XXII. FILARIAL INFECTIONS
GENERAL CONSIDERATIONS
The filarial worms are thread-like nematodes, with a thin cylindrical oesophagus, which live in various parts of the body and may or may not give rise to disease conditions. It is one of the most remarkable facts in animal parasitology that a person may harbor numerous adult filariae and myriads of embryos without in any way manifesting symptoms of the infection. In most of the filarial worms the female has a double uterus with the uterine opening near the anterior extremity.
It has been proposed to designate the filarial embryo by the term microfilaria, reserving the generic name Filaria for the adult parasite. This may be convenient for differentiation but zoölogical nomenclature does not permit different names for adults and embryos. While there have been almost 20 different filarial species reported for man there is, in some instances, doubt as to the correctness of the observation, and again, a well recognized species has at times been considered as a new species and given a new name.
From a practical standpoint we need only consider: (1) Filaria bancrofti; the adult of which lives in the lymphatic glands and vessels while the sheathed embryos (which from their appearance in the blood only at night are called Filaria nocturna) obtain access to the peripheral blood vessels.
Various well-known conditions are caused by this parasite, such as elephantiasis, varicose groin glands, chyluria, etc. This infection was formerly stated to be caused by Filaria sanguinis hominis.
(2) Loa loa, the adult of which wanders about in the subcutaneous tissues, characteristically in the region of the eyes, while the sheathed embryo is found in the blood during the day, hence Filaria diurna.
Calabar swellings, irregular febrile conditions and the disagreeable sensations incident to the wanderings of the worm are clinical features of this infection.
-----------+--------------------+--------------------+------------------- | Adults | Embryos | Remarks -----------+--------------------+--------------------+------------------- |Male 40 by 0.1 mm. |Sheathed, 300 by 7.5|Transmitted by | Female 90 by 0.28 | microns. Distance | mosquitoes, Culex | mm. Smooth cuticle.| from head to V spot| fatigans and Filaria | Bulbous anterior | 90 microns; to | Stegomyia pseudo- bancrofti | extremity. | break in cells 50 | scutellaris. | Occupy lymphatic | microns. Tail | Causes | glands and vessels.| rather straight. | elephantiasis, | | Terminal cells do | lymph scrotum, | | not fill up tail | chyluria, etc. | | end. Nocturnal | | | periodicity in | | | peripheral | | | circulation. | -----------+--------------------+--------------------+------------------- |Male 27 by 0.3 mm. |Sheathed, 240 × 7 |Transmitted by | Female 55 by 0.4 | microns. Distance |species of a biting | mm. Cuticle tuber- | from head to V spot| fly—Chrysops. | culated. Anterior | 65 microns; to | Causes calabar Loa loa | extremity like | break in cells | swellings. Worms | truncated cone. | 40 microns. Cork- | often visit ocular | Wanders in | screw tail which is| region. | subcutaneous | completely filled | | tissues. | up with terminal | | | cells. Diurnal | | | periodicity in | | | peripheral | | | circulation. | -----------+--------------------+--------------------+------------------- |Male 40 by 0.07 mm. |Without sheaths, 200|Transmitting agent | Female 75 by 0.1 | by 5 microns. Post-| not surely known. | mm. Cuticle smooth.| erior two-thirds | Mosquitoes and Acanthoch- | Tip of tail shows 2| tapers to blunt | ticks suggested. eilonema | triangular | ending. Distance | No pathogenicity. perstans | processes. Found | from head to V spot| | about root of | 49 microns; to | | mesentery. | break in cells 34 | | | microns. Persists | | | in circulation both| | | day and night. | -----------+--------------------+--------------------+------------------- |Male 30 by 0.14 mm. |Without sheaths, 250|Method of trans- | Female usually | by 7.5 microns. | mission unknown. Onchocerca | fragmented. | Found in cyst-like | Causes small volvulus | Possibly 75 by 0.36| spaces of tumors. | cystic tumors, | mm. Cuticle | Not in peripheral | under skin of | striated. Found | circulation. | thorax | coiled up in | | especially. | cyst-like tumors | | | under skin. | | -----------+--------------------+--------------------+------------------- |Male from Leiper’s |Without sheaths. 600|Embryos swallowed | monkey 22 mm. | × 20 microns. Long | by Cyclops. Man | Female 80 to 90 cm.| slender tail. | drinks water | long by 1.6 mm. | Cuticle striated. | containing Dracunculus| wide. Smooth white | Extruded from break| Cyclops. medinensis| body. Anchoring | in skin of patient.| | hook at tail end. | | | Female lives in | | | subcutaneous | | | tissue of lower | | | extremity. | | -----------+--------------------+--------------------+-------------------
(3) Onchocerca volvulus. The males and females of this parasite are found coiled up in channeled connective tissue tumors of the subcutaneous tissues.
The sheathless embryos have been surely found only within these tumors and not in the blood.
(4) Acanthocheilonema perstans. This parasite does not seem to give rise to clinical manifestations except possibly to cause an irregular fever.
The adult is found in the retroperitoneal connective tissue or fat, while the sheathless, blunt-tailed embryo is found in the blood, both by day and night, hence perstans. The adult forms are found in the tissues behind the abdominal aorta and at the attachment of the mesentery.
(5) Dracunculus medinensis. The female of this parasite, about 36 inches long and 1/15 inch in diameter, travels to the subcutaneous tissues of the extremities and boring through the skin causes a small surface erosion.
An unimportant filarial worm which has been found only in the West Indies and British Guiana is known as Filaria demarquayi or F. ozzardi. The embryos have sharp tails and are without a sheath. The parasite is not known to produce symptoms.
HISTORY
Filaria bancrofti.—While elephantiasis was frequently described by ancient writers yet the confusion between Elephantiasis Graecorum, a term applied to leprosy, and Elephantiasis Arabum, or the filarial condition, made the question of the nature of the skin thickenings very indefinite.
The thickenings due to leprosy and those connected with filariasis were separated clinically by observers during the 17th and 18th centuries, Hilary, in 1750, having accurately described the progress of that form of elephantiasis connected with elephantoid fever and lymphangitis. In 1863 Demarquay discovered filarial embryos in the exudate of a chylous hydrocele and three years later Wucherer, in Brazil, found similar nematode larvae in the urine of a case of haematochyluria. Commencing with the year 1863 Lewis carried on a series of investigations in Calcutta in which he found these embryos not only in the urine of patients with chyluria but as well in the lymph and blood of those affected with elephantiasis. He called the parasite Filaria sanguinis hominis, a name still frequently employed by medical writers.
In 1876 Bancroft, in Australia, discovered the adult filarial worms in a lymphatic abscess, hence the name Filaria bancrofti. In 1878 Manson, in China, demonstrated the mosquito transmission of the disease as well as the phenomenon of nocturnal periodicity. Manson’s idea, however, was that the fully developed embryo escaped from the body of the infected mosquito at the time of the death of the insect and that man contracted the infection in drinking water.
The investigations of Low and more recently those of Fülleborn and Bahr and others have shown that the larvae escape by way of the mosquito’s proboscis and enter the skin of man.
Loa loa.—The knowledge of a filarial infection of the region of the eye seems to date from the time of Magellan. Although the disease is now confined to the west coast of Africa, cases were reported from the West Indies by Mongin and Bajou during the 18th century. These cases were in slaves who had contracted the infection in Africa.
In 1891 Manson noted the presence of the larval forms which showed a diurnal periodicity in the peripheral blood.
Dracunculus medinensis.—Ancient Egyptian writings would indicate that the disease was well known in those times. It is believed that the fiery serpent of the wilderness, which afflicted the Children of Israel, was an infection of this sort.
The prevalence of dracontiasis, as the infection is generally termed, in Arabia, was well known to the Greeks and Romans.
Fedschenko, in 1870, noted the transmission of the disease by species of Cyclops.
Onchocerca volvulus was first discovered in 1893, in peculiar tumors of the natives of the Gold Coast.
Acanthocheilonema perstans was first found by Manson, in 1891, in the blood of natives of the Congo.
Daniels also found these embryos, along with those of F. demarquayi, in the blood of natives of British Guiana.
FILARIA BANCROFTI
GEOGRAPHICAL DISTRIBUTION
This parasite has been found in almost all tropical and subtropical countries. It is quite prevalent in the West Indies and has been found in some of the Southern states of the U. S. It is very common in some of the South American countries as well as in Central America. The infection is widespread in Arabia, India and China. Africa, especially the West Coast, and Australia, particularly in Queensland, are parts of the world where the infection prevails.
It is especially in some of the Pacific islands, as Samoa and Fiji, that it is extraordinarily prevalent. Bahr has stated that Fijians in the proportion of 27% show filarial embryos in their blood. In 25% of these natives clinical manifestations of the disease exist but the embryos are absent from the peripheral circulation. In other words more than one-half of the population show absolute evidence of infection.
LIFE HISTORY
It is a well-known fact that filarial embryos may be present at night in the peripheral blood of persons not showing a single symptom of filariasis and again, in those with marked elephantiasis, varicose groin glands or chyluria there may be an entire and permanent absence of embryos in the blood. When certain mosquitoes bite persons having embryos in the blood they take into their stomachs the sheathed embryos of F. bancrofti. Flu states he has succeeded in infecting the following mosquitoes: C. fatigans, S. scutellaris, M. ludlowi and M. rossii. The most suitable carriers proved to be C. fatigans and S. scutellaris. Large numbers of larvae perish in anopheline mosquitoes.
The following developmental cycle has been demonstrated for Culex fatigans and Stegomyia pseudoscutellaris. Bahr has found that if there are too many embryos taken up by the mosquito the insect is apt to die, as the result of too heavy an infection; so that a person harboring many filarial embryos may be less dangerous than one with a smaller number. Upon reaching the stomach of the mosquito the sheath of the embryo becomes fixed in the viscid blood contents and the embryo itself by active motions is able to force itself from its sheath. This escape usually occurs within two hours but may take longer. The free embryo then bores its way through the stomach walls and within twenty-four hours has reached the thoracic muscles of the mosquito. Within forty-eight hours the embryo begins to broaden and the anterior and posterior V spots to become more prominent. About the end of the first week there commences the formation of an alimentary canal, by which time the developing larva is about 0.5 mm. long. When the larva is about 0.6 mm. long an ecdysis apparently takes place. Later on these larvae develop 3 or 4 terminal papillae and make their way to the fleshy labium of the mosquito’s proboscis. An occasional larva may enter other structures than the labium but in such case they would be unable to effect an entrance to their definitive host, man. These larvae in the proboscis are about 1.5 mm. long and about 20 microns broad.
The mosquitoes have two terminal processes, the labella, separated from the labium by a thin membranous partition called Dutton’s membrane. The larvae, having completed their developmental cycle in the mosquito, which takes about three weeks, and moving down the labium, break through this membrane when it is put upon a stretch by the wide separation of the labella at the time of feeding on the part of the mosquito. It was formerly supposed that the larvae entered man through the puncture made by the biting parts of the mosquito, but Bahr has shown by experiments that they effect an entrance through the intact pores of the skin as does the ancylostome larva.
These larvae upon entering the human host reach the lymphatic vessels or glands and in this definitive host (man) the females are fertilized by the males and give off sheathed larvae from the uterine opening near the anterior end of the worm.
The sheath is simply the egg membrane which from being oval at first becomes stretched by the developing embryo to finally become a long, narrow sac encasing the fully developed embryo as it exists in man. From the lymph stream they reach the general circulation. In a case of a man with filarial embryos in his peripheral circulation, who committed suicide one morning, Manson found the embryos, in large part, contained in the vessels of the lungs. There were 675 embryos per slide in blood from the lungs for one from blood from the spleen or liver. It would thus appear that during the day, when the embryos are absent from the peripheral circulation, they retire to the lungs. In the case of the filarial embryo of persons in the Pacific Islands there does not appear to exist any periodicity. Bahr thinks this absence of nocturnal periodicity to be connected with the habits of its principal intermediary host, Stegomyia pseudoscutellaris, which feeds by day. Culex fatigans feeds at night.
With the filarial embryos found in patients in the Philippines there is also a lack of nocturnal periodicity. In the opinion of Ashburn and Craig the Philippine filarial worm is a new species, Filaria philippinensis.
Walker, however, recently examined four adult filarial worms in the Philippines and was unable to note any differences from F. bancrofti.
PATHOLOGY AND MORBID ANATOMY
The adult worms may exist in numbers and over long periods of time give off great numbers of embryos into the peripheral circulation without there being any evidence of disease in the patient. There is apt to be at such time a marked eosinophilia. The process by which the fibrosis of lymph channels with obstruction to the flow of lymph occurs is unknown. Some think that with the pouring out of embryos inflammatory processes, bacterial or otherwise, may be set up. We know that there is a tendency for these adults to die and become calcified, in this way bringing about lymphatic obstruction.
Bahr notes the influence of adult filariae in producing an increase in connective tissue in glands and considers such glands as less resistant to bacterial infection.
Manson has an idea that some factor may cause the female to give off immature embryos, which being oval, and of considerable width, may block the lymphatics.
It has often been claimed that various cocci were the exciting factors in the lymphangitis associated with filariasis. Recently Dutcher has reported the isolation of an organism resembling B. subtilis as the cause of filarial lymphangitis (Bacillus lymphangiticus).
As the result of the lymphangitis and blocking of the channels the embryos cannot reach the peripheral circulation; hence when obstruction does occur and symptoms of lymph stasis appear, there may be an absence of embryos in the circulation.
It is now well established that patients with elephantiasis very rarely show embryos in the peripheral circulation, and this fact should be better understood because there is a tendency to negative a filarial diagnosis when embryos are absent from the peripheral circulation.
These lymph channel obstructions may at one time cause dilatations or varices and at another bring about solid oedemas of the tributary parts. The treatment will be considered under each special form of the disease. It may be stated however that salvarsan, arsenophenylglycin and other similar remedies have been without special effect in destroying the filarial worms.
CLINICAL MANIFESTATIONS
Not only is it important to understand that elephantiasis and other manifestations of filarial infection may and usually do exist without there being embryos in the peripheral blood of the patient, but also, that a high percentage of a population may show filarial embryos in their blood and yet never or with extreme rarity show any of the signs of filarial disease. These people, with abundant embryos in their blood, usually show no disturbance of health. In the Philippines one may rarely see a case of chylocele but usually there is nothing clinical to note.
Johnson, in examining 400 people, in Charleston, S. C., found 19% with filarial embryos, yet only 5% showed any symptoms of filariasis. Croll states that 11.5% of 4000 Europeans admitted to the Brisbane Hospital (Australia) showed filarial infection but practically none had symptoms. In South Queensland cases of lymphangitis, chyluria and varicose groin glands are occasionally seen and rather frequently hydrocele and filarial abscesses. There is an absence of elephantiasis.
Elephantoid Fever
The febrile accessions that accompany the recurring attacks of lymphangitis in elephantiasis, lymph scrotum and other filarial manifestations, are very important because they may lead to errors in diagnosis.
Thus in Barbadoes, where there is no malaria, a condition in which there occurs a high fever of sudden onset with rigors and associated erysipelatous redness of leg or scrotum, accompanied by lymphangitis and painful lymphatic glands, has given a suggestion of a malarial paroxysm. The tense inflamed area, after several days, shows an exudation of lymph and the redness disappears, but with some resulting thickening of the affected tissues. Such attacks may terminate with profuse sweating.
The treatment of the condition is such as would be advisable for ordinary lymphangitis—rest in bed, elevation of the part, laxatives and local applications.
Lymph Scrotum
This condition is apt to set in with fever. The scrotal tissues are somewhat tense and reddened and may show numerous lymphatic varices which when pricked with a needle, give exit to lymph which may or may not contain filarial embryos. The lymph continues to exude for a long time. Erysipelatous manifestations are not uncommon. With recurring attacks the scrotal tissues become more and more hypertrophied and may go on to elephantiasis of the scrotum.
Ordinarily local applications with suspension of the scrotum is the proper treatment. Should the thickening increase to a great extent the blubbery tissues may be excised, care being exercised to avoid the testicles and to bring together sound tissue for the enclosing flaps. These wounds usually heal readily, although there may be delay in healing from the outpouring of lymph in cases where the flaps include diseased tissue.
Varicose Groin Glands
Swellings which come on rather slowly and insidiously may involve the inguinal or femoral groups of glands of one or both sides. The epitrochlear glands may also be involved. The skin over the enlarged, rather doughy glands can be freely moved but the glands themselves are bound down to the deeper tissues. Elephantoid fever may set in associated with local manifestations of pain and redness.
If such glands are punctured with a hypodermic needle lymph, which may contain embryos, exudes. This test together with their slow disappearance on lying down and slow return on assuming the upright position should differentiate hernia. When the contents of a hernial sac are omental there is some difficulty in diagnosis. As a rule it is not advisable to interfere surgically in this filarial condition.
Filarial Abscesses
As a rule injury to the adult filarial worms, which results in their death, is not followed by abscess formation but such termination may occur. These abscesses have been found deeply seated in the extremities. Wise and Minett in a careful examination of 28 such cases found evidences of adult filariae in 22 cases. In 21 of these abscesses, infections with streptococci or staphylococci were demonstrated. Very interesting also is the finding of filarial worms in deep-seated abdominal abscesses.
As regards location, these filarial abscesses were found 31 times in the pelvis of the kidney, 18 times in the epididymis, 12 times in the retro-peritoneal tissues, 25 times in the inguinal glands, 4 times in the ilio-psoas muscles and 8 times in the lymphatic vessels.
They regard the endemic funiculitis to which attention has been directed by Castellani as simply a similar process involving the tissues about the spermatic cord. The treatment of filarial abscesses is similar to that of other abscesses.
Chyluria
As the result of obstruction of the lymphatic vessels varices may form in the bladder lymphatics and, as the result of their rupture, milky urine may be passed. If the thoracic duct be occluded the urine will show an abundance of fat, while if the obstruction exists only in other lymphatics, the milky fluid will be found to show but little fat. Blood is usually present in chyluria so that the urine will show an pinkish tinge.
Chylous urine coagulates rapidly and we have in such a specimen of urine, upon standing, an upper fatty layer and pinkish sediment at the bottom, with a clot between.
The sediment shows lymphocytes and at times filarial embryos. When the exudate is lymph mixed with blood the term haematolymphuria would be a better one.
Clots may form in the bladder and give rise to obstruction to the flow of urine from the bladder.
The appearance of the chyluria is often preceded by heaviness about the loins and pains in the region of the bladder.
The morning urine in such a case is apt to be clear while that passed later in the day is milky in appearance.
A feature of chyluria is its tendency to disappear and reappear so that when treating such a case one should be conservative in considering the treatment as effecting a cure.
It is difficult to understand why chyluria should be common in India and China while almost unknown in the filarial infections of the Pacific islands.
In treating a case of chyluria one should enjoin rest in bed, laxatives and a restriction of fluids and fats. Patients subject to the condition should refrain from active exercise and other conditions which might cause fatigue. Drugs are of little value.
Filarial Orchitis and Hydrocele
The condition rather resembles an attack of epididymitis. As a result of recurring attacks hydrocele develops. The fluid may be lymphous or chylous in appearance and upon microscopical examination may show filarial embryos. These filarial hydroceles seemed to be the most common manifestations of the disease as observed in the Philippines. These hydroceles or chyloceles do not become very large but may require tapping.
Elephantiasis
As the result of recurring attacks of lymphangitis the tissues of the affected part show the effects of lymphatic obstruction by an hypertrophy of the skin and subcutaneous tissues. It would seem that the combination of lymphatic obstruction and bacterial infection is necessary for the production of elephantiasis. The skin of a part affected with elephantiasis is rough and the hair scanty. In addition to the lymphoedema of the part there is a great increase in the connective tissue.
On account of the lymphatic stasis incision into the blubbery tissue causes the outpouring of much lymph.
Elephantiasis of the lower extremities is by far the most common situation, giving us probably 90% of such affections. In Fiji elephantiasis of the upper extremities is quite common.
Other favorite sites are the scrotum, vulva, breasts and penis. Rarely the scalp or areas about neck or trunk may show involvement.
Surgical treatment is the one usually followed. When an extremity becomes too much of a burden, amputation may be indicated. The employment of the method of lymphangioplasty, which consists in the introduction of silk threads into the subcutaneous tissues, to make a channel to the normal lymphatics, does not seem to have been attended with any degree of success or at any rate permanent results. These wounds tend to become infected and if this does not occur the new channels are speedily obliterated.
Castellani recommends the use of Merck’s fibrolysin in injections of from 2 to 4 cc. daily, for three to six months. After each injection the part is tightly bandaged with flannel or rubber bandages. The injections may either be made into the affected part or into the gluteal region. Massage prior to the bandaging may give better results. When the limb becomes smaller and the skin smoother, long strips of skin and subcutaneous tissue may be dissected out and the adjacent edges sutured.
In considering the advantages of operation in elephantiasis of the scrotum it is usually stated that the only question involved is the removal of a burdensome mass which in no way is a source of danger to the life of the patient. At the same time such patients are subject to attacks of elephantoid fever, a condition not without its dangers. There is one factor not usually brought forward and that is the remarkable effect of a successful operation on the mental state of the patient. This is well shown in the accompanying illustrations of the patient before and after operation. If sexual deficiencies are of so powerful an influence on persons of education how much greater must they weigh on an uneducated native with but few of the higher interests of life.
Prior to operation the patient should be kept in bed for a day or so to lessen the amount of fluid and to secure relaxation of tissues. Thorough scrubbing with soap and water the day of and the day before the operation and the use of alcohol as an antiseptic are important. Some prefer iodine.
For the operation the lithotomy position is employed. An assistant supports the scrotal tumor wrapped in a sterile towel. Fauntleroy, whose method I give, does not recommend a tourniquet to the base of the tumor as in his opinion it assists but little in controlling haemorrhage and endangers asepsis. Haemostats answer better and as the vessels which give most trouble are deeply situated the elastic cord would not affect them. In some cases there is very little bleeding. The upper part of the pear-shaped tumor usually affords sufficient sound skin next the thighs for the flaps. As a rule the elephantoid tissue does not involve the upper 2 or 3 inches of the skin anteriorly, which is thus available to cover in the base of the penis. In addition to this covering for the penis we have a long prepuce which has been considerably stretched so that after removing all elephantoid tissue there is enough sound prepuce remaining to cover the distal 2 or 3 inches, so that usually there is sufficient sound skin for a 5-inch penis.
The flaps which are to cover the penis and testicles should be mapped out with shallow incisions and care must be exercised that only sound skin is included in these flaps. A horseshoe shaped incision is made commencing at the left side of the base of the tumor about 1 inch from the thigh and about at the level of the penis in health. The incision is carried downward and passes just below the opening of the penis on the tumor surface. A similar incision on the right side completes the horseshoe curve. Next a downward incision in the sound skin is made over the posterior surface of the tumor, thus encircling the base of the scrotum. The anterior horseshoe incision is now deepened to free the penis, care being taken not to injure the spermatic cord. Next the incisions are deepened laterally until the testicles are reached. The testicles are usually in the center of the tumor imbedded in a blubbery tissue from which they can be easily stripped. The remains of the gubernacula are then hooked up and cut close to the testicles. The tunicae vaginales are often thickened and contain fluid which has to be drawn off.
In 60% of Fauntleroy’s cases it was necessary to remove one testicle on account of extensive disease. One must also bear in mind the possibility of hernial complications and undescended testicle.
A sound is now introduced into the urethra and the septum of the scrotum divided close to the sheath of the penis, then dissecting away the blubbery tissue. At this stage there may be considerable bleeding.
The testicles and spermatic cords are then dissected away from the tunicae vaginales. The penis is now freed by a circular incision around and above the opening in the anterior part of the mass. The remainder of the horseshoe flap is now dissected up and the penis freed. The proximal covering for the penis is made from this horseshoe flap which is stitched to the distal one shaped from the prepuce, carefully trimmed of elephantoid tissue.
The lateral flaps are brought together with linen or silk-worm gut sutures leaving space for a drainage tube and we thus form a new scrotum for the testicles.
The mortality is usually given as 5% but Fauntleroy did not lose a case among 149 such operations, the tumors varying from 10 to 85 pounds in weight.
Chylous Hydrocele
Filarial affections of the tunica vaginalis or the testicle itself are not rare. In the milky fluid obtained by tapping such a hydrocele we may find filarial embryos.
Besides chylous hydrocele we may have a chylous ascites or a chylous diarrhoea. Where there is no obstruction to the thoracic duct there is less fat and the condition is more properly a lymphocele rather than a chylocele. The same distinction is applicable to the other conditions connected with lymphatic varices due to lymphatic obstructions other than that of the thoracic duct.
LABORATORY DIAGNOSIS
The blood from a needle prick of the finger tip or the lobe of the ear can be examined as a fresh preparation. It is advisable to make a vaseline ring around the drop of blood on the slide and then apply a cover-glass. Such a preparation will permit of the examination of the living embryos for a day or more.
Smear preparations may be made by the Ehrlich method of drawing cover glasses apart or by the Daniels method on slides. Some prefer making a thick smear of a drop of blood and, after it has dried, carefully to dehaemoglobinize it with water and then staining with dilute haemotoxylin. Staining with Leishman’s or Wright’s stain gives beautiful pictures. Fixation with methyl alcohol or with heat, by burning off a film of alcohol, and then staining with Giemsa’s stain or some haematoxylin preparation, is to be recommended. On the whole I consider haematoxylin the most desirable staining reagent, as such preparations hold their color for a long time. The paper-like sheaths are seen as if twisted about the larvae with their violet-stained cells. One should note a break in the violet-stained cell column which is 50µ from the head end of F. bancrofti and 40µ for L. loa.
A V spot is seen posterior to the break in the cell column and shows best with very light staining.
The break in the column of the cell nuclei marks the position of the nerve ring, which is distant from the head one-fifth the total length. The anterior spot, below the break in the cell column, is distant about 30% of the total length. It is the location of the excretory pore. In F. bancrofti the cell nuclei extend to 95% of length, thus differing from those of L. loa, which fill up the tail end. At about 82% of the length from the head is located the anal pore.
Ruge’s thick film method for malarial parasites gives excellent results in staining filarial embryos. Either the Giemsa or haemotoxylin staining may be employed.
Embryos may be found in the lymph from varicose groin glands or in the exudate from a chylous hydrocele, as well as in the urinary sediment from a case of chyluria.
The failure to find embryos in no way negatives the existence of a filarial infection.
Adult filariae, either alive or dead and calcified, may be found in the lymphatic glands or in the contents of filarial abscesses.
The blood shows an eosinophilia.
LOA LOA
This filarial infection is at present only known for the West Coast of Africa. In the Cameroons and in Old Calabar the infection is quite common.
As noted in the table previously given, the adults which are a little more than an inch long have cuticular protuberances or bosses, about 12 to 15 microns in height. The sheathed embryo is very similar to that of F. bancrofti, but has a more twisted tail and shows a complete filling up of the tail end with rather elongated cells. The lines of the curves of the embryo show irregularities and are not the smooth lines characteristic of F. bancrofti embryos.
The periodicity is diurnal, for which reason the parasite was originally termed F. diurna.
Leiper has reported two species of Chrysops, one of the tabanid biting flies, as transmitting agents and considers that the embryos undergo development in the salivary glands of the fly.
The life history is not well understood but as a rule a period of several years elapses after infection before adult filariae or filarial embryos are found. Again, for some reason, adult filariae may be noted and when extracted be found full of embryos and yet embryos not be found in the peripheral circulation.
The adults are noted for their tendency to move about in the subcutaneous connective tissues having been found in such tissues in the region of scalp, trunk, penis and extremities.
Most frequently, however, they are noted in the tissues about the region of the eyes and even under the conjunctivae, from which location they have been frequently extracted. It is this which has caused the name Filaria oculi to be given the worm.
The course of the wandering worm is usually marked by an oedematous track. In his own case, recently reported by a medical man, the first symptoms were transient painless swellings about the joints, associated with stiffness. Various diagnoses, such as rheumatism, erythema nodosum and angioneurotic oedema were made in his case. Although two adult filariae were removed at different times the blood examinations were negative for embryos.
As a rule the appearance of the worms in the subcutaneous tissues is characterized by itching sensations and a feeling of tension. Warmth causes them to appear in the superficial tissues while cold makes them confine themselves to the deeper structures. Eosinophilia is rather pronounced.
=Calabar Swellings.=—Although we have no absolute proof that these usually painless swellings, which occur rather suddenly on various parts of the body having only a thin layer of connective tissue, as forearms, face, ankles, hands, are connected with an infection with L. loa, yet such is the general view. These swellings are about the size of a hen’s egg, do not pit on pressure and last for about three days. There is marked tension over the swellings and they may itch greatly.
Rarely does one note more than one swelling at a time. Eosinophilia is quite marked during the attacks. Manson thinks the oedema results from the extrusion of embryos from the female at the site of the swelling. Ward considers the cause to be toxic material excreted by the worm.
There is very little of importance in connection with treatment. When the worms, which travel in the tissues about the eye, at the rate of about ½ inch per minute, are noted, some local anaesthetic may be used and the worm seized with forceps and extracted through a small incision. Elliot recommends the application of hot fomentations to the eye and upon the appearance of the worm under the conjunctiva to instill cocaine solution, seize the worm with forceps and then pass a silk ligature through the conjunctival fold taking in the worm. The ligature is tied and an incision made through which the worm is extracted. Cooling local applications, or an ichthyol ointment, may be applied to the Calabar swellings.
ONCHOCERCA VOLVULUS
This name is given to a filarial worm, found principally on the West Coast of Africa, which causes the formation of subcutaneous tumors. In certain localities as many as 10% of the population may be infected. More recently the parasite has been reported from Guatemala.
It is supposed that the adult worms cause an inflammation of the lymphatic vessel in which they may lie and that a formation of new connective tissue results, giving rise to a tumor-like mass, which is most often found in the axilla or about the sides of the thorax. This tissue stroma encompasses the worms except for the anterior extremity of the female, with its uterine opening, and the posterior extremity of the male carrying the spicules, which ends lie loose in a sort of cyst-like dilatation, which is filled with a viscid fluid swarming with unsheathed embryos. These tumor-like masses cause very little discomfort, last indefinitely and do not tend to ulcerate.
It was formerly thought that these larvae were absent from the peripheral circulation but more recent investigations in cases of onchocerciasis have shown sheathless larvae in the blood, which had the characteristics of those in the contents of the tumors. Such findings, however, are of extreme rarity, the blood examination being almost invariably negative.
The cysts are usually found on the sides of the chest and are quite superficial, with the skin freely movable over them. They may be as large as a hen’s egg but usually are smaller. They are also found over trochanters or along the crests of the ilium.
Dubois states that the embryos may be found in juice from puncture of groin glands.
The tumors are easily enucleated.
In the American infections the tumours are more common in the regions near the eye and it has been thought that certain cases of keratitis may be due to onchocerciasis.
DRACUNCULUS MEDINENSIS
The disease caused by infection with this parasite is usually termed dracontiasis and the parasite Dracunculus medinensis or the Guinea worm.
The geographical distribution includes India, Arabia, the West Coast of Africa and Brazil.
Life History.—The male has not surely been seen in man so that the pathological condition is entirely connected with the female worm. Almost invariably the female worm, which measures about two feet long by 1/12 inch broad, tends to wander down to the connective tissue structures of the lower extremity. In about 10% of the cases the worm may present elsewhere, as scrotum, back or arms. At the posterior extremity there is a sort of anchoring hook.
With the anterior extremity the worm presses against the overlying skin and causes the formation of a blister-like lesion.
This vesicle later on bursts and, if water is applied to the spot, a delicate tube, the uterus, is extruded and there exude a few drops of a milky fluid, which swarms with the sharp-tailed, striated, sheathless embryos. It is thought that the pouring forth of embryos, when water touches the part, is in order that the embryos may reach the water of a pool through which the infected native may be wading. Once in the water of such a pool, the larvae are swallowed by Cyclops and gaining the body cavity of this little crustacean, they continue to develop for about one month.
During this period there are two ecdyses, the first after about two weeks, when the tail becomes blunt.
When one takes these infected cyclops into the stomach, by drinking water containing them, the cyclops is killed by the gastric juice and the Guinea worm larva breaks out of the dead intermediary host and bores its way through the stomach wall and possibly goes to the tissues about the retroperitoneal region. As a matter of fact we are in ignorance of the exact cycle which goes on, until the fertilized female, with her embryo-distended uterine tube, reaches the lower extremity. A cross section of the female shows the body of the worm to be almost entirely made up of uterus, with an insignificant alimentary canal pressed to one side.
The period of incubation is from 8 to 12 months.
Usually there are no other symptoms than discomfort from the blister and a feeling of heaviness about the affected extremity. At times there may be pain and fever. The parasite may fail to gain exit to the skin surface or die before reaching maturity. In such cases she may become calcified or give rise to abscess formation. The x-ray plate may show a convoluted cord-like structure with frequent breaks in the line.
Treatment.—By douching the point of exit we may cause the uterus to empty itself in about three weeks. At that time we may commence extraction by intermittent traction by winding the worm around a large toothpick or similar object. If undue force is exerted the worm may break off and abscess formation or sloughing result.
Macfie has reported success in treating 23 cases of dracontiasis with tartar emetic. He gave 1 grain intravenously every other day and found that it was not necessary to give more than 6 grains in the course of treatment. The inflammation quickly yielded and the discharge from the sore ceased rapidly.
XXIII. THE SCHISTOSOMIASES
GENERAL CONSIDERATIONS
There is a group of diseases, caused by trematodes of the family Schistosomidae, to which we apply the name schistosomiasis. The Schistosomidae differ from other human flukes (Trematoda) by not being hermaphroditic and by having nonoperculated eggs. From these eggs a ciliated embryo (miracidium) emerges which gains entrance to certain species of molluscs. In this intermediate host the miracidium gives rise to a sporocyst, which latter forms daughter sporocysts. These emerge from the mother cyst and enter the digestive gland of the mollusc and produce cercariae.
These cercariae show an absence of a pharynx and upon the rupturing of the sporocyst are discharged from the mollusc and furnish the infecting stage for penetrating the skin of man or other animal.
There are those who think the entrance is effected through mucous membranes, especially those of the mouth, genitalia and anus and even the nasal mucosa.
It is generally admitted that infection by drinking water, containing the ciliated embryos, is impossible, owing to the rapidity of their destruction by solutions of HCl of similar strength to that of the gastric juice.
Infecting mice with S. japonicum cercariae from snails mashed on the abdominal surface of the mouse, it was found by Suyeyasu that after penetrating the skin the cercariae went to the right heart by way of venous and lymphatic channels. From the pulmonary vessels they penetrate the lungs and go by way of the mediastinum or pleura to the diaphragm which they penetrate and make their way to the abdominal cavity next penetrating the liver and entering the portal vein.
It is probable that the earlier stages of development take place in the portal vein and that having reached maturity the female attaches herself to the male and together they go, by way of the inferior mesenteric vein, to the haemorrhoidal or vesical terminals. The male is in the shape of a narrow leaf, about ½ inch long with a ventrally turned oral sucker and a closely adjacent ventral sucker. The female is a somewhat longer and cylindrical worm almost an inch in length and, like the male, has two suckers. There is a dark brown zig-zag stripe which shows prominently in the posterior part of the female and outlines the blood-filled intestinal tract. When the female applies herself to the ventral surface of the male there is an infolding of the sides of the flattened surface giving the male a cylindrical outline and resulting in the formation of a canal containing the female (gynaecophoric canal).
The males of the flukes which cause the vesical (Schistosoma haematobium) and the rectal (Schistosoma mansoni) involvement are covered externally with small tubercles and have a ventral sucker only slightly larger than the oral one. The Japanese schistosome (Schistosoma japonicum) is slightly smaller, has a smooth surface and shows a prominent pedunculated ventral sucker of much larger size than the oral one.
Both suckers are larger than those of the other species.
The eggs of S. haematobium have a terminal spine and measure from 115 to 175 by 60 microns; those of S. mansoni have a lateral spine and measure from 110 to 125 by 50 microns while those of S. japonicum are devoid of spinous projections and measure about 100 by 70 microns.
Clinically, the three infections differ as will be noted further on.
Looss claims that the two tuberculated species are identical and that the lateral spined egg is the product of an unfertilized female. He has more recently regarded the egg as produced parthenogenetically. Other helminthologists have noted slight anatomical differences as to ovaries and testicles so that the consensus of opinion is that vesical and rectal bilharziases are caused by different species of the genus Schistosoma.
Recently Leiper has found cercariae showing the absence of a pharynx (characteristic of the genus) in a Japanese mollusc. Such molluscs were teased out in water and laboratory bred mice immersed therein. One of these mice was killed a month later and adult schistosomes were found in the portal vessels. Leiper has also found cercariae showing absence of pharynx in four different species of molluscs in Egypt. With such molluscs he was able to infect white rats and other animals. He states that infection with these cercariae from the mollusc host can bring about infection either by way of the mouth or through the skin. Sodium bisulphate in a strength of 1 to 1000 killed these cercariae almost immediately.
It would therefore seem proven that all human schistosome infections take place following cercarial and not miracidial development. As proof that S. haematobium and S. mansoni are different species, Leiper notes that mice infected by molluscs of the genus Bullinus showed schistosomes with terminal spined eggs, the ovary lying in the lower half of the female. The male had four or five large testes. In mice infected by molluscs of the genus Planorbis, the eggs were lateral spined, the ovary was in the anterior half of the body and the male had eight small testicles.
The mollusc host of S. japonicum is Blanfordia nosophora. The shell of this snail is of cornucopia shape.
As these flukes are found in the blood vessels they are often referred to as the blood flukes.
HISTORY
Vesical schistosomiasis has undoubtedly existed in Egypt since ancient periods as vesical calculi are frequent in the mummies of various dynasties. Ruffer has found calcified schistosome ova in the kidney of a mummy.
The French troops suffered greatly from the disease in 1800. It was Bilharz in Cairo, in 1851, who first associated the haematuria with the presence of the parasite and it is from his name that we get the designation bilharziasis or bilharziosis for the disease.
In 1903, Manson found lateral spined eggs in a patient from the West Indies who was suffering from rectal rather than bladder symptoms. In 1907 Sambon, considering the points of difference between the eggs and the involvement of rectum rather than bladder, established a new species, S. mansoni.
In the West Indies, as shown by the reports of Surgeon Holcomb from Porto Rico, rectal bilharziasis is rather common.
For a number of years Japanese physicians had noted the existence of a disease characterized by splenic and hepatic enlargement, ascites and cachexia. In August, 1904, Katsurada discovered ova with a ciliated embryo in the stools of patients with this disease. He found schistosomes in the portal vessels of dogs and cats containing eggs similar to those seen in the human cases. He named this trematode S. japonicum. In November, 1904, Catto discovered the parasite at an autopsy on a Chinaman. In 1910 Lambert, in China, described a disease, which he called urticarial fever, and a short time afterward Houghton established the connection between this disease and the more advanced stages of Japanese schistosomiasis.
PATHOLOGY
The pathological lesions are almost entirely due to the irritation of the eggs with resulting connective tissue increase or ulcerative processes. For some reason these flukes select the inferior mesenteric vein and make their way to the vesical plexus of veins in the case of S. haematobium and to the haemorrhoidal vessels for the other species. At times the ova or worms may be carried over to the systemic veins by way of the channels of anastomosis. In the terminal vessels the female gives off the eggs which penetrate the adjacent mucosa giving rise to inflammatory thickenings and the extrusion of the irritating eggs into the lumen of the bladder or rectum.
In the bladder these terminal spined eggs cause haematuria and form the nucleus for vesical calculi. The mucosa may also show wart-like excrescences. If the eggs are swept back through the portal vessels to the liver an interlobular cirrhosis results which would seem to be due entirely to the irritation of these egg emboli and not to toxic products of the worms themselves. Marked ureteral and kidney lesions may result as complications of cystitis or primarily from irritation by ova. In women the vagina, vulva and cervix uteri may show papillomatous thickenings. Bilharzial lesions of the male urethra are not uncommon and may lead to fibroid thickenings and fistula.
In searching for the flukes at autopsy we should make a longitudinal slit in the portal vein and with a spoon scoop out the blood and search for the parasites in a glass dish.
In the intestinal form of schistosomiasis the rectum may be studded with polypoid tumors which when projecting from the anus may ulcerate and lead to a diagnosis of cancer of the rectum. In sections from these masses great numbers of lateral spined eggs may be found.
The connective tissue increase is in the submucosa. The gut section may also present small abscess-like areas.
Eggs have been found in the appendix as well as in the large intestines and the small intestine has been found involved in one case. In rare instances ova have been found in the lungs, spleen and even in the brain and spinal cord.
By digesting selected tissues in 4% NaOH at 75°C. and centrifuging one may find eggs which otherwise would be overlooked. Statistics from Cairo usually note 30 to 40% of infection in natives but Ferguson employing all methods found 61% infected at autopsies on 600 males. In all forms of schistosomiasis but particularly in the Japanese infection, eosinophilia is pronounced.
In Japanese schistosomiasis the intestines may show thickenings at the site of aggregations of eggs. In the liver a marked interlobular cirrhosis occurs with numerous eggs in the connective tissue increase. Rarely, eggs may lodge in the brain, giving granuloma-like areas. The irritating eggs may also give rise to similar areas in the lungs.
SYMPTOMATOLOGY
Vesical Schistosomiasis or Endemic Haematuria
This form of the disease is chiefly found in Egypt, Syria, Uganda and South Africa. It is caused by S. haematobium and the period of incubation is approximately six months.
The first symptoms are pricking sensations about urethra and slight haematuria which comes on at the end of the act of micturition. Excesses or fatigue are apt to increase the haematuria. The diagnosis is made by finding the ova in the sediment of the centrifuged urine.
Symptoms of cystitis and even pyelitis may follow the early bladder and urethral manifestations. Pain in the back or symptoms suggesting renal colic may be present. Anaemia and physical weakness gradually develop. An important sequel is vesical calculus. It is a question whether the eggs or some other product of the infection form the nucleus of such a stone. Not only can stone be recognized by cystoscopy but rather distinctive are small, glazed yellowish nodules with areas of granulation tissue. Papillomatous growths may also be seen upon cystoscopy.
Perineal fistulae in the male and vaginitis in the female may be noted.
When reinfection does not occur the haematuria tends slowly to disappear but recovery does not usually take place for several years. The vesical schistosome (S. haematobium) often causes pathological changes in the rectum so that a case may show both vesical and rectal symptoms. The rectal schistosome (S. mansoni) does not give rise to vesical trouble.
Rectal Schistosomiasis
While terminal spined eggs may be found in rectal lesions, but usually combined with lateral spined eggs, in countries where the vesical form of the disease exists, yet there are many parts of the world where, with the exclusive existence of an intestinal bilharziasis, only lateral spined eggs are found. The infection resulting from S. mansoni is the sole one in the West Indies, Congo Free State and in North-eastern South America.
The symptoms are usually those of a chronic dysentery with more or less tenesmus and straining. Prolapse is a common result and is the cause of the ulcerations which may cause the disease to be diagnosed as cancer. Cirrhosis of the liver is more apt to occur than in pure vesical schistosomiasis.
Most writers fail to mention other than the later manifestations of rectal bilharziasis, the earlier symptoms being overlooked or attributed to other causes. The same was true of Japanese schistosomiasis in which the initial “urticarial fever” was only recognized as connected with the late manifestations of liver cirrhosis and ascites a few years ago.
In 1916 Lawton noted in a number of Australian soldiers, encamped in Egypt, a fever of about 7 to 10 days’ duration in which the evening rise approximated 103°F. A diarrhoea and abdominal pain accompanied the fever and along with this a cough and patchy consolidation. Most of the cases showed urticaria which lasted from one to seven days. All cases showed a well marked eosinophilia. The diagnosis, but frequently only after prolonged and continued search, was made by the finding of the lateral spined eggs of S. mansoni. The period of incubation in these cases seemed to be from one to three months.
Japanese Schistosomiasis
This is also called Katayama disease and in its early stages urticarial fever or Yangtse fever. It is caused by the nontuberculated species, S. japonicum, which is characterized by the egg without a spine.
Laning, in a study of 7 well-controlled cases, has shown that the disease sets in after two or three days from the time of exposure to infection, by wading through paddy fields or still waters of infected ponds or lakes. The disease occurs in China, Japan and possibly in the Philippine Islands.
The course of the disease may be divided into 3 stages: the 1st, that of urticarial, pulmonary and febrile manifestations, which lasts about a month; the 2d, where ova begin to show in the small mass of bloody mucus which may cap the stool, and finally the 3d stage with cirrhosis of the liver, ascites, cachexia and death.
In the 1st stage we have headache and an evening rise of temperature to about 101°F. or 102°F. Shortly after the onset urticarial lesions, which may be 2 or 3 inches in diameter, may appear and disappear on various parts of the body.
The pulse rate is usually low. Very characteristic and early manifestations are those of the pulmonary involvement. Here oedematous patches may give the signs of crepitation and consolidation to rapidly disappear and reappear in another part of the lungs.
These pulmonary manifestations and the associated fever frequently cause a diagnosis of broncho-pneumonia to be made. A dry hacking cough appears early and with the fever, etc., may make one think of tuberculosis. The urticarial lesions often cause a diagnosis of ptomaine poisoning to be made. The blood examination shows a marked eosinophilia, of from 30 to 60%.
The 2d stage shows more or less intestinal disturbance with at times bloody mucus containing ova. The ova may not be present for long intervals or may never be found. Where reinfection does not take place the patient tends to recover but if exposure to infection be kept up then the 3d stage sets in with rather marked dysenteric manifestations, emaciation, anaemia, ascites, dropsy and a terminal cachexia.
The bladder never seems to be involved in Japanese schistosomiasis. The eggs, however may be carried to the brain and produce symptoms of Jacksonian epilepsy.
LABORATORY DIAGNOSIS
This consists in the search for ova in the centrifuged urine of vesical bilharziasis or in the bloody mucus of the intestinal manifestations of the disease. If one adds water to the urine the ciliated embryo will be noticed to break out of the shell in a few minutes and move about actively as if in search for some host.
The eosinophilia is of great diagnostic value and is usually associated with an increase in the leucocyte count.
Fairley has introduced a complement fixation reaction in diagnosis, using an extract of the livers of infected snails as antigen. The reaction appears early in the infection but disappears in the later stages. It is a group reaction as the livers of Bullinus answer for the S. mansoni serum as well as for the specific S. haematobium serum.
PROPHYLAXIS
Bathing should be allowed only in filtered water, there being an absence of the infecting cercariae in such a supply.
Then, too, if a water which does not contain fresh water snails is stored for three or four days the cercariae which might have been present in the freshly pumped up water will have died out, such free cercariae only surviving for about this period. The gastric juice will destroy cercariae so that it would seem impossible for an infection to occur by the alimentary tract atrium with the exception that cercariae might bore their way through the buccal mucosa as well as through the skin. The sterilization of the urine of cases of vesical bilharziasis and of the faeces in other forms should be carried out where practicable. It is now considered practicable to eradicate carriers of the infection with antimony treatment.
TREATMENT
The most important matter is to avoid places where the infection is known to exist. If one must wade through infected waters the body should be protected by canvas or other closely woven garments.
Of various treatments, having in view the destruction of the worm, such as salvarsan, etc., none seem to have been of any value except antimony.
Robertson has reported relief of symptoms from the administration of 2 grains of thymol dissolved in half a drachm of benzine. The treatment is continued for a few weeks. Others have not had good results from this treatment. Local treatment is necessary in treating the cystitis and prolapse of rectum. Operative procedures are indicated where calculi exist.
The results obtained by treatment with tartrate of antimony during the past three years justify us in considering bilharziasis as a disease which has a specific for its cure. Almost all cases will yield to a course of intravenous injections of from one-half to two grains of the drug, commencing with the smaller dose. The drug should be well diluted (25 to 50 cc. sterile saline). Some use a 1% solution but the higher dilutions are safer from a standpoint of avoiding phlebitis. Intravenous injections are made twice weekly and the total amount of drug given during the course should rarely exceed 25 to 30 grains. For details see under treatment of leishmaniasis.
XXIV. MINOR HELMINTHIC INFECTIONS
PARAGONIMIASIS
General Considerations
This is an infection with a trematode, Paragonimus westermanni (P. ringeri) (Distoma pulmonale). It is rather common in some parts of Japan and Formosa.
Arce has recently reported cases of paragonomiasis in three Peruvians who had been in contact with Japanese immigrants.
In 1880, Baelz found the ova in the sputum of a case of haemoptysis in a Japanese, as did also Manson in a Chinaman. Manson’s case subsequently died and when autopsied showed in his lungs a fluke which was responsible for the eggs seen by Manson. The fluke itself is a little more than ⅓ of an inch (8 mm.) long and is almost round on transverse section, there being, however, some flattening of the ventral surface. The acetabulum is conspicuous and opens just anterior to the middle of the ventral surface.
The branched testicles are posterior to the laterally placed uterus and the genital pore opens below the acetabulum. The branched ovary is opposite the uterus on the other side.
It is rather flesh-like in appearance and is covered with scale-like spines. The flukes are usually found in tunnels in the lungs, the walls of which are thickened connective tissue. These tunnels result from hypertrophy of the bronchioles. There may be also cysts formed from the breaking down of adjacent tunnel walls. In addition to lung infection with this fluke, brain, liver and intestinal infections may be found.
The life history and mode of infection of man, further than the miracidium stage, has been unknown until recently. If the eggs in the sputum are shaken up with water and the water renewed from time to time a ciliated embryo or miracidium develops after a few weeks and, at this time if one presses on a cover-glass covering some of these more mature ova, the miracidium will break through the operculated extremity of the egg and swim about actively in the surrounding water.
Nakagawa has found that the miracidia infest certain fresh water molluscs and become cercariae in this first intermediate host. From this host the cercariae go to certain fresh water crabs and encyst in this second intermediate host, either in the liver or in the gills. In Japan one of these crab hosts, Potamon dehaanii, is eaten both raw and cooked.
Experimental feeding of puppies on infected crabs brought about infection with the lung fluke. It is thought that the fluke, after leaving the cyst, goes through the intestine to the abdominal cavity. Thence it perforates the diaphragm and enters the pleural cavity, finally penetrating the lung to become encysted there. The lung is the favorite site but wandering flukes may invade other tissues and organs even invading the central nervous system.
Besides man, dogs, cats and especially hogs may be infected.
Symptomatology, Diagnosis and Treatment
The case is usually considered as one of chronic bronchitis on account of the occurrence of cough and morning expectoration of a gelatinous sputum which is usually brownish. It is popularly known as endemic haemoptysis for the reason that after violent exertion, or at times without manifest reason, attacks of haemoptysis of varying degrees of severity come on. The signs on percussion are usually insignificant while those on auscultation at the time of haemoptysis are often marked. The symptoms often disappear for months to again reappear.
The course of the disease is very chronic, often lasting many years. As a rule the patient is fairly well nourished although recurring attacks of haemoptysis may bring on a rather marked anaemia. Jacksonian epilepsy has been reported as occurring in paragonomiasis, the ova being found in cysts of the brain. There is some question as to whether some of the reports as to paragonomiasis may not have been connected with infections with Japanese schistosomiasis.
The diagnosis of endemic haemoptysis is readily made by finding the operculated eggs in the more or less sanguinolent sputum. These eggs are of a light yellow color and average 90 × 65 microns. One often sees Charcot-Leyden crystals in the sputum.
As prophylactic measures we should forbid uncooked crabs or crayfish. The sputum should be sterilized.
The treatment is entirely symptomatic.
CLONORCHIOSIS
This is an infection due to a trematode, Clonorchis endemicus (Opisthorchis sinensis). It is also referred to as human liver fluke disease. It is true that the common liver fluke of sheep, Fasciola hepatica, may occur in man but such infections are rare, only 23 cases having been reported. Another liver fluke of ruminants is the lancet fluke, Dicrocoelium lanceatum, but it is also unimportant for man, only 7 cases having been reported.
Clonorchis infections are common in China and Japan, the fluke being about ½ inch long by ⅛ inch wide. There is considerable dispute as to whether we have a pathogenic and nonpathogenic Clonorchis; the name C. endemicus applying to the former and C. sinensis to the latter.
Looss considered the nonpathogenic C. sinensis to be larger (13-19 mm.), to show pigment in its parenchyma and to have breaks in the vitelline glands. C. endemicus was reported as smaller (10 to 13 mm.), and without pigment or breaks in the continuity of the vitellaria.
The eggs of this fluke show slightly concave bending of the sides at the operculated end and are about 30 × 16 microns. These flukes are found within the thickened bile ducts and may be present in great numbers. They may invade the pancreas as well as the liver.
These flukes are found in dogs and cats as well as man.
This fluke is supposed to produce most serious symptoms as indigestion, swelling and tenderness of liver, bloody diarrhoea, ascites, oedema and a fatal cachexia.
The course of the disease is insidious and chronic with periodic improvement.
As a matter of fact, many physicians in China attribute very little pathogenic importance to it. The disease is diagnosed by the presence of the ova in the stools. The source of infection is probably through the eating of uncooked fish.
Kobayashi has examined various molluscs and fish for trematode larvae. He succeeded in infecting nine kittens and two cats by feeding them with certain fresh water fishes whose flesh contained trematode larvae. These fishes were found in districts where human distomiasis was common.
Further experiments by Kobayashi have shown that the larval flukes leave the cyst and start for the biliary passages. When the flukes are very numerous the size is smaller. Maturity is reached in four weeks. This investigator believes that the primary intermediate host is a mollusc as cercariae found in these hosts are very similar to the larval forms found in fish.
He does not consider that there are two species concerned in Clonorchis infections, as he has found variations in continuity of vitellaria in small as well as large flukes. Number of parasites present influences size. Age influences pigment production.
Another human fluke, Opisthorchis felineus, inhabits the gall bladder and bile ducts of man and it is stated that the infection is quite common in Siberia.
It is also a parasite of cats and dogs.
Both Clonorchis and Opisthorchis have the testicles in the posterior end with the uterus anterior. The testicles of Clonorchis are branched (dendritic) while those of Opisthorchis show as two lobes. In Dicrocoelium the lobed testicles are anterior to the uterus, which fills up the posterior end of the fluke.
The mode of infection as well as the life history is not known but is probably connected with the eating of raw fish.
The symptoms are similar to those caused by C. endemicus.
The fluke has two-lobed testicles as against the dendritic one of C. endemicus.
INTESTINAL DISTOMIASIS
The most important intestinal fluke is undoubtedly Fasciolopsis buski. It is now thought that this infection is more common than was previously stated. Goddard states that more than 5% of stools examined in Shaohing, China, show eggs of this parasite. It is a very large fluke with an acetabulum 4 times the diameter of the oral sucker. It is characterized by a very long and prominent cirrus.
F. buski and Fasciola hepatica are much alike in size and outline. The acetabulum of the latter is only 1.6 times the diameter of the oral sucker and the alimentary tract shows branching which is best seen in the cone-shaped projection of its anterior extremity. F. hepatica is a liver fluke rarely found in man.
F. buski is found in China, Assam and India. It is a parasite of hogs as well as man. The eggs measure from 80 to 120 microns, are nearly colorless and have a thin shell with a very small operculum.
The symptoms are chiefly those of a chronic diarrhoea followed by anaemia and wasting. The stool is light yellow in color, exceedingly offensive and does not contain blood. Goddard thinks that they live in the upper part of the small intestines.
The life history is unknown but Goddard states that fresh water snails are much eaten by the people of Shaohing. Nakagawa notes that the eggs of Fasciolopsis hatch in two to three weeks. The miracidia penetrate various species of snails in which the cercariae may encyst and infect pigs eating such snails. The cercariae may also leave the snail and encyst on blades of grass, to later infect an animal feeding on the grass, this latter method of infection resembling that of Fasciola hepatica.
Noc has reported success with treatment with thymol and Goddard with beta-naphthol.
Other intestinal flukes such as Cladorchis watsoni, Gastrodiscus hominis, Heterophyes heterophyes, and Fascioletta ilocana are of less importance. Heterophyes is probably a rather common parasite but owing to its very small size (2 mm.) has been generally overlooked at autopsy.
STRONGYLOIDES STERCORALIS
It was formerly supposed that a chronic form of diarrhoea in Cochin China was due to an infection with the parthenogenetic female of Strongyloides stercoralis. It is now known that the parasite is widely distributed over the tropical and subtropical world and that it rarely gives rise to manifest symptoms although some observers regard it as capable of producing diarrhoea and more or less anaemia.
It seems to be capable of setting up quite an eosinophilia at the time the adult female is penetrating the crypts of Lieberkühn, so that it is probably of pathogenic importance.
The parasitic or intestinal form (also known as Anguillula intestinalis) is represented only by females. These are about 1/12 of an inch (2 mm.) long and reproduce parthenogenetically. They have a pointed, four-lipped mouth, and a filariform oesophagus which extends along the anterior fourth of the body. The uterus contains a row of 8 to 10 elliptical eggs which stand out prominently in the posterior part of the body by reason of being almost as wide as the parent worm.
They usually live deep in the mucosa and the embryos emerge from the ova laid in the mucosa. The embryos escape from the eggs while still in the intestines, so that in the faeces we only find actively motile embryos. The eggs, which are strung out in a chain, never appear in the faeces except during purgation. As they greatly resemble hookworm eggs this is a point of great practical importance.
In fresh faeces we find hookworm eggs and Strongyloides embryos. The embryos are rather common in stools in the tropics. These embryos have pointed tails and are about 250 × 13 microns. They have a double oesophageal bulb. They are about 250 microns when they first emerge but may grow until they approximate 500 microns in the faeces. The mouth cavity of the embryo of the hookworm is about as deep as the diameter of the embryo at the posterior end of the mouth cavity; that of Strongyloides is only about one-half as deep as the diameter. If the temperature is low, below 15°C., these rhabditiform embryos develop into filariform embryos, which form the infecting stage.
It has been demonstrated by Fülleborn that infection of man takes place through the skin. If the temperature is warm, 25° to 35°C., these embryos develop into the free-living form. In this we have males and females, with double oesophageal bulbs, the male about 1/30 of an inch (¾ mm.) long with an incurved tail and 2 spicules and the female about 1/25 inch (1 mm.) long with an attenuated tail. These copulate and we have produced rhabditiform larvae, which later change to filariform ones. At this time the length is about 550 microns. These start up the parasitical generation.
For treatment thymol is usually recommended. Stiles speaks highly of sulphur.
XXV. TABLE OF IMPORTANT ANIMAL PARASITE DISEASES
PROTOZOAL DISEASES
-----------------+--------+----------+-----------+----------------------- Parasite | Defin. | Inter- | Important | Transmission and | host | mediate | reservoir | pathogenicity | | host | of virus | -----------------+--------+----------+-----------+----------------------- Entamoeba |Man. |Not |Man-carrier|Cysts in food or water. histolytica. | | required.| stage | Flies may act as | | | (feces). | carriers. Ingestive. | | | | Amoebic dysentery. -----------------+--------+----------+-----------+----------------------- Balantidium coli.|Man |Not |Man-carrier|Transmission probably | (hogs).| required.| stage | same as for E. | | | (hogs). | histolytica. Found | | | | in those having care | | | | of hogs. Ingestive. | | | | Balantidium dysentery. | | | | Anaemia. -----------------+--------+----------+-----------+----------------------- Lamblia (Giardia)|Man |Not |Man-carrier|Transmission probably intestinalis. | (mice | required.| stage | same as for E. | and | | (mice and | histolytica. Rat | rats). | | rats). | feces on human food | | | | important. Ingestive. | | | | Lamblia dysentery. | | | | Giardiasis. -----------------+--------+----------+-----------+----------------------- Spiroschaudinnia |Louse |Man.(*) |Man |Cyclical development in (Spironema) | (P. | | (blood). | louse. Bite puncture recurrentis, | vesti- | | | contaminated by carteri, etc. | menti).| | | crushed louse. (louse group.) | | | | Relapsing fever. -----------------+--------+----------+-----------+----------------------- Spiroschaudinnia |Tick |Man.(*) |Man |Excretions of tick (Spironema) |(species| | (blood). | contaminating duttoni, novyi. |of | | | tick-bite. Tick (Tick group.) |Ornith- | | | fevers. Relapsing |dorus or| | | fever. |Argas). | | | -----------------+--------+----------+-----------+----------------------- Treponema |Man. |Not |Man. |T. pallidum. Usually (pallidum and | | required.| | venereal. Syphilis. pertenue). | | | | T. pertenue. Flies or | | | | contact. Yaws. -----------------+--------+----------+-----------+----------------------- Leptospira |Man |Not |Rat. |Common infection of ictero- | (rat). | required.| | rats. Present in haemorrhagiae. | | | | blood. Excreted in | | | | urine. Ingestion. | | | | Weil’s disease. -----------------+--------+----------+-----------+----------------------- Leptospira |Mosquito|Man. |Man |Cyclical development icteroides. |(Stego- | | (blood). | in mosquito--12 |myia | | | days. Inoculative. |calopus)| | | Yellow fever. -----------------+--------+----------+-----------+-----------------------
PROTOZOAL DISEASES (Continued)
-----------------+--------+----------+-----------+----------------------- Parasite | Defin. | Inter- |Important | Transmission and | host | mediate |reservoir | pathogenicity | | host |of virus | -----------------+--------+----------+-----------+----------------------- Leptospira |Man |Not |Rat. |Man inoculated by morsus-muris. | (rat). | required.| | bite of infected rat. | | | | Rat bite fever. -----------------+--------+----------+-----------+----------------------- Trypanosoma |Fly |Man. |Man--game |Cyclical development gambiense |(Glossina| | animals? | in tsetse fly. and rhodesiense.|species)| | (blood). | Inoculative. Sleeping | | | | sickness. -----------------+--------+----------+-----------+----------------------- Schizotrypanum |Lamus |Man. |Man. |Cyclical development cruzi. |megistus| | | in bug. Inoculative. | | | | Brazilian | | | | trypanosomiasis. -----------------+--------+----------+-----------+----------------------- Leishmania |Not |Man. |Man. |L. donovani—Bed bug? (donovani, | surely | | | kala-azar. L. infantum infantum, and | known. | | | —dog flea? infantile tropica). | | | | leishmaniasis. L. | | | | tropicum--biting | | | | insects? Oriental | | | | sore; American | | | | leishmaniasis. -----------------+--------+----------+-----------+----------------------- Plasmodium |Mosquito|Man (with |Man (blood)|Cyclical development malariae, |(Anoph- | schiz- | (with | in mosquito—12 vivax and | eline | onts). | gametes). | days. Inoculative. falciparum. |species)| | | Malaria. -----------------+--------+----------+-----------+----------------------- Rickettsia |Man. |Louse (P. |Man (blood)|Cyclical development in prowazeki. | | vesti- | | louse. Bite puncture | | menti). | | inoculated by | | | | louse feces. Typhus | | | | fever. -----------------+--------+----------+-----------+----------------------- Dermacentroxenus |Man |Tick |Goats and |Excretions of tick rickettsi. |(goats, |(Dermacen-| rodents. | contaminating |rodents,|tor ander-| | tick-bite. Rocky | etc.). |soni). D. | | Mountain fever. | | venustus.| | -----------------+--------+----------+-----------+----------------------- Bartonella |Man. |Unknown. |Man (blood)|Transmission unknown. bacilliformis. | | | | Species of | | | | Phlebotomus suggested. | | | | Oroya fever. -----------------+--------+----------+-----------+-----------------------
NOTE.—(*) Some authorities give man as definitive host of Spiroschaudinnia (Spironema). Diseases often classified as filterable virus ones of protozoal affinity are (1) Dengue. Cause unknown. Transmitted by Stegomyia species. (2) Pappataci fever. Cause unknown. Transmitted by Phlebotomus species. Other protozoal diseases are (1) Tsutsugamushi. Probably a protozoan. Transmitted by Kedani mite. (2) Trench fever. Probably Rickettsia. Transmitted by louse.
HELMINTHIC DISEASES—TREMATODES
-------------+--------+-------------+-----------+----------------------- Parasite | Defin. |Intermediate |Important | Transmission and | host | host |reservoir | pathogenicity | | |of virus | -------------+--------+-------------+-----------+----------------------- Clonorchis |Man |1st, snail |Man. |Not definitely known. sinensis. | (cats, | (Melania | | Eating raw fish. |dogs and| libertina)? | | Ingestive. Human liver | hogs). | and 2d, fish| | fluke disease. -------------+--------+-------------+-----------+----------------------- Opisthorchis |Man |1st, mollusc.|Cats and |Man infected by eating felineus. | (cats | 2d, fish. | dogs. | raw fish. Ingestive. | and | | | Liver fluke | dogs). | | | disease. -------------+--------+-------------+-----------+----------------------- Fasciolopsis |Man |Possibly 1st,|Hog. |Not definitely known. buski. | (pig). | mollusc. | | Intestinal | | Cercariae | | Distomiasis. | | encyst on | | | | grass. | | -------------+--------+-------------+-----------+----------------------- Heterophyes |Man |1st, probably|Dogs and |Not definitely known. heterophyes.| (dogs | mollusc. | cats. | Intestinal Distomiasis. | and | 2d, probably| | | cats). | fish. | | -------------+--------+-------------+-----------+----------------------- Paragonimus |Man |1st, snail. |Cats, dogs |Eating raw crabs ringeri. | (dogs, | 2d, crab. | and hogs. | containing cercariae. |cats and| | | Ingestive. Lung fluke | hogs). | | | disease. -------------+--------+-------------+-----------+----------------------- Schistosoma |Man. |Snail |Man |Bathing or drinking haematobium.| | (Bullinus). | (urine). | water containing | | | | cercariae. Penetrative. | | | | Vesical bilharziasis. -------------+--------+-------------+-----------+----------------------- Schistosoma |Man. |Snail |Man (feces)|Bathing or drinking mansoni. | | (Planorbis).| | water containing | | | | cercariae. Penetrative. | | | | Rectal bilharziasis. -------------+--------+-------------+-----------+----------------------- Schistosoma |Man. |Snail |Man (feces)|Bathing or drinking japonicum. | |(Blanifordia)| domesticated | water containing | | | animals). | cercariae. Penetrative. | | | | Katayama disease. -------------+--------+-------------+-----------+-----------------------
NOTE.—Rare trematodes of man are (1) Fasciola hepatica. Chiefly disease of sheep. Cercariae from snail (Limnea) encyst on grass. (2) Dicrocoelium lanceatum. Chiefly disease of cattle. (3) Heterophyes nocens. A very small intestinal fluke of man. (4) Metagonimus yokogawai. Another very small intestinal fluke of man. Intermediate hosts: mollusc and gold fish. (5) Echinostoma ilocanum. A rare intestinal fluke of the Philippines. (6) Two genera of Paramphistomidae—Cladorchis and Gastrodiscus. Intestinal flukes.
HELMINTHIC DISEASES (Continued). NEMATODES
-------------+--------+-------------+-----------+------------------------ Parasite | Defin. |Intermediate |Important | Transmission and | host | host |reservoir | pathogenicity | | |of virus | -------------+--------+-------------+-----------+------------------------ Filaria |Man. |Mosquito |Man |Indirect in mosquito. bancrofti. | | (various | infected | Mature larva | | species). | (blood). | penetrates skin. | | | | Elephantiasis, etc. -------------+--------+-------------+-----------+------------------------ Loa loa |Man. |Fly. Species |Man |Probably indirect (F. loa). | | of Chrysops | infected | (cyclical) in Chrysops. | | (mangrove | (blood). | Probably inoculative. | | flies). | | Ocular filariasis, etc. -------------+--------+-------------+-----------+------------------------ Acantho- |Man. |Not |Man |Transmission by cheilonema | | definitely | infected | mosquitoes and ticks perstans (F.| | known. | (blood). | suggested. No perstans). | | | | pathogenicity. -------------+--------+-------------+-----------+------------------------ Dracunculus |Man. |Species of |Man |Larvae enter cyclops. medinensis. | | cyclops. | infected | Infected cyclops in | | | (subcuta- | drinking water. | | | neous | Ingestive. Guinea | | | tissue). | worm infection. -------------+--------+-------------+-----------+------------------------ Onchocerca |Man. |Not |Man |Possibly Glossina. volvulus (F.| | definitely | (blood?). | Subcutaneous tumor volvulus). | | known. | | and lymphangitis. -------------+--------+-------------+-----------+------------------------ Strongyloides|Man. |Not required.|Man (feces)|Parasitic filariform stercoralis.| | | | larva penetrates skin. | | | | Pathogenicity doubtful. -------------+--------+-------------+-----------+------------------------ Necator |Man. |Not required.|Man (feces)|Encysted strongyloid americanus | | | | larvae penetrate skin. and | | | | Ancylostomiasis. Ancylostoma | | | | duodenale. | | | | -------------+--------+-------------+-----------+------------------------ Trichinella |Man (rat|Hog (man and |Hog |Encysted larva in raw spiralis. | and | rat). | (muscle). | or insufficiently | hog). | | | cooked pork. Ingestive. | | | | Trichinosis. -------------+--------+-------------+-----------+------------------------
NOTE.—Ascaris, Trichuris and Oxyuris do not require intermediate host. With Ascaris and Trichuris, larva gradually develops in egg passed in faeces. Infection by ingestion of embryo-containing eggs. Embryo-containing eggs contaminate fingers from crushing female Oxyuris in perineal region.
HELMINTHIC DISEASES. CESTODES
-------------+--------+-------------+-----------+----------------------- Parasite | Defin. |Intermediate |Important | Transmission and | host | host |reservoir | pathogenicity | | |of virus | -------------+--------+-------------+-----------+----------------------- Dibothrio- |Man. |1st, cyclops?|Man |Eating raw fish cephalus | | 2d, fish. | (feces), | containing pleocercoid latus. | | | dog and | larvae. Broad Russian | | | cats. | tapeworm disease. -------------+--------+-------------+-----------+----------------------- Hymenolepis |Man. |Not required.|Children |Man intermediate and nana. | | | (feces). | definitive host. | | | | Ingestive. Dwarf | | | | tapeworm disease. -------------+--------+-------------+-----------+----------------------- Taenia |Man. |Cattle (ox). |Man (feces)|Eating insufficiently saginata. | | | | cooked beef containing | | | | cysticerci. Ingestive. | | | | Beef tapeworm | | | | disease. -------------+--------+-------------+-----------+----------------------- Taenia |Man. |Hog. |Man (feces)|Eating insufficiently solium. | | | | cooked pork containing | | | | cysticerci. Ingestion. | | | | Pork tapeworm | | | | disease. -------------+--------+-------------+-----------+----------------------- Taenia |Dog. |Man, sheep |Dog (feces)|Dogs infected at echinococcus.| | and hogs. | | abattoir. Hydatid | | | | disease. -------------+--------+-------------+-----------+-----------------------
NOTE.—Rare cestodes of man are (1) Dipylidium caninum. A parasite of the dog with louse or flea as intermediate host. (2) Hymenolepis diminuta. A parasite of rats. Intermediate host in insects. (3) Species of Davainea. Intermediate host possibly cockroach. These cestodes are probably accidental parasites of man.
ARTHROPODAN DISEASES
--------------+---------------------------+------------------------------ Parasite | Life history | Disease and manifestations | | and remarks --------------+---------------------------+------------------------------ Linguatula |Adult in nasal cavity of |Porocephaliasis. Man may serrata | dogs, etc. Eggs in nasal | harbor adult or larva. Larvae (Lingua- | mucus contaminate grass. | usually in lungs or liver tulidae). | Rabbits, cattle infected. | and do not seem to cause | Larvae in liver, lungs. | symptoms. --------------+---------------------------+------------------------------ Porocephalus |Adults in lungs of snakes. |Porocephaliasis. Larvae wander armillatus | Eggs contaminate water | in abdominal cavity or lungs (Lingua- | or food. Larvae in liver, | in which latter they produce tulidae). | lungs, etc., of lions, | a chronic bronchitis which | monkeys, man, etc. | may resemble phthisis. --------------+---------------------------+------------------------------ Demodex |All stages passed within |Demodectic acariasis. Causes a folliculorum | hair follicles or | resistant itch in dogs. In (Demodicidae).| sebaceous cysts especially| man, may invade eyelids or | about nose. Adult may | meibomian glands, and has | wander. | been reported as causing | | various forms of dermatitis. --------------+---------------------------+------------------------------ Sarcoptes |Female lives in burrow of |Scabies. Burrows show as scabei | skin giving off eggs which| blackish lines, especially (Sarcoptidae).| hatch into larvae. | between fingers, flexor | | surfaces of arms and penis. | | Itching worse at night. --------------+---------------------------+------------------------------ Pediculoides |Female lives on wheat straw|Grain itch. The mites leave ventricosus | worm or grain moth. Larval| wheat straw or grain and (Tarson- | mites develop inside | attack harvesters or those emidae). | mother. | sleeping on straw mattresses. | | Attack upper trunk, neck and | | arms. Erythematous or | | vesicular eruption with | | constitutional symptoms. ---------------+--------------------------+------------------------------ Microtrombidium|Adults live in fields or |Autumnal erythema. The larval pusillum | woods. The larval mite | mites known as red bug or (Trombidoidae).| lives on grasshoppers or | jigger attack man causing a | small rodents. | severe itch. ---------------+--------------------------+------------------------------ Dermanyssus |Mites live in chicken |Poultryman’s itch. The mites gallinae | houses and feed on fowls. | attack man producing (Gamasidae). | | eczematous dermatitis on | | backs of hands and forearms. --------------+---------------------------+------------------------------ Dermacentor |Adults live on cattle, |Tick paralysis. The bite of venustus | sheep, etc. May bite man. |this tick or Ixodes holocyclus (Ixodidae). | | may produce paralysis in | | sheep. An ascending type of | | paralysis due to tick bites | | has been several times noted | | in man, chiefly in children. --------------+---------------------------+------------------------------ Pediculus |Adults live on clothing or |Pediculosis—Phthiriasis. humanus | hair and feed on man. | Produce skin irritation with (Insecta, | | later on pigmentation Pediculidae).| | (Vagabondismus). --------------+---------------------------+------------------------------ Dermatophilus |Impregnated female |Sandflea or chigoe penetrans. | penetrates skin of man or | infestation. Site of penetr- (Sarco- | animals, especially toes | ation shows as black spot psyllidae). | and feet. | with whitish induration | | surrounding it. Apt to form | | ulcers. --------------+---------------------------+------------------------------
ARTHROPODAN DISEASES (Continued)
--------------+---------------------------+------------------------------ Parasite | Life history | Disease and manifestations | | and remarks --------------+---------------------------+------------------------------ Dermatobia |Eggs of fly become attached|A cutaneous myiasis. Larva at cyaniventris | to mosquitoes or ticks. | first club shaped (ver (Oestridae: | These latter bite man and | macaque), later worm shaped Bot Flies). | larva penetrates skin. | (torcel). Larva causes a | | swelling with black opening. | | May invade eye. --------------+---------------------------+------------------------------ Hypoderma |Larvae of this or other |Creeping eruption. Larva lineata | flies burrow under skin. | migrans. The burrows make (Oestridae). | | zig-zag lines on face or | | soles of feet. Causes | | itching. --------------+---------------------------+------------------------------ Chrysomyia |Fly deposits eggs in |Screw worm infection. Nasal macellaria, | nostrils. Larvae wander to| myiasis. Larvae in their and C. dux | nasal sinuses. May invade | wandering destroy tissues of Muscidae). | aural canal. | nasal cavities, or of ear, Oestrus ovis | | and may cause death. May (Oestridae). | | infest wounds or vagina. C. | | macellaria causes American | | nasal myiasis, C. dux causes | | Indian nasal myiasis and O. | | ovis causes African nasal | | myiasis. --------------+---------------------------+------------------------------ Ochromyia |An African fly, which |Larvae bore under skin, (Cordylobia) | deposits eggs on children | causing boil-like lesions anthropophaga| and animals. | with central opening. Larvae (Muscidae). | | mature in two weeks. --------------+---------------------------+------------------------------ Auchmeromyia |An African fly deposits |Congo floor maggot. The bite luteola | eggs on floors of native | is not painful. (Muscidae). | huts. Larvae bite man. | --------------+---------------------------+------------------------------ Calliphora |Blow and bluebottle flies, |Larvae may be cause of obscure vomitoria | depositing eggs on tainted| abdominal conditions; may be and Lucilia | meats. Larvae may be found| found in nasal cavities, caesar and L.| in feces. | causing serious symptoms, or serricata | | in ear. (Muscidae). | | --------------+---------------------------+------------------------------ Musca |Eggs presumably deposited |Larvae have been found in male domestica | near genitalia or ear. | urethra and in the ear. (Muscidae). | | --------------+---------------------------+------------------------------ Sarcophaga |Viviparous. Larvae are |Larvae gain access to wounds, carnaria | deposited on decaying | nasal cavities, etc., at (Sarcoph- | flesh (wounds, orifices | times causing death. Commonly agidae). | of body). | found in intestinal myiases. | | May occur in vagina. --------------+---------------------------+------------------------------ Anthomyia |Larvae deposited in body |Occasionally reported as found pluvialis | orifices. | in ear. (Anthomyidae).| | --------------+---------------------------+------------------------------ Fannia |Eggs deposited near |Symptoms of urinary irritation canicularis | external genitalia and | or obstruction. Has been (Anthomyidae).| larva penetrates urethra. | found in gastro-intestinal | | tract. --------------+---------------------------+------------------------------
SECTION V
INFECTIOUS GRANULOMATA OF THE TROPICS
XXVI. YAWS OR FRAMBOESIA
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—Some authorities think that a disease described by the Arabian physicians of the 10th century was yaws, but the first description of what was undoubtedly yaws was that of Oviedo, who in the 16th century described such an affection as existing in the West Indies. Bontius, later on, noted the existence of the disease in the East Indies as well as in the West Indies.
It is known that yaws often occurred in epidemic form on board the slave ships and it is thought that this disease may have been an African importation into the new world.
=Geographical Distribution.=—Yaws is essentially a disease of tropical regions.
In Africa it is very prevalent in the equatorial region, especially in the Congo Free State. It is also found more rarely in Tripoli and Algiers and to a less extent in the Sudan region. It is common in the West Indies and tropical America.
In Asia it is very prevalent in the Malay Peninsula, Siam, the East Indian Islands and in the Philippines. It does not exist in Japan. In many of the islands of the Pacific it is exceedingly prevalent, particularly in Samoa. It is also present in Northern Australia.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—In view of the fact that many great authorities, especially J. Hutchinson, insisted upon the syphilitic nature of yaws it was a matter of great interest when Castellani, in 1905, discovered the causative organism which is characterized by the same sharp-cut, corkscrew spirals that are noted with the syphilitic spirochaete discovered by Schaudinn in the same year. Treponema pertenue is found in the epidermis of the yaws granuloma and has been demonstrated in lymphatic glands and spleen. Although it has not been demonstrated in the blood, through microscopical examination, it must exist there as monkeys infected with the blood of yaws patients develop the lesions of yaws in which the spirochaetes are present. Another name for the organism is Spirochaeta pallidula; this however is only a synonym.
Inoculation experiments as well as clinical manifestations show yaws and syphilis to be distinct. Thus Charlouis, in 1881, inoculated a native suffering from typical yaws wistations of syphilis followed. There have been many instances of the development of yaws, naturally and by inoculation, in those affected with syphilis. Nichols has shown that a rabbit which had been infected intratesticularly with T. pallidum and then cured by salvarsan did not show immunity to T. pertenue when the latter was used to infect the testicle.
In the monkey inoculation over the eyebrow gives a flat dry and scaly lesion with syphilitic material while yaws inoculation gives a softer, more oedematous one.
Levaditi and Nattan Larrier have noted that monkeys which had been inoculated with syphilis were immune to yaws inoculation but yaws monkeys could be infected with syphilis, thus indicating that yaws was a mild form of syphilis. In Guam, it has recently been shown that 68% of cases of gangosa, a disease supposed to be a tertiary form of yaws, give a positive luetin reaction. This would indicate a close relationship between yaws and syphilis.
Salvarsan is more specific for yaws than it is for syphilis and the percentage of positive Wassermann tests is as great in yaws as in syphilis.
Notwithstanding the above points, which would indicate a close relationship, all authorities are now agreed that clinical and pathological evidence show the two diseases to be separate entities.
=Epidemiology.=—Charlouis inoculated 32 Chinese prisoners with scrapings from yaws lesions. The disease developed in 28 of them, first showing itself at the site of inoculation.
Paulet inoculated 14 negroes with yaws material and after a period of incubation of from twelve to twenty days a primary lesion appeared, to be followed by the generalized eruption. In naturally acquired yaws the period of incubation is from three to six weeks. These experiments are in line with the known fact that any skin abrasion which comes in contact with a yaws lesion becomes infected, as when the mother nurses an infant with lesions on its face and develops a yaws lesion at the site of some fissure about the nipple.
Yaws shows a striking limitation to the tropics and in a disease so communicable by direct contact it seems remarkable that it does not spread from the occasional case introduced into temperate regions. In the tropical world it seems limited to low level areas. Another feature of yaws epidemiology is the vastly greater susceptibility of colored races, even those of mixed white blood showing a certain degree of immunity.
All evidence is against a congenital form of yaws.
In particular are flies important factors in the transmission of the disease, transferring the secretions from yaws lesions to abrasions or ulcers on the skin of healthy persons.
The greater the attention to personal hygiene the less probable is the spread of yaws, so that Europeans are rarely infected while the disease may be prevalent in the native population.
In countries where it is prevalent it is chiefly a disease of children, the adults possessing immunity as the result of attacks in childhood.
PATHOLOGY
The primary yaws lesion is histologically the same as the lesions of the generalized eruption of the second stage. In these lesions we fail to find the endothelial proliferations and perivascular round cell infiltrations so characteristic of syphilis. There is great thickening of the interpapillary pegs of the epidermis which dip down deeply into the corium. Areas are noted in the epithelium containing swollen degenerated epithelial cells, polymorphonuclears and granular débris. There is marked oedema in the corium with dilatation of the blood vessels and lymphatics.
There is less oedema of the corium in yaws than in a syphilitic condyloma thus accounting for the greater dryness of the former. The main point in the pathology of a yaws lesion is the predominating involvement of the epidermis and the comparatively slight change in the corium.
In a Levaditi-stained specimen the spirochaetes are found in the epidermal layers instead of in the corium as with syphilis.
The visceral organs and central nervous system are not affected although Harper has reported cases of tabes and general paresis in Fijians following yaws. He excludes syphilis.
SYMPTOMATOLOGY
It is usual to consider the clinical course of yaws as exhibiting two stages, the primary one, which comes on from 2 to 5 weeks after introduction of the virus and is characterized by a papular initial lesion, which later shows the fungoid appearance of a typical yaws tubercle, and the secondary stage in which yaws lesions similar to the initial one develop as a generalized eruption.
Some authorities recognize a tertiary stage in which gumma-like nodules, with subsequent ulceration, appear. There is much evidence to indicate that a destructive ulceration of the nasopharyngeal region, in natives of Guam, is a tertiary manifestation of yaws.
The Primary Stage.—During a period of incubation, averaging three weeks, vague digestive troubles, nocturnal headache, joint pains and an irregular fever may be noted which often abate upon the appearance of the initial papule at the site of inoculation. There may be enlargement and tenderness of the lymphatic glands about the time of the appearance of the eruption. This initial lesion may be single or there may be several papules grouped together. In some cases it may be impossible to get any history of a primary lesion or it may have been overlooked. The primary lesion is almost invariably extra-genital and it has the same appearance as the lesions of the secondary stage, thus differing from syphilis.
The yaws lesion, whether primary or secondary, starts as a papule which in a few days enlarges to the size of a small pea. It is conical and surrounded by an inflammatory areola. At this time the thickened epidermis begins to crack and a yellowish sero-purulent fluid exudes from the underlying fungoid base. They bleed easily but are not painful. It is this fungoid yellowish or yellowish-red tubercle which has been thought to resemble a raspberry, hence the name framboesia. French authors liken it to a fig which has been turned inside out. The moist or crusting surface soon shows an underlying ulcer, which may dry up leaving a pigmented spot or become exuberant and appear as a mass of fungating granulations, 1 to 2 inches in diameter. Such lesions are given the name “mother yaw.”
The Secondary Stage.—In from six weeks to three months after the appearance of the initial lesion, which may have dried up and left only a scar, or which more commonly is still present, there again set in malaise, headache and joint pains with an irregular inconstant fever.
The secondary eruption is made up of lesions having the same character and course as the primary yaws tubercle. In the general eruption, the papules appear frequently in the region of the junction of skin and mucous membrane as about mouth, nose and anus. In such regions they may become very moist and resemble the mucous patches of syphilis.
Besides their location on face and about the perineal region they are numerous on neck, arms, legs, and buttocks. They are rare on the trunk and scalp.
In their ordinary locations the yaws tubercles are not painful unless pressed firmly but when located on the palms of the hands or soles of the feet the thick skin of these regions exerts pressure so that in such situations the lesions are painful.
In this stage yaws does not involve mucous membranes or affect the viscera.
The secondary stage lasts from 3 or 4 months to 2 or 3 years, the yaws tubercles coming out in successive crops in long standing cases.
The Tertiary Stage.—Daniels noted in the Fiji Islands destructive lesions of the naso-pharyngeal region which he thought might be associated with a preceding yaws attack. He noted cutaneous lesions which resembled lupus vulgaris. Boissiere has noted not only the nasopharyngeal lesions and lupus-vulgaris-like ones but also tibial involvement, joint swellings and dactylitis.
Numa Rat describes various tertiary manifestations. There may be subcutaneous nodules about ankle or leg which soften and may produce bone lesions and deformities. He notes destructive lesions of nares, pharynx and palate which may set in years after an attack of yaws. His description of the process starting as an ozoena or sore throat followed by destruction of the uvula, velum palati and septum nasi is much like gangosa. Howard has noted the greater frequency of destructive lesions of the nasopharynx in those parts of Africa where yaws is prevalent than in parts where syphilis prevails.
According to Castellani the characteristic lesions of tertiary yaws are gummatous nodules and deep ulcerations. Such ulcerations may give rise to contractures.
In Guam the view now prevails that the condition known as gangosa is a form of tertiary yaws.
Other than a moderate anaemia there is very little in the blood of yaws which differs from the normal.
Peculiar Types of Yaws.—When yaws tubercles develop in the palms of the hands or soles of the feet we have a very painful and incapacitating condition resulting. The pressure of the thick unyielding epidermis on the tubercles beneath gives rise to marked pain, thus differing from tubercles on other parts of the body. Eventually these tubercles break through and the affected sole may have a worm-eaten appearance. The name “crab yaws” is a common one for such a condition involving the soles of the feet and is so-called from the difficulty in walking which has a resemblance to the locomotion of a crab. In some cases the yaws tubercles adjoin one another to form a circle enclosing unaffected skin. Such an arrangement of lesions is often described under the name of “ringworm yaws.”
DIAGNOSIS
=Clinical Diagnosis.=—Bromide eruptions may greatly resemble yaws but the history of the taking of the drug and the effect upon withdrawal should differentiate.
Syphilis and Yaws.—Degorce gives a very complete table of the points of difference between syphilis and yaws, some of the more important of which are the following:
YAWS
1. Primary lesion of soft consistency, or very little infiltrated, with granulating or pimply surface, situated almost invariably extragenitally, resembling the secondary lesions. Lymphadenitis not marked.
2. Roseola resembling that of syphilis but rarer.
3. Secondary cutaneous lesions at first in the form of conical elevations of a light red color, not infiltrated at base, appearing in close groups. The lesions are similar to those of syphilis, namely, on the scalp in the form of encrusted papules; on thin-skinned regions in the form of ulcerating papules, and in the case of the palm of the hands and plantar surface of the feet, in the form of simple papules.
4. Circinate lesions with the edges more raised than in syphilis, covered with yellow crusts.
5. On the face lesions of the same type, but more striking and with irregular projections.
6. Cutaneous lesions do not itch.
7. Perionychia similar to that of syphilis, but occasionally giving rise to pimply lesions.
8. Alopecia has not been described.
9. Lesions in the buccal and pharyngeal mucosa often absent. No erythema. No typical mucous patches. Sometimes fissures at the angles of the mouth. The typical lesions are raised, pure white and occasionally covered with intact epithelium.
10. Lesions with prominent edges or even pustular with yellowish crusts, occasionally also ulcerations resembling mucous patches.
11. Similar condylomata, but larger and more raised.
SYPHILIS
1. Primary lesion infiltrated and indurated, with flat and smooth surface, ordinarily situated on the genital organs; often accompanied by abundant lymphadenitis. Phagedenic processes frequent.
2. Roseola present.
3. Secondary cutaneous lesions papular from the first, dark red, infiltrated and fairly regularly scattered.
4. Circinate lesions with pink edges, slightly raised, with fine scales.
5. Seborrheic syphilides on the face.
6. Cutaneous lesions do not itch.
7. Perionychia present.
8. In syphilis, alopecia rather the exception.
9. Lesions in the buccal and pharyngeal mucosa are not numerous and are slight in degree. Erythema of the soft palate and pharynx occurs. Mucous patches. Ulcers of the lips and at the angles of the mouth.
10. In the glans, prepuce or vulva, the lesions are more or less typical mucous patches.
11. Moist condylomata at the margin of the anus.
The authorities generally discuss extensively the points of distinction between yaws and syphilis. This is probably more connected with possible relationship than practical importance in diagnosis.
=Laboratory Diagnosis.=—The staining of the juice from yaws tubercles by the India ink method or with Giemsa’s stain is the usual procedure.
Baermann gives the percentage of positive Wassermann reactions in untreated, clinically positive cases, as 80 to 100%; in treated cases, 50%, and in the latent ones as from 35 to 40%. In an examination of the serum of 281 cases of gangosa, Halton obtained 37.3% positive Wassermann reactions. Kerr found that 73.8% of 2,429 natives of Guam had had yaws, usually in childhood.
Among other diseases which may be confused with yaws, particularly as regards the nasopharyngeal ulcerations of tertiary yaws, may be mentioned American cutaneous leishmaniasis. The differentiation rests in finding Leishmania tropica in such lesions.
Sections from a yaws tubercle treated and sectioned according to Levaditi’s method show the treponemata in the region of the thickened interpapillary pegs of the epidermis.
PROGNOSIS
This is almost entirely favorable as regards danger to life. The death rate is approximately ½ of 1% and such fatalities generally occur in young children in whom secondary infections develop on the site of the ulcerating yaws lesions.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—Daniels thinks the frequency of infection about the angles of the mouth, which frequently show fissures, is explained by the exchange of particles of food or other substances by children, thus transferring the infection.
Of course care should be taken to prevent articles of clothing contaminated with yaws discharges from acting as infecting agents.
The main point in prophylaxis is to prevent flies from having access to abrasions on the skin, so that all cuts or sores should be protected by dressings. The sound skin is a barrier to infection.
=Treatment.=—It can certainly be stated that in salvarsan we have an absolute specific for yaws, the results which obtain in a few days being almost miraculous when one considers the protracted normal course of the disease.
The drug is given intravenously although neosalvarsan intramuscularly is more convenient for those not prepared to give intravenous injections.
The methods of administration are exactly as for the treatment of syphilis. The drug gives best results when used early in the course of the disease.
Doses of 0.4 gram of salvarsan usually suffice and frequently one dose effects a cure. The dose for women, children and thin individuals should be less than for strong adult men. Atoxyl does not seem to be effective in yaws. In other words the methods of treatment are the same for the two treponemata, except that the effect of salvarsan may be termed specific for yaws and less so for syphilis. Bergen found that about 4% of cases treated with salvarsan or neosalvarsan relapsed. The average time to effect a cure was eleven days.
Many of the older writers have reported the value of mercury in the treatment of yaws but the present view is that this drug has very little if any place in the therapy of the disease. Potassium iodide does seem to be a very useful drug in the absence of opportunity for obtaining some arsphenamine product. Where the specific remedy cannot be secured the next best treatment is Castellani’s yaws mixture. The formula for the preparation is the following:
Tartar emetic one grain (0.06 gm.) Potassium iodide twenty grains (1.3 gms.) Sodium salicylate ten grains (0.6 gm.) Sodium bicarbonate fifteen grains (1 gm.) Chloroform water and syrup one ounce (30 cc.)
The above is a single dose and it is given well diluted about three times daily. This treatment is continued for about a week and after an interval of another week is resumed according to the response to such treatment. In children between seven and fifteen years the dose is reduced one-half and for younger children correspondingly. It would seem well to start treatment with a smaller dosage than the standard one, being guided by the ability of the patient to stand an increase in the dose of the drugs.
For local treatment use antiseptic dusting powders as iodoform or boric acid.
XXVII. GANGOSA
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—It is known that in 1828 a Spanish Commission, investigating the diseases of the Ladrone Islands, reported the existence, in those islands, of a disease which was called gangosa, by reason of the muffled character of the voice, the Spanish word gangosa meaning muffled voice. The Commission recommended that cases of this disease, as well as those with leprosy, be isolated, thus showing that the disease was differentiated from leprosy at that time.
Daniels, who studied similar naso-pharyngeal lesions in Fiji, considered the disease as a sequel of yaws and stated that if it were not a stage of yaws it was probably a separate and distinct disease. Leys, who studied gangosa in Guam, in 1904, gave it the name rhino-pharyngitis mutilans and described it as a disease sui generis.
=Geographical Distribution.=—The disease is very prevalent in Guam, and is also present in other islands of the Caroline group. It exists in Fiji and many cases have been reported by Numa Rat from the island of Dominica, in the West Indies. Cases have also been reported from the Philippines and Ceylon.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The two most prominent views as to its etiology are that it is a sequel of either yaws or syphilis. The fact that gangosa responds to antisyphilitic treatment is no proof as to its luetic origin because yaws yields equally well to such remedies.
Gangosa cases also give a considerable percentage of positive Wassermann reactions, 105 positives in 281 cases. Halton who made these tests found 100% positive reactions in cases of yaws and 46% of positives in those who had had yaws several years previously.
The main points against the syphilitic nature of the disease are absence of either congenital or acquired syphilis among the natives of Guam. There is an absence of Hutchinson’s teeth and interstitial keratitis. Leys states that neither primary nor secondary syphilis had been seen in a native of Guam during a year in which a very large number, including several prostitutes, had been treated. Recently a positive luetin reaction has been obtained in 253 out of 369 cases of gangosa, of which 143 were papular type reactions, 65 pustular and 45 torpid reactions (taking ten days or more for the reaction to manifest itself). The syphilitic and yaws antigens seem to be reciprocal so that these tests do not throw out yaws. The great stumbling block of the advocates of the luetic etiology has been to show the presence of syphilis among the people of Guam. Under tropical ulcer it will be noted that Jeanselme failed to find the eye or teeth signs of congenital syphilis among natives of Indo-China with the disease.
Kerr, who has been an advocate of the yaws etiology, has shown that of 315 cases of gangosa, 205 could show yaws scars and knew where the mother yaw had been and of the entire 315 only 18 claimed never to have had yaws and failed to show scars.
Rossiter, who observed active ulcerations of the nasal septum and hard palate in the case of a two-year old Samoan child, following yaws, states that he found yaws treponemata in smears from the ulcerated areas.
=Epidemiology.=—If gangosa is a sequel of yaws then the same factors which are operative for yaws apply to gangosa.
PATHOLOGY
Sections made from the ulcerating margins of the nasopharyngeal lesions have failed to show treponemata when stained by Levaditi’s method. In sections of such tissue stained by Giemsa’s method I noted a rather marked infiltration with lymphocytes and a great number of mast cells. Fordyce has noted the presence of giant cells.
From the histological study one can only state that the lesions present the characteristics of the granulomata.
A remarkable feature of the disease is the rapidity with which ulceration destroys cartilage and bone. The nasal duct seems to be prone to attack and it is through this channel that the process reaches the eye to bring about its destructive tendency in that organ.
Of 81 cases studied by McLean and Mink the eye was involved in 21. The larynx was involved in 33 of these cases. It is the frequent perforation of the hard palate that gives these patients the nasal voice, whence the name of the disease is derived.
SYMPTOMATOLOGY
Patients with the disease have rarely been observed prior to the full development of the mutilating ulcerations. In a few cases, however, it was noted that a patch of membrane first appeared in the region of the soft palate. This membrane rapidly became honeycombed and an examination three or four days later showed underneath a deep ulcer, surrounded by an area of marked congestion.
The ulcerating process advances rapidly, destroying bone as well as soft parts. The process seems to extend from within outward, giving a funnel-shaped loss of tissue. The ulceration advances upward and forward, destroying the nasal septum and structures forming the tip of the nose, leaving the upper lip as the lower border of this external opening.
The active process tends to become quiescent in one or two years, the cases then showing extensive loss of tissue with cicatricial borders. Occasionally active ulceration may again set in after a period of quiescence.
The voice character is that of any case where there is a perforation of the hard palate and is not distinctive of the victims of this disease.
During active ulceration there is a malodorous sero-purulent discharge which makes the patients very objectionable. These cases seem to suffer very little impairment of the general health even when the process is active.
Although the destructive lesions about the nasopharynx and the region of the face are the most striking ones it would appear that similar ulcers on the extremities are of the same nature as those more prominently situated.
In an examination of the blood of 10 of these cases in Guam I did not observe any abnormal findings, other than an eosinophilia, which was present to an equal degree in those unaffected. Musgrave and Marshall reported a slight leucocytosis in their case.
DIAGNOSIS
Gangosa is chiefly to be differentiated from leprosy, syphilis and lupus vulgaris. Its more rapid course should distinguish it from leprosy and lupus and the history from syphilis.
TREATMENT
Odell found that a thorough antisyphilitic treatment cured these ulcerations. He used mercurial injections. Recently salvarsan has been used with striking curative results. It has been thought that local application of tincture of iodine was effective in stopping the progress of the early ulcerations but this would seem doubtful, it being advisable immediately to give salvarsan.
On account of the offensive odor of the discharge solutions of permanganate of potash have generally been used.
XXVIII. MYCETOMA
GENERAL REMARKS
Various destructive processes of different parts of the body, but more commonly of the foot, which are caused by invasion and growth of fungi are generally designated mycetomas. Chalmers and Archibald have studied these conditions most carefully and have grouped most of them under maduro-mycoses and actinomycoses. The mycetomas are characterized by the presence of fungi in the form of grains composed of hyphae, and at times chlamydospores, imbedded in a matrix. These grains may be imbedded in the tissues or present in the discharge from the sinuses. Eosinophile bodies are usually present. The maduro-mycoses have grains with large segmented mycelial filaments, possessing well defined walls and usually chlamydospores. We have white or yellow, black and red ones according to the colour of the grains. The actinomycoses have very fine nonsegmented mycelial filaments with ill-defined walls and no chlamydospores. We have black, yellow and red grain actinomycoses. In addition to the mycetomas we recognize paramycetomas and pseudomycetomas, the former of which show fungi which do not show any grain formation and the latter failing to have present either fungi or eosinophile bodies. The pseudomycetomas are associated only by reason of clinical resemblance.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—The disease was first described by Kaempfer about 200 years ago, but at that time was often confused with elephantiasis. The first exact clinical description of the disease, with its pathology, in which was noted the fungus nature of the granules given off in the discharges from the sinuses, was that of Vandyke Carter, whose studies were carried on from forty to fifty years ago.
=Geographical Distribution.=—The name Madura foot takes its origin from the great prevalence of the affection about Madura, in the Madras Presidency of India. It is less frequent in other parts of India. It also occurs in Ceylon. The disease is rather widespread in Africa, having been reported from Algiers, Tripoli, Tunis, Egypt and the Sudan as well as from Madagascar. Cases have also been reported from Italy and Greece in Europe and from the West Indies and some of the South American countries. Several cases have been reported from North America and Sutton, in 1913, reported two cases from Kansas, one in a Mexican and one in a native of Texas.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—The disease is caused by the penetration of certain species of fungi into the tissues of the foot, although rarely the hand or some other part of the body may be affected. These species of fungus develop in granulomatous areas from which sinuses lead to the surface of the foot, in the discharges from which are found small granules resembling those found in the discharges from actinomycosis lesions.
As a rule only one kind of fungus is found in a single case. The most common infection is that due to Discomyces madurae (Nocardia madurae) which is the fungus of the fish-roe-like granules of the pale or white variety of mycetoma. These, like the fungus of actinomycosis, Discomyces bovis, show a felted mycelium in the center and peripheral club-like structures. These granules are yellowish-white and vary in size from a pin’s head to a small pea. The mycelial threads are very narrow, 1 to 1½ microns. It grows aerobically and the cultures show slender mycelial threads which are Gram-positive. This is the organism of Carter’s white mycetoma.
Other species of the pale, white or ochroid group of mycetoma fungi are Indiella mansoni (Brumpt’s white mycetoma), Nocardia asteroides (Musgrave and Clegg’s white mycetoma), Sterigmatocystis nidulans (Nicolle’s white mycetoma) and several others.
The cases caused by the black varieties are more rare and are characterized by the presence in the discharges from the sinuses of black gunpowder-like grains.
These hard, brittle, irregular grains are caused by various species of fungi of which the best known is Carter’s black mycetoma (Madurella mycetomi). This species was cultured by Wright and first shows a grayish growth, later becoming black. Other black varieties of mycetoma are due to various other fungi. Bouffard’s black variety is caused by Aspergillus bouffardi. DeBeurmann’s black mycetoma has as cause Sporotrichum beurmanni.
Besides the white and black varieties we also have a red variety of mycetoma. The fungus grains are quite small and reddish in color. It is not an uncommon infection in certain parts of Africa, as Senegal. The cause is Nocardia pelletieri.
Boyd and Crutchfield have noted an ascomycete in an American case, with white granules, to which has been given the name Alleschiria boydii.
=Epidemiology.=—We know very little about the occurrence of these mycetoma fungi, other than in man. It is thought that such fungi lead a saprophytic existence on thorns or blades of grass or spine-like grains of various cereals. Thus Nicolle’s case in Tunis started from a puncture wound by a grain of barley.
As the vast majority of such cases are noted in the feet, and as such cases are chiefly in those who work barefooted, it seems reasonable to consider that the fungi are introduced on some puncturing object and the external wound having healed development goes on in the deeper structures.
PATHOLOGY
In more than 75% of cases of mycetoma the foot is the only part infected. More rarely there is involvement of hands, knees and buttocks.
The affected part shows nodules on the external surface which connect with the granulomatous lesions of the interior of the foot by sinuses. In advanced cases there may be a network of sinuses and cyst-like dilatations which are filled with a viscid fluid packed with the small fish-roe granules in the white variety or the gunpowder grains of the black mycetoma. The bony structures of the foot may undergo disintegration as well as muscular and areolar tissue so that on cutting into such a foot there is nothing normal remaining—simply a cheesy mass.
In the early granulomatous areas are found the actinomyces-like granules surrounded by an area of mononuclear and polymorphonuclear infiltration. Giant cells are occasionally found. There is an inflammatory oedema. Externally we have connective tissue cells and a fibrous wall. The blood vessels show endothelial proliferation and thrombosis.
SYMPTOMATOLOGY
The disease usually begins in the sole of the foot with the formation of firm swellings about ½ inch in diameter. The cases are rarely seen at this stage, the natives waiting before seeking medical advice until the nodule has softened and begun to discharge the viscid fluid with the various-colored granules floating in it. As stated before, the soft, yellowish-white, fish-roe-like granules are most commonly observed, the more friable, hard, gunpowder-like grains less so. The nodules continue to form and to break down until the foot has become greatly enlarged, the under surface bulging out in a convex mass with the toes and heels appearing as if raised up. The dorsal surface is also puffed up and studded with broken down nodules, and the sides well rounded. There is no increase in the length of the foot. This swollen distorted foot is borne on a thin peg-like leg which makes the size of the foot more striking. Very rarely cases have been reported where the hand or thigh have been involved.
If one probes the discharging sinuses bone may or may not be felt according to the advancement of the degenerative changes. There is rarely pain or bleeding following the probing.
It is more from the onerous burden of carrying around this fungoid mass of a foot, 3 or 4 times the normal size, than pain, that the patient complains of.
Uncomplicated cases do not show fever and the occasional enlargement of lymphatic glands is probably connected with bacterial infections.
There are never visceral metastases in mycetoma as is true of the nearly related actinomycosis.
The process shows no tendency to heal naturally or under treatment but fortunately does not extend, the process being confined to a foot or a hand. The joints are rarely if ever invaded. Unless the sinus-riddled member is amputated the drain on the patient gradually exhausts him and death ensues in ten or fifteen years.
DIAGNOSIS
The distorted appearance of the foot or hand, riddled with sinuses discharging a viscid fluid containing the variously colored granules, which upon microscopical examination are found to be sclerotia of fungi, is absolutely diagnostic. As regards recognition of the causative fungus one should culture the discharge or grains on maltose agar, potato or rather dry blood serum. The recognition of species of fungi is a very difficult matter, even for an expert.
PROGNOSIS
This is absolutely unfavorable as regards the relief of the condition but as regards life it is not unfavorable provided the drain on the system is gotten rid of by amputation of the part.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—The wearing of shoes in the fields or forests would seem to be the best means of protection against small wounds from thorns, splinters and the like.
Then, too, any such wound which might occur should be treated with tincture of iodine.
=Treatment.=—It is usual to try the effects of curetting the lesions and if taken early enough this may have effect. As a rule the process goes on but is limited to the member attacked so that amputation of the diseased part brings about a cure. Iodide of potash is of no value. X-ray treatment seems to be of value in relieving the pain and in lessening the discharge from the sinuses but is of questionable curative effect. It might be of greater value if tried early in the disease.
XXIX. GRANULOMA VENEREUM
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—It is generally stated that Daniels first noted the disease in British Guiana, in 1896, but Daniels regards the disease previously described by Macleod from India under the designation “serpiginous ulceration of the genitals,” as referring to granuloma venereum.
=Geographical Distribution.=—Cases of the disease have been chiefly reported from British Guiana and the West Indies. It is now recognized, however, that it occurs in India, China and Northern Australia as well as in some of the islands of the Pacific. It also occurs in Northern and Central Africa.
Grindon has reported 3 cases from the United States.
ETIOLOGY
Various spirochaetes have been reported as present in the lesions. The finding by Wise of spirochaetes resembling Treponema pallidum has not been generally accepted.
Donovan has reported the presence, in scrapings from the ulcerations, of an oval bacillus (1½ × 2 microns) which was contained in large phagocytic cells. There were sometimes several such bodies in a single cell.
Flu has recently reported the presence in plasma cells as well as occasionally in other cells of a capsulated organism which he believes related to the Friedlander group. His cultural work has not been conclusive. It is probable that this capsulated organism is merely a secondary invader.
There is also a suggestion of the cellular reaction characteristic of the chlamydozoa.
The disease is rather more common in women than in men and is rarely seen before the period of puberty. It is thought that it is transmitted by sexual intercourse.
PATHOLOGY
The pathological process manifests itself as a small round cell infiltration of the superficial portion of the corium. The growth is well supplied with blood vessels. Giant cell formation and caseation have not been noted. There is an abundance of plasma cells.
There is a marked tendency to the formation of fibrous tissue.
SYMPTOMATOLOGY
The disease usually first shows itself as a papule or vesicle on the penis or labia minora. The process extends and the thin epidermal layer rubs off leaving a surface of granulations which bleed easily and give off a creamy discharge which is frequently very offensive.
The process usually extends from the penis to the groins by continuity and thence down the inner surfaces of the thigh. When the glans penis is involved there may be a fungating growth suggestive of epithelioma. In the female the process extends from the labia minora into the vagina and also to the labia majora and thence to the perineum and perianal region. Recto-vaginal fistulae often result. The process extends more rapidly and markedly when invading mucous membranes.
While the granulomatous process is advancing there is frequently cicatrization of the areas previously invaded forming a scar tissue which breaks down easily. There is little pain or itching and the general health is not impaired.
There is no enlargement of the lymphatic glands. Although the process extends by continuity yet it may also pass to parts in contact with the diseased area. While healing of affected skin tends to occur that of mucous membrane does not.
There is really very little tendency to ulceration.
DIAGNOSIS
It is usual to suspect a syphilitic process but the absence of gland involvement and secondary manifestations of syphilis negatives this.
It may be suggestive of tuberculous or epitheliomatous processes. The marked chronicity and tendency to scarring are striking.
TREATMENT
Excision of the entire granulomatous area going well into the normal skin has been thought by some to be the only cure.
Ordinary antisyphilitic treatment does not seem to have any effect and the good reports that have been made as to therapeutic success with salvarsan may have been due to diagnosing a syphilitic process as granuloma venereum. Radiotherapy has been recommended.
Local treatment with antiseptic or deodorant washes or ointments is necessary in these cases.
Antimony Treatment.—Breinl reports success in treatment by using tartar emetic injections. This treatment is now the standard one and the drug is given intravenously as described under treatment of leishmaniasis. It is also recommended to apply locally compresses soaked with a ½% solution of tartar emetic.
SECTION VI
TROPICAL SKIN DISEASES
XXX. TROPICAL ULCER
GENERAL CONSIDERATIONS
Under the names tropical phagedaena or tropical ulcer various skin lesions have been described, from all parts of the tropics, which vary greatly in etiology and symptomatology.
These skin ulcers are most frequently observed on the dorsum of the foot or front of the leg but may appear on the hands or forearms and have rarely been reported from other parts of the body.
There is no doubt but that many of the cases reported as tropical ulcer are really manifestations of tertiary syphilis.
Jeanselme has noted the insignificant manifestations of the secondary stage of syphilis in natives of Indo-China and the malignancy of the tertiary ones as regards the skin lesions. In fact a striking feature of the late stages of syphilis in the natives of the tropical world is the frequency and severity of skin lesions and the rarity or absence of involvement of the central nervous system to produce tabes or general paresis.
Again congenital syphilis is common in most tropical countries which have been visited by white men for long periods and Jeanselme has noted the rarity in natives so affected of interstitial keratitis and Hutchinson’s teeth, signs upon which medical men are apt to base a diagnosis of such a condition.
Again, Butler, studying the serological side of 27 ulcerations which clinically could be diagnosed as tropical ulcer, obtained strongly positive Wassermann tests in 26, or 96 per cent. of the cases. Shattuck found that about 94% of the chronic ulcerations of the Philippines could be ascribed to syphilis.
Besides syphilis one must bear in mind the possibility of the ulcers being a manifestation of tertiary yaws, a condition which also gives a high percentage of positive Wassermann tests.
In Guam, the natives separate the ulcerations about the lower extremities from the naso-pharyngeal ones by designating the former cases llagosos and the latter gangosas. It is probable that the leg ulcers are manifestations of the same disease as the naso-pharyngeal ones whether it be syphilis or yaws. These ulcers of the leg in Guam as well as those studied by Butler in the Philippines would certainly be classed as tropical ulcers.
There are undoubtedly many cases which can be explained by infections with ordinary pyogenic organisms of the skin which are enabled to get a foothold in an abrasion or other minor wound, in a person whose resistance has been reduced by such cachexia-producing diseases as malaria, dysentery or ancylostomiasis.
Indeed some authorities attach special importance to the tibial ulcers found in advanced cases of hookworm disease. Some of the sores are due to irritating applications used by the natives of many countries as setons. In many instances the sores are from neglected wounds.
Vincent has called attention to the association of the fusiform bacillus and delicate spirillum, better known in connection with Vincent’s angina, in smears from tropical ulcers.
Such findings have also caused many to consider tropical ulcer as related to hospital gangrene. There is no doubt but that smears from the dirty membranous deposit on these ulcers do frequently show the fusiform bacillus and at times the spirillum, but we also frequently find various fungi in such smears. Very few hold that these have anything to do with the production of the ulcer.
Inoculation experiments have as a rule been indefinite in result.
LeDantec has incriminated a very large Gram-negative bacillus which was noncultivable.
Prowazek believes that he has found the cause in a spirochaete which possesses fewer turns and these more widely separated than those of the spirochaete of syphilis. The association with the fusiform bacillus has also been noted.
Wolbach and Todd note the frequent finding of spirochaetes in tropical ulcers and attach considerable importance to a spirochaete with abruptly tapering ends. The name of Spirochaeta schaudinni has been given to the organism. They also generally found associated micrococci and bacilli as well as the fusiform bacillus.
Other than the noting of granulation tissue and the presence of plasma and small round cells there does not seem to be anything definite in the histopathology of tropical ulcer. This is what one might expect in view of the lack of definite knowledge of the condition.
Veld sore.—Under the name of Veld sore we have a form of tropical ulcer which is common in various desert regions.
These ulcerations may appear on the face as well as on the dorsal surfaces of the hands or forearms or on the lower extremities. They seem to arise from infections of abrasions of the exposed parts. In the early stages of the lesion the diphtheria bacillus has been frequently isolated and some of the cases have been followed by diphtheritic palsies. It would appear that these lesions have at times been those of cutaneous diphtheria. Such cases were reported by Craig in cases in the Sinai desert. The simultaneous existence of cases of ordinary faucial diphtheria should make one suspicious of the real nature of such ulcerations. Skin diphtheria is more frequent than is generally considered.
SYMPTOMATOLOGY
These ulcers are most frequently found on the dorsum of the foot, over the shin and about the external malleolus. More rarely they involve the dorsum of the hand or back of the wrist.
In the multiplicity of clinical descriptions from various parts of the tropics we obtain two types of ulceration.
One is that of a rather chronic ulcer, which slowly develops from a painless swelling, which is not unlike a gummatous process. Surrounding the swelling there is a circumscribed, reddened, glazed area of skin. After two or three weeks the swelling begins to soften and a serous fluid exudes from its summit.
Ulceration, with the frequent formation of a membrane-like deposit, now sets in and later on we have a more or less punched-out ulcer showing indurated margins. There may be no impairment in the health of those with this type of ulcer.
The other type is generally seen in persons who are much debilitated or suffering from some cachectic state. In the earliest stages these sores seem to resemble an area which has been excoriated and inoculated with vaccine virus, there being a rather dry, angry-looking spot of erythema. This within a few hours may be surrounded by a circle of vesicles beyond which is an encircling inflammatory areola.
There is marked subjective pain and tenderness. The serum from the vesicles fails to show any bacteria and the cellular contents are made up almost entirely of polymorphonuclear leucocytes. Within a few hours to one or two days the area within the ring of vesicles is converted into a dark gray to black pultaceous diphtheroid membrane which when detached shows underlying fungating granulations, covered with greenish-yellow pus. This membrane, if stripped off, tends to reform with great rapidity (twenty-four to forty-eight hours), and in many respects resembles the membrane of diphtheria except for its dark color.
These ulcerations extend with great rapidity and even when showing a tendency to heal may suddenly, from a point along the margin, proceed to form a new area of ulceration, extending somewhat as would a ringworm. When the original site of ulceration fails to heal during a period of several weeks, the edges become rather indurated but do not show the punched-out or undermined characteristics of the first type.
These cases last for months and are far more tantalizing than the former type of ulceration for the reason that from time to time they show a strong tendency to heal, the process clearing up almost entirely, when suddenly the former area of the ulceration is equalled or exceeded.
TREATMENT
Many of these ulcerations yield readily to salvarsan and in such cases we naturally think of a syphilitic or framboesial etiology.
Castellani has recommended a protargol ointment, 5 to 10%, which is applied to the ulcer after previous flushing with hydrogen peroxide or other antiseptic lotion.
At times thorough cauterization with pure carbolic acid followed by neutralization with alcohol may shorten the process.
Iodide of potash benefits some cases but has no effect on others and the same is true of mercurial treatment.
An 8% ointment of scarlet red should be tried on these sores when treatment with ordinary applications fails.
XXXI. TINEA IMBRICATA
GENERAL CONSIDERATIONS
This form of tropical ringworm is chiefly found in the islands of the South Pacific and in the Malay Archipelago. It is also found in Southern China and quite recently has extended to Southern India and Ceylon. Recently it has been reported from Brazil.
On account of the disease having been carried from the Tokelau Group to Samoa it is often designated tokelau.
Manson was the first to recognize the affection as due to a fungus which he demonstrated microscopically in the scales.
He was also able to transmit the disease by inoculation experiments and found that after about ten days a raised, brownish spot appeared at the site of inoculation. This spot increased in size until when about ¼ inch in diameter its central portion became detached, thus giving rise to several thin, rosette-like scales, free at the center but still attached peripherally. The fungus advances peripherally, leaving a smooth surface within. Again there is a similar process developing in the original central spot to again form a circle of scales within the older and more peripheral circle. The process is repeated until several rings of scales are formed each originating from the central focus as concentric ripples form on water from the fall of a pebble.
These scale circles are from ⅛ to ½ inch apart and give a festooned appearance to the affected skin. It was formerly supposed that the causative fungus was Aspergillus concentricus but Castellani has demonstrated that fungi of this genus, when present, are merely accidental. He has isolated in cultures what he considers the causative fungus, Endodermophyton concentricum. He treated scales for ten minutes with absolute alcohol and then placed single scales in a series of tubes of maltose bouillon.
The fungus grows between the rete malpighii and the external epidermal layers forming a network of mycelial threads, about 3 microns broad.
Another fungus cultured from tinea imbricata scales is Endodermophyton indicum. Inoculation of this organism in pure culture produced the disease.
The characteristics of the genus Endodermophyton are: The growth of a mycelial network between the rete malpighii and the superficial epidermal layers; in cultures only mycelial filaments are found; there are no conidia-bearing hyphae.
The fungus is also called Trichophyton concentricum.
When this skin disease is introduced into a country with high relative humidity and fairly uniform temperature, between 80° and 90°F. it spreads with great rapidity.
A dry climate or one showing considerable variations in temperature is not favorable for its spread.
SYMPTOMATOLOGY
The clinical characteristic of this form of ringworm is the presence of rosette-like lesions of several concentric circles of shingle-like, papery scales which are fixed peripherally and free toward the center, thus, from its imbrications, suggesting the name given it by Manson.
If one passes the finger over the affected surface from without inward there is no sensation of roughness but if passed from the center outward the free borders of scales cause a sensation of roughness.
As these circles extend peripherally they meet the peripheral rings of other circles so that various curves appear which give the general appearance of watered silk.
The flaky scales are of tissue paper thinness and are of a dirty, brownish-gray color.
The general health of the patient is not affected but the itching is very severe.
There is an entire absence of inflammation about this ringworm thus differentiating it from the more common tropical ringworms. Again the axillae and crotch are much more rarely affected than in other ringworms as is also true of the face, palms of hands and soles of feet. The scalp is never affected.
Some claim that the fungus never invades the nails but Manson states that this frequently occurs. The presence of the fungus in a scale treated with 10% solution of sodium hydrate differentiates the scales from those of ichthyosis.
Tinea intersecta is somewhat similar to tinea imbricata when first appearing, showing dark brown patches but it never shows the concentric rings. The ordinary ringworms present inflammatory characteristics.
TREATMENT
A thorough preliminary scrubbing with soap and water in order better to expose the fungus to curative applications is important.
For treatment Manson recommends iodine liniment. This contains 12½% of iodine as against 7% for the tincture. The liniment has also 3½% of glycerine which is not an ingredient of the tincture. Both tincture and liniment have 5% of potassium iodide. The application of the tincture does not seem to be as satisfactory as the liniment, the stronger preparation being more effective.
Chrysarobin is very effective but very irritant and has to be used with care. An application of a 5% solution of chrysarobin in chloroform to the affected area, then painting it over with a 50% aqueous solution of ichthyol, often gives good results.
Some prefer a 2% to 5% ointment of chrysarobin. Chrysarobin produces a conjunctivitis if used near the eyes. Again if absorbed it may act as a renal irritant.
Castellani strongly recommends the use of resorcin in tincture of benzoin (60 to 120 grains of resorcin in 1 ounce of tincture of benzoin). Either remedy alone has very little effect, the combination being necessary. The application is made once or twice daily. In addition to this treatment the patient should be scrubbed with sand-soap and hot water twice a week.
As regards prophylaxis the clothing should be boiled. The natives attach value in preventing the disease to anointing the body with cocoanut oil.
XXXII. TINEA CRURIS
GENERAL CONSIDERATIONS
Under the name “dhobie itch” this fungus affection is probably better known to Europeans than any other tropical skin disease. This name dhobie or washerman’s itch has been given on account of associating it with the infection of the underclothing while being washed in the pools or streams along with the garments of those who have this skin disease. This, like every other widespread view, has probably some foundation but cannot be verified. It is the eczema marginatum of Hebra.
This affection is caused by various species of Epidermophyton. This genus differs from Trichophyton in that it never invades the hair or hair follicles.
The species which have been more frequently reported are Epidermophyton cruris, E. perneti and E. rubrum. The mycelium is about 4 microns broad and the spores about 5 or 6 microns. All of these fungi can be cultured on Sabouraud’s maltose agar, growth appearing in about a week, except E. perneti, which grows more rapidly.
SYMPTOMATOLOGY
The favorite site is the crotch although the axillary region is also frequently involved. The process starts as a papule but these rapidly develop and give rise to an angry red, swollen patch with sharply delimited margins. These red, festooned patches are usually limited to the perineum, scrotum and inner surfaces of the thighs.
The itching is unbearable and many secondary infections or eczematous lesions result from the fierce scratching of the parts.
If the patient goes to a cooler place the process subsides to return when he comes back to the hot moist climate where the infection was originally contracted.
In some cases the fungus invades the region between the toes and gives rise to intolerable itching and from secondary bacterial infections to a condition known as “Mango toe.”
It has seemed to me that when one has a coccal infection engrafted upon the fungus one the condition becomes what might be termed fulminating, so rapidly does the itch extend.
TREATMENT
When the process is markedly inflammatory mild applications are indicated, such as calamine lotion (30 grains each of calamine and zinc oxide with 5 or 10 drops of carbolic acid in 1 ounce of saturated solution of boric acid).
A 10% to 15% solution of sodium hyposulphite can, however, be used on the area even when markedly inflammatory.
Iodine applications are too irritating for the region of the scrotum.
An ointment of resorcin, 20 to 30 grains with 1 dram of sulphur to the ounce, may be tried. If chrysarobin be used it should be applied with greatest care as noted under tinea imbricata. Many advocate applications of solutions of salicylic acid in alcohol, 2% to 5%.
Manson’s dusting powder of equal parts of boric acid, zinc oxide and starch should be freely used.
XXXIII. PINTA
GENERAL CONSIDERATIONS
This is a parasitic skin affection due to various species of fungi. It is only found in the tropical portion of the new world, and is especially prevalent in Colombia, where it has been estimated 4% of the population have the disease. It is also found in Mexico, Central America and some of the other countries of South America as well as Colombia.
Other names for the disease are caraate and mal de los pintos. At first it was thought that the different colors shown by the eruption were due to varying depths of the proliferating fungi in the skin layers but it is now known that the explanation is in a variety of species in the different types of pinta.
The pure violet pinta is caused by Aspergillus pictor while the grayish-violet one is due to Penicillium montoyai. A species of Monilia causes the white variety and different species of Montoyella a black and a red variety respectively. The genus Montoyella is stated by Castellani to have both slender and thick mycelial threads, from the thicker of which spring delicate hyphae terminating in pear-shaped conidia.
Material scraped from the lesions and mounted in liquor potassae shows the fructification terminations characteristic of Aspergillus or Penicillium in the violet or gray-violet varieties while the white, black and red ones only show mycelial threads and scattered spores. These pinta species of fungi can be cultivated on Sabouraud’s medium.
Montoya thinks that the pinta fungi lead a saprophytic existence in the waters of mines or other places with a constant high temperature, and states that he has obtained pure cultures from such sources.
SYMPTOMATOLOGY
The spots of the eruption are generally first noted on the hands or face and are rather rough, dry and only slightly raised. Itching is quite marked and the scratching probably is largely responsible for the gradual spread of the affection over the body generally.
The palms of the hands, soles of the feet and nails are never involved. The course is essentially chronic and shows no tendency to spontaneous cure.
The red pinta is that most often found in white people, the patches being of brick-red color.
The white pinta may not only be caused by a species of Monilia but it may represent an area formerly invaded by a species producing some other color and then dying out leaving a vitiligo-like area.
The violet pinta is quite common among miners, while the black one is the type which more often appears in the black population. The black varieties may show either a pure black or a violet-black color.
TREATMENT
Local applications of iodine preparations or of chrysarobin seem most effective. The resorcin sulphur ointment noted under tinea cruris is best for the face.
XXXIV. MINOR TROPICAL AFFECTIONS OF THE SKIN
DERMATOPHILIASIS
This is a skin infection due to the penetration of the region about the feet and especially the toes by the female sand flea or chigoe. It is also sometimes called the jigger. This flea is a member of the subfamily Sarcopsyllinae which differs from the ordinary flea subfamily in that the impregnated female becomes fixed in the tissues of the host instead of developing her eggs in a free state. The proper name for this flea is Dermatophilus penetrans, synonym Sarcopsylla penetrans. It is found abundantly in Central America and Northern South America as well as in the West Indies. It is also found in East and West Africa as well as India and is apparently rapidly spreading over the tropical world.
This flea attacks not only man but many wild and domesticated animals as well, and in particular the pig. The males and females live in dry sandy soil and feed on the blood of various mammals. The importance of the parasite is that upon impregnation the female ceases to lead a free existence but burrows into the tissues of man or other host and becomes enormously distended with eggs. There is some question as to whether these eggs are extruded by the female or whether they are set free in the ulceration process which tends to occur around the imbedded flea. The eggs develop into 13-segment larvae, which form a cocoon from which the insect comes out in about ten days.
The female flea tends to burrow into the skin about the sides of the toe nails, although more rarely boring into other parts of the body as penis, scrotum, thighs or hands. Finally only the tip of the abdomen projects. This marks the black spot which is noted in the tense itching area which is quite white unless bacterial infection starts up inflammation.
The swelling is about the size of a small pea by the end of five or six days. Ulceration is the usual termination of the infection if untreated and such ulcers may be very intractable or form a favorable soil for infection with the tetanus bacillus. Quiros has estimated that 250 deaths from tetanus occurred in Costa Rica in 4 years from infection of nigua (sand flea) ulcerations.
Well-made shoes are most important in prophylaxis and the best treatment is to enucleate the egg-distended flea with a needle and then touch the cavity with pure carbolic acid followed by neutralization with alcohol. It is astonishing how expert the natives become in dissecting out these insects.
TROPICAL IMPETIGO
Under the designation pemphigus contagiosus Manson describes a very common skin disease of the tropics. The condition, however, is not pemphigus. A bacteriological examination shows in the smear great numbers of pus cells containing phagocytized diplococci. Wherry has named the organism Diplococcus pemphigi contagiosi. As a matter of fact, culturally, this organism is the common Staphylococcus pyogenes aureus.
It is also a matter of common observation that this organism when in pus cells of active inflammatory processes shows a diplococcus morphology rather than a staphylococcal one.
These staphylococcal lesions which do not start in the hair follicles are often designated as “pyoses.”
The disease is markedly contagious in children and is strikingly autoinoculable so that unless the first lesion is taken in hand immediately the eruption may become generalized. A small spot of erythema first appears which rapidly becomes vesicular, the bleb covering the entire spot, so that there is practically no surrounding inflammatory areola.
The diaphanous covering rubs off with the slightest touch and leaves underneath a raw-looking surface which extends peripherally to form an angry-looking red patch an inch or more in diameter. In adults it rarely affects parts other than the axilla or crotch.
The general health of the child is practically unaffected.
The usual treatment is with bichloride lotions followed by a dusting powder of equal parts of boric acid, starch and zinc oxide. I have found, however, that an ointment of ammoniated mercury, 2% to 5% according to age, is the most satisfactory treatment.
Tropical Boils.—It is interesting that the same organism responsible for this more fulminating lesion should be the one responsible for the common cosmopolitan boil and in fact boils are exceedingly common in the tropics. These boils may be larger and with a greater tendency to widespread distribution and in some regions they are so common as to have a regional designation (Nile boils). The staphylococcus of tropical impetigo seems to have greater virulence than that of the boils. Autogenous vaccines are often most successful in the treatment of boils.
PIEDRA
This is a fungus disease of the hairs in which small nodules form along the shaft. They are about the size of the nits of head lice but more or less surround the hair instead of projecting off at an angle as do the ovoid lice nits. These little masses are black in color and very hard, hence the name piedra—stone. The disease is chiefly found in Colombia and is thought to be due to the application, by the women, of a mucilaginous preparation to their hair. If an infected hair be examined in liquor potassae the nodule will be found to be made up of faceted bodies matted to the side of or, at times, encircling the hair. These bodies are the spores of Trichosporum giganteum.
Besides piedra there are also other nodular affections of the hairs due to species of Nocardia. Chalmers has recently reported several cases of trichonocardiasis where the axillary hairs were matted together and the skin of the region inflamed. Castellani called attention to this condition in 1911 and reported a narrow, bacillus-like fungus as the cause, Nocardia tenuis. The nodules are rather soft and may be yellow, black or red in color. Microscopical examination shows the fungus.
Chalmers had excellent results by treating the affected hairs with a 2% formalin solution in alcohol. At night a 2% ointment of sulphur was applied. A 5% alcoholic solution of salicylic acid has also been recommended.
CUTANEOUS MYIASES
=Ver Macaque.=—The best known of these myiases is that due to the larva of a botfly (Oestridae), Dermatobia cyaniventris.
The larva is at first club shaped and in this stage is called ver macaque. Later on it becomes worm shaped and is then called torcel in Venezuela or berne in Brazil. The natives of most of the countries where the infection is found have called the larvae “mosquito worms” or “gusano de zancudo” and they have even incriminated large mosquitoes belonging to the genus Psorophora as being responsible for the infections.
Surcouf has noted that these fly larvae have been found cemented to mosquitoes of the genus Janthinosoma by a glue-like substance. These mosquitoes are vicious biters and evidently the young larvae escape from the eggs attached to the mosquito and enter the wound made by the biting parts of the mosquito. Some have thought that D. cyaniventris deposits its eggs in a glue-like material on the leaves of plants and that they stick to mosquitoes flying about such plants. From the facts that these eggs apparently only become attached to this particular mosquito, and further in that the eggs are attached in a constant manner with the hatching end outward, it would seem that the mother fly must in some way seize the mosquito and deposit her eggs on it. As the larva grows in the subcutaneous tissues of man or other animals a tumor-like swelling develops with a central orifice, toward which the posterior extremity of the larva points and through which it takes air into its spiracles.
It has been stated that the eggs of D. cyaniventris may be conveyed by ticks.
The swelling somewhat resembles a blind boil and may be as large as a pigeon’s egg.
These botfly boils tend to break down and discharge a sero-purulent fluid and it is supposed that the larva, when mature, escapes as a result of the disintegration of the tumor.
In Brazil they make tobacco juice applications which cause the larva to protrude and then squeeze it out. The injection of a little chloroform into the larva with a hypodermic syringe, prior to its extraction with a forceps, makes the process less painful.
=The Screw Worm.=—This is the larva of a bluebottle fly, Chrysomyia macellaria, which differs from the common bluebottle fly, Lucilia, by having 3 black lines on scutum. This muscid fly lays 200 to 300 eggs in wounds or orifices having offensive discharges, as from nose, ears, etc. The larvae burrow into the adjacent tissues and cause frightful destruction of all soft parts. The mature larvae are a little more than ⅔ inch long and have circlets of spines around each of the 12 segments.
This infection is especially common in tropical and subtropical America and is important in animals as well as man.
In Yount’s 23 cases 18 were of nasal myiasis; the mortality for the 23 cases was 15% and for the nasal ones 22%. Irrigation with chloroform water or a 5% carbolic acid or compound cresol solution gives the best results in treatment. If the larvae reach the sinuses it may be necessary to open them to get at the parasites.
CREEPING ERUPTION
This is a skin affection which is also called larva migrans on account of its being due to the burrowing of more or less undetermined fly larvae in the subcutaneous tissues. In their advance, which is at the rate of from one to several inches daily, they leave a raised pinkish line. The burrow is approximately ⅙ inch in diameter. The disease is most common in Southern Russia but is also found in Africa, Asia and South America. Looss considers that hookworm larvae, when penetrating the skin, may produce similar lesions.
TUMBU FLY DISEASE
This African myiasis is due to the penetration of thighs or buttocks by the larvae of Cordylobia anthropophaga. The appearance of the tumefied area is quite similar to that of the tumor of Dermatobia cyaniventris and the treatment is similar.
CRAW-CRAW
This is a rather chronic papular skin disease which is reported from the west coast of Africa. These papules may be as large as a small pea and are quite hard. They are found chiefly on legs and arms. The proximal lymphatic glands may be enlarged.
Undoubtedly many of the cases called craw-craw are scabies. In fact the Africans give the name to a host of different skin affections. O’Niel thought he had found a filarial larva in one of his cases and Nielly incriminated a nematode larva of the Anguillulidae family. The cause is unknown and the disease very intractable to treatment.
SECTION VII
TROPICAL DISEASES OF DISPUTED NATURE OR MINOR IMPORTANCE
XXXV. VERRUGA PERUVIANA AND OROYA FEVER
It is thought that Oroya fever was the disease which proved so fatal to Pizarro’s army in the 16th century. In 1870, great interest was aroused in these diseases on account of their prevalence in the workmen constructing the railroad from Lima to Oroya, a town in the Andes. At this time there was much conflict of opinion as to whether the two diseases were identical. In 1885, Carrion, a medical student of Lima, inoculated himself with the blood from a verruga lesion and died from Oroya fever about one month later. As the result of this it seemed to be established that infection with verruga material would produce the serious first-stage fever and many call the fever Carrion’s disease. Consequently these two diseases have, until recently, been considered as two stages of the same disease, the usual idea being that Oroya fever is the first stage, following which, provided the patient does not die from this very fatal fever, there sets in an eruption which is the second or verruga stage. In order to reconcile the observations of the development of the eruptive stage without a severe, febrile, preliminary one of three or four weeks, it was considered that the first stage might be exceedingly mild.
Strong and his colleagues, however, inoculated a volunteer with material from verruga lesions and sixteen days later the eruption appeared without the preliminary fever and anaemia that are so characteristic of Oroya fever, and it is now recognized that they are two distinct entities.
OROYA FEVER
GENERAL CONSIDERATIONS
Oroya fever is an acute, infectious disease, often terminating fatally, caused by the Bartonella bacilliformis, and characterized by an insidious onset, irregular fever, pains in the bones and a rapidly developing anaemia of the pernicious anaemia type.
The disease is chiefly found in towns situated in narrow, wind-protected valleys of the west side of the Andes, at elevations of from 3000 to 9000 feet. Townsend has suggested that a species of Phlebotomus, P. verrucarum, which is very prevalent, may be the transmitting agent. This investigator believes that verruga and Oroya fever are the same disease. It may be stated that malaria and enteric fevers, as well as verruga, are common in the localities where Oroya fever prevails and much of the confusion in the literature of Oroya fever is due to failure to differentiate the better known conditions. Strong noted that Oroya fever was common from January to April, particularly towards the close of the warm, rainy season. Cases were rare in April and May and did not occur in the months of June, July and August. He notes that verruga was not uncommon at the time when Oroya fever was not occurring. Concomitant infection with Oroya fever and verruga may occur but this is also true of malaria or malaria and verruga may exist at the same time.
Barton isolated a paratyphoid bacillus from the blood of a patient, besides which other bacteria have also been isolated. In 1909, Barton noted certain rod-like organisms in the red cells of Oroya fever patients which he considered protozoal in nature.
Strong and his colleagues found in the blood of Oroya fever cases rod-shaped forms in the red cells, varying from 1 to 2 microns in length, the red cells containing from 1 to 30 of these elements.
A study of sections of lymphatic glands of severe fatal cases showed great numbers of these bodies packed in the endothelial cells. These cells rupture and set free the organisms.
Intravenous inoculation of blood containing these elements into monkeys and rabbits was negative in result. Strong failed to cultivate the organism. These organisms were considered as intermediate between bacteria and protozoa. They are closely related to Grahamella and the Harvard commission has proposed the name Bartonella bacilliformis. In many ways they resemble piroplasms, especially Theileria.
PATHOLOGY
At autopsy the skin shows the pale yellowish waxy hue of pernicious anaemia. The lymphatic glands are somewhat enlarged and may be oedematous. The heart is flabby and ecchymoses may be present in the pericardium. The spleen is enlarged, shows numerous infarctions and contains large amounts of pigment in the form of yellowish masses or granules deposited between the splenic cells and in the endothelial leucocytes. This pigment is like melanin in not giving the iron reaction. The liver likewise is enlarged, shows areas of toxic degeneration and contains moderate amounts of pigment. The femoral marrow is soft and dark red. Microscopically, the endothelial cells of the lymphatics distended with the causative organisms were particularly noted by Strong.
SYMPTOMATOLOGY
The incubation period is about three weeks and the onset of the disease is marked by malaise and apathy, to be followed by a rapidly developing anaemia, of the pernicious anaemia type, with an irregular fever of a remittent character fluctuating between 100° and 102°F. and only exceptionally going up to 104°F., and pains in head, joints and bones. The tenderness over the bones is undoubtedly associated with the marked changes going on in the bone marrow and is particularly marked over the sternum.
The patient rapidly develops a very severe anaemia and death results in 20 to 40% of cases in two or three weeks. Delirium is often noted.
The spleen and the lymphatic glands are somewhat enlarged. Associated with the profound anaemia there may be oedema of legs and about joints and functional cardiac murmurs. The kidneys do not seem to be affected. There may be a diarrhoea in the later stages of the disease. There is no eruption in uncomplicated cases.
The most important findings in the disease are those in connection with the blood examination. The rod-shaped organisms, which are thought to be the cause of the disease, are somewhat difficult to observe in fresh blood preparations. They show definite motility within the red cells, particularly after warming the blood slide. The motion is a rather gliding one. In Romanowsky-stained preparations the 1 to 2 micron-long rods within the red cells may occur singly or in numbers of 4 or 5. V-shapes are frequently seen. The rod shows a bluish staining with a deep purplish-red chromatin-stained granule at one extremity. Rounded, oval or pear-shaped forms may also be seen.
While the parasites are present in great numbers in severe cases they may be very scarce in mild forms of the disease.
Very striking is the rapidly developing anaemia which frequently shows a red cell count of less than a million within a few days. Normoblasts are quite numerous and fulminating cases show numerous megaloblasts.
Polychromatophilia and poikilocytosis are noted.
In the red cells we have the picture of a rapidly developing pernicious anaemia The color index is above 1.
The leucocytes number about 20,000 of which 60 to 70% are neutrophiles. Immature neutrophiles, as the metamyelocyte, are very common.
PROPHYLAXIS AND TREATMENT
The transmitting agent not being known we are in the dark as to prevention. Evidence points to some arthropod biting at night as the incidence of the disease decreased when those working in the Oroya fever zone were compelled to leave the valleys before sundown. The treatment is largely one of nursing although some have reported favorably from the intravenous administration of salvarsan.
VERRUGA PERUVIANA
GENERAL CONSIDERATIONS
Verruga peruviana is an infectious eruptive disease, caused by an unidentified virus, lasting two or three months, and characterized by successive eruptions exhibiting two types of lesion,—the miliary and the nodular,—both of which show a pronounced tendency to ulceration and haemorrhage. The eruption of verruga somewhat resembles that of yaws and it was at one time suggested that verruga was simply yaws as influenced by high altitude. Strong and his colleagues found that they could infect rabbits intratesticularly and that lesions resembling those of man could be produced in dogs and monkeys by cutaneous and subcutaneous inoculations. The virus has been transmitted from monkey to monkey. The monkey is not as susceptible to the virus as man and the rabbit and dog less so. Inoculation of the monkey is not followed by a generalized eruption. The Wassermann reaction was negative. In extracts from the granulomatous lesions they found a very active haemolysin. It will be remembered that animals are not susceptible to Oroya fever blood inoculations.
From the fact that it is possible to inoculate a person by rubbing verruga material on a scarified surface it would seem that the infection might be transmitted by insects.
As regards the pathology of verruga, Cole has noted involvement of the lymphatic channels, which become obstructed by a cellular exudate, around which lymphatics are found plasma cells and fibroblasts. There is marked dilatation of the capillary blood vessels. The structure of these granulomatous tumors is very vascular, almost cavernous, hence the tendency to haemorrhage. The haemolysin may also be operative in the liability to haemorrhage.
Strong and his colleagues found the early lesions to consist of newly formed blood vessels lying in an oedematous connective tissue. The endothelial cells lining them may be in more than one layer. Around these blood vessels we have aggregations of cells which are considered as angioblasts. These angioblasts show frequent mitotic figures. There is a resemblance to a fibrosarcoma.
SYMPTOMATOLOGY AND TREATMENT
The period of incubation is about two weeks as shown by experimental inoculation but may be as long from the standpoint of clinical observation as forty days. At the onset we have rather severe pains of joints, especially the knees, ankles and wrists, together with a fever sometimes reaching 104°F. but usually not above 100°F. Following the eruption, the temperature usually subsides to normal in a few days. The eruption shows two types, the one with numerous, small, wart-like lesions, not exceeding the size of a small pea (2 to 5 mm.)—the miliary type, and the other, with less numerous but much larger nodular masses—the nodular type. The latter type is more rarely seen than the former.
The Miliary Type.—The eruption is most abundant on the face and extensor surfaces of the extremities and less common on the trunk. In this type a pink macule appears which rapidly takes on a bright red color and becomes nodular. These nodules may be flat or somewhat pedunculated and bleed easily. At first smooth and shiny, it later on shrivels up without leaving a scar. This form of the eruption may involve the mucous membranes, as of conjunctivae, nose, pharynx, etc. In children the disease is usually of a mild type.
The Nodular Type.—The nodular eruption develops slowly and the lesions may become as large as a pigeon’s egg. They tend to become strangulated and then show as ulcerating, fungating masses which are a source of danger from haemorrhage. The nodular eruption does not invade mucous membranes and is usually confined to the regions of joints, as flexures of elbows, knees, etc.
The eruptions tend to come out in crops and the duration of the disease extends over two or three months.
Treatment.—The ordinary principles of cleanliness apply to the care of the lesions to prevent secondary infections. When the large tumor-like masses begin to ulcerate or become gangrenous they should be excised. It must be remembered that dangerous bleeding may occur at unexpected times, for which reason the patients should be provided with styptics or compresses to prevent serious loss of blood.
XXXVI. DENGUE AND DENGUE-LIKE FEVERS
DEFINITION AND SYNONYMS
=Definition.=—Dengue is an epidemic disease due to an ultramicroscopic, filterable virus which has been stated to be transmitted by Culex fatigans. More recent work points to Stegomyia.
It is characterized by an initial three or four-day febrile paroxysm of very sudden onset, a remission, which comes on about the fourth day and a terminal rise of temperature for two or three days—the saddle-back temperature course.
Backache and pains about the muscular attachments at the joints and especially a marked postorbital soreness are important features.
An eruption appears about the third or fourth day. Leucopenia and polymorphonuclear reduction are constantly noted. Apathy and a mild neurasthenic state may continue into convalescence.
=Synonyms.=—Dandy Fever (the word dengue is supposed to be derived from the Spanish equivalent of dandy or denguero), Break-bone Fever, Bouquet. German. Dengue-fieber.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—While Hirsch gives the credit for the first mention of the disease to the chronicler Gaberti, who described a disease with certain resemblances to dengue as existing in Cairo in 1779, yet, for the reason that certain clinical features of this epidemic would hardly appear to belong to dengue, as we now know it, there would seem to be good ground upon which to give the credit of priority to Benjamin Rush, who, under the designation break-bone fever, gave us a true picture of dengue as it manifested itself in Philadelphia in 1780.
Gaberti was particularly impressed with the knee involvement so that from his description the disease was known as the disease of the knees. He further noted swelling of the fingers and that the pains continued for more than a month. The sudden onset and the sweating would seem to belong to relapsing fever as well as to dengue and in support of the view that the disease described by Gaberti might have been relapsing fever we have the statement of Sandwith that bone pain, chiefly of the knee, is the symptom most complained of by the Egyptian native with relapsing fever.
Boylon, who reported an outbreak of an epidemic disease in Batavia in 1780 stated that everybody was attacked and that the symptoms were almost the same as those ushering in plague—headache, lassitude and pains in the joints. He noted, however, that this epidemic had no bad consequences, patients getting rid of it in three days under moderate diet and copious beverages.
Ashburn and Craig, in 1907, proved that the disease could be transmitted by injections of blood, unfiltered as well as filtered.
=Geographical Distribution.=—The disease may occur in epidemic form in almost any part of the tropical or subtropical world. It is very common in the countries about the China Sea and in the West Indies.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—One can only state that the disease is caused by a filterable virus which is present in the patient’s blood from the second to the fifth day. Graham reported a piroplasm-like organism as the cause but other workers have failed to confirm this. Reports as to bacterial causative organisms have not been verified. Cleland and his colleagues inoculated guinea pigs and rabbits without result and were unable to find spirochaetes. Couvy has reported the presence of short spirochaetes in the blood 2 or 3 hours before the onset of the fever,—never later. They had two or three turns and fine extremities.
=Epidemiology.=—As regards the epidemiology of dengue there seems to be a general acceptance of the idea that dengue is transmitted by the common culicine mosquito of the tropics, Culex fatigans. There is not, however, that definiteness which attaches to the transmission of yellow fever by Stegomyia calopus or to pappataci fever by Phlebotomus papatasii, in both of which a certain period of development of the unknown filterable virus in the arthropod host is necessary before the insects become capable of transmitting the infections.
It will be remembered that in the nine experiments as to dengue transmission, conducted by Ashburn and Craig, the authors threw out five of the cases for such reasons as previous immunity or refusal of the experimental mosquitoes to bite. Of the four remaining volunteers only one developed dengue. This man, however, had been on duty at the Division Hospital in Manila and the statement is made that he had not been exposed to the disease so far as could be determined. This of course rather militates against the value of this isolated experiment and furthermore the mosquitoes which bit him had fed on the blood of a dengue patient only two nights previously. If this is to be considered as a valid experiment, we must believe that only a short sojourn of the virus in the mosquito is requisite, which is rather at variance with the twelve days for the yellow fever virus and eight days for that of pappataci fever.
In the recent Australian epidemic (1916) experiments failed to show C. fatigans capable of transmitting the disease. Stegomyia, however, gave success in 4 out of 7 cases, the volunteers developing dengue in from six to nine days after being bitten.
Stegomyia mosquitoes are often termed the domesticated ones, since they are observed to breed and pass their lives in the immediate environment of man and further to be distinctly urban, rather than rural, in their distribution. For their breeding places they choose artificial collections of water, such as cisterns, barrels, pails, bottles and cans, in or near dwellings.
These mosquitoes are small in size, silver-striped, vicious feeders and very alert. The female alone bites, blood apparently being necessary for ovulation. It feeds especially during the morning and afternoon hours,—much less commonly at night unless there is a light. The life history of Stegomyia is discussed more fully under yellow fever.
As regards the transmission of the disease by blood filtered through a diatomaceous filter it will be remembered that Ashburn and Craig, by proving this fact, placed the dengue virus in the same category with the filterable viruses of the two diseases just considered. Cleveland found the virus in the washed cells as well as in the serum. The virus maintains its potency for several days outside the body it being present in the blood at periods of from 18 to 90 hours.
Lavinder injected dengue blood from cases in the second to fifth day into rhesus monkeys without noting any variation in their temperature or blood findings.
Graham in Beirut carried out some experiments, one of which would seem almost positively to demonstrate mosquito transmission. He took mosquitoes which had fed on dengue patients, to a village in the mountains where no case of dengue existed. He caused these mosquitoes to feed on two natives of the village and both men became sick with dengue four and five days respectively after being bitten by the mosquitoes. Graham’s claims to have noted piroplasma-like organisms in dengue blood have not been verified and do not receive credence.
The most convincing evidence as to mosquito transmission of dengue is that afforded by the absence of dengue in Port Said during the years 1906 and 1907 notwithstanding the prevalence of the disease in adjacent parts of Egypt. This was attributed to the absence of mosquitoes, these having been destroyed in the fight to make Port Said malaria-free. This campaign was commenced in May, 1906.
Other species of culicine mosquitoes, among which may be noted Stegomyia, have been incriminated. In the Philippines I was convinced that Culex microannulatus might transmit the disease as well as C. fatigans. In one of his experiments Graham claimed to have produced dengue by injecting an emulsion of the salivary glands of a mosquito which had fed on a dengue patient one or two days previously.
PATHOLOGY
As death almost never occurs from the disease there is nothing to note other than the marked leucopenia.
SYMPTOMATOLOGY
After a period of incubation of from four to fifteen days the disease manifests itself with striking suddenness, in fact the patient can generally recall almost the hour of the onset.
The temperature rapidly rises and in a few hours reaches a maximum of from 102° to 105°F. Associated with this primary fever we have frequently a blotchy congestion of the face—the so-called initial rash.
We also have intense headaches, principally supraorbital and postorbital. The pulse rate is slightly accelerated at first but soon becomes slow and may fall to 50 from the fourth to fifth day.
There is no involvement of the joints, and the so-called joint pains are really pains of the muscular insertions about the joints.
The backache of dengue is usually a well marked feature. Pain on motion of the eyeballs is a prominent symptom—it is a deep soreness.
Insomnia, characterized by frequent dropping off to sleep to be awakened immediately by disturbing dreams, is often noted.
The depression, mental and physical, is altogether out of proportion to the lack of seriousness of the disease.
Malaise and anorexia are marked. Constipation is the rule at first.
About the third or fourth day the temperature drops to normal or about that and remains so lowered for from twelve hours to three days. At this time the patient feels much better and views his affection in a less serious light. After this variable intermission the temperature rises to possibly a greater height than primarily, although as a rule it is less marked. This interval, or intermission, separating two periods of fever gives us a chart designated “saddle-back.” There may be only one rise of fever.
This second febrile attack is attended with pains and possibly greater depression than the first accession. It is usually, however, of shorter duration and during this period the terminal rash appears. This is the most characteristic feature of the disease. It generally manifests itself about the dorsal surface of hands and feet advancing up forearms and legs. Later on it may involve all extremities, face and trunk. The eruption is much like that of measles but lacks the dusky red appearance of the measles rash. It may however be punctiform and thus resemble the rash of scarlet fever.
With the appearance of the terminal rash we may have crises such as profuse sweating or marked diarrhoea or epistaxis.
The desquamation is furfuraceous in character and may be attended by marked itching.
In some patients (European) there is a rosy carmine flush of palms of hands and soles of feet. Some authorities have reported glandular enlargements in dengue.
Convalescence is apt to be protracted, being especially characterized by malaise and nervous depression, practically neurasthenia.
Leucopenia and polymorphonuclear percentage reduction appear by the second day.
Clinical Types.—In different epidemics it is noted that some one clinical feature may seem outstanding. Of these we may note:—
(1) The pulse rate is slow for the temperature rise, thus reproducing a phenomenon common in yellow fever (Faget’s law). It is in recent epidemics particularly that clinical descriptions have recorded the frequency of a very slow pulse, most of the older authorities having noted a pulse rate which corresponded to the elevation of temperature.
(2) In some epidemics the feature of glandular swelling is prominent, while in others the swelling is so slight as to be overlooked.
(3) The characteristic “saddle-back” temperature chart seems lacking in the general run of cases in certain outbreaks. It is possible that such epidemics, showing atypical temperature curves, may have been due to phlebotomus fever, or seven-day fever, instead of dengue.
(4) In some epidemics, the rash is insignificant or very slight in most cases. This observation is possibly dependent on the ephemeral character of the eruption in certain groups of cases.
(5) From the chart Fig. 138, analyzing the symptoms in one epidemic, it will be noted that Lane observed cold, clammy, dusky extremities in 17 per cent of his cases. This is an unusual finding.
Symptoms in Detail
Onset and the Temperature Chart.—Dengue probably sets in more abruptly than any other disease. The temperature chart is typically saddle-back.
The Pains.—Very marked soreness deeply seated about the place of origin of the ocular muscles so that every movement of the eyeballs is at once complained of as giving pain.
General pains all over the body, more especially of the back and about tendinous insertions of the muscles which cause the pains to be referred to the joints. The knee-joint pains are probably the most frequent. The rachialgia may be as great as that in variola or yellow fever.
The Eruption.—The characteristic eruption does not appear until about the time of the intermission or with the accession of the terminal fever.
The fall of fever about the third or fourth day is often attended by a critical epistaxis, sweat or diarrhoea, to be succeeded by an intermission of from one to three days of a feeling of well-being. About this time or with the secondary rise of fever the true dengue rash appears. It is at first noted about the bases of the thumbs and extending over the dorsal surfaces of the wrists. Almost simultaneously a measles-like rash appears over the dorsal and internal surfaces of the big toe extending to the ankle, especially over the internal malleolus. Later on the elbows and knees may be involved or the rash may cover thickly the entire body. A carmine flush of the palms of the hands and soles of the feet is not uncommon. A furfuraceous desquamation with much itching at times follows the eruption. The so-called primary eruption is nothing more than an initial flushing of the face, it is ephemeral. The true dengue rash may also be quite ephemeral but usually it lasts for two or three days, or possibly four or five days.
The Nervous System.—Besides the headaches we have insomnia and depression which extends through convalescence. Apathy is marked.
The Blood.—This shows a leucopenia of about 4000 from shortly after the onset together with a reduction of the percentage of polymorphonuclears to about 45%. During the attack the eosinophiles are decreased but there is an increase during convalescence.
DIAGNOSIS
The two diseases with which dengue can be most easily confused are influenza and yellow fever. In fact when the great pandemic of influenza (1890) first made its appearance in France, many regarded it as an atypical form of dengue.
The respiratory involvement of influenza and the eruption and comparatively slow pulse of dengue are the principal points of difference. It must be remembered that affections in the tropics, diagnosed as influenza, have shown but slight respiratory symptoms, the cases being more of a nervous or intestinal type. The eruption of dengue may fail to appear or be missed in the study of the case. The blood findings should aid in differentiation from influenza as is also true of yellow fever, a disease which likewise has blood findings of practically a normal character. Other than the blood picture we have in yellow fever (1) albuminuria, coming on about the second day, and (2) jaundice appearing about the third day. In dengue the eruption appears from the third to the fifth day. Albuminuria is absent in dengue.
Dengue may be mistaken for measles, but the early coryza, Koplik spots and marked rash, first appearing about the face, should differentiate.
In scarlet fever the rapid pulse, angina and leucocytosis should be sufficiently differentiating.
Confusion with articular rheumatism may arise when the pain about wrists, knees and ankles has been mistaken for true joint involvement.
The headache and backache of smallpox may be confusing until the eruption about the forehead appears. The leucopenia of dengue is the main differential point in these first three days of doubt.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—This would seem to rest entirely upon the question of destruction of mosquitoes and prevention of the mosquito from biting a patient. In dengue the virus is apparently in the blood for four or five days so that screening of patients is necessitated for a longer period than for yellow fever or phlebotomus fever.
=Treatment.=—The malaise and depression are generally so great that the patient keeps his bed voluntarily. A light diet is indicated although the anorexia is so marked that it is difficult to persuade a patient to take food.
Cold spongings, provided the patient is not disturbed by being moved, are of value for the insomnia. Phenacetine may be given for the relief of the headache and backache. It is rarely necessary to give morphine.
During convalescence tonics are indicated and if there is any condition where a good wine is of value, it is in this, to counteract the terrible depression. It has been suggested that adrenal insufficiency may account for the asthenic, protracted convalescence and from this standpoint adrenalin has been recommended.
DENGUE-LIKE FEVERS
PHLEBOTOMUS OR PAPPATACI FEVER
=Etiology and Epidemiology.=—This fever, which is often called three-day fever, on account of its running its course in this period, is caused by a filterable virus. This virus only seems to be in the blood of the patient’s peripheral circulation during the first twenty-four hours of the illness, blood abstracted toward the end of the second day and injected into a well person failing to reproduce the disease.
If the blood is filtered through a Pasteur candle F, the filtrate will set up an attack just as well as the unfiltered blood, in this respect being like dengue and yellow fever. Couvy reports having found spirochaetes in the blood 3 hours and 24 hours after the onset.
The transmitting agent is a moth midge, Phlebotomus papatassii. This midge, as is true of the psychodid family, to which it belongs, is very hairy. It has long slender legs and narrow wings. The proboscis is as long as the head and the lancets project beyond the labium.
The female alone bites, which act takes place chiefly at night; cool, moist, shady places, away from sleeping rooms, being preferred in the day time. The insect is a persistent, vicious feeder, difficult to escape from, as mosquito nets offer no protection. It takes from six to eight days after feeding on a patient in the first day of the fever before the midge is capable of transmitting the disease, this being in accordance with the twelve-day developmental period in the mosquito, that holds for yellow fever. Doerr thinks that the pappataci virus may be transmitted hereditarily by the insect to the egg.
At present, of the genera of the three families of midges, only Phlebotomus is known to transmit disease. P. papatasii transmits phlebotomus fever in the Balkans. P. minutus is the host at Aden. Another species, P. perniciosus, can transmit the disease. These moth midges are 2 mm. in length and have the body densely covered with long yellow hairs. The second longitudinal vein has three distinct branches. The antennae have 16 restricted joints and the proboscis is as long as the head. The species of Phlebotomus are separated by slight variations in wing venation, palpal lengths, etc., thus the second segment of palpi of P. papatasii is a little longer than the third one, while with P. perniciosus these segments are of equal lengths. In P. minutus the second segment is only half the length of the third. The insect lays about 40 eggs in damp dark places. The period of metamorphosis from egg to insect is about one or two months, according to temperature.
Phlebotomus larvae die out in dry soil and very wet earth is unfavorable. Moderate moisture and protection from light seem necessary for their development. The remains of dead insects also seem to make good breeding places. It is in cracks of old damp brick or stone walls that the female most often deposits her eggs. Caves are also selected.
Blood seems necessary for the fertilization of the eggs but lizard blood seems more common in the stomach of P. minutus than human blood. They have also been observed to feed on other reptilian bloods. The female insect has been kept alive in captivity up to forty-six days.
Cases first appear in the late Spring and the disease becomes epidemic during the Summer.
An attack produces quite an immunity.
The disease has chiefly been studied in the Balkan States but undoubtedly it is widespread.
The disease is almost never fatal so that we know nothing of its pathology.
=Symptomatology.=—The symptoms will answer perfectly for cases of dengue one sees in a dengue epidemic in which, instead of the saddle-back course of fever, we have a three-day primary rise and then a fall to normal without any secondary fever rise. Cases of phlebotomus fever are occasionally reported where the fever continues seven or eight days.
The symptoms as usually given are as follows: After a period of incubation of from three to six days there is an abrupt onset with congested face and injected conjunctivae. There is pain in head, eyes and back. There is marked malaise with great depression of spirits. There is anorexia with coated tongue and rarely vomiting and diarrhoea. There may be some congestion of the pharynx and even a slight bronchitis. So much in common with influenza has it clinically that a synonym is summer influenza. The liver and spleen are normal. Mental depression is frequently noted. Epistaxis is rather common.
There is a leucopenia and polymorphonuclear percentage decrease. The two points which are chiefly advanced in its clinical differentiation from dengue are (1) slow pulse, a bradycardia, and (2) only three days of fever and absence of eruption.
SEVEN-DAY FEVER
Rogers first described a dengue-like fever which occurred in India during the summer months as seven-day fever. The fever course was at times typically saddle-back and again would be of continuous type. A pulse relatively slow for the temperature is generally recorded, together with sudden onset and general malaise. The spleen is at times enlarged and there is a definite leucopenia and polynuclear percentage reduction. The eruption is only occasionally present (about 10%) and is an erythema which makes its appearance on the extensor surfaces of the forearm about the fourth day after the onset.
=Etiology.=—In cases similar clinically to the seven-day fever of Rogers, Ido, Ito and Wani have found a spirochaete resembling that of infectious jaundice and designated Leptospira hebdomadalis. It can be differentiated from L. icterohaemorrhagiae by immunity reactions. It is found in the blood during the fever period and young guinea pigs can be infected by such blood either subcutaneously or by mouth. The organism can be cultured by Noguchi’s method. The spirochaete is to be found in the urine towards the end of the disease and the urine is probably the source of infection. In Japan field mice seem to be the carriers of this spirochaete. In about 3% of such rodents the spirochaete can be found in the urine and the disease is limited to the sections in which the field mice are found. There is practically no mortality and the treatment is symptomatic.
SAND-FLY FEVER, AND THREE-DAY FEVER
These dengue-like fevers of India are practically identical clinically with phlebotomus fever. The usual idea is that dengue epidemics are far more explosive in character than is true of epidemics transmitted by the sand-fly.
The strongest point in differentiation of sand-fly fever and dengue is that neither confers any immunity for the other disease.
The distinctions of enlarged glands and break-bone pains are often advanced as characteristic of dengue and not of sand-fly fever. I have never observed other than slight glandular enlargement in dengue cases.
SIX-DAY FEVER
Deeks has described a disease from Panama with a dengue-like clinical course.
There were but slight changes from normal in the pulse rate or blood findings. Some of the cases showed a late scarlatiniform eruption.
It was considered that the continuous fever for six days and the enlargement of the spleen, which accompanied the disease, differentiated it from dengue.
XXXVII. TSUTSUGAMUSHI
DEFINITION AND SYNONYMS
=Definition.=—This is an acute febrile disease caused by the bite of the larval Kedani mite of the region where the infection prevails. The onset is characterized by headache and giddiness, a rather rapidly rising temperature and swelling of the lymphatic glands draining the region in which is situated a small necrotic ulcer marking the site of the bite. With injected conjunctivae, continuous fever and hyperaesthesia, the disease goes on for about a week when a macular eruption appears about face, then chest, extremities and trunk. About ten days after the appearance of the eruption there is a fall of fever by lysis.
=Synonyms.=—Flood fever, Japanese River fever, Kedani mite disease. Shimamushi.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—There are records which would indicate that the disease has been known for more than 1000 years.
=Geographical Distribution.=—It is only in the western part of the island of Nippon, when the banks of the Shinanogawa are inundated each spring, that we find the disease. The disease is supposed to be confined to Japan although Ashburn and Craig have thought a disease observed by them in the Philippines as possibly identical.
ETIOLOGY AND EPIDEMIOLOGY
The cause is unknown, but has been attributed by some to various bacteria and by others to a protozoon.
Nagayo attaches importance to piroplasm-like forms found in the spleen and lymphatic glands.
Kawamuro and his colleagues could not demonstrate any organism by any method of examination. The virus is in the blood and even as small an amount as 0.001 cc. may infect a monkey although 0.1 cc. is usually required. The virus is present also in the enlarged lymph glands. Heating the blood at 50°C. for 10 minutes destroys the virus. Recently Hayashi has reported as cause minute rod, ring-shaped or spheroid bodies which when stained with Giemsa’s stain are brought out in the lymphocytes and endothelial phagocytes of lymph nodes and spleen. They also occur in the blood plasma and in severe cases in red blood cells. He has transmitted the disease to monkeys, guinea pigs and rabbits. These bodies resemble bacteria, in this respect resembling the organisms of typhus and spotted fever of the Rocky Mountains. Hayashi regards the organism as resembling Theileria parva and Bartonella bacilliformis, and believes he has shown the field mouse to be a reservoir of the virus.
The disease is not communicable from person to person and only follows the bite of a larval mite, Trombidium akamushi (Leptotrombidium akamushi). This is a minute orange-red arachnoid which can scarcely be seen with the naked eye. This mite is only a source of danger in the region of the inundated river banks, its bite not producing the disease elsewhere.
Persons harvesting hemp during August are liable to contract the disease if bitten by the larval mite.
The mite is found in large numbers on the ears of field mice, these hosts, however, not appearing to be suffering from any particular disease.
PATHOLOGY
Other than the local ulcer and the swollen regional glands, there is little that is definite. The spleen shows enlargement and there is also swelling of the mesenteric glands. The lower part of the ileum may show injection.
SYMPTOMATOLOGY
=A Typical Case.=—About one week after receiving the bite of the larval mite, which may not have been noticed by the patient, there develop chilliness, giddiness and headache, with a rising temperature. In two or three days from the onset, painful glands are noticed in certain regions as of groin, axilla or neck. From these glands we can often by following inflamed lymphatics find the small necrotic ulcer which is often located in the armpit or in the region of the genitals. There is a dark red areola about the ulcer which is only slightly tender. The glands are not very much enlarged and are not excessively tender. There may be general glandular enlargement following that of the primary swellings. The pulse rate is only from 80-100, notwithstanding the rise of the fever to 104°F. or even 105°F.
The body is decidedly hyperaesthetic and the conjunctivae are injected. There is frequently deafness. About the seventh day a macular eruption appears first on the face and then spreads to chest, extremities and trunk. The eruption never becomes petechial. The tongue becomes dry and cracked. There is often a cough. The blood shows a leucopenia. The eruption disappears in from seven to ten days and the fever becomes remittent or intermittent and, after a few days, reaches normal. Parotitis may occur as a complication.
Schüffner has described a similar disease from Sumatra. The mortality is, however, only 3% as against the 30% in Japan. He thinks it is transmitted by a tick. In his cases the necrotic ulcer and glandular enlargements were followed by a roseola which reached its maximum on the eighth to tenth day and was most marked on the trunk and flanks. The nervous symptoms resembled typhoid fever and there was a lymphocytosis.
Symptoms in Detail
The Nervous System.—There is marked giddiness and headache at the onset. Hyperaesthesia of the body is quite characteristic. There is often delirium at night. Deafness is frequently noted.
The Cutaneous System.—A small necrotic ulcer about ⅙ inch in diameter, with a dusky red areola, is noted at the site of the bite of the larval mite. The healing of the ulcer is delayed well on into convalescence.
About one week after the onset a dusky macular eruption appears first on the face (cheeks), then going to the chest, legs, forearms and trunk. It is not marked on neck, arms or thighs. It never becomes petechial.
Fever Course.—The temperature, which on the first day or two reaches only 101° to 103°F., becomes later on higher and continuous. About the tenth day from the appearance of the eruption it begins to fall, becoming remittent and then intermittent.
The Lymphatic System.—Very characteristic is the swelling of the glands proximal to the initial ulcer. The connecting lymphatics may be inflamed. Later on other glands may show slight swelling and tenderness.
The spleen is usually enlarged.
The Blood.—There is no change in the red cells but there is a leucopenia.
DIAGNOSIS
In the differential diagnosis the limited geographical distribution should prevent error and, in particular, where one has the initial necrotic ulcer, with enlargement of the glands draining the region in which it is located, there should be little confusion. Of course plague may have a primary vesicle or ulcer with enlargement of neighboring glands; these glands however are matted together and are exquisitely tender.
Then too the eruption of tsutsugamushi and the early and more stuporous state of plague should differentiate, even without the aid of the laboratory.
It is usual to consider tsutsugamushi, typhus fever and spotted fever of the Rocky Mountains as having many characteristics in common. These diseases may best be differentiated by the fever course and eruption as shown in the following table:
------------------+-------------------------+--------------------------- | Fever course | Eruption ------------------+-------------------------+--------------------------- Tsutsugamushi |Fever increases each day |Begins on face, then chest, | until reaching maximum | legs, forearms and trunk. | about 4th or 5th day. | Does not become petechial. | Fall by lysis after | First appears about 7th | fading of eruption. | day. ------------------+-------------------------+--------------------------- Tabardillo. |Onset and termination |Begins on abdomen, sides of Typhus fever. | of fever characterized | chest, thence going to Brill’s | by considerable | extremities. Petechial disease. | abruptness. | tendency. First appears | | about 5th day. ------------------+-------------------------+--------------------------- Spotted fever |Gradual rise during a |Begins on forearms and leg. of the Rocky | week with lysis. | Petechial tendency. May Mountains. | | have gangrene of prepuce | | and scrotum. First appears | | on 2d to 5th day. ------------------+-------------------------+---------------------------
TREATMENT
There is no specific treatment. It may be necessary to use drugs to combat the insomnia.
The serum of monkeys which have recovered from the disease seems to have some value.
XXXVIII. SPOTTED FEVER OF THE ROCKY MOUNTAINS
DEFINITION AND SYNONYMS
=Definition.=—The disease is chiefly reported from certain sections of the states of Montana and Idaho. The virus is not filterable and is probably bacterial in nature and is transmitted solely by the tick, Dermacentor andersoni, which arthropod host gets its infection from certain rodents of the section serving as virus reservoirs.
Maxey described the disease as follows: “An acute endemic, noncontagious, but probably infectious febrile disease, characterized clinically by a continuous moderately high fever, severe arthritic and muscular pains and a profuse, petechial eruption in the skin, appearing first on the ankles, wrists and forehead but rapidly spreading to all parts of the body.”
=Synonyms.=—Rocky Mountain fever. Tick fever of the Rocky Mountains. Black fever. Blue disease.
HISTORY AND GEOGRAPHICAL DISTRIBUTION
=History.=—The disease was first noted in the Snake River Valley of Idaho, about 1893, and in the Bitter Root Valley of Montana, about 1890. There is some evidence that the disease may have existed among the Indians prior to the advent of white settlers in the Bitter Root Valley. The disease was first described by Doctor M. W. Wood, U. S. A., in 1896. It is interesting to note that the first white settlers of the Bitter Root Valley suffered from what was considered a very fatal form of “black measles.”
In 1902 Wilson and Chowning reported that the disease was due to a piroplasm of the squirrel and that it was transmitted to man by the bite of a tick (Dermacentor venustus). Later Ashburn and others, while accepting the tick transmission, failed to corroborate the piroplasm etiology.
It is chiefly to Ricketts that we owe much of our detailed knowledge of the epidemiology of the disease.
The work of McClintic and Frick along lines of prophylaxis has given us practical measures for the control of the disease.
The views of Ricketts, Wolbach and Frick as to etiology are discussed under that heading.
=Geographical Distribution.=—The two best known regions of prevalence of the disease are the Bitter Root Valley of Montana and the Snake River Valley of Idaho. It is also reported from limited sections of Washington, Oregon and California, as also from Nevada and Utah.
In Wyoming it is rather widely distributed.
ETIOLOGY AND EPIDEMIOLOGY
=Etiology.=—Wolbach states that he has noted certain bacterial forms in the endothelial cells of the blood vessels of guinea pigs infected with the virus, as well as a very general distribution in infected ticks.
There are two morphological types—one, a chromatic-staining lanceolate diplococcoid organism, found in the circulating blood as well as in the endothelial cells, the other type—a blue-staining rod-shaped form.
Ricketts noted certain chromatin-staining bacteria, in man and in eggs of infected ticks, which were about 1 micron long by ⅓ micron broad, showed chromatin staining, were about the size of B. influenzae, and appeared as two lanceolate-shaped bodies. These bodies are now considered as belonging to the Rickettsia group of organisms. Wolbach has named the organism of spotted fever of the Rocky Mountains Dermacentroxenus rickettsi. In infected guinea pigs Wolbach found these bodies particularly abundant in the endothelial cells.
Frick has also found bodies within the red cells of human cases and infected guinea pigs, as well as extracellularly, which showed chromatin-staining characteristics, there often being an elongated reddish body joined on to a larger blue-staining protoplasm.
In 1902 Wilson and Chowning reported the finding of piroplasm-like bodies in the blood of human cases of Rocky Mountain Spotted Fever. Ricketts proved that the virus was not filterable. A tick, Dermacentor andersoni transmits the disease.
=Epidemiology.=—The transmitting tick, D. andersoni (D. venustus) lives on the domesticated animals of the region of geographical distribution of the disease. Ricketts showed that the reservoir of the virus was to be found in ground squirrels, chipmunks, mountain rats, etc., and that ticks feeding on these rodents become infected and transmit the disease to man. The guinea pig, white rat and monkey are also susceptible.
The virus can be propagated indefinitely in guinea pigs without loss of virulence by weekly blood inoculations in another animal. The virus seems to be transmitted by the salivary secretion of the tick and a tick once infected remains infective for the remainder of life.
Frick succeeded in obtaining anaerobic cultures from infected blood of a bacillus, somewhat resembling the B. typhi exanthematici of Plotz. These bacteria, however, did not show complement fixation with immune serum and were nonpathogenic to guinea pigs.
Spotted fever is a disease of rural districts and tends to give only one case to a house, thus indicating the negative rôle of bedbugs, lice, etc. It is at the time when ticks are most abundant, in the months of the spring, that the disease makes its appearance. The virus is in the blood during the entire febrile course.
PATHOLOGY
The cadaver shows marked jaundice with petechial spots on extremities and trunk.
There is marked venous engorgement and the blood is very dark and fluid.
In the blood vessels we have proliferation of the endothelial cells leading to thrombosis.
Ricketts noted enlargement of the lymph glands. The spleen is three or four times the normal size and is quite firm. Microscopically it shows extensive endothelial cell proliferation. The kidneys are enlarged and congested. Gangrene of the prepuce and scrotum are often noted.
SYMPTOMATOLOGY
The period of incubation is from five to ten days when the disease sets in with considerable abruptness, with more or less marked rigors, headache, malaise and severe pains of the larger joints, but without inflammatory changes.
Some cases present a prodromal period lasting a day or so with malaise and chilly sensations followed by the symptoms noted above. Hyperaesthesia and photophobia are apt to be present during the course of the disease.
The eruption first appears from the second to the fifth day as macules about the wrists and ankles, thence spreading over the extremities and extending to the trunk. These macules tend to become petechial.
The Pulse.—The pulse is not very rapid (90-110) and the fever steadily rises day by day from the initial 102°F to reach a maximum of about 105°F. by the end of a week or so. A toxaemic condition appears early.
A stuporous state is fairly common but in many cases the mind is clear throughout the course.
The spleen is palpable early in the disease and is quite firm, not soft like the spleen of typhoid fever.
The kidney involvement shows itself early as an albuminuria.
Constipation is rather a constant feature.
Icterus and vomiting tend to come on later in severe cases.
Gangrene.—Gangrene of the tonsils, scrotum and prepuce are more common in the milder type of the disease, as seen in Idaho, than in the more severe one of Montana.
There is leucocytosis early in the disease, falling to about 10,000 after a few days. There is an increase in the large mononuclears. The eosinophiles are decreased in percentage.
DIAGNOSIS
The association of a tick bite and proper geographical distribution is of prime importance. The more sudden onset, joint pains and negative Widal differentiate it from typhoid fever.
Typhus fever shows more marked abruptness of onset and decline of fever than does Rocky Mountain fever. The guinea pig, while susceptible to both infections, is more easily infected with this disease than with typhus fever.
As a matter of fact there are marked clinical resemblances between typhus fever and Rocky Mountain fever. Tsutsugamushi and trench fever also have points of resemblance.
PROGNOSIS
It is very remarkable that the disease should rather constantly give a mortality approximating 75 to 90% in western Montana and only about 5% for Idaho.
Where the nervous manifestations are marked the prognosis is more unfavorable. Death tends to occur in the second week and patients living through this week have a good chance for recovery. The death rate is greatest in old people and least in young children.
PROPHYLAXIS AND TREATMENT
=Prophylaxis.=—Dermacentor andersoni requires a long time to become attached and feed on the human host—at least one or more hours—hence inspection of one’s person for ticks after returning from exposure and removing those found would tend to prevent infection.
When these ticks attach themselves to the wool of grazing sheep, 87% seem to die, possibly from the effect of the fat in the wool.
Again such sheep can be dipped for further destruction of the ticks.
=Treatment.=—Just as with typhus fever the most important point in the care of the patient is good nursing. The room should be darkened and quiet maintained. Cool sponging lowers the temperature and is a tonic for the nervous disorders. An ice cap is good for the headache. The diet should be liquid and water should be given freely on account of the tendency to renal involvement.
There is a tendency to heart failure so that the recumbent position is demanded and cardiac stimulants indicated.
Michie and Parsons found sodium citrate of greatest benefit in treating infected guinea pigs and recommended it for human cases. It is to be used intravenously and about 60 cc. of a 5% solution given twice daily. Immune sera were tried out by Ricketts, but without result.