. R. Acad. Sci., Paris, 1863, lvii, p. 157.

BÜTSCHLI, O. Zur Kenntn. der Fischpsorosp., Zeitschr. f. wiss. Zool., 1881, xxxv, p. 629.

COHN, L. Über die Myxospor. von Esox lucius u. Perca fluviatilis, In.-Diss., Königsberg, 1895, u. Zool. Jahrb. Anat., 1895, ix.

-- Zur Kenntnis der Myxospor., C. f. B., P. u. Inf., 1902, i Abt. Orig., xxxii, p. 628.

CREPLIN, J. C. H. Beschreibung der Psorosporm. des Kaulbarsch. nebst Bemerkung über die der Plötze, Arch. f. Naturg., 1842, viii, 1, p. 61.

DOFLEIN, F. Stud. z. Nat. d. Prot.: III, Über Myxospor., Zool. Jahrb., Anat., 1898, xi, p. 281.

DUJARDIN, F. Hist. nat. des helm., Paris, 1845, p. 643.

GURLEY, R. On the Classification of the Myxosporidia, Bull. U.S. Comm. of Fish and Fishermen, 1891, Washington, 1893, p. 407.

-- The Myxosporidia or Psorosperms of Fishes and the Epidemics produced by them, Rep. U.S. Comm. of Fish and Fishermen, 1892, Washington, 1894, p. 65.

HOFER, B. Die sogen. Pockenkrankh. d. Karpfen, Allg. Fisch.-Ztg., 1896, pp. 2, 28; 1902, p. 22.

JOSEPH, H. Chloromyxum protei n. sp., Arch. f. Protistenkde., 1907, viii, P· 398.

LAVERAN, A., and F. MESNIL. Sur une myxosp. des voies biliaires de l’Hippocampe, C. R. Soc. Biol., Paris, 1900, lii, p. 380.

-- -- Sur la multiplic. endog. d. Myxosporidies, C. R. Soc. Biol., Paris, 1902, liv, p. 469.

LEYDIG, F. Über Psorosperm. u. Gregarinen, Arch. f. Anat. u. Phys., 1851, p. 221.

LIEBERKÜHN, N. Über d. Psorosp., Arch. f. Anat. u. Phys., 1854, p. 349.

LUDWIG, H. Über d. Myxospor. d. Barben in d. Mosel, Jahresber. d. Rhein. Fisch.-Ver., 1888–89, p. 27.

LÜHE, M. Cystodiscus immersus Lutz., Verh. d. D. zool. Ges., 1899, p. 291.

MERCIER, L. Phénomènes de sexualité chez le Myxobolus pfeifferi, C. R. Soc. Biol., Paris, 1906, lx, p. 427.

MÜLLER, J. Über eine eigent. krankh. paras. Bildung mit specif. organis. Samenkörp., Arch. f. Anat. u. Phys., 1841, p. 477.

MÜLLER, J., and A. RETZIUS. Über paras. Bildungen, ibid., 1842, p. 193.

PERUGIA, A. Sulle myxosp. d. pesci marini, Bull. scientif., Ann. xii-xiii, 1889–90, p. 10.

PFEIFFER, L. Die Protoz. als Krankheitserreger, 2. Aufl., Jena, 1891.

-- Unters. über d. Krebs, Jena, 1892.

PLEHN, M. Über die Drehkrankh. der Salmoniden, Arch. f. Protistenkde., 1905, v, p. 145.

RAILLIET, A. La maladie d. barbeaux de la Marne, Bull. soc. centr. d’aquicult. France pour 1890, ii, p. 117.

SCHRÖDER, OL. Eine neue Myxosporidienart aus den Kiemen von Acerina cernua, Arch. f. Protistenkde., 1906, vii, p. 186.

SCHUBERG, A., and O. Schröder. Myxosp. a. d. Nervensyst. u. d. Haut der Bachforelle, Arch. f. Protistenkde., 1905, vi, p. 47.

THÉLOHAN, P. Rech. sur les Myxospor., Bull. scientif. France et Belg., 1895, xlvi, p. 100.

-- Observ. sur les myxosp. et essai de classific. d. ces. org., Bull. soc. philom., Paris, 1892 (8), iv, p. 165.

WELTNER, W. Über Myxospor. in d. Eiern v. Esox lucius, Sitzungsber. Ges. naturf. Frde., Berl., 1892, p. 28.

ZSCHOKKE, F. Myxospor. d. Gattg. Coregonus, C. f. B., P. u. Inf., 1898 (i), xxiii, p. 602; Mitt. nat. Ges., Lucerne, 1898, 2, p. 205.

ORDER. Microsporidia (pp. 184 to 186).

BALBIANI, G. Rech. sur les corpusc. de la pébrine, Journ. de l’Anat. et de la Phys., 1866, iii, p. 599.

-- Etud. sur la maladie psorosperm. des vers à soie, ibid., 1867, iv, pp. 263, 329.

BOLLE, J. Der Seidenbau in Japan, Budapest, Wien, Leipzig, 1898, p. 94.

GLUGE. Tumeurs enkystées observées sur la peau des épinoches, Bull. Acad. roy. de Belg., 1838, v, p. 772.

HENNEGUY. Note sur un paras. d. muscl. du Palaemon rectirostris, Mém. soc. philom. à l’occas. du centenn. de sa fondat, Paris, 1888.

HENNEGUY and THÉLOHAN. Myxospor. par d. muscl. chez quelq. crust. décap., Ann. microgr., Paris, 1892, iv, C. R. Soc. Biol., Paris, 1892 (9), iv, C. R. Acad. Sci., Paris, 1892, cxiv.

HESSE, E. Sur une nouv. microsp. tétraspor. du genre Gurleya, C. R. Soc. Biol., Paris, 1903, lv, p. 495.

-- Sur la prés. d. microsp. du genre Thelohania chez les insectes, C. R. Acad. Sci., Paris, 1903, cxxxvii, p. 418.

-- Thelohania legeri n. sp., microsp. nouv. d. larves d’Anopheles maculipennis Meig., C. R. Soc. Biol., Paris, 1904, lvii, p. 570.

-- Sur Myxocystis mrázeki, microsp. par de Limnodrilus hoffmeisteri Clap., C. R. Soc. Biol., Paris, 1905, lviii, pp. 12–15.

KOROTNEFF, A. Myxosporidium bryozoides, Z. f. w. Zool., 1892, liii, p. 591.

KULAGIN, N. Zur Entw. v. Glugea bombycis Thél., Zool. Anz., 1898, xxi, p. 469.

LEBERT, H. Über die gegenwärtig herrsch. Krankh. des Insects d. Seide, Berl. entom. Ztschr., 1858, ii, p. 149.

LEYDIG, FR. Zur Anat. v. Coccus hesferidum, Z. f. w. Zool., 1854, v, p. 11.

-- Zum fein. Bau d. Arthropoden, Arch. f. An. u. Phys., 1855, p. 397.

-- Über Paras. nied. Tiere, Arch. f. path. Anat., 1858, p. 280.

-- Der Parasit in der neuen Krankh. d. Seidenraupe, Arch. f. Anat. u. Phys., 1863.

LUTZ, A., and A. SPLENDORE. Über Pebrine u. verw. Microspor., C. f. B., P. u. Inf., 1903, i Abt., xxxiii, p. 150.

MONIEZ, R. Note sur des paras. d. helm., Bull. scient. du Départ. du Nord, 1879 (2), ii, p. 304.

-- Observ. pour la revis. d. microsporid., C. R. Acad. Sci., Paris, 1887, civ, p. 1312.

MRÁZEK. Sporozoenstudien: II, Glugea lophii Dofl., Sitzungsber. k. böhm. Ges. der Wiss., math.-nat. Kl., 1899, Prag, 1900.

PASTEUR, L. Etude sur la maladie des vers à soie, Paris, 1870.

PÉREZ, CH. Sur une nouv. microsp. paras. d. Carcinus maenas, C. R. Soc. Biol., Paris, 1904, lvii, p. 214.

PERRONCITO, E. Il coccidio jalino ed il microsp. poliedrico nell’ uomo, Giorn. Accad. Med., Torino, 1902, Ann. 65, p. 378.

PFEIFFER, L. Beitr. zur Kenntn. d. pathog. Gregar.: I, Die Microsporidien und die Fleckenkrankh. (Pébrine) d. Seidenspinners, Zeitschr. f. Hyg., 1888, iii.

STEMPELL, W. Über Thélohania mülleri (L. Pfr.), Zool. Jahrb. Anat., 1902, xvi, p. 235.

-- Über Nosema anomalum Moniez, Arch. f. Protistenkunde., 1904, iv, p. 1.

VANEY, C., and A. CONTE. Sur une nouv. microsp., Pleistophora mirandellae, paras. de l’ovaire d’Alburnus mirandella Blanch., C. R. Acad. Sci., Paris, 1901, cxxxiii, p. 644.

ORDER. Actinomyxidia (p. 187).

Some earlier literature will be found quoted in:--

CAULLERY, M., and F. MESNIL. Recherches sur les Actinomyxidies, I, Arch. f. Protistenkde., 1905, vi, 3, p. 272.

ORDER. Sarcosporidia (pp. 187 to 194).

BERTRAM, A. Beitr. zur Kenntn. d. Sarcosp., Zool. Jahrb., 1892, v, p. 581.

BLANCHARD, R. Sur un nouv. type d. Sarcospor., C. R. Acad. Sci., Paris, 1885, c, p. 1599.

-- Note sur les Sarcospor. et sur un ess. d. classif. d. ces sporoz., Bull. Soc. Zool. France, 1885, x, p. 244.

DAMMANN, C. Psorosp.-Krankh. beim Schaf., Arch. f. path. Anat., 1867, xli, p. 283.

EECKE, J. VAN. Sarcosporidien, Geneesk. Tijdschr. v. Nederl.-Indie, 1892, xxxii; Jaarsverl. Labor. path. An. en Bact. te Weltevreden (1892), Batavia, 1893.

FORET, P. Observ. rel. au dével. de la cuticle chez le Sarcocystis tenella, Arch. d’Anat. Micr., 1903, vi, p. 86; C. R. Soc. Biol., Paris, 1903, lv, p. 1054.

HESSLING, V. Histol. Mittheil., Zeitschr. f. wiss. Zool., 1854, v, p. 189.

KOCH, M. Über Sarcosporidien, Verh. V. intern. Zool. Congr., Berlin, Jena, 1902, p. 674.

-- Die experimentelle Übertrag. d. Miescherschen Schläuche, Berl. klin. Wochenschr., 1904, li, p. 321.

KORTÉ, W. E. de. On the Presence of Sarcosporidia in the Thigh Muscle of Macacus rhesus, Journ. of Hyg., Cambridge, 1905, v, p. 451.

LAVERAN, A., and F. MESNIL. Morph. d. sarcospor., C. R. Soc. Biol., 1899 (x), vi, p. 245.

LEISERING and WINKLER. Psorosp.-Krankh. beim Schaf., Ber. üb. Veterin.-Wesen, Königr., Sachsen, 1865; Arch. f. path. Anat., 1865, xxxvii, p. 431.

MANZ, W. Beitr. z. Kenntn. d. Miescherschen Schläuche, Arch. mikr. Anat., 1867, iii, p. 345.

MIESCHER, F. Über eigent. Schläuche in d. Musk. einer Hausmaus, Ber. über die Verh. d. naturf. Ges., Basel, 1843, v, p. 198; Reprinted in Verh. d. V. internat. Zool.-Congr., Berlin, Jena, 1902, p. 679.

PIANA, G. P. Fasi evol. d. Sarcosp., La clinica veter., 1896, p. 145; C. f. B., P. u. Inf. (1), xx, p. 39.

PLUYMERS, L. Des sarcosp. et de leur rôle dans la pathog. d. myositis, Arch. Méd. exp. et d’Anat. pathol., 1896, p. 761; C. f. B., P. u. Inf. (1), xxii, p. 245.

RAINEY, G. Structure and Development of Cysticercus Cells as found in the Muscles of the Pig, Phil. Trans. Roy. Soc., 1858, cxlvii, p. 111.

RIECK, V. Sporozoen als Krankheitserreger, Deutsche Zeitschr. f. Thiermed. u. vergl. Path., 1889, xiv, p. 75.

RIEVEL and BEHRENS. Beitr. zur Kenntn. d. Sarcosp. und deren Enzyme, C. f. B., P. u. Inf., 1903, i Abt. Orig., xxxv, p. 341.

RIVOLTA. Dei paras. veget., Torino, 1873; Giorn. an., fis. e pat. d. anim., 1874, vi, p. 25.

SCHNEIDEMÜHL, G. Über Sarcosporidien, Thiermed. Vortr., Leipzig, 1897, iii, p. 11.

SIEBOLD, C. Th. v. Zusatz [zu Hessling. histol. Mittheil.], Zeitschr. f. wiss. Zool., 1854, v, p. 199.

SIEDAMGROTZKY, O. Psorosp. in d. Musk. d. Pferde, Wochenschr. f. Thierheilkde. u. Viehz., 1872, xvi, p. 97.

SMITH, TH. The Production of Sarcosporidia in the Mouse by Feeding Infected Muscle Tissue, Journ. Exp. Med., Baltimore, 1902, vi, p. 1.

-- Further Observations on the Transmission of Sarcocystis muris by Feeding, Journ. Med. Res., 1905, xiii, p. 429.

STILES, CH. W. Notes on Parasites: 18, Presence of Sarcosporidia in Birds, U.S. Dept. of Agric., Bur. of An. Ind., Bull. 3, 1893, p. 79.

Sarcosporidia observed in Man (pp. 193, 194).

BARABAN and ST. REMY. Sur un cas d. tub. psorosp. obs. chez l’homme, C. R. Soc. Biol., Paris, 1894 (x), i, p. 201.

-- -- Le parasitisme d. sarcosp. chez l’homme, Bibliogr. anat., 1894, p. 79.

BRAUN, M. Zum Vork. d. Sarcosporid. b. Menschen, C. f. B. u. Par., 1895 (1), xviii, p. 13.

KARTULIS. Über pathog. Protoz. b. Menschen, Zeitschr. f. Hyg., 1893, xiii, p. 1.

LINDEMANN. Über d. hygien. Bedeutung d. Gregarinen, Deutsche Zeitschr. f. Staatsarzneikde., 1868.

ROSENBERG. Ein Befund von Psorosp. im Herzmuskel d. Mensch., Zeitschr. f. Hyg., 1892, xi, p. 435.

VUILLEMIN, P. Le Sarcocystis tenella, paras. de l’homme, C. R. Acad. Sci., Paris, 1902, cxxxiv, p. 1152.

ORDER. Haplosporidia (pp. 194 to 197).

CAULLERY, M., and F. MESNIL. Rech. sur les Haplosporidies, Arch. de Zool. exp., 1905, sér. iv, iv, p. 101, in which a good bibliography is given.

MINCHIN, E. A., and H. B. FANTHAM. Rhinosporidium kinealyi n. g., n. sp., a New Sporozoon from the Mucous Membrane of the Septum Nasi of Man, Quart. Journ. Micros. Sci., 1905, xlix, p. 521.

*Class IV.--Infusoria* (pp. 198 to 210).

BÜTSCHLI, O. Studien über ... die Conjugation d. Infusorien, Abh. d. Senckenb. naturf. Ges., 1876, x.

EHRENBERG, CH. G. Die Infusionsthierchen als vollkommene Organismen, Leipz., 1838.

GUIART, J. Sur un nouv. infus. paras. de l’homme, C. R. Soc. Biol., Paris, 1903, lv, p. 245.

HERTWIG, R. Über die Conjugation d. Infusorien, Abh. kgl. bayer. Akad. d. Wiss., 1889, ii, Kl., xvii.

KENT, SAV. A Manual of the Infusoria, London, 1880–1882.

MAUPAS, E. Rech. expér. sur la multipl. des Infusoires ciliés, Arch. Zool. exp., 1888 (2), vi.

-- Le rajeunissement karyogamique chez les Ciliés, ibid., 1889, vii.

STEIN, FR. V. Der Organismus der Infusionsthiere, Leipz., 1859–1867.

Balantidium coli (pp. 200 to 204 and 637).

ASKANAZY, M. Pathog. Bedtg. d. Bal. coli, Wien. med. Wochenschr., 1903, liii, p. 127; Verh. d. D. path. Ges., v (1902), Berlin, 1903, p. 224.

CASAGRANDI, O., and P. BARBAGALLO. Bal. coli s. Param. coli, Catania, 1896, 8vo.

COLLMANN, B. Fünf Fälle von Bal. coli im Darm d. Mensch., In.-Diss., Kgsbg., Pr., 1900.

EHRNROTH, E. Z. Frage der Pathogenität d. Bal. coli, Zeitschr. f. klin. Med., 1903, xlix, p. 321.

GRASSI, B. Signif. patol. d. prot. par. dell’ uomo, Atti Accad. Lincei, Rendic., 1888 (4), iv, Sem. 1, p. 86.

JANOWSKI, W. Ein Fall von Bal. coli im Stuhl, Zeitschr. f. klin. Med., 1897, xxxii, p. 415. (With copious literature compiled by Shegalow, Solowjew and Klimenko.)

KLIMENKO, W. Beitr. z. Pathol. d. Bal. coli, Beitr. z. path. Anat. u. allg. Path., 1903, xxxiii, p. 281.

KOSLOWSKI, J. J. Zur Lehre v. d. Infus., die als Paras. im Verdauungskan. d. Mensch. vork., Arch. f. Verdauungskrankh., 1905, xi, p. 31.

KOSSLER, K. Ein Fall von Balantidium-Colitis, Wien. med. Wochenschr., 1906, lvi, p. 522.

MAGGIORA, A. Microsk. u. bacter. Beob. während einer epid. dysent. Dickdarmentzdg., C. f. B. u. Par., 1892, xi, p. 181.

MALMSTEN, P. H. Infusorien als Intestinalthiere b. Mensch., Arch. f. path. Anat., 1857, xii, p. 302.

NAGEL. Üb. ein. Fall v. Infusorienenteritis, Münch. med. Wochenschr., 1905, No. 44.

SHEGALOW, J. P. Ein Fall von Bal. coli bei einem 5 jähr. Mädchen, Jahrb. f. Kinderhlkde., 1899, xlix, p. 425.

SIEVERS, R. Über Bal. coli im menschl. Darm u. dessen Vork. in Schwed. u. Finland, Arch. f. Verdauungskrankh., 1900, v. Abstracted in C. f. B., P. u. Inf., 1900 (1), xxviii, p. 328.

SIEVERS, R. Zur Kenntn. d. Verbreit. v. Darmparas. d. Menschen in Finland, Helsingfors, 1905; Festschr. f. Palmén, No. 10.

SOLOWJEW. Bal. coli als Erreger chron. Durchfälle, C. f. B., P. u. Inf., 1901 (1), xxix, pp. 821, 849. [Solowjew’s additional communication that appeared in “Wratsch,” 1901, Nos. 12 and 14, as well as in the “Russki Wratsch,” 1902, No. 14, has been translated into German by Klimenko (l. c.).]

STOKVIS, B. J. Paramaecium in sputa, Nederl. Tijdschr. v. Geneeskde., 1884 (2), xx.

STRONG, R. P., and W. E. MUSGRAVE. Preliminary Note of a Case of Infection with Balantidium coli, Bull. Johns Hopkins Hosp., Baltimore, 1901, xii, p. 31.

-- -- The Clinical and Pathological Significance of Balantidium coli, Dept. of Int. Bureau, Govt. Labor. Biol., Manila, No. 26, 1905, p. 1.

WLAJEFF, G. Zur Frage d. Ätiol. u. Behandlg. d. Dysenterie, Wracebraja Gaseta, Kemmern, 1905, xii, p. 913; abstracted in C. f. B., P. u. Inf., 1906, i, Ref. xxxvii, p. 757.

WOIT, O. Drei neue Fälle von Bal. coli i. menschl. Darm., Deutsch. Arch. f. klin. Med., 1898, lx, p. 363.

Balantidium minutum (pp. 204 and 637).

JAKOBY, M., and F. SCHAUDINN. Üb. zwei neue Infus. i. Darm. d. Mensch., C. f. B., P. u. Inf., 1899 (i), xxv, p. 487.

SCHULZ. Colpoda cucullus im Darm d. Mensch., Berl. klin. Wochenschr., 1899, No. 16, p. 353.

Nyctotherus (pp. 204 to 206 and 637).

CASTELLANI, A. Observations on some Protozoa found in Human Fæces, C. f. B., P. u. Inf., 1905, i Abt. Orig., xxxviii, p. 66.

JAKOBY, M., and F. SCHAUDINN. Über zwei Infus. i. Darm d. Mensch., ibid., 1899 (1), xxv, p. 487.

KRAUSE, P. Üb. Infus. im Typhusstuhle nebst Beschreibg. einer bisher noch nicht beob. Art. (Balantidium giganteum), Deutsch. Arch. f. klin. Med., 1906, lxxxvi, p. 442.

Chlamydozoa (pp. 207 to 210).

BOSC, F. J. Les malad. bryocytiques (malad. à protozoaires), II, La maladie vaccinale (Plasmodium vaccinæ), C. f. B., P. u. Inf., i Orig., xxxvi, p. 630; xxxvii, pp. 39, 195.

-- Les malad. bryocyt., III, La variole et son parasite (Plasmodium variolæ), ibid., xxxix, pp. 36, 129, 247, 389, 594.

CALKINS, G. N. The Life-history of Cytoryctes variola, Journ. Med. Research, Boston, 1904, xi, p. 136.

COUNCILMAN, MAGRATH, BRINCKENHOFF, TYZZER, SOUTHARD, THOMPSON, BANCROFT and CALKINS. Studies on the Pathology and on the Etiology of Variola and of Vaccinæ, Journ. Med. Research, Boston, 1904, xi, 1, 1904.

GORINI, C. Über die bei der mit Vaccine ausgef. Hornhautimpf. vorkomm. Zelleinschlüsse, C. f. B., P. u. Inf., 1900, i, Abt. xxviii, pp. 233, 589; 1902, i Orig., xxii, p. 111.

GUARNIERI, G. Ric. sulla patogenesi ed etiol. dell’ inf. vacc. e variolosa, Arch. sci. med., Torino, 1892, xvi.

-- Ulteriori ric. sulla etiol. e sulla patog. della inf. vacc., Clinica moderna, Firenze, 1897, iii.

HÜCKEL. Die Vaccinekörperchen, Beitr. z. pathol. Anat. u. z. allg. Path., Supp. II, 1898.

LOEFF, A. VAN DER, in Weekbl. van het Nederl. Tijdschr. v. Geneeskde., 1886, No. 46.

MÜHLENS, P., and M. HARTMANN, Zur Kenntnis d. Vaccineerregers, C. f. B., P. u. Inf., 1906, i Orig., xxxxi, pp. 41, 203, 338, 435.

PRÖSCHER, F. Über d. künstl. Züchtung eines “unsichtbaren” Mikroorgan. aus der Vaccine, C. f. B., P. u. Inf., 1906, i Orig., xl, 3, p. 337.

PROWAZEK, S. Unters. üb. d. Vaccine, I, Arb. a. d. kais. Gesundheitsamt, 1905, xxii, p. 535.

-- Unters. üb. d. Vaccine, II, ibid., 1906, xxiii, p. 525.

SALMON, P. Rech. sur l’infect. dans la vaccine et la variole, Annal. Inst. Pasteur, 1897, xi, No. 4.

SCHULZE, F. E. Cytorrhyctes luis Siegel, Berl. klin. Wochenschr., 1905, No. 21.

SCHULZE, W. Impfungen mit Luesmaterial an Kaninchenaugen, Klin. Monatsbl. f. Augenheilkde., 1905, xliii.

-- Das Verhalten der Cytorrhyctes luis in der mit Syphilis geimpften Kanin cheniris, Beitr. z. path. Anat. u. z. allg. Path., 1906, xxxix, p. 180.

SIEGEL, J. Zur Kritik der bisherigen Cytorrhyctesarbeiten, C. f. B., P. u. Inf., 1906, i Orig., xlii, pp. 128, 225, 321, 480.

WASIELEWSKI, V. Beitr. z. Kenntnis d. Vaccineerregers, Zeitschr. f. Hyg., 1901, xxxviii, p. 212.

*(B) PLATYHELMINTHES* (pp. 211 to 359, 638 to 698 and 753 to 755).

*Class II.--Trematodes* (pp. 212 to 282, 638 to 644, 753, and 754).

[N.B.--The literature, which is very comprehensive, has, up to the year 1892, been quoted and critically examined in Braun’s monograph on the Trematodes: Bd. iv, Abth. i, of Bronn’s “Klass. u. Ord. d. Thierreichs,” Leipz. Of works that have appeared later it is not possible to do more than enumerate the following.]

BETTENDORF, H. Musculatur u. Sinneszell. d. Tremat., Zool. Jahrb. Anat., 1897, x, p. 307.

BLOCHMANN, F. Die Epithelfrage bei Cestoden u. Trematoden, Hamburg, 1896.

BRAUN, M. Arten d. Gattg. Clinostomum, Zool. Jahrb., 1900, Syst. xiv, p. 1.

-- Trematoden d. Chelonier, Mitt. zool. Mus. Berlin, 1901, ii, p. 1.

-- Trematoden d. Chiroptera, Annal. K. k. naturh. Hofmus., Wien, 1900, xv, p. 217.

-- Zur Kenntn. d. Tremat. d. Säugeth., Zool. Jahrb., 1901, Syst. xiv, p. 311.

-- Fascioliden d. Võgel, ibid., 1902, xvi, p. 1.

BRUGGE, G. Zur Kenntn. d. Excretionsgefässsyst. d. Cestoden u. Tremat., Zool. Jahrb. Anat., 1902, xvi, p. 208.

FISCHOEDER, F. Die Paramphistomiden d. Säugeth., Zool. Jahrb., 1903, Syst. xvii, p. 485.

GRONKOWSKI, C. V. Zum feineren Bau d. Tremat., Poln. Arch. f. biol. u. med. Wiss., 1902, i.

HEIN, W. Zur Epithelfrage d. Tremat., Zeitschr. f. wiss. Zool., 1904, lxxvii, p. 546.

LOOSS, A. Die Distomen unserer Fische und Frösche, Stuttg., 1894; Bibl. zool., xvi.

-- Rech. faune paras. de l’Egypte, I, Mém. Inst. égypt., 1896, iii, p. 1.

-- Weit. Beitr. z. Kenntn. d. Tremat.-Fauna Ägypt, Zool. Jahrb., 1900, Syst. xii, p. 521.

-- Über neue u. bekannte Tremat. aus Seeschildkröten, ibid., 1902, xvi, p. 411.

MACLAREN, W. Beitr. z. Kenntn. einig. Tremat., Jen. Zeitschr. f. Naturw., 1903, xxxviii, p. 573.

MONTICELLI, F. S. Stud. tremat. Endopar., I, Zool. Jahrb., 1893, Suppl. iii.

ROEWER, C. F. Beitr. z. Histogenese v. Cercariaeum helicis, Jen. Zeitschr. f. Naturw., 1906, xli, p. 185.

SCHUBMANN, W. Eibildung u. Embryonalentw. v. Fasciola hepatica, Zool. Jahrb. Anat., 1905, xxi, p. 571.

ZIEGLER, H. E. Das Ectoderm d. Plathelminthen, Verh. D. zool. Ges., 1905, p. 35.

Watsonius watsoni (pp. 234, 235).

CONYNGHAM, H. F. A New Trematode of Man, Brit. Med. Journ., 1904, ii, p. 663; Lancet, 1904, ii, p. 464.

SHIPLEY, A. E. Cladorchis watsoni (Conyngham), a Human Parasite from Africa, Thompson, Yates and Johnston Lab. Report, Liverpool, 1905, vi, 1, p. 129.

Gastrodiscus hominis (pp. 236, 237).

GILES, G. M. A Report of an Investigation into the Causes of the Disease known in Assam as Kála-azár and Beriberi, Shillong, 1890, p. 125.

LEUCKART, R. Die Paras. d. Mensch., 2. Aufl., ii, p. 450, where the first discovery is reported in greater detail.

LEWIS, T. R., and MCCONNEL. A New Parasite Affecting Man, Proc. Asiatic Soc., Bengal, 1876, p. 182.

Fasciola hepatica (pp. 237 to 244, and 638).

AMMON. Klin. Darst. d. Krankh. d. menschl. Auges, Dresden, 1838.

BOSSUAT, E. Les helminth. dans le foie, Arch. de Paras., 1902, vi, p. 186. [The author is in error when he writes “The name Dist. sibiricum originated from M. Braun”!]

COE, W. R. Bau des Embryos v. Dist. hep., Zool. Jahrb. Anat., 1896, ix, p. 561.

DUFFEK, E. Dist. hep. beim Mensch., Wien. klin. Wochenschr., 1902, p. 772.

GAIDE, cf. under Clonorchis sinensis (p. 787).

GESCHEIDT and AMMON. Die Entoz. d. Auges, Zeitschr. f. Ophth., 1833, iii, P. 405.

GREEFF, R. Über d. Vork. v. Würmern im Auge, Arch. f. Augenheilkde., 1907, lvi, p. 334.

HAVET, J. Contrib. à l’étud. d. syst. nerv. d. Trémat., La Cellule, 1900, xvii, p. 351.

HENNEGUY, L. F. Rech. sur la mode de form, de l’œuf du Dist. hep., Arch. d’anat. micr., 1906, ix, p. 47.

KHOURI, A. Le Halzoun, Arch. de Paras., 1904, ix, 1, p. 78.

KÜCHENMEISTER, F. On Animal and Vegetable Parasites of the Human Body, translated by E. Lankester, London, 1857.

LEUCKART, R. Z. Entw. d. Lebereg., Arch. f. Naturg., 1882, i, p. 80.

LUTZ, A. Lebensgesch. d. Dist. hep., C. f. B. u. P., xi, p. 783; xiii, p. 320.

MALHERBE. Progr. méd., 1898, vii, No. 4.

MARCINOWSKI, K. Das untere Schlundgangl. von. Dist. hep., Jen. Zeitschr. f. Naturw., xxxvii, 1903, p. 544.

NORDMANN, A. V. Mikrograph. Beitr. z. Naturgesch. d. wirbellos. Thiere, Berlin, 1832, ii, p. 9.

PALLAS, P. S. De infestis viventibus intra viventia, Diss. in., Lugd., Batavia, 1760.

SAITO, S. Beitr. z. Kenntn. d. geogr. Verbr. d. Dist. hep., C. f. B., P. u. Inf., 1906, i Orig., xli, p. 822.

SCHAPER. Die Leberegelkrankheit. d. Schafe, Deutsche Zeitschr. f. Tiermed., 1890, xvi, p. 1.

SOMMER, L. Anat. d. Leberegels, Z. f. w. Zool., 1880, xxxiv, p. 539.

STIEDA, L. Beitr. z. Anat. d. Plattw.: I, Arch. f. Anat. u. Phys., 1867, p. 52.

-- Über d. angebl. inneren Zusammenhang d. männl. u. weibl. Org. b. Tremat., ibid., 1871, p. 31.

STILES, C. W. Frogs, Toads and Carp as Eradicators of Fluke Diseases, Ann. Rep. Bur. of Anim. Ind., 1901, Wash., 1902, xviii, p. 220.

THOMAS, P. The Life-history of the Liver Fluke, Quart. Journ. Micros. Sci., 1883, xxiii, p. 99.

[N.B.--A bibliography of cases has been compiled by Davaine (1877), Leuckart (1889–1894), Moniez (1896), Blanchard (1889), and Huber (1895), in addition to Khouri (l. c.).]

Fasciola gigantica (pp. 244, 245).

COBBOLD, TH. SP. Description of a New Trematode Worm (Fasciola gigantica), Edin. New Phil. Journ., 1855, N.S. ii, p. 262.

-- Entozoa, an Introduction to the Study of Helminthes, London, 1864, pl. i.

GOUVEA, H. DE. La distomatose pulm. par la douve du foie, Thèse, Paris, 1895.

LOOSS, A. Rech. sur la faune de l’Egypte, Mém. Inst, égypt., 1896, iii, p. 33.

-- Obs. à prop. d’une note ... C. f. B., P. u. Inf. (1), 1898, xxiii, p. 459.

RAILLIET, A. Sur une forme partic. de douve hépat. prov. de Senegal, C. R. Soc. Biol., Paris, 1895, 10e sér., ii, p. 338.

Fasciolopsis buski (pp. 245, 246, and 638).

BUDD, G. On Diseases of the Liver, London, 1852.

COBBOLD, T. SP. On the Supposed Rarity of ... Dist. crassum, Journ. Linn. Soc., 1875, xii, p. 285; Obs. on the Large Human Fluke, Veterinarian, 1876.

GILES, G. M., cf. under Gastrodiscus hominis (p. 784).

LANKESTER, E. Manual of Animal and Vegetable Parasites (Küchenmeister), London, 1857, App. i, B. p. 437.

LEIDY, J. On Distomum hepaticum, Proc. Acad. Nat. Sci., Philadelphia, 1873, P· 364.

ODHNER, TH. Fasciolopsis buski, C. f. B., P. u. Inf., i Orig., xxxi, p. 573.

Fasciolopsis rathouisi (pp. 246, 247).

POIRIER, P. Note sur une nouv. esp. de Dist. paras. de l’homme, Arch. Zool. exp., 1887 (2), v, p. 203.

Paragonimus ringeri (pp. 249 to 251, 639 and 640).

BAELZ, E. Über paras. Haemopt., Centralbl. f. med. Wiss., 1880, p. 721.

-- Über einig. neue Paras. d. Mensch., Berl. klin. Wochenschr., 1883, p. 234.

INOUYE, J. Über d. Dist. ringeri Cobb, Zeitschr. f. klin. Med., 1903, l, p. 120, with list of Japanese literature.

JANSON, J. Die bish. in Japan bei Schweinen gef. Paras., Mitt. d. Ges. f. Natur- u. Völkerkde. Ostasiens, 1897, Heft 59–60.

KATSURADA, F. Beitr. z. Kenntn. d. Dist. westerm., Beitr. z. path. Anat. u. z. allg. Path., 1900, xxviii, p. 506.

KERBERT, C. Zur Trem.-Kenntn., Zool. Anz., 1878, i, p. 271.

-- Beitr. z. Kenntn. d. Tremat., Arch. f. mikros. Anat., 1881, xix, p. 519.

MANSON, P. Dist. ringeri, Med. Times and Gaz., 1881, ii, p. 8; 1882, ii, p. 42.

MIURA, M. Fibr. Tuberkel verurs. durch Parasiteneier, Arch. f. path. Anat., 1889, cxvi.

MONTEL, R. Distomiase pulm. en Cochinchine, Annal. d’ Hyg. et de Méd. Col., 1906, ix, p. 258.

RAILLIET, A. Paras, des anim. domest. du Japon, Le Natural., 1891, xii, p. 143.

STILES, C. W. Notes on Parasites, No. 26; Dist. (Mesogon.) westermanni, Discovery of a Parasite of Man, new to the United States, Vet. Journ., 1894, p. 107.

STILES, C. W., and A. HASSALL. Notes on Parasites, No. 50: A Muscle Fluke in American Swine, XVI Ann. Rep., Bur. of Anim. Industry (1899), Wash., 1900, p. 559.

-- No. 51, The Lung Fluke in Swine, ibid., p. 560.

TANIGUCHI. Ein Fall von Distomum-Erkrankung des Gehirns mit dem Symptomenkomplex von Jacksonscher Epilepsie, Arch. f. Psych, u. Nervenheilk., 1904, xxxviii, No. 1.

WARD, H. B. Dist. westerm. in den Vereinigten Staaten, C. f. B. u. P., 1894, xiv, p. 362; 1895, xvii, p. 304.

YAMAGIVA, K. Lungendistomenkrankh. in Japan, Arch. f. path. Anat., 1892, cxxvii; Zur Ätiologie der Jacksonschen Epilepsie, ibid., 1890, cxix.

Ophisthorchis felineus and Metorchis truncatus (pp. 252 to 255, 261 and 262).

ASKANAZY, M. Über Inf. d. Mensch. mit Dist. felin. in Ostpreussen u. ihren Zusammenhang mit Leberkrebs, C. f. B., P. u. Inf. (1), 1900, xxviii, p. 491; Verh. d. Deutsch. path. Ges., 1900, iii, p. 72.

-- Die Ätiologie u. Path. d. Katzenegelerkrankg. d. Mensch., Deutsche med. Wochenschrift, 1904, xxx, p. 689; Verh. d. Ver. f. wiss. Heilkde. i. Königsb. i. Pr., 1904, iii, p. 3.

-- Weitere Mitteil. üb. d. Quellen d. Inf. mit Dist. felineum, Schrift d. Phys.-oek. Ges., Königsberg i. Pr. (1905), 1906, xlvi, p. 127.

BRAUN, M. Die Leberdistomen d. Hauskatze u. verw. Arten, C. f. B. u. Par., 1893, xiv, p. 381.

-- Über ein für den Menschen neues Distomum, ibid., 1894, xv, p. 602.

CHOLODKOWSKY, N. Icones helm. hom., II, St. Petersb., 1898, Taf. xi, 115.

KAMENSKY, G. Not. helm., I, Charkow, 1900.

KHOLODKOWSKY, N. Sur quelq. rar. paras. de l’homme en Russie, Arch. de Paras., 1898, i, p. 354.

RIVOLTA. Sopra una spec. di Distoma nel gatto e nel cane, Giorn. anat., fisiol. e pat. d. animali, 1884, xvi, p. 20.

WARD, H. B. On Dist. fel. in the United States, Vet. Mag., 1895.

-- Notes on Parasites of the Lake Fish: III, On the Structure and the Copulatory Organ in Microphallus, Stud. Zool. Lab., Univ. Nebraska, May, 1901, p. 174.

WINOGRADOFF, K. Ein neues Dist. a. d. menschl. Leber, Nachr. v. d. k. Tomskischen Univ. (1891), 1892, iv, p. 116; Ein zweiter Fall von Dist. sib., ibid., p. 131.

-- Über Würmer, welche im menschl. Körper paras., ibid. (1892), 1893, v.

ZWAARDEMAKER, H. Cirrhosis parasit., Arch. f. path. Anat., 1890, cxx, p. 197.

Amphimerus noverca (p. 258).

COBBOLD, T. SP. Synopsis of the Distomidæ, Journ. Linn. Soc., London, 1859, Zool., v, p. 8; Further Observations on Entozoa, with Experiments, Trans. Linn. Soc., London, 1862; xxiii, p. 349, pl. 33, figs. 1 and 2.

LEWIS, T. R., and D. CUNNINGHAM. Micros. and Phys. Res., XI Ann. Rep. San. Comm. Govt. India, Calcutta, 1872, Appendix C, p. 168.

MCCONNELL, J. F. P. On the Dist. conj. as a Human Entozoon, Lancet, 1876, i, p. 343; 1878, i, p. 476.

Clonorchis sinensis and Cl. endemicus (pp. 258 to 261, 640, and 641).

BAELZ, E. Über einige neue Parasiten des Menschen, Berl. klin. Wochenschr., 1883, p. 235.

BLANCHARD, R. Lésions du foie déterm. par la prés. des Douves, Arch. de Paras., 1901, iv, p. 581.

COBBOLD, T. SP. The New Human Fluke, Lancet, 1875, ii, p. 423.

GAIDE. De la distomatose hépatique au Tonkin, Ann. d’Hyg. et de Méd. Colon., 1905, viii, p. 568; abstracted in Arch. f. Schiffs- u. Trop.-Hyg., 1906, x, p. 256.

IJIMA, J. Dist. endemicum, Journ. Coll. Sci., Imp. Univ., Japan, 1886, i, p. 47.

INOUYE, Z. Über d. Distom. spathulatum, Arch. f. Verdauungskrankh., 1903, ix, p. 107.

KATSURADA, F. Beitr. z. Kenntn. d. Dist. spathulat., Beitr. z. path. Anat. u. z. allg. Path., 1900, xxviii, p. 479.

LOOSS, A. On some Parasites in the Museum of the School of Trop. Med., Liverpool, Ann. Trop. Med. and Par., 1907, i, p. 123.

MCCONNELL, J. F. P. Remarks on the Anatomical and Pathological Relations of a New Species of Liver-fluke, Lancet, 1875, ii, p. 271; 1878, i, p. 406.

MCGREGOR. A New Form of Paralytic Disease Associated with the Presence of a New Species of Liver Parasite, Lancet, 1877, i, p. 775.

MOTY. Lésions anat. prod. par le Dist. sinense, C. R. Soc. Biol., Paris, 1893, p. 224.

SAITO, S. Über den Eiinhalt d. Dist. spathul. u. d. morphol. Beschaffenh. seines Embryos, C. f. B., P. u. Inf., i Orig., 1906, xlii, p. 133.

Heterophyes heterophyes (pp. 262 to 264).

BLANCHARD, R. Note prél. sur le Dist. heterophyes, C. R. Soc. Biol., Paris, 1891 (9), iii, p. 792.

LOOSS, A. Über d. Bau von Dist. heteroph. u. D. fraternum n. sp., Cassel, 1894.

LOOSS, A. Not. z. Helminth. Ägypt., I, C. f. B., P. u. Inf., 1896 (1), xx, p. 836.

-- Weitere Beitr. z. Kenntn. d. Tremat.-Fna. Ägypt., Zool. Jahrb., Syst. 1899, xii, p. 699.

-- Notz. z. Helminth. Ägypt, V, C. f. B., P. u. Inf., 1902, i Orig., xxxii, p. 886.

SANDWITH, F. M. Dist. heterophyes in a Living Patient, Lancet, 1899, ii, p. 888.

SIEBOLD, C. TH. V. Beitr. zur Helminth. hum., Z. f. wiss. Zool., 1852, iv, p. 52.

DICROCŒLIUM DENDRITICUM (pp. 266, 267).

ANGLAS, J., and E. de Ribaucourt. Etude anat. et hist. du Dist. lanceolatum, Ann. Sci. Nat., 8vo, sér. xv, 1902, p. 313; cf. Zool. Centralbl., 1902, ix, p. 840.

ASCHOFF, L. Ein Fall von Dist. lanc. i. d. menschlichen Leber, Arch. f. path. Anat., 1892, cxxx, p. 493.

BRERA, V. L. Memor. fis.-med. sopra i princ. vermi di corpo, Roma, 1811.

DUBINI, A. Entozoograf. umana, Milano, 1850.

GALLI-VALERIO, B. Notes de parasitol., B, Paras. anim. (4) Œufs de Dicr. lanc. dans les fèces de l’homme, C. f. B., P. u. Inf., 1905, i Orig., xxxix, p. 239.

HOLLACK, J. Z. Kenntn. der sexuellen Amphitypie bei Dicrocoel., C. f. B., P. u. Inf., 1902, i Orig., xxxii, p. 867.

KAMENSKY, S. Notes helm. No. 2, Sur la prés. réelle du Dicroc. lanceol. chez le chien, Trav. Soc. Nat. Univ. Charkow, 1902, xxxvi, p. 63.

MEHLIS, C. F. S. Observ. anat. de Dist. hep. et lanceol., Gotting., 1825.

PIANA, G. P. Le cercarie d. moll. stud. in rapp. colla pres. del Dist. epat. e D. lanc., La clinica veter., 1882, v.

WALTER, G. Beitr. zur Anat. und Histol. einig. Tremat., Arch. f. Naturg., 1858, xxiv (1), p. 269.

ZSCHOKKE, F. Selt. Paras. des Menschen, C. f. B. u. P., 1892, xii, p. 500.

Schistosoma hæmatobium (pp. 270 to 277 and 641 to 644).

BALFOUR, A. Eosinophilia in Bilharzia dis. and Dracontiasis, Lancet, 1903, ii, p. 1649.

BEYER, H. G. A Second Chinese Case of Infection with the Asiatic Blood Fluke, Amer. Med., 1905, x, p. 578.

BILHARZ, TH. Beitr. zur Helminth. hum., Z. f. w. Zool., 1852, ii, pp. 53, 454.

CATTO, J. Schistosoma cattoi, a New Blood Fluke of Man, Brit. Med. Journ., January 7, 1915; abstracted in C. f. B., P. u. Inf., 1906, i, Ref. xxxvii, p. 617.

CHAKER, M. Et. sur l’hématurie d’Egypt, Thèse, Paris, 1890.

CHATIN, J. Obs. sur le dével. et l’org. du proscol. de la Bilh., Ann. sc. nat. Zool., 1881 (6), xi.

FRITSCH, G. Zur Anat. d. Bilh. haemat., Arch. f. mikr. Anat., 1888, xxxi, p. 192.

FUJINAMI, A. Weitere Mitt. über die path. Anat. d. sog. Katayama-Krankh. und der Krankheits-Er. ders., Kyoto Igaku Zassi, March 1, 1904. (In Japanese, with German abstract.)

FUJINAMI, A., and J. KON. Beitr. z. Kenntn. der pathol. Anat. der sog. Katayama-Krankheit, ibid., 1904, i, 1; abstracted in C. f. B., P. u. Inf., 1905, i, Ref. xxxvi, p. 499.

GUNN. Bilharzia Disease, Journ. Amer. Med. Assoc., 1906, No. 14; abstracted in C. f. B., P. u. Inf., 1907, i, Ref. xxxix, p. 217.

KARTULIS. Vorkommen d. Eier von Dist. haemat., Arch. f. path. Anat., 1885, xcix, p. 139.

-- Weitere Beitr. z. path. Anat. d. Bilharz., ibid., 1898, clii, p. 474.

KASAI, K. Unters. über die sog. Katayama-Krankh., Mitt. der med. Ges., Tokio, 1904, xviii, p. 4; abstracted in C. f. B., P. u. Inf., 1905, i, Ref. xxxvi, p. 499.

KATSURADA, F. Schistosomum japonicum, ein neuer menschl. Paras., durch welchen eine endem. Krankh. in versch. Gegend. Japans verursacht wird, Annot. zool. japon., 1904, v, 3, p. 147.

LAHILLE, A. La bilharziose intest. aux Antilles, Ann. d’Hyg. et de Méd. Colon., 1906, ix, p. 262.

LETULLE, M. Bilharziose intestinale, Arch. de Paras., 1905, ix, p. 329.

LOOSS, A. Beob. über Eier und Embr. v. Bilh., in Leuckart: Die Paras. d. Menschen, 2. Aufl., i, p. 521.

-- Bemerkungen zur Lebensgeschichte der Bilh. haem., C. f. B. u. P., 1894, xvi, pp. 286, 340.

-- Rech. faun. paras. de l’Egypt, Mém. Inst. égypt., 1895, iii, p. 158.

-- Zur Anat. und Histol. d. Bilh. haem., Arch. f. mikr. Anat., 1895, xlvi, p. 1.

-- Bilharziosis, Handb. d. Tropenkrankh., 1905, i, p. 93.

-- Schistosomum japonicum, eine neue asiatische Bilharzia d. Menschen, C. f. B., P. u. Inf., 1905, i Orig., xxxix, p. 280.

LORTET and VIALLETON. Etud. sur la Bilh. hæm., Paris, 1895; Ann. de l’Univ. de Lyon, 1894, ix.

OGAWA. Beitr. zur Kenntn. der Katayama-Krankh., Kyoto Igaku Zassi, 1904, i, p. 3; with German abstract.

RAILLIET, A. Obs. sur l’embr. du Gynæcoph. hæm., Bull. Soc. Zool. France, 1892, xvii, p. 101.

RÜTIMEYER, L. Über Bilharzia-Krankheit, Mitt. klin. u. med. Inst. d. Schweiz., i, 1894, xii, p. 871.

SCHEUBE, B. Ein neues Schistosomum beim Menschen, Arch. f. Schiffs- u. Tropen-Hyg., 1905, ix, p. 150.

SONSINO, P. Ric. s. sviluppo d. Bilh., Giorn. R. Ac. med., Torino, 1889, xxxii, p. 380.

STILES, C. W. The New Asiatic Blood Fluke ... of Man and Cats, Amer. Med., 1905, ix, p. 821.

WILLIAMSON. Bilharzia hæmatobium in Cyprus, Brit. Med. Journ., 1902, p. 956.

WOOLLEY, P. G. The Occurrence of Schistosoma japonicum vel cattoi in the Philippine Islands, Philipp. Journ. Sci., 1906, i, p. 83.

*Class III.--Cestodes* (pp. 282 to 359 and 644 to 674).

[An almost complete collection of the literature relating to Cestodes up to 1895 is to be found in Braun’s monograph on the tapeworms in Bronn’s “Klassen und Ordnung des Thierreiches,” iv, p. 2; of later books the following may be mentioned.]

BARTELS, E. Cysticercus fasciolaris, Anat., Beitr. zur Entw. und Umwandl. in Taenia crassicollis, Zool. Jahrb. Anat., 1902, xvi, p. 511.

BLANCHARD, R. Sur quelq. Cest. monstr., Progr. méd., 1894 (2), xx.

BLOCHMANN, F. Die Epithelfrage bei Cestoden und Tremat., Hambg., 1896.

BOAS, J. E. V. Triplotaenia mirabilis, Zool. Jahrb., 1902, Syst. xvii, p. 329.

BRANDES, G. Teratol. Cestoden, Ztschr. f. d. ges. Nat., Halle, 1899, p. 105.

BUGGE, G. Zur Kenntn. der Excretionsgefäss-Syst. der Cestoden und Tremat., Zool. Jahrb. Anat., 1902, xvi, p. 177.

CHILD, C. M. Abnormality in Moniezia expansa, Biol. Bull. Woods Holl., 1902, iii, pp. 95, 143.

COHN, L. Zur Anat. und Syst. der Vogelcestoden, Nov. Act. Acad. Caes. Leop.-Carol. Nat. Cur., Halle, 1901, lxxix, No. 3.

DRAGO, U. Azione sperim. dei succhi diger. sull’ involucro della ova di alc. Tenie, Arch. de Paras., 1906, x, p. 321.

FUHRMANN, O. Ein getrenntgeschlechtlicher Cestode, Zool. Jahrb., 1904, Syst. xx, p. 131.

GROHMANN, W. Die Abnormitäten in den Progl. der Cestoden, Inaug.-Dissert., Giessen, 1906.

KUNSEMÜLLER, F. Zur Kenntnis der polycephalen Blasenwürmer, insbesondere des Coenurus cerebralis Rud. und des C. serialis Gerv., Zool. Jahrb. Anat., 1903, xviii, p. 507.

LÜHE, M. Zur Anat. und Syst. der Bothrioceph., Verhandl. der Deutsch. zool. Ges., 1899, p. 30.

-- Review of Braun’s Bothr.-Syst., C. f. B., P. u. Inf., 1902, i Orig., xxi, p. 318.

MESSINEO, G. Sul veleno conten. in alcune Tenie dell’ uomo, Atti Accad. Gioenia sci. nat., Catania, 1901 (4), xiv, No. 6.

MINGAZZINI, P. Sul vario modo di fissaz. delle Tenie alia parete intest., Rich. Labor. anat., Roma, 1904, x, p. 5.

RÖSSLER, P. Über den fein. Bau der Cysticerken, Zool. Jahrb. Anat., 1902, xvi, p. 423.

SAINT-RÉMY, G. Dévelop. embr. Taenia serrata, Arch. de Paras., 1901, iv, p. 143.

SCHAAF, H. Zur Kenntn. der Kopfanlage der Cysticerken, insbes. des Cysticercus der Taenia solium L., Zool. Jahrb. Anat., 1906, xxii, p. 435.

SPENGEL, J. W. Die Monozootie der Cestoden, Ztschr. f. w. Zool., 1905, lxxxii, p. 252.

STILES, CH. W. Revision of Ad. Tapeworm of Hares and Rabbits, Proc. U.S. Nat. Mus., 1896, xix.

STILES, C. W., and A. HASSALL. Tapeworms of Poultry, U.S. Dept of Agric., Bur. of Anim. Ind., 1896, Bull. 12.

VIGENER, J. Über dreikant. Bandwürmer a. d. Fam. d. Taeniiden, Jahrb. nass. Ver. f. Naturke., Wiesb., 1903, p. 115.

ZERNECKE, F. Unters. über d. fein. Bau d. Cestod., Inaug.-Diss., Rostock, 1895.

Dibothriocephalus latus (pp. 310 to 315, and 658).

(a) Anatomy.

BÖTTCHER, A. Studien über den Bau des Bothr. latus, Arch. f. path. Anat., 1864, xxx, p. 97; 1869, xlvii, p. 370.

ESCHRICHT, D. F. Anat.-phys. Untersuchung. über die Bothrioceph., Nov. Act. Ac. Caes. Leop.-Carol. nat. curios., 1841, xix, Suppl. ii.

SCHMIDT, F. Beitr. z. Kenntn. d. Entwickl. d. Geschlechtsorg. d. Cestoden, Z. f. w. Zool., 1888, xlvi, p. 155.

SOMMER, F., and L. LANDOIS. Beitr. z. Anat. d. Plattw.: I, Bothr. latus, Z. f. w. Zool., 1872, xxii, p. 40.

STIEDA, L. Zur Anat. d. Bothr. latus, Arch. f. Anat. u. Phys., 1864, p. 174.

(b) Development of Embryos.

BERTOLUS. Sur le dévelopm. du Bothrioceph. de l’homme, C. R. Acad. Sci., Paris, 1863, lvii, p. 569.

KNOCK, J. Die Naturg. d. breiten Bandw. mit bes. Berücks. sein. Entw., Mém. Acad. d. Sci., St. Pétersbourg, 1862 (7), v, p. 5; Journ. de l’Anat., 1879, vi, p. 140.

SCHAUINSLAND, H. Die embryon. Entw. d. Bothrioceph., Jen. Zeitschr. f. Naturw., 1885, xix, p. 520.

(c) Infection.

ALESSANDRINI, G. Bothr. latus Br. nella prov. di Roma, Boll. soc. zool. ital., 1906, ser. 2, vii, p. 231.

BRAUN, M. Zur Frage d. Zwischenwirth. von Bothr. latus, Zool. Anzeiger, 1881, iv, p. 593; 1882, v, pp. 39, 42, 194; 1883, vi, p. 97.

-- Bothriocephalus latus u. seine Herkunft., Arch. f. path. Anat., 1883, xcii, p. 364.

-- Zur Entwickel. d. breit. Bandw., Würzburg, 1883.

-- Salm oder Hecht? Berl. klin. Wochenschr., 1885, xxii, p. 807.

-- Über den Zwischenwirth des breit. Bandw., eine Entgegnung an Küchenmeister, Würzburg, 1886.

-- Bothriocephalus-Finnen im Hecht des St. Petersb. Fischmarktes, St. Petersb. med. Wochenschr., 1892, xvii, No. 28.

-- Helminth. Notizen, I, C. f. B. u. Par., 1893, xiv, p. 802.

GRASSI, B., and FERRARA. Zur Bothriocephalusfrage, D. med. Wochenschr., 1886, p. 699.

GRASSI, B., and G. ROVELLI. Contrib. allo studio d. svil. d. Bothr. latus, Giorn. R. Accad. Med., 1887, No. 11.

-- -- Bandwürmerentwickelung, C. f. B. u. Par., 1888, iii, p. 173.

IJIMA, J. The Source of Bothr. latus in Japan, Journ. Coll. Sci., Imp. Univ., Tokio, 1888, ii, 1, p. 49.

KÜCHENMEISTER, F. Wie steckt sich der Mensch mit Bothr. latus an? Berl. klin. Wochenschr., 1885, xxii, pp. 505, 527.

-- Die Finne des Bothrioceph. u. seine Übertrag. a. d. Menschen, Leipzig, 1886.

-- Weit. Bestätigung meiner Behamptung, die Finne des Hechts hat nichts mit Bothr. latus zu thun, D. med. Wochenschr., 1886, p. 551.

LEUCKART, R. Zur Bothriocephalusfrage, C. f. B. u. Par., 1887, i, pp. 1, 33.

LÖNNBERG, E. Über das Vork. d. breit. Bandw. in Schweden, C. f. B. u. Par., 1892, xi, p. 189.

PARONA, E. The Bothr. latus in Lombard., Rend. R. Istit. Lomb., 1886 (2), xix, fasc. 14.

-- Sulla quest. d. Bothr. latus, Gazz. med.-ital.-lomb., 1887.

SCHROEDER, A. V. Wie bek. die Einwohner St. Petersb. d. breit. Bandw., St. Petersb. med. Wochenschr., 1892, xvii, No. 22.

-- im Wratsch, 1894, No. 12; 1895, No. 15; Jesched. journ. prakt. med., 1896, Nos. 19 and 27; abstracted in C. f. B. u. Par., xvi, p. 314; xviii, p. 24; xx, p. 621.

ZSCHOKKE, F. Weit. Zwischenwirthe des Bothr. latus, C. f. B. u. Par., 1888, iv, p. 417; 1890, vii, pp. 393, 435.

(d) Geographical Distribution Statistics.

BAVAY. Sur la prés. du Bothr. latus à Madagascar, Bull. Soc. Zool. France, 1890, xv, p. 134.

BENEDEN, E. VAN. Sur la prés. en Belgique du Bothr. latus, Bull. Acad. roy. Belg., 1886, 3e sér., xi, 8, p. 265.

BERKELEY, W. N. A Case of Bothriocephalus with Remarks on the Occurrence of Bothriocephalus in America, Med. Rec., New York, 1903, lxiii, p. 355.

BOLLINGER, O. Über das autochth. Vork d. Bothr. latus in München nebst Bemerk. über die geogr. Verbreitung der Bandw., Dtsch. Arch. f. klin. Med., 1885, xxxvi, p. 277.

GRUSDIEFF, S. S. Zur Frage der Verbreit. tier. Darmparas. bei der Schuljugend, Wratsch, 1891, No. 13.

HAHN, L. Le Bothriocéph., son dével., ses migrat., sa distrib. géogr. et sa prophyl., Gaz. hebd. méd. et chir., 1885 (2), xxii, p. 450.

HUBER, J. Über die Verbreitung der Cestoden in Schwaben., Ber. d. naturhist. Ver., Augsburg, f. 1886, p. 85.

KERBERT, E. Bothr. latus Br. (in Nederland), Nederl. Tijdschr. v. Geneeskde., 1889, i, p. 424; Handel van het II Nederl. Nat. en Geneesk. Congr., Leiden, 1889.

KESSLER, D. A. Beitr. z. Statistik der Eingeweidew. bei den Einwohnern Petersburgs, Wratsch, 1888, pp. 109, 128.

KIAER, F. C. Baendelorm hos mennesk. i Norge, Tidsskrift. f. pr. med., Kristiania, 1889, p. 1; abstracted in C. f. B. u. Par., 1889, v, p. 353.

KRABBE, H. 300 Tilfälde af bändelorm hos mennesket jagt. i Danmark, Nord. med. Arkiv, 1887, xix, 1.

-- Über das Vork. von Bandw. beim Menschen in Dänemark, ibid., 1905, Abt. ii, i, No. 2.

LEON, N. Note sur la fréq. des Bothrioc. en Roumanie, Bull. Soc. d. Sci. de Bucarest, 1904, xiii, p. 286.

NICKERSON, W. S. The Broad Tapeworm in Minnesota, Journ. Amer. Med. Assoc., 1906, p. 711.

SCHOR, M. Contrib. à l’ét. du Bothr. latus dans le canton de Vaud, Thèse, Lausanne, 1902; abstracted in C. f. B., P. u. Inf., 1903, Abt. i, Ref. xxxiii, p. 286.

SIEVERS, R. Zur Kenntnis der Verbreit. von Darmparas. des Menschen in Finnland, Festschr. f. Palmén, No. 10, Helsingfors, 1905.

SZYDLOWSKI. Beitr. zur Mikroskopie der Faeces, Inaug.-Diss., Dorpat, 1879.

VANLAIR, C. Un nouv. cas de bothriocéphalie en Belg., Bull. Acad. roy. Belg., 1889, 3e sér., xviii, p. 379.

WELLMAN, C. Notes on Tropical Diseases of the Angola Highlands, New York Med. Journ., August 12, 1905, and Phil. Med. Journ., September 2, 1905.

WILLSON, R. N. Bothr. latus ... Amer. Journ. Med. Sci., Philadelphia, 1902, p. 262.

ZAESLIN, TH. Über die geogr. Verbreit. u. Häufigkeit der Entozoen in der Schweiz, Corresp.-Bl. f. schweiz. Ärzte, 1881, xi, p. 673.

ZSCHOKKE, F. Der Bothr. latus in Genf, C. f. B. u. Par., 1887, i, pp. 377, 409.

(e) Bothriocephalus Anæmia.

ASKANAZY, M. Über Bothrioceph.-Anämie und die progn. Bedeutung d. Megaloblast, Ztschr. f. klin. Med., xxvii, p. 492.

BABES, V. Über den Bothr. latus und die Bothr.-Anämie, Arch. f. path. An., 1895, cxli, p. 204.

FÉDOROV, N. L’anémie bothriocéph., Arch. de Paras., 1902, vi, p. 207.

ISAAC, S., and VAN DEN VELDEN. Eine specif. Präcipitinreaktion bei Bothr. latus beherb. Menschen, Dtsche. med. Wchschr., 1904, xxx, p. 982.

MESCHEDE. In: Tagebl. d. 45. Vers. dsch. Naturf. u. Ärzte in Leipzig, 1872, p. 186; Ztschr. f. Psych., 1874, xxx, p. 109.

MÖLLER, W. Stud. öfv. de hist, förändr. i. dig.-Kan.... vid Bothrioc. anaem., Helsingfors, 1897.

NEUBECKER, O. Bothrioc.-Anämie ohne Bothrioceph., Inaug.-Diss., Königsb., 1898.

REYHER, G. Beitr. zur Ätiol. u. Heilbark. der pernic. Anämie, Dtsch. Arch. f. klin. Med., xxix, p. 31.

ROSENQUIST, E. Über den Eiweissstoffwechsel bei der pernic. Anämie, mit spezieller Berücks. der Bothrioc.-Anämie, Ztschr. f. klin. Med., 1903, xlix, p. 193.

RUNEBERG, J. W. Bothr. latus und pernic. Anämie, ibid., 1886, xli, p. 304.

SCHAPIRO, H. Heilung der Biermerschen pernic. Anämie durch Abtreibung von Bothr. latus, Ztschr. f. klin. Med., 1889, xiii, p. 416.

SCHAUMANN, O. Zur Kenntnis der sog. Bothr.-Anämie, Berlin, 1894.

THOMSON, W. G. A Case of Dibothriocephalus latus Infection causing Pernicious Anæmia with Complications; Recovery, Med. News, 1905, lxxxvi, p. 635.

ZINN, W. Tödl. Anämie durch Bothr. latus, D. med. Wchschr., 1903, xxix, p. 264.

(f) Duration of Life.

BREMSER. Über lebende Würmer im leb. Menschen, Wien, 1819.

LEUCKART, R. Die Paras. d. Mensch., &c., Leipz., 1881, 2. Aufl., i, 2; and Arch. f. Naturg., 40. Jahrg., 1874, ii, p. 446.

MOSLER, F. Über Lebensdauer u. Renitenz d. Bothr. latus, Arch. f. path. Anat., 1873, lvii, p. 529.

Dibothriocephalus cordatus (pp. 315, 316).

BRAUN, M. Berichtig. betr. d. Vork. v. Bothr. cordatus in Dorpat, Zool. Anz., 1882, v, p. 46.

LEUCKART, R. Jahresb. üb. d. wiss. Leist. i. d. Naturgesch. d. nied. Thiere f. 1861–62, Arch. f. Naturgesch., 29. Jahr., 1863, p. 149.

-- Die menschl. Paras., 1863, i, p. 437.

Diplogonoporus grandis (pp. 316, 317).

BLANCHARD, R. Not. sur les paras. de l’homme, IV, C. R. Soc. Biol., Paris, 1894 (10), i, p. 699.

IJIMA and T. KURIMOTO. On a New Human Tapeworm, Journ. Coll. Sci., Imp. Univ., Tokio, 1894, vi, p. 371.

KURIMOTO, T. Diplogonoporus grandis, Zeitschr. f. klin. Med., 1900, xl, p. 1.

Sparganum mansoni (pp. 317, 318, and 659).

COBBOLD, P. SP. Description of Ligula mansoni, Linn. Soc. Journ. Zool., Lond., 1883, xvii, p. 78.

IJIMA, J., and MURATA. Some New Cases of the Occurrence of Bothriocephalus ligula, Journ. Coll. Sci., Imp. Univ., Tokio, 1888, ii, p. 149.

LEUCKART, R. Demonstr. eines selt. menschl. Entoz., Tagebl. 57, Vers. d. Naturf. u. Ärzte zu Magdeburg, 1884, p. 321.

-- Die Paras. d. Mensch., 2. Aufl., i, p. 941.

MANSON, P. Case of Lymph Scrotum associated with Filariæ and other Parasites, Lancet, 1882, ii, p. 616.

MIYAKE, H. Beitr. z. Kenntn. d. Bothrioc. ligul., Mitt. Grenzgeb. Med. u. Chir., 1904, xiii, p. 145.

STILES, C. W., and L. TAYLER. A Larval Cestode of Man ... U.S. Dept. of Agric., Bur. of Anim. Ind., Bull. No. 35, Wash., 1902, p. 47.

Sparganum proliferum (pp. 318 to 320).

IJIMA, J. On a New Cestode Larva Parasitic in Man, Journ. Coll. Sci., Imp. Univ., Tokio, 1905, xx, Article 7.

Dipylidium caninum (pp. 320 to 323 and 659 to 661).

(a) Anatomy and Development.

DIAMARE, V. Il genere Dipylidium, Atti R. Accad. sci. fis. e met. Napoli, 1893, 2 ser., ii, No. 7.

GRASSI, B., and G. ROVELLI. Embryol. Forsch. an Cestoden, C. f. B. u. Par., 1889, v, p. 370.

-- -- Ric. embryol. sui Cestodi, Atti Gioen. sci. nat., Catania, 1892, 4 ser., iv.

MELNIKOW, W. Über d. Jugendzust. d. Taen. cucum., Arch. f. Naturg., 1869, xxxv, i, p. 62.

SONSINO, P. Ric. s. ematoz. del cane e sul ciclo evol. d. T. cucum., Atti soc. tosc. sci. nat., 1888, x, p. 1.

STEUDENER, F. Unters. über d. fein. Bau d. Cestod., Abh. nat. Ges., Halle, 1877, xiii, p. 295.

(b) Case Histories (New Cases Only).

ASAM, W. Taenia cucumerina bei einem Kinde, Münch. med. Wochenschr., 1903, l, p. 334.

BOLLINGER, O. Über T. cucum. beim Mensch., Deutsch. Arch. f. klin. Med., 1905, lxxxiv, p. 50.

BRANDT, E. Zwei Fälle von T. cucum. beim Mensch., Zool. Anz., 1888, xi, p. 481.

FRERIKS, B., and C. W. BROERS. Een T. cucum. bij een Kind, Weekbl. Nederl. Tijdsch. v. Geneesknde., 1904, Deel. ii, p. 33.

HOFFMANN, A. Taen. cucum. bei einem 4 Monate alten Kinde, Jahrb. f. Kinderheilkde., 1887, N.F. xxvi.

KÖHL, O. Taen. cucum. bei einem sechs Wochen alten Kinde, Münch. med. Wochenschr., 1904, li, p. 157.

KRÜGER, F. In St. Petersb. med. Wochenschr., 1887, No. 41.

ROSENBERG, L. Zehn Bandwürm. bei einem vierzehn Monate alten Kinde, Wien. med. Wochenschr., 1904, liv, p. 427.

SONNENSCHEIN, G. Taen. cucum. s. elliptica bei einem sechs Monate alten Kinde, Münch. med. Wochenschr., 1903, No. 52.

TRIIS. In Nord. Med. Arkiv., 1884, xvi, No. 6.

ZSCHOKKE, F. Ein neuer Fall von Dipylidium caninum beim Mensch., C. f. B., P. u. Inf., 1903, i Abt., xxxiv, p. 42.

-- Dipyl. canin. als Schmarotz. d. Mensch., ibid., 1905, i Orig., xxxviii, p. 534.

Hymenolepis nana (pp. 323 to 326, 661 and 662).

BLANCHARD, R. Hist. zool. et méd. d. Téniad. du genre Hymenolepis, Paris, 1891.

CAPAZZO, Z. Due casi di T. nana, Riv. clin. pediatr., 1904, ii, p. 829.

CARRER, C. Un caso di T. nana, Riv. venet. sci. med., 1905, xxii, T. xliii, 2, p. 509.

COMINI, E. Epilessia rifl. da T. nana, Gazz. d. osp., 1887, viii, p. 174.

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Davainea (?) asiatica (pp. 330 and 662).s

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Tænia solium and T. saginata (pp. 331 to 336, 338 to 342, and 662 to 674).

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Tænia marginata (p. 338).

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Tænia serrata (p. 338).

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Tænia africana (pp. 342, 343).

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-- Helminth. vom Ufer d. Nyassasees, Jen. Zeitschr. f. Naturw., 1900, xxxv, p. 420.

Tænia confusa (pp. 343, 344).

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Tænia echinococcus (pp. 344 to 347).

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*(C) NEMATHELMINTHES* (pp. 360 to 470, 674 to 698, 754, and 755).

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Rhabditis pellio (p. 377).

BAGINSKY. Haemoglobinurie mit Auftreten von Rhabditiden im Urin, Deutsche med. Wochenschr., 1887, p. 604.

OERLEY, L. Die Rhabditiden und ihre medic. Bedeutung, Berlin, 1886.

PEIPER and WESTPHAL. Über d. Vorkom. v. Rhabditiden im Harne bei Haematurie, Centralbl. f. klin. Med., 1888, ix, p. 145.

SCHEIBER, S. H. Ein Fall von mikrosk. kleinen Rundwürm. i. Urin eines Kranken, Arch. f. path. Anat., 1880, lxxxii, p. 161.

Rhabditis nieillyi (p. 378).

GLATZEL. Drei Monate im Serra Hadji Hospital zu Dar-es-Salam, Arch. f. Schiffs- u. Tropen-Hyg., 1906, p. 284.

KÜNNEMANN. Rundwürmer (Rhabditis strongyloides) als Ursache eines Hautausschlages beim Hunde, Deutsche tierärztl. Wochenschr., 1905, No. 24.

NIELLY. Un cas de dermatose paras. obs. pour la première fois en France, Arch. méd. nav., 1882, xxxvii, pp. 337, 488; Bull. Acad. Méd., 1882 (2), xi, pp. 395, 581.

O’NEILL, J. On the Presence of a Filaria in Craw-craw, Lancet, 1875, i.

SCHNEIDER, J. G. Nematodenembr. i. d. Haut d. Hundes, In.-Diss., Basel, 1891.

WHITTLES, J. D. A Case of General Infection by a Nematode accompanied by Hypertrophic Gingivitis, Lancet, 1903, i, p. 1435; 1903, ii, p. 57.

Rhabditis sp. (pp. 378, 379).

FRESE, O. Über mikroskop. Würmer (Rhabditiden) im Magen einer Ozaenakranken, Münch. med. Wochenschr., 1907, No. 11.

Anguillula aceti (p. 379).

HENNEBERG, W. Zur Biologie des Essigaales. Berlin, 1900, Deutsche Essigind. Institut für Gährungsgewerbe, 1899, Nos. 45–52; 1900, Nos. 1–5.

PALLECHI, P. Sulla resistenza vitale dell’ Anguillula dell’ aceto, Boll. Mus. Zool. ed Anat. comp., Genova, 1893, No. 17.

STILES, CH. W., and W. A. Frankland. A Case of Vinegar Eel (Anguillula aceti) Infection in the Human Bladder (eleven miscellaneous papers on animal parasites), U.S. Dept, of Agric., Bur. of Animal Ind., Bull. No. 35, Washington, 1902, p. 35.

Strongyloides stercoralis (pp. 380 to 384, 674, 675, and 755).

ASKANAZY, M. Über Art und Zweck der Invasion der Anguillula intestinalis in die Darmwand, C. f. B., P. u. Inf., 1900, i Abt., xxvii, p. 569.

BAVAY. Sur l’Anguillule stercorale, C. R. Acad. Sci., Paris, 1876, lxxxiii, p. 694.

-- Sur l’Anguillule intestinale, ibid., 1877, lxxxiv, p. 266.

BRAUN, M. Bemerk. üb. d. sporad. Fall von Anguill. intest. in Ostpreussen, C. R. Acad. Sci., Paris, 1899, xxvi, p. 612.

BROWN, PH. K. Report of Three Cases in which Embryos of the Strong. intest. were found in the Stool, Boston Med. and Surg. Journ., 1903, cxlviii, p. 583.

CHAUVIN. L’Anguillule stercorale dans la dysenterie des Antilles, Arch. Méd. Nav., 1878, xxix, p. 154.

DURME, P. VAN. Quelq. notes sur les embryons de Strongyloides intestin. et leur pénétrat par la peau, Thompson Yates Lab., Liverpool, 1902 (2), iv, p. 471.

GRASSI, B. Sovra l’Anguillula intestinale, Rend. Istit. lomb. sc. e lett., 1879 (2), xii, p. 228.

GRASSI, B., and C. PARONA. Sovra Anguillula intest., Arch. sci. med., 1879, iii, p. 10.

GRASSI, B., and R. SEGRÈ. Nuove osserv. sull’ eterogonia del Rhabdon. intest., Atti R. Accad. d. Lincei Rendic., 1887 (4), iii, p. 100.

KURLOW, M. V. Anguillula intestinal. als Ursache akuter, blut. Durchfälle beim Menschen, C. f. B., P. u. Inf., 1902, i Orig., xxxi, p. 614.

LEICHTENSTERN, O. Über Anguillula intestinalis, Deutsche med. Wochenschr., 1898, No. 8, p. 118.

-- Zur Lebensgeschichte d. Ang. int., C. f. B., P. u. Inf., 1899, xxv, p. 226.

-- Stud. üb. Strongyl. intest. nebst Bemerk. üb. Ancylost. duodenale, Arb. kais. Gesundheitsamt, 1905, xxii, p. 309.

LEUCKART, R. Über d. Lebensgesch. d. sogen. Anguillula stercoralis, Ber. d. math.-phys. Class. d. k. sächs. Ges. d. Wiss., 1883, p. 85.

LOOSS, A. Die Wanderung der Ancylostomum- u. Strongyloides-Larven von d. Haut nach dem Darm, C.R. 6me Congr. intern. de Zool., Berne, 1904 (1905), p. 225.

NORMAND, A. Sur la maladie dite diarrhée de Cochinchine, C. R. Acad. Sci., Paris, 1876, lxxxiii, p. 316.

-- Mém. sur la diarrh. de Cochinchine, Arch. Méd. Nav., 1877, xxvii, p. 35.

-- Du rôle étiol. de l’anguillule dans la diarrh. de Cochinchine, ibid., 1878, xxx, p. 214.

PAPPENHEIM. Ein sporad. Fall von Ang. intest. in Ostpreussen, C. f. B., P. u. Inf., 1899, i Abt., xxvi, p. 608.

PERRONCITO, E. Obser. sur le dévelop. de l’Anguillula intestinalis, Journ. de l’Anat. et de la Physiol., 1887, xvii, p. 499.

-- Il Rhabdonema strongyloides Leuck., Anguillula intestinalis e Pseudorhabditis stercoralis, Giorn. R. Accad. di Med., Torino, 1906, p. 3.

PRICE, MARSHALL LANGTON. Occurrence of Strongyloides intestinalis in the United States, Journ. Amer. Med. Assoc., 1903, xli, p. 713.

ROVELLI, G. Ric. s. org. genit. d. Strongyloides, Como, 1888.

SCHLÜTER, H. Zur Kenntn. d. Anguillula-Erkrank. b. Menschen, In.-Diss., Kiel, 1905.

SEIFERT. Über Anguillula stercoralis, Sitzungsber. phys.-med. Ges., Würzburg, 1883, p. 22.

SONSINO, P. Tre casi d. mal. du Rhabdonema intest. _o Rhabdonemiasi_, Suppl. d. Riv. gen. ital. di Clinica med., July 20, 1891.

STRONG, R. P. Cases of Infection with Strongyloides intestinalis; First reported cases in North America, Johns Hopk. Hosp. Rept., 1901, x, p. 91.

STURSBERG. Über Anguillula intestinalis, Sitzungsber. niederrh. Ges. f. Natur- u. Heilkde., Bonn., 1905, p. 28.

TEISSIER, P. Nouv. contrib. à l’étude de l’Anguill. stercoralis; Anguillulose experim. de la grenouille, Arch. Méd. expér., 1896, p. 358.

TESTI, A. Contrib. allo studio dell’ anguillulosi intest., Riv. crit. di clin. med., 1904, v, Nos. 6–8.

THAYER, W. G. On the Occurrence of Strongyloides intestinalis in the United States, Journ. Exper. Med., 1901 (1), vi, p. 75.

ZINN, W. Über Anguillula intestinalis, C. f. B., P. u. Inf., 1899, i Abt., xxvi, p. 696.

Gnathostoma siamense (pp. 384, 385).

LEVINSEN, G. M. R. Om en ny rundworm hos mennesket, Vidensk. meddel. fra. naturh. Foren., Kjöbenhavn, f. 1889, p. 323; abstracted in C. f. B., P. u. Inf., 1890, viii, p. 182.

Dracunculus medinensis (pp. 386 to 390, 675, and 676).

BASTIAN, A. On the Structure and Nature of the Dracunculus, Trans. Linn. Soc. Lond., 1863, xxiv, p. 101.

BLANCHARD, R. Malad. paras., paras., paras. animaux, Paris, 1895, p. 768.

CHARLES, R. H. Hist. of the male Filaria medin., Sci. Mem. Med. Offi., Army of India, Calcutta, 1892, vii.

COPPOLA, N. Filaria medin. nella Colon. Eritrea, Giorn. med. del R. esercito, 1906, liv, p. 92; abstracted in Arch. f. Schiffs- u. Tropen-Hyg., 1906, x, p. 518.

FEDSCHENKO. Bau u. Entw. d. Filaria, Ber. d. k. Ges. d. Frd. d. Nat., Anthrop. u. Ethnogr., 1879, viii (1), p. 71.

LEUCKART, R. Die menschlichen Parasiten, 1876, 1. Aufl., ii, p. 644.

MANSON, P. On the Guinea-worm, Brit. Med. Journ., London, 1895, ii, p. 1350; Lancet, 1895, ii, p. 309.

-- The Life-span of Filaria medinensis, Brit. Med. Journ., 1903, ii, p. 10.

MOSLER, F. Über die medic. Bedeutung d. Medinawurmes, Wien, Leipzig, 1885.

PLEHN, F. Die Kamerunküste, Berlin, 1898, p. 294.

POWELL, S. A. The Life-span of the Guinea-worm, Lancet, 1904, i, p. 76; Brit. Med. Journ., 1904, i, p. 73.

RAILLIET, A. De l’occurr. de la Filaire de Médine chez les animaux, Bull. Soc. Zool. France, 1889, xiv, p. 73.

VORTISCH, H. Erfahrungen über einige spezifische Krankheiten an der Goldküste, Arch. f. Schiffs- u. Tropen-Hyg., 1906, x, p. 537.

Filaria bancrofti (pp. 390 to 403, and 676 to 678).

ANNETT, H. E., J. E. DUTTON and J. H. ELLIOT. Report of the Malaria Expedition to Nigeria, II, Filariasis, Liverpool, 1901.

BANCROFT, TH. On the Metamorphosis of the Young Form of Filaria bancrofti in the body of Culex ciliaris, Proc. Roy. Soc. N. S. Wales, 1898, xxiii, p. 48; 1901, xxxv.

BIONDI, D. Chiluria da Filaria sanguinis hominis nocturna in Europa, Atti Accad. d. Lincei, January 12, 1903 (5), p. 538.

BLANCHARD, R. Transmiss. de la filariose par les moustiques, Arch. de Paras., 1900, iii, p. 280.

BOURNE, G. A. Note on Filaria sanguinis hominis with description of a Male Specimen, Brit. Med. Journ., 1888, No. 1429.

COBBOLD, T. S. The Life-history of Filaria bancrofti, Journ. Linn. Soc., London, 1879, xiv, p. 356.

DEMARQUAY. Note sur une tumeur de bourse ... renferm.... des helm. némat., Gaz. méd., Paris, 1863 (3), xviii, p. 665.

LEWIS, T. R. On a Hæmatozoon inhabiting Human Blood, Calcutta, 1872; 2nd. edit., 1874.

-- The Pathological Significance of Nematode Hæmatozoa, Calcutta, 1874.

LINSTOW, V. Über die Arten d. Blutfil. d. Menschen, Zool. Anz. 1900, xxiii, p. 76.

LOW, G. C. A Recent Observation on Fil. nocturna in Culex, Brit. Med. Journ., 1900, i, p. 1456.

-- The Development of Filaria nocturna in Different Species of Mosquitoes, Brit. Med. Journ., London, 1901, i, p. 1336.

-- Malaria and Filaria Diseases in Barbados, West Indies, Brit. Med. Journ., 1901, ii, p. 687.

LYNCH, G. W. A. Note on the Occurrence of Filaria in Fijians, Lancet, 1905, i, p. 21.

MAITLAND, J. Note on the Etiology of Filariosis, Brit. Med. Journ., 1900, ii, p. 537.

MANSON, P. The Filaria sanguinis hominis ... London, 1883.

-- The Metamorphosis of Fil. sanguinis hominis in the Mosquito, Trans. Linn. Soc., Lond., 1884 (2), ii, pp. 10, 367.

-- The Filaria sanguinis and Filariasis, Trop. Diseases, New Edit., London, 1903, p. 545.

PENEL, R. Les filaires du sang de l’homme, 2e édit., Paris, 1905; abstracted in Arch. de Paras., 1905, ix, p. 187.

SCHEUBE. Die Filariakrankheit, Volkmanns Samml. klin. Vortr., 1883, No. 232.

SIBTHORPE. On the Adult Male of Filaria sanguinis hominis, Brit. Med. Journ., 1889, No. 1485.

SOLIERI, S. Chiluria da Filaria bancrofti in Europa, Atti Accad. fisiocrat. sci., 1904 (4), xv, p. 429.

TANIGUCHI, N. Über Filaria bancrofti, C. f. B., P. u. Inf., 1904, i Abt. Orig., xxxv, p. 492.

THIESING, H. Beitr. zur Anat. der Filaria sang. hom., Inaug.-Diss., Basel, Leipzig, 1892.

TRIBOUDEAU. Note sur la Filaria aux îles de la Société, C. R. Soc. Biol., Paris, 1903, lv, p. 996.

VINCENT, G. A. Observations on Human Filariasis in Trinidad, Brit. Med. Journ., 1902, i, p. 189.

ZIEMANN, H. Beitr. z. Filariakrankh. d. Menschen u. d. Tiere in d. Tropen, Dtsche. med. Wchschr., 1905, No. 11.

Filaria demarquayi (pp. 403 and 404).

DANIELS, C. W. Filariæ and Filarial Disease in British Guiana, Brit. Med. Journ., 1898, ii, p. 878.

-- Adult Form of Filaria demarquayi, Journ. Trop. Med., 1902, v, p. 357.

GALGEY, O. Filaria demarquayi in St. Lucia, Brit. Med. Journ., 1891, i, p. 145.

LOW, G. S. Notes on Filaria demarquayi, ibid., 1902, i, p. 196.

MANSON, P. On Certain New Species of Nematode Hæmatozoa occurring in America, ibid., 1897, ii, p. 1837.

OZZARD, A. T. Description of a Female Form of the Filaria demarquayi, Journ. Trop. Med., 1902, v, p. 259.

Filaria (?) conjunctivæ (pp. 404 to 406).

ADDARIO, C. Si di un nemat. dell’ occhio umano, Ann. d. ottalmol., 1885, xv.

ALESSANDRINI, G. Nuovo caso di Filaria conjunctivæ Add., Boll. soc. zool. ital., 1906, 2a ser., vii, p. 233.

BABES, V. Über einen neuen Parasiten d. Menschen, Med.-chir. Ctrlbl., Wien, 1879, xiv, p. 554.

-- Über einen im menschl. Peritoneum gefund. Nemat., Arch. f. path. Anat., 1880, lxxxi, p. 158.

GRASSI, B. Filaria inermis, ein Parasit d. Menschen, d. Pferdes u. d. Esels, C. f. B. u. Par., 1887, i, p. 617.

Agamofilaria oculi humani (p. 406).

GESCHEIDT. Die Entozoen des Auges, Zeitschr. f. Ophthalmol., 1833, iii, p. 405.

KRAEMER, A. Die thier. Schmarotzer des Auges, Graefe-Saemischs Handb. d. ges. Augenheilkde., Leipz., 1899, x, 2, chap. xviii.

KUHNT, H. Extract. ein. neuen Entozoon a. d. Glaskörper, Arch. f. Augenheilkde., 1891, xxiv, p. 205.

NORDMANN, A. V. Mikrograph. Beitr. z. Naturgesch. d. wirbellos. Thiere, Berlin, 1831, Heft 1, p. 7; Heft 2, p. 9.

Agamofilaria labialis (p. 407).

PANE. Nota su di un elminte nematode, Annal. Accad. degli aspiranti naturalisti, Napoli, 1864 (3), iv.

Filaria (?) romanorum-orientalis (p. 407).

SARCANI, A. Filaria romanorum orientalis, Wien. med. Presse, 1888, No. 7, p. 222.

Filaria (?) kilimaræ (p. 407).

KOLB, G. Filaria kilimaræ in Britisch-Ostafrika, Arch. f. Schiffs- u. Tropen-Hyg., 1898, ii, p. 28.

Filaria (?) sp.? (p. 407).

CHOLODKOWSKY, N. A., in Wratsch, 1896, No. 3.

-- Über einige selten beim Menschen vork. Parasit., Sitzgsber. St. Petersb. naturf. Ges., 1897, p. 185.

Mikrofilaria powelli (p. 407).

PENEL, R. Les filaires du sang de l’homme, 2e ed., Paris, 1905, p. 126.

POWELL, A. A Species of Blood Filaria, probably hitherto undescribed, Brit. Med. Journ., 1903, i, p. 1145.

Setaria equina (pp. 408, 409).

BLANCHARD, R. Traité de Zool. méd., Paris, 1890, ii, p. 16.

BRERA. Mem. phys.-med. sopra i princip. vermi del corpo umano, Crema, 1811, p. 31.

DEUPSER. Zur Entw. d. Filaria papillosa, Zool. Anz., 1892, xv, p. 129; In.-Diss., Breslau, 1894.

LINSTOW, V. Beobacht. an neuen u. bekannten Nemathelm., Arch. f. mikr. Anat. u. Entw., 1902, lx, p. 222.·

TREUTLER, F. A. Observat. pathol.-anat. auct. ad helminthol. humani corporis continentes, Lipsiae, 1793.

Loa loa (pp. 409 to 414, and 678).

BILLET, A. Un nouv. cas de Filaria loa male, C. R. Soc. Biol., Paris, 1906, lxi, p. 507.

BLANCHARD, R. La Filaire sous-conjonctivale, Progr. Méd., Paris, 1886 (2), iv, pp. 591, 611.

-- Nouveau cas de Filaria loa, Arch. de Paras., 1899, ii, p. 504.

BRUMPT, E. La Filaria loa est la forme adulte de la microfilaire designée sous le nom Filaria diurna Mans., C. R. Soc. Biol., Paris, 1904, lvi, p. 630.

GAUTHIER, C. Microfilaires du sang coincidant avec une filaire de l’œil, Semaine méd., 1905, p. 176; C. R. Soc. Biol., Paris, 1905, lviii, p. 632.

HABERSHON, J. H. Calabar Swellings on the Upper Congo, Journ. Trop. Med., 1904, vii, p. 3.

LINON, J., and PÉNAUD. Un cas de Filaria loa avec oedèmes intermitt., microfil. dans le sang, l’urine et la salive, C. R. Soc. Biol., 1906, lxi, p. 510.

LOOSS, A. Zur Kenntnis des Baues der Filaria loa G., Zool. Jahrb., 1904, Syst. xx, p. 549.

LUDWIG, H., and TH. SAEMISCH. Über Filaria loa im Auge des Menschen, Z. f. w. Zool., 1895, lx, p. 726.

MANSON, P. The Filaria sanguinis hominis major and minor, Two New Species of Hæmatozoa, Lancet, 1891, i, p. 4; Ctrlbl. f. allg. Path., ii, p. 298.

-- Geographical Distribution of Filaria sanguinis hominis diurna ... Trans. VII. Int. Cong. of Hyg. and Demography, London, 1891, i, p. 79.

MONGIN. Observ. sur un ver trouvé sous la conjonctive à Maribaron, île St.-Domingue, Journ. de Méd., Chirurg., Pharmacie, Paris, 1770, xxxii, p. 338.

PENEL, R. Les Filaires du sang de l’homme, 2e édit., Paris, 1905, p. 127.

PLEHN, F. Die Kamerunküste, Berlin, 1898, p. 296.

SAMBON, L. W. Remarks on the Individuality of Filaria diurna, Journ. Trop. Med., 1903, vi, p. 26.

THOMPSTONE, S. W. Calabar Swellings, Journ. Trop. Med., 1899–1900, ii, p. 89.

WARD, H. B. The Earliest Record of Filaria loa, Zool. Ann., 1906, i, p. 376; Med., London, 1902, v, p. 381; vi, p. 26.

-- Studies on Human Parasites in North America: I, Filaria loa, Stud. Zool. Lab., Univ. Nebraska, 1906, No. 63.

WURTZ, R., and A. CLERC. Nouv. observ. de Filaria loa, Arch. Méd. exp. et d’Anat. path., 1905, xvii, p. 261.

Acanthocheilonema perstans (pp. 414 to 416).

CHRISTY, C. The Distribution of Sleeping Sickness; Filaria perstans ... in East Equatorial Africa, Rep. Sleeping Sickness Comm., London, 1903, ii, p. 1.

DANIELS, C. W. The Filaria sanguinis hominis perstans found in the Aboriginals of British Guiana, Brit. Guiana Med. Ann., 1897, p. 28.

-- Discovery of the Parental Form of a British Guiana Bloodworm, Brit. Med. Journ., 1898, i, p. 1011.

DANIELS, C. W. The Filaria ozzardi and their Adult Form, Brit. Guiana Med. Ann., 1898, x, p. 1.

-- Filariæ and Filarial Disease in British Guiana, Brit. Med. Journ., 1898, ii, p. 878.

-- The Probable Parental Form of a Sharp-tailed Filaria found in the Blood of the Aboriginals of British Guiana, ibid., 1899, i, p. 1459.

-- The Sharp-tailed Filaria in British Guiana, Journ. of Trop. Med., 1899–1900, ii, p. 11.

-- Filariasis in British Central Africa, Journ. Trop. Med., 1901, p. 193.

FIRKET, C. M. Filariose du sang chez les nègres du Congo, Bull. Acad. Roy. méd. Belg., 1895 (4) ix; abstracted in C. f. B., P. u. Inf. (1), xix, p. 791.

HENRY. Remarks on Filaria, Proc. Acad. Nat. Sci., Philadelphia, 1896, p. 271.

HODGES, A. Sleeping Sickness and Filaria perstans in Busoga, Journ. Trop. Med., 1902, v, p. 298.

LOW, G. C. Filaria perstans, Brit. Med. Journ., London, 1903, i, p. 722.

MANSON, P. Cf. under Loa loa and Filaria demarquayi (pp. 805, 806).

OZZARD, A. T. A Supposed New Species of Filaria sanguinis hominis found in the Interior of British Guiana, Brit. Guiana Med. Ann., 1897, p. 24.

PENEL, R. Cf. under Loa loa (p. 806).

ZIEMANN, H. Über das Vorkommen von Filaria perstans und von Trypanosomen beim Schimpansen, Arch. f. Schiffs- u. Tropen-Hyg., 1902, vi, p. 362.

-- Beitr. zur Filariakrankheit d. Menschen u. d. Tiere in d. Tropen, Dtsche. med. Wchschr., 1905, No. 11.

Dirofilaria magalhāesi (p. 417).

BLANCHARD, R. Maladies parasitaires ... Paris, 1895, p. 782.

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