L. THE FAECES AND THE ALIMENTARY TRACT IN TROPICAL DISEASES…

L. THE FAECES AND THE ALIMENTARY TRACT IN TROPICAL DISEASES

THE FAECES

It is advisable to examine a stool macroscopically before taking up the microscopical examination. Pus or blood in stools may often be noted without the aid of the microscope.

The normal stool is sausage-shaped and soft.

The mucus of bacillary dysentery is opaque and grayish from the great number of pus and phagocytic cells. It is well to remember that Charcot-Leyden crystals, which are practically always absent from bacillary dysentery stools, are not infrequent findings in the amoebae-containing stools; of course, these crystals appear in other intestinal parasite infections.

In obstruction of the common bile duct we have acholic, whitish, foul-smelling stools. If the putty color be due to bacterial change exposure to the air will restore the brownish tinge.

Sprue stools are whitewash to putty-colored, pultaceous, and filled with air bubbles. The amount is excessive.

A very practical way of obtaining amoebae is to pass a rectal tube or a piece of drainage tube with fenestrations into the bowel, and amoebae may be found in the mucus filling the perforations in the tube.

Ordinarily the stool is best collected in quart fruit jars and examined as soon after evacuation as possible. The wooden spatula-like tongue depressors are well adapted for handling the specimen.

In examining a stool, it is well to color the drop of faeces, which is to be covered with the cover-glass, with a small loopful of ½% solution of neutral red. If diluting fluid is used, it should be salt solution, and not water. The neutral red tinges the granules of the endoplasm of amoebae and flagellates a very striking brown-red color, thus differentiating them from vegetable cells or body cells.

Encysted protozoa are difficult to diagnose, unless one possesses considerable experience. In examining for encysted amoebae as well as for bringing out the number of flagella of flagellates I now use the following method: Take a clean slide and make a vaseline line across it about 1 inch from the end. A drop of the iodine solution is placed on the slide about ½ inch from the vaselined line and a suitable portion of the faeces to be examined is emulsified in it. The edge of a square cover-glass is then applied to the vaselined line and allowed to drop on the preparation. By pressure suitable thicknesses of fluid can be examined. There is an absence of current motion.

Epithelial cells are generally more or less disintegrated. In the mucus of bacillary dysenteric stools, however, large intact phagocytic cells are frequent, which may be mistaken for encysted amoebae, and the polynuclear cell count averages 90% as contrasted with the average polynuclear count of 7.5% in amoebic dysentery.

When a smear preparation is desired, we may smear out a fragment of mucus and stain by Romanowsky’s or Gram’s method. Beautiful preparations may be made by mixing the faeces with water, then centrifuging for one minute. This throws down vegetable débris and crystals. Now decant the supernatant fluid, which holds the bacteria in suspension, and add an equal amount of alcohol. Again centrifuge, decant, and smear out and examine the bacterial sediment.

Simply taking a small mass of faeces and emulsifying it with a wooden toothpick on a concave slide in 70% alcohol—then, after the sediment settles, taking up a loopful with platinum loop from the surface and smearing out, gives a very satisfactory smear. Gram’s method, with dilute carbol fuchsin counterstaining, gives the best picture.

To culture for typhoid, dysentery, cholera, or other bacteria, take up the material in a tube of sterile bouillon and smear it out with a swab over a lactose litmus agar plate or an Endo or Conradi-Drigalski plate. Before streaking the plates they should be very dry on the surface. This can be best done by pouring the melted agar into a plate with a circular piece of filter-paper in the lid and placing in the incubator for one-half hour to dry. The filter-paper absorbs the moisture. Then inoculate the surface of the plate with the faecal material.

=Teague Medium.=—We have formerly preferred the Endo plate for typhoid work and the lactose litmus agar when culturing for dysentery bacilli. More recently we have obtained most satisfactory results with the Teague medium. The colon colonies, after eighteen hours, are deep black and opaque while the typhoid-dysentery group show colorless, transparent colonies.

The medium is prepared as follows: Nutrient agar is made in the usual way, containing 1.5% agar, 1% Witte’s peptone, 0.5% sodium chloride, and 0.5% Liebig’s meat extract, to the liter of distilled water. It is cleared with egg-white, placed in flasks, and sterilized in the Arnold sterilizer on three successive days. The reaction is brought to plus 0.8. The agar is melted and saccharose 0.5% and lactose 0.5% are added. The medium is then heated for ten minutes in the Arnold. To every 50 cc. of the medium are added 1 cc. of 2% yellowish eosin and 1 cc. of 0.5% methylene blue. The mixture is shaken and plates poured. Eosin solution should be added first.

=Occult Blood.=—In performing the test for occult blood, one should exclude the possibility of blood reaching the bowels from an extraneous source, such as ingested foods, mouth, nose, lungs and vagina, and the absence of interfering substances should be ensured. An absolute milk diet, or, at least, a diet containing neither meat nor green vegetables, is indicated for two or three days prior to the test, and all medication should be suspended. The technique noted on page 524 should be followed scrupulously when dealing with faeces.

It has been suggested that the absence of occult blood from the faeces may be accepted as an indication of cure in ancylostomiasis.

=Ova in Faeces.=—It is in the faeces we examine either for the parasites or for their ova in connection with practically all the flukes, except the lung fluke and the bladder fluke; for intestinal taeniases and for practically all the round-worms, except the filarial ones.

In the tropics, the examination of the faeces exceeds in value that of urine and is possibly more important than blood examinations.

=Helminthiasis Statistics.=—There is one point in connection with the statistical reports as to the presence of intestinal parasites in a given section of the tropics that I desire to emphasize.

Because a limited district shows a certain prevalence of intestinal parasites we should not conclude that the entire country from which such findings emanate shows a similar extent and type of infection. Take for instance the Philippine Islands.

In 1910, there were made in Cavite Province 932 stool examinations upon specimens from cases of sick people and of these only such patients as it was thought required such an examination for diagnostic reasons were made to bring such a specimen of faeces.

Of the 932 examinations, 135 or 14.4% failed to show the presence of intestinal parasites or their ova. The remaining positive examinations gave findings as follows:

-------------------+----------------------+--------------- Organism | Number of infections | Per cent. -------------------+----------------------+--------------- Ascaris | 627 | 67.2 Trichocephalus | 607 | 65.1 Flagellates | 135 | 14.4 Amoebae | 111 | 10.9 Hookworm | 23 | 2.4 Taenia saginata | 3 | 0.3 Balantidium | 1 | 0.1 Strongyloides | 1 | 0.1 -------------------+----------------------+---------------

At Bilibid Prison, Garrison encountered amoebic infection in 23% of the cases. In the medical survey of Taytay, his findings were 2.7%. Rissler and Gomez report only 0.39% of amoebic infection in their examinations in Las Piñas and no cases showing such infections in Tuguegarao and Santa Isabel. Such numbers are in striking contrast with those of former investigators, some of whom have reported as high a percentage of infection as 70.

Our findings as regards flagellates (14.4%) corresponded fairly closely with those of Garrison, namely, 21% at Bilibid and 5.5% at Taytay.

Garrison, for Trichocephalus infection, obtained 59% at Bilibid and 77% at Taytay; Rissler and Gomez give 53% at Las Piñas; 25.9% at Tuguegarao, and 6.23 at Santa Isabel. Our findings were 65.1%.

As regards Ascaris we found a higher rate of infection than for any other parasite (67.2%). Garrison encountered 26% at Bilibid and 82.9% at Taytay. The percentages of Rissler and Gomez are 77, 73, and 60 respectively for Las Piñas, Tuguegaroa, and Santa Isabel.

Garrison noted at Bilibid an incidence second only to Trichocephalus for hookworm infection, namely 52%. His percentage of infection at Taytay was 11.6. Rissler and Gomez found 11.14% of all cases examined infected with hookworms at Las Piñas, 8.01% in Tuguegarao, and 45.38% in Santa Isabel. We noted only 2.4% for Cavite, San Roque, and Caridad.

Our findings as regards Strongyloides (0.1%) were far below those reported by Garrison at Bilibid (3%) and at Taytay (0.7%). Rissler and Gomez found 2.24% infected in Las Piñas, but no cases were encountered in Tuguegarao and Santa Isabel. The same factors influencing hookworm infection in this locality may be operative for Strongyloides. Garrison found 0.2% of the individuals examined at Taytay to be infected with ciliates, while Gomez and Rissler failed to find such infections at Tuguegarao or Santa Isabel. We found a single case in the 932 examinations.

THE ALIMENTARY TRACT

The Mouth

In pellagra we have moist fissuring at the angles of the mouth with a large indented tongue with central coating and bare tip and sides. There is often a glairy mucus covering these red borders on the side. The fungiform papillae are prominent. Later on the tongue may become fissured and uniformly red. The buccal mucosa shows a carmine flush. The gums are tender but there is not the tendency to aphthous ulcers one sees in sprue. The flow of saliva is frequently increased.

In sprue there is at first great sensitiveness of the buccal mucosa so that articles of moderate pungency give rise to painful burning sensations. The tongue becomes quite sore with vesicle formation along borders and tip which soon turn into ulcers. Ulcerations also occur on the buccal mucosa, particularly at the site of the posterior upper and lower molar teeth (Crombie’s ulcer).

The congestion causes a great increase in mucus especially about the faucial pillars and pharynx. Ulcers are common about the fraenum of the tongue. While the tongue is coated at first with red ulcerated tip and sides it later becomes bare of any coating, red and finally even glazed as though varnished. It is at times fissured.

Onyalai.—A very peculiar disease of Portuguese West Africa and possibly the Soudan region, known as onyalai is characterized by the appearance of blood-distended vesicles of the mucosa of the cheeks and hard palate. The tongue is often swollen. The skin may show haemorrhages and haematuria is not infrequent. The mouth blebs vary in size from that of a split pea to a diameter of ½ inch or more. The cause is unknown.

Herpes labialis is not so common in tropical as in temperate climate malarias. It is absent in plague pneumonia.

In leprosy the nodules which form on the inside of the cheeks and fauces tend to show ulceration and thickenings. The discharges from the ulcerations in the nose, especially that on the vomer, reach the pharynx and such leprosy bacilli-containing discharges may be expectorated and cause one to consider the material as coming from the lungs.

In yellow fever the bleeding from the gums usually precedes the black vomit.

In kala-azar and possibly in malaria we may have gangrenous conditions of the cheek, as cancrum oris.

In the miliary type of verruga we may have the granulomatous lesions appearing on the mucous membranes of the mouth.

In typhus fever the mouth is strikingly foul with marked sordes covering the teeth. The dry brown tongue in this disease is known as the “parrot tongue.”

We may rarely have parotid gland enlargement in Malta fever, malaria and tsutsugamushi.

Parotitis is not uncommon in typhus fever. A type of parotitis which differs from mumps in not being contagious has been reported from the Philippines.

Stomach and Oesophagus

Very important in diagnosis is a tenderness in the pyloric end of the stomach, which is brought out by attempting to palpate the epigastric region. It is marked in yellow fever and acute pernicious beriberi as well as in blackwater fever and bilious remittent fever. We also frequently have epigastric tenderness, extending to the right, in ancylostomiasis.

Hookworms patients are often “pot-bellied” and the craving for eating unusual articles, as earth, may be connected with the gastric hyperacidity which the patient desired to neutralize with alkaline earth.

Sprue gives a flatulent dyspepsia with gaseous eructations.

Pellagra gives eructations and pyrosis and very common is a burning sensation going up from the stomach along the line of the oesophagus.

The esophagus is raw in sprue so that swallowing is painful.

Nausea and Vomiting

So many diseases are attended with nausea, besides those in which nausea is accompanied by rather constant vomiting, that it would hardly seem advisable to consider it alone. At the same time the slight nausea which often accompanies bacillary dysentery, as one of the manifestations of toxaemia, is of value in differentiating this type of dysentery from the amoebic one.

In yellow fever there may be early vomiting of whitish or bile-stained mucus but the well-known black vomit is a later feature, only occurring after the fourth day when the other haemorrhagic manifestations set in.

Bilious vomiting is the feature in bilious remittent fever which causes the patient the greatest distress.

In blackwater fever the frequent retching and bilious vomiting tend to exhaust the patient and the persistent vomiting of green bile often precedes death.

Bilious vomiting may be quite a feature of the icteric type of relapsing fever.

Vomiting sickness.—There is a disease known as vomiting sickness which has been noted in Jamaica. It occurs chiefly in children and has a sudden onset with marked vomiting followed by cerebral symptoms and great mortality. Some have thought the disease to be yellow fever but the fever and jaundice of that disease are absent. Scott has thought it to be epidemic cerebro-spinal meningitis, but more recently has suggested that it is possibly due to the eating of some poisonous substance, plant or otherwise, and that it is not an infectious disease. It is now recognized as due to ackee poisoning.

Vomiting is often a sign of dangerous vagal involvement in acute pernicious beriberi. Some consider that the extreme dilatation of the right heart, pressing on the stomach, may be the excitant of this vomiting.

The vomiting of cholera follows the diarrhoea. The material vomited may be of the same character as the rice-water stools.

In ptomaine poisoning vomiting precedes the diarrhoea.

Rarely a liver abscess may burst into the stomach, in which case we would have the vomiting of pus. Of course the more common route is by the lungs in which case the chocolate-colored liver abscess pus would be coughed up instead of vomited up.

The Intestinal Tract

It is usual to consider constipation as a clinical feature of such diseases as plague, yellow fever, Malta fever, beriberi and tsutsugamushi, as well as typhus fever.

Abdominal pains are most often connected with dysenteric conditions and it is customary to state that the greater the tormina, or intestinal griping, the nearer is the dysenteric process to the caecum.

In cholera the cramping of the abdominal muscles may follow that of the calf muscles.

In sprue we may have a doughy sensation on palpating the abdomen due to the fermenting contents of the intestine.

In the algid type of pernicious malaria the abdominal griping may be severe.

Tenesmus is the condition which along with tormina gives a diagnosis of some form of dysentery.

In rectal schistosomiasis the thickenings and blood extravasations, resulting from the eggs extruded by the fluke, may give rise to prolapse of the rectum. This may also occur in severe bacillary dysentery and in a disease of British Guiana and Venezuela, known as epidemic gangrenous rectitis, prolapse and gangrene of the rectum may occur. The symptoms are those of gangrenous dysentery.

Diarrhoea

The chronic diarrhoeas of the tropics are often associated with amoebic dysentery and in such cases we generally get a history of recurring attacks of diarrhoea separated by periods of constipation.

In sprue the condition generally sets in as a morning diarrhoea, very profuse and painless. Hill diarrhoea also shows frequent stools of whitish color from early morning until about noon.

The typical stool of sprue is a gas-permeated, putty-colored, offensive mass, extraordinarily copious.

In cholera the rice-water stool, which is not attended by pain, causes an unusual sense of prostration even at the onset of the stage of evacuation.

In pellagra we often have a recurring diarrhoea or mild manifestations of dysentery.

The stool of pellagra is darker and less copious than that of sprue and shows only a normal fat content while that of sprue is very fatty—as much as 30% of ingested fat appearing in the sprue stool as against the 5% for the normal one.

In Japanese schistosomiasis, following the stage of urticarial fever, we have our best diagnostic means in examining the blood-tinged bit of mucus capping the stool for the spineless ova of the fluke.

The fluke diseases of the liver and intestines give rise to various disturbances. The diagnosis is by the finding of the specific ova.

In infections with Strongyloides stercoralis there may be vague manifestations of neurasthenia and diarrhoeal disturbances. Cochin China diarrhoea was once thought to be a Strongyloides infection.

Infections with amoebae, intestinal flagellates and ciliates are discussed under dysentery.

Intestinal flagellates are so common in the stools of well people in the tropics that one should be very careful in assigning a pathogenic rôle to them.

It is now generally accepted that Lamblia (Giardia) can bring about exhausting diarrhoeas.

Intestinal Myiases

In the tropics vague intestinal disturbances or violent abdominal cramping may be brought about by dipterous larvae in the intestinal canal. The symptoms may be those of a dysentery and may be attended with fever and malaise. The biliary tract also may be invaded. For a more detailed statement of the several myiases, see Chapter XXV.

The larvae usually obtain access to the alimentary tract in food taken in by the mouth. Flies of the genus Sarcophaga are prone to deposit their larvae on food, especially meat that is somewhat tainted. Other flies, as Musca or Anthomyia, may lay their eggs on food. Flies of the genus Anthomyia tend to lay their eggs on plants.

It is possible for a fly to deposit its eggs or larvae about the anus while the man is at stool.

Great care must always be observed to assure one’s self that fly larvae, which may be present in the stool, have not originated from larvae deposited on the stool subsequent to its passage.

DETERMINATION OF DIPTEROUS LARVAE

There are certain points in the anatomy of dipterous larvae which must be considered in recognition of the genus or family of the flies concerned in the various myiases. The broad extremity is the posterior one and the tapering one the anterior. The dark hook-like processes, which may be in pairs or fused, project from the anterior or head end and above them is a pair of projecting papillae. The second segment from the head has on either side projecting hand or fan-like structures with varying numbers of terminal divisions, 4 to 40 or more. These are the anterior spiracles.

The large terminal segment has on its posterior surface two chitinized plates with 3 slits of various architecture in each. These are the posterior stigmal plates and are the structures we pay particular attention to in identification. In the early larval stages there is only one slit; in the second stage there are two. It is only in the fully developed larval stage that we note the characteristic 3 slit stigmal plates. The presence or absence of a rounded protuberance or button at the base of each stigmal plate should be looked for. The area carrying the stigmal plates may be sunken to form a pit. (See Fig. 135.)

KEY TO LARVAE OF THE MYIASES. (BANKS.)

1. Body with lateral and dorsal spinose processes Homalomyia. Body without such processes 2 2. Body ending in two fleshy processes; rather small species 3 Body truncate or broadly rounded at end 4 3. Processes bearing the stigmal plates; body about 5 mm. long Drosophila. Processes not bearing the stigmal plates; body 10 mm. or longer Piophila. 4. But one great hook; posterior stigmal plates with winding slits; no distinct lateral fusiform areas; tip of body with few if any conical processes Muscinae. With two great hooks; slits in the stigmal plate not sinuous 5 5. No tubercles about anal area; no distinct processes around stigmal field 6 Distinct tubercles above anal area; often processes around stigmal field; lateral fusiform areas usually distinct 7 6. Stigmal plates on black tubercles; lateral fusiform areas distinct Ortalidae. Stigmal plates barely if at all elevated; lateral fusiform areas indistinct; stigmal plates often contiguous or nearly so; slits long and subparallel Trypetidae. 7. Slits in stigmal plates rather short, and arranged radiately 8 Slits slender and subparallel to each other 9 8. Two tubercles above anal area; stigmal field with distinct processes around it Anthomviidae. Four or more tubercles above anal area; slits of stigmal plates usually pointed at one end Muscinae. 9. A button to each stigmal plate; slits rather transverse to body Calliphorinae. No button to stigmal plates, slits of one plate subparallel to those in opposite plate; plates at bottom of a pit Sarcophagidae.

A specimen of stool containing fly larvae may be incubated in a moist chamber in order to obtain the imago for species determination.

Spotted a typo or a problem in this chapter? Tell us

LI. THE JOINTS, BONES AND MUSCLES IN TROPICAL DIAGNOSIS

In considering the diagnostic significance of bone and joint manifestations of tropical diseases, it is essential that the practitioner in the tropics bear in mind the cosmopolitan arthropathies.

It should be remembered that lesions of joints may accompany or follow almost all infectious diseases, and that it is often impossible to ascertain if the lesions be due to the actual presence of organisms within the joint or to the action of toxic substances elaborated elsewhere; so that infectious arthritis is broadly defined as arising from the presence within the body of a focus of infection. This definition is further expanded to include joint affections of intestinal origin, and also those in which neither the causal organism nor its focus of origin is discoverable, but which by analogy we unhesitatingly recognize as being due to an infective agent.

It is to be noted that the lesions of arthritis may develop either in the intra-articular membranes or in the bony parts adjacent to a joint, and that they may remain confined to their primary site or eventually extend to involve other tissues.

INFECTIOUS ARTHRITIS

A. Of known etiology.

May be acute or chronic. Examples are: Gonorrhoea, typhoid, tuberculosis, bacillary dysentery, pneumococcus infections, pyogenic cocci, filariasis, Malta fever, secondary to any recognized focus.

B. Of unknown etiology.

May be acute or chronic: Examples are: Acute articular rheumatism, rheumatoid arthritis, four types beginning with acute symptoms, one type having insidious onset. These are often due to unidentified foci.

NONINFECTIOUS ARTHRITIS

A. Traumatic.

1. Acute, due to known traumatism.

2. Chronic, generally static in origin, or due to chronic strain or irritation. Possibly includes villous arthritis of the knee and hypertrophic arthritis in the young.

B. Trophic.

1. Metabolic. Examples are gout, psoriasis and probably hypertrophic arthritis.

2. Senile.

3. Neuropathic. Examples are tabes, leprosy, syringomyelia, Raynaud’s disease, and scleroderma.

4. Arteriosclerotic.

C. Blood dyscrasias, as haemophilia, anaemias and scurvy.

D. Toxic, as lead poisoning.

The diseases of more peculiar importance for the tropics in which joint involvement must be considered in the diagnosis are the following:

Malta Fever.—This infection offers a good example of a disease in which joint symptomatology is of diagnostic and therapeutic importance. A prolonged typhoid-like course with sudden and painful swelling of various joints, hip, shoulder, ankle or costo-vertebral articulations, if occurring in the endemic area of Malta fever, would at once make one suspect this disease. Typhoid does not give painful joints, dengue is not accompanied by joint swelling, while gonorrhoeal polyarthritis will be accompanied by other evidence of gonorrhoeal infection.

The neuralgias, sciaticas and painful joints, together with the sweats which exhaust the sufferer from Malta fever, often tempt both patient and physician to resort to narcotics. Acute or subacute effusion into one or more joints is present in at least 40 per cent of cases of Malta fever according to Rogers. The Malta fever joint is not red, which fact, taken with its evanescent character, differentiates it from the arthritis of acute rheumatic fever.

Dengue.—Sporadic dengue is difficult to diagnose. In an epidemic the characteristic pains referable to tendinous insertions about joints are present in at least 50 per cent of cases and is of great diagnostic value. There is no swelling of the joints although the turgescence of the skin over them may give the impression of an arthritis. The intensity of pain varies from a feeling of muscular soreness to excruciating pain when muscles or joints are actively moved. Passive movement is not usually painful. In addition to the rachialgia, bone and joint pains, some writers have described swelling of the joints. This in my experience is unusual. Joint pains are so characteristic that they distinguish dengue from all other eruptive fevers.

Joint pains during convalescence may produce stiffness and crippling continuing for many weeks after the cessation of fever.

Relapsing Fever.—Bone, muscle and joint pains are practically always present in this disease. In addition rachialgia and headache are prominent symptoms and the aching gnawing pains in loins or nape of neck may make one think of beginning smallpox, dengue or yellow fever. There is no swelling of the joints in relapsing fever. As in dengue the pains in the neighborhood of the joints may be quite persistent.

Yaws.—This disease gives us bone, joint and muscle lesions similar to those of syphilis. From the mother lesion to the tertiary framboesioma the course and symptoms of the two diseases are similar. Thus we may have the flying pains and osteocopic pains of the early days of infection and, as later events, chronic synovitis, frambroesial infiltration of perisynovial membranes, frambroesial infiltration of synovial membranes, chondro-arthritis, epiphysitis and chronic frambroesial periostitis. These pathological processes cause such conditions as we know under the names dactylitis, saber shin, mutilating oro-rhino-palato-pharyngeal ulcerations, Parrot’s nodes and cranio-tabes.

The uncomplicated framboesioma must be pathologically similar to the gumma. Certainly the later effects of bone and joint destruction and scarring are wonderfully like some of the middle-age European descriptions “when lues was in flower.” In framboesial disease the damage from bone destruction or from contracture following cicatrization may be so complete as to render useless a finger, a hand, one of the large joints or even a whole extremity.

Bacillary Dysentery.—As far back as the 17th century (Sydenham) it was noted that joint pains or actual arthritides were occasional complications of dysentery. We now know that the bacterial types of dysentery are those most likely to show joint complications. Because the joint fluid in these lesions is usually sterile, it is assumed that they are the effect of toxins (or a toxin) produced by B. dysenteriae. Of the two hypothetical toxins of the dysentery bacillus one is supposed to produce neuritis and joint complications. Arthritides are more common in some epidemics than in others and with certain strains of bacilli than with others. The Shiga strain is the worst offender in this regard. Manson reports 27% of joint involvement in one epidemic.

Clinically, dysenteric arthritis is more apt to affect one of the larger joints, the knee, ankle and hip, being most affected. The elbow, wrist or shoulder joint may be affected, though this is unusual. The pain and swelling may be an incident of the early part of the attack. Usually it comes on when the acute symptoms are abating or as a sequela. The joint is distended with effusion and this involves the ligaments around the joint. Given an arthritis in the course of a frank dysentery there is nothing it could ordinarily be confused with. It is well to remember, however, that patients with dysentery may have also a concurrent gonorrhoea or arthritis from some focal infection. The dysenteric rheumatism ordinarily completely subsides with the cure of the colitis.

In hepatic abscess following amoebic colitis pain of some type is a frequent symptom. Rheumatic-like pains and swelling of the hands occur rarely, rapidly disappearing when the abscess is evacuated.

Filariasis.—Maitland and Bahr have noted a synovitis which is apparently a complication of filariasis. Bahr has found a fibrotic ankylosis often to follow such a joint condition. The synovitis may be followed by pus formation with serious or fatal outcome.

Guinea Worm Disease.—Very rarely the female Dracunculus may penetrate a joint and cause synovitis or arthritis.

Leprosy.—Occasionally there is joint involvement, especially of the wrist and ankle joints, in which erosion of the cartilage and bone dislocation occur giving us a condition similar to the Charcot joint.

It will be remembered that the Charcot joint is most often seen in tabes and may give one of the greatest joint swellings. As a rule only one joint, usually knee or hip, is involved in tabes and the affection is generally painless. The progress may be acute, subacute or chronic. Syringomyelia, a disease which may be confused with leprosy, may also show joint involvement, usually of the upper extremity.

BONE AFFECTIONS

Mycetoma.—As the result of the invasion of an extremity—usually the foot—with the causative fungi, disorganization of the tissues involved takes place. The granulomatous process invades muscles and bones and as a result of the sinus formation we have the bones converted into a softened, cheesy mass. This disintegration of bone and other tissues is attended with little or no pain. The granules discharging through the sinuses make for a proper diagnosis.

Goundou.—In goundou the nasal bones and the nasal processes of the superior maxilla are the seat of symmetrical swellings of the nature of an hypertrophic osteitis. These exostoses may be quite large so that there is interference with vision. There is little or no pain connected with the bony growths and there is no invasive tendency.

Big Heel.—There has been observed in natives of the Gold Coast an affection of the os calcis somewhat like that involving the superior maxillary bones in goundou. The disease begins with pain and tenderness of one or both heels. The enlargement may involve only one os calcis or affect both bones. There is no joint involvement but locomotion is interfered with. There are periods of improvement which are followed by return of the pains.

Ainhum.—In this disease there is thinning or absorption of the bones of the toe. A fibrous cord replaces the bony structures.

Oroya Fever.—In this very serious disease of certain areas of Peru the bone pains may be excruciating. These bone pains are especially marked in the sternum but also involve the long bones.

Trench Fever.—Pain over the shin bone is a prominent complaint in this affection so that the term “trench shin” has been employed.

Relapsing Fever.—Bone pains, especially referred to the knees, are complained of by patients with the bilious typhoid of Griesinger. This is a type of relapsing fever occurring in Egypt.

Leprosy.—The bone affections of leprosy are considered under the muscles.

MUSCLE INVOLVEMENT

Leprosy.—In this ancient disease the course of which is marked by anaesthesia, atrophy, absorption and accidents (cigarette burns, etc.), the lesions of bones, joints, muscles and indeed of all other tissues are, in great part, due to infiltration of nerves by the organism of leprosy. The effects are secondary and trophic on the one hand, and on the other partly due to secondary infection of the leproma by various bacterial agents. Leprosy was for centuries confused with other diseases in which ulceration and mutilation are features. The value of mercury in differentiating syphilis, the recognition of the importance of anaesthesia in this disease, together with the discovery of the bacillus of leprosy and of the etiological factors of several other confusing diseases, have made of leprosy one of the easiest of all diseases to diagnose correctly. It is, however, essentially a laboratory diagnosis.

In nerve leprosy we often get atrophy of the small muscles of the hand and of the muscles of the forearm. The contracture which takes place under these circumstances gives the “claw hand.” In tubercular and mixed forms of leprosy we may get in addition trophic disturbances of the fingers and toes and also extraneous infections which may ultimately result in amputation of fingers or toes. This process, going on over a considerable time or being repeated, results often in stumping of fingers or hands or toes and feet.

In addition to these openly destructive processes there is often seen in leprosy a condition of subcutaneous absorption of all the tissues. In this way the distorted finger nail may come to occupy a seat over the knuckle or even (though rarely) further up the back of the hand or arm. Briefly in leprosy we have, as representing the pathology, muscular atrophy from nerve involvement, periostitis and arthritis, interstitial absorption of bone and contractures resulting in mutilation of fingers, toes, hands and feet from trophic disturbance and intercurrent bacterial infection.

Beriberi.—In this disease we have muscular atrophies, especially of the muscles innervated by the peroneal and ulnar nerves, similar to those following other forms of peripheral neuritis.

Amoebiasis.—There have been reported very rarely disintegrating lesions of muscles and cutaneous tissues in which amoebae have been found.

Heat Cramps.—In those working in firerooms or steel-mills, the excessive heat to which they are subjected may cause various manifestations of heat prostration, among which the painful muscle cramps are prominent. These cramps are similar to those which are such a feature of Asiatic cholera and in each instance are supposed to be the result of dehydration of muscle tissue.

Trichinosis.—Acute muscle pain is a feature of the stage of muscle penetration by the larval Trichinella spiralis. In the disease we have a fever suggestive of typhoid fever and oedema about the face. A marked eosinophilia is characteristic. Another helminthic parasite which may invade the muscles of man is the larval Taenia solium. This must be of extreme rarity because infection with the adult T. solium is most rare and it is only accidental that the embryonic stage would occur in man. It is a fact that the common tapeworm of man, Taenia saginata, is found in the human host only as a sexually mature parasite in the intestines; there is never a cysticercus stage in the muscles.

Myositis purulenta tropica.—We may have a suppurative myositis with a single abscess formation or with disseminated foci or a diffuse purulent infiltration. The attending fever and toxaemia are similar to those attending any deep abscess formation. Abscess formation in the muscles has been reported from various parts of the tropics, especially the Gold Coast. It is possible that F. bancrofti infections are concerned in some of these conditions.

Filariasis.—Filarial abscesses were found in the ilio-psoas muscles in four cases. Wise and Minett found evidences of adult filarial worms (F. bancrofti) in 22 out of 28 deep-seated abscesses, which were examined by them.

Spotted a typo or a problem in this chapter? Tell us

LII. NEUROLOGICAL CONSIDERATIONS IN TROPICAL DISEASES

There is a great tendency in the tropics to ascribe neurological manifestations to beriberi or malaria. It must be acknowledged, however, that various sensory and motor phenomena, which may show themselves from time to time, in those who have suffered from beriberi, are common and prove sources of confusion in diagnosis. Tropical sunlight with its ultra-violet rays had a vogue which held sway for a brief period as explaining most nervous conditions in Europeans in the tropics. At present we are inclined to believe that excesses in eating and drinking and late hours may be more potent in the production of nervous breakdowns than are factors less cosmopolitan.

While syphilis is rampant in many parts of the tropical world the usual views are that the luetic neurological manifestations, so common in temperate climates, are more or less nonexistent. At the same time it would seem advisable with this point in view to study the cases attributed to other causes along the line of laboratory investigations of the cerebro-spinal fluid.

Clinically there are many points of difference between syphilis as seen in the native races of tropical regions and as observed in Europeans at home, and it would seem advisable to do more work along the line of spinal fluid examinations. The examination of the spinal fluid for syphilis should include a Wassermann test using several concentrations ranging from 0.2 to 1.0 cc., a globulin estimation, cell count and Langes colloidal gold reaction,—the last not being necessary however, unless positive findings are obtained in one or more of the other tests. Of course the most important test is the Wassermann of the spinal fluid and every one should bear in mind the marked complement fixation power of the spinal fluid of paretics. In such a fluid we almost always obtain a positive reaction where quantities of 0.2 cc. or less are employed, while with locomotor ataxia or cerebro-spinal lues amounts of 0.5 to 1 cc. are generally required to give a positive test. It is not necessary to inactivate spinal fluid.

These tests can only be carried out in a well equipped laboratory and the same is true of the colloidal gold one. The tests for cell increase and globulin increase, however, can be made by anyone prepared to do ordinary clinical laboratory work.

The normal spinal fluid is as clear as water, has a specific gravity of about 1.010 and is under a pressure of about 5 to 7 mm. of mercury or 60 to 100 mm. of water. The sugar content is about 0.07% and the proteid content about 0.03 to 0.04%.

CEREBRO-SPINAL FLUID EXAMINATIONS

To withdraw spinal fluid for bacteriological examination or cytodiagnosis we use a sterile needle about 4 inches long for an adult, preparing the skin as described for blood cultures from a vein (see page 516). The patient is placed on the left side with knees drawn up and head and shoulders carried forward to give the greatest possible space between the spinous processes by arching the spine. A line at the level of the iliac crests passes between the third and fourth lumbar vertebrae. Select a point midway between the spinous processes of these lumbar vertebrae and enter the needle two-fifths of an inch to the right of this point, pushing the needle inward and upward. Collect the material in two or three sterile test tubes, to avoid contamination of the entire sample by a drop of blood which may come out in the first portion. The presence of blood in very slight amount interferes with cytodiagnosis and globulin tests and, if present in more than a trace, it makes the colloidal gold test practically worthless. Make cultures on blood serum at the earliest possible moment. Centrifugalize a portion of the fluid at high speed and examine the sediment for bacterial content. After the puncture the patient should drink a glass or so of water and remain in bed for a day, preferably with the head lower than the feet.

In general terms, excluding syphilis, it may be stated that:

1. A lymphocytosis indicates a tuberculous or poliomyelitis process. With these diseases, the fluid will probably be clear.

2. An abundance of polymorphonuclear and eosinophilic leucocytes indicates an infection with pyogenic organisms, in which cloudy fluid is the rule.

Meningism shows very few cells.

Trypanosomiasis gives a cellular increase very similar to syphilis. In the work of the French Sleeping Sickness Commission five cells per cubic millimeter was taken as normal.

Not only may trypanosomes be found in the spinal fluid, when they mark the setting in of the “sleeping sickness” stage of trypanosomiasis, but a case has been reported of the presence of Trichinella embryos in the spinal fluid. Recently a few cases have been reported of anthrax meningitis, in which anthrax bacilli have been found in the spinal fluid.

=Cell Count.=—A method of examination considered by neurologists as of differential diagnostic value is to count the number of cells in a cubic millimeter of the cerebro-spinal fluid. The technic is to use a gentian-violet-tinged 3% solution of acetic acid. This is drawn up to the mark 0.5, and the cerebro-spinal fluid is then sucked up to 11. After mixing, the cell count is made with the haemacytometer.

Count all the cells appearing in the entire ruled area (9 large squares) and add one-sixth of this number to find the approximate total number of cells per cubic millimeter of spinal fluid examined as above. It is advisable to make the cell count of the fluid as soon after obtaining it as possible, the cells tending to degenerate or adhere to the glass of the tube. The latter can be minimized by vigorous shaking before withdrawal of the fluid for counting. Normally we have only two to ten cells per cubic millimeter, but in tabes and general paresis this is increased to 50 or 100 cells, greatest at onset of disease.

Pleocytosis.—Miller gives the following table as to pleocytosis:—

AVERAGE INCIDENCE OF LYMPHOCYTOSIS IN THE SPINAL FLUID

(Plaut, Relim and Schottmuller)

--------------------+-----------+------------------------------------- Clinical diagnosis | Frequency,| Remarks | per cent. | --------------------+-----------+------------------------------------- Cerebro-spinal lues | 85-90 | Counts often over 100—may reach | | 1000 per c.mm. --------------------+-----------+------------------------------------- Tabes dorsalis | 90 | Counts usually under 100. --------------------+-----------+------------------------------------- General paresis | 98 | Counts average 30-60 cells per c.mm. --------------------+-----------+------------------------------------- Secondary lues | 30-40 | Moderate increase as a rule. --------------------+-----------+------------------------------------- Multiple sclerosis | 25 | Border-line counts. --------------------+-----------+------------------------------------- Cerebral haemorrhage| {Frequency| Cerebral tumors | { is | Cellular increase is apt to be a Sinus thrombosis | { variable| very moderate one. --------------------+-----------+-------------------------------------

Globulin Increase Tests.—Noguchi’s butyric acid test is very satisfactory, but because of the objectionable odor of the butyric acid, we use the Ross-Jones and Pandy tests routinely in our laboratory.

For the Ross-Jones method, one cc. of saturated solution of ammonium sulphate is placed in a small test tube and one cc. of spinal fluid placed on top of this column. If globulin increase is present a turbid ring appears within a few seconds at the junction. Normally there is no sign of a ring. This test is a modification of Nonne’s Phase 1 reaction. For Pandy’s test, prepare a saturated solution of carbolic acid crystals in distilled water. Place 1 cc. of this reagent in a small test-tube and add 1 drop of spinal fluid. In a normal fluid, only the faintest opalescence is observed; but in a fluid with globulin increase a smoke-like white cloud develops instantly where the drop comes in contact with the reagent.

=Colloidal Gold Test (Lange’s).=—It is now generally accepted that this test is more diagnostic of general paresis than any other single test. The color changes in the first five tubes (1-10 : 1-160) are so constant that the term “paretic curve” is applied to such findings. Of less diagnostic value are the so-called cerebro-spinal lues curves where the color changes, though of less intensity than the paretic ones, are most marked in the third, fourth, fifth and sixth tubes (1-40 to 1-320). In various types of meningitis, other than luetic, the color changes are at times more marked in the tubes with the higher dilutions of spinal fluids (from 1-320 to 1-2560).

The paretic curve of the colloidal gold test generally runs parallel with a spinal fluid Wassermann and globulin increase. This agreement does not exist at all constantly for positive blood serum Wassermann tests and increased cell counts.

It may be stated that this test is of more importance in paresis than any single one of the four reactions of Nonne, viz.: (a) blood serum Wassermann; (b) spinal fluid Wasserman; (c) globulin increase, and (d) increased cell count of spinal fluid (pleocytosis). Of course, all of these tests should be carried out.

Test.—The test is carried out by preparing a series of ten test tubes containing dilutions of spinal fluid in 1 cc. of normal saline, ranging from 1-10 to 1-5120, and adding 5 cc. of the colloidal gold reagent to each tube and to a control tube containing salt solution alone. The successful application of the test is dependent upon (a) care in the preparation of the reagent; (b) absolute cleanliness of all glassware used, and, (c) on the entire absence of blood from the spinal fluid. Before using a new colloidal gold solution, it should be tested with spinal fluid of known reaction, so that it may be discarded if too sensitive or not sufficiently so. The color changes usually start almost immediately and if there is no change evident in half an hour, there will probably be none later. The maximum change occurs after several hours, so that readings are made after the tubes have stood overnight at room temperature. The proper color of the control in tube 11 should be salmon-red or old rose and the fluid should be perfectly transparent. When the color is changed in tubes containing dilutions of the spinal fluid we record one showing a bluish tint as 1. When the change is to a lilac we record it as 2. A distinct blue is marked as 3 and a pale blue as 4. When decolorization is complete there is the highest color change, which is noted as 5.

Mastic Test.—The mastic test as devised by Cutting is apparently of value as an aid in the diagnosis of syphilis of the nervous system. The test is made by treating six dilutions of spinal fluid in test tubes with an alcoholic extract of pure gum mastic, diluted with distilled water before using. Its great value lies in the ease of preparation from an effective gum mastic, and in the keeping qualities of the stock alcoholic extract. After standing at room temperature for twelve to eighteen hours or at 37°C., for six to twelve hours, readings are made. In positive cases (paresis) the mastic will be precipitated in the first one, two, three or four tubes (higher in strongly positive cases) leaving the supernatant fluid clear, with the mastic as a white flocculent precipitate at the bottom of the tube. In some positive reactions the opalescence of the fluid persists with a fine white precipitate at the bottom. The control tube must remain unchanged.

SHOWING THE AVERAGE FREQUENCY OF THE VARIOUS REACTIONS IN SYPHILIS OF THE CENTRAL NERVOUS SYSTEM (MILLER)

-----------------------+---------------+----------------+--------------- | Paresis | Tabes dorsalis | Cerebro-spinal | per cent. | per cent. | syphilis -----------------------+---------------+----------------+--------------- Blood Wassermann | 98-100 | 70 | 70-80 Spinal fluid Wassermann| 97 | 60-80 | 85-90 Pleocytosis | 98 | 85-90 | 85-90 Positive globulin test | 100 | 90-95 | 90-95 Colloidal gold test | 98-100 | 85-90 | 75-80 | Paretic curves| Luetic type of | Luetic curve | | curve | -----------------------+---------------+----------------+---------------

Other Chemical Constituents.—Normally the fluid reduces Fehling’s or Benedict’s qualitative copper solutions. It is well for one to gain experience with the degree of reduction to be normally expected as the test is but slightly marked. Quantitatively, the reducing substance is equivalent to 60-70 mg. glucose per 100 cc.

The urea is practically the same as in the blood, parallels any change in the latter, and has the same significance. Creatinine is about half that of the blood, and has apparently no clinical significance. Uric acid is present in still smaller proportion.

DELIRIUM AND COMA

It is difficult to make a sharp distinction between a disease showing delirium and one showing coma as delirious states tend to be followed by coma or such conditions may alternate.

In yellow fever the alert, suspicious mental state may give way to one of marked delirium requiring close watching to prevent the patient throwing himself from his bed.

In plague there is more of a mild delirious state in which the patient has a great tendency to wander about. The mental state is rather that of an intoxicated person with the thickness of speech and retardation of mental processes.

Typhus fever and spotted fever of the Rocky Mountains tend to produce stuporous states.

A delirious state, especially at night, is often noted in tsutsugamushi.

Rat bite fever also tends to show delirium.

In the ordinary paroxysm of malignant tertian there is quite a tendency to flightiness during the prolonged hot stage. In the cerebral types of pernicious malaria there may be violent delirium followed by coma or the patient may be comatose from the onset of the paroxysm. Such conditions are often mistaken for sun stroke. In the comatose form of malaria we have a high temperature with sighing or stertorous breathing and at times Cheyne-Stokes respiration.

Following upon the algid stage of cholera we may have a stage of reaction without the disappearance of anuria, in which a typhoid state, with low muttering delirium or even with an acute delirious state, supervenes.

Toward the end of the sleeping sickness stage of trypanosomiasis we have a subnormal temperature with a comatose state.

Comatose states following upon the acute confusional psychoses of pellagra are not uncommon. Pellagra may show an acute collapse delirium.

In heat stroke we may have either delirium or coma. There is no more difficult problem encountered in the tropics than the one of differentiating cerebral malaria from heat stroke.

Oroya fever is frequently accompanied by delirium.

In typhus fever (tabardillo) delirious or stuporous states are to be expected about the end of the first week or even earlier. This is a disease in which the clouding of the consciousness is almost as marked as in plague. Delirium is more apt to occur at night.

In very toxic cases of bacillary dysentery there may be a mild delirium.

=Insomnia.=—Sleeplessness or, at any rate, a condition where the patient only dozes is often seen in dengue. This mental alertness and wakefulness may also be noted in yellow fever. In malaria, possibly connected with quinine administration, we may have marked insomnia although cases have been reported of insomnia due to malaria which has been relieved by quinine.

Just as cardiac decompensation from any cause will be attended by a distressing insomnia so is this also a feature of beriberi where cardiac involvement is marked.

Liver abscess may be attended with insomnia.

Malta fever is often attended with a weariness from suffering with the various joint and nerve pains so that insomnia is often marked.

Even in trypanosomiasis insomnia may be present at first. Insomnia is also one of the early neurasthenic manifestations of pellagra.

=Somnolence.=—The disease in which this symptom is best known is sleeping sickness. The patient may go to sleep lying in the bright sunlight or in the midst of eating a morsel of food. These cases can be easily aroused but quickly drop off to sleep afterwards. They often deny that they were asleep. Later on in sleeping sickness the patient may sleep from 24 to 36 hours continuously and a more marked tendency to somnolence may be present by day than by night.

In the prodromal stage of leprosy somnolence is often marked and accompanied by a sensation of unaccountable weakness. Sweatings and accessions of fever may also be noted at this time.

In plague the rather stuporous state of the patient may give the impression of somnolence.

CEPHALALGIA, RACHIALGIA AND OTHER PAINS

Yellow fever is marked by pains in the lumbar region, the coup de barre of the French. It is as if the patient had been beaten over the small of the back with a bar of iron. The headache is rather orbital and is often excruciating. There are also frequently heavy, dull pains of the extremities.

Blackwater fever also has marked pains in the lumbar region giving expression to the kidney damage done by the haemoglobin detritus plugging the tubules.

In all forms of malaria, but especially in the paroxysms of malignant malaria, there are severe headaches and pains in the extremities. Intermittent neuralgia is often regarded as malarial.

Dengue gives rise to a marked post-orbital soreness rather than pain. There is also a marked rachialgia with pains in the limbs often referred to the regions of the joints, which, however, are not swollen.

In Malta fever the neuralgias, especially sciatica, often associated with suddenly appearing, painful joint swellings, are prominent features.

In trypanosomiasis headache is often marked, together with a characteristic deep hyperaesthesia, so that the striking of a limb against a hard object gives rise to excruciating pain, there being, however, a delay in the experiencing of the painful sensation.

In relapsing fever the headache is often intense with pains in the back and bones.

In cholera one of the most striking phenomena of the disease is the terrible cramping of the muscles, especially those of the calves and feet. These pains actually torture the patient. Cramps of abdominal muscles as well as those of extremities are often noted in heat stroke in men in firerooms.

In beriberi there is often pain in the epigastric region so that the slightest touch causes great distress. This epigastric tenderness is also a feature of yellow fever. The calf muscles are also markedly hyperaesthetic in beriberi.

In leprosy the neuralgic pains may be very severe while the nerves are being pressed upon by the connective tissue increase of the endoneurium and perineurium. Mention has been made of excruciating pains of toes, especially the big toe, even suggesting gout.

The excruciating pains of Oroya fever are connected with the changes taking place in the bone marrow. There is probably more rapid alteration in the blood picture in this disease than in any other. It might be designated a fulminating pernicious anaemia.

Pain on pressure on dorsal or lumbar spine is common in pellagra.

Plague may be associated, during the first day or two, with an excruciating headache. This may even be prodromal but tends to disappear with the rapidly developing stuporous state of the patient.

In typhus fever boring headache, oppressive rather than lancinating, is a feature of the first days. It is usually frontal or temporal.

In malignant tertian the headache is often quite intense during the prolonged hot stage. The headache of malaria is usually frontal or suboccipital.

In trench fever we may have a cutaneous hyperaesthesia over the shins. Rocky Mountain fever shows joint pains.

TREMORS AND CONVULSIONS

It is in trypanosomiasis that we have the most important tremor. It is the fine tremors, which first are noticeable in the tongue and later in hands and even legs, that mark the onset of the stage of sleeping sickness with the trypanosomes in the cerebro-spinal fluid. At times an intention tremor may be noted in advanced cases of sleeping sickness. In addition we have epileptiform seizures in sleeping sickness.

In cerebral manifestations of pernicious malaria there is a type characterized by epileptiform convulsions.

In the acute stage of Brazilian trypanosomiasis we may have almost any type of cerebral or cord lesion.

Tremors of tongue and hands may be present in the second stage of pellagra.

Fibrillary tremors have been noted in the main-en-griffe of beriberi but tremors of the tongue and hands, so common in alcoholic neuritis, are rare in beriberi.

Convulsive seizures are not uncommon in the hyperpyrexial type of heat stroke.

In infantile beriberi the child often becomes rigid. There is not a true convulsion but such cases are at times thought to have meningitis.

In schistosomiasis and paragonomiasis as well as in infections with the larval stage of Taenia solium we may have brain involvement and manifestations of Jacksonian epilepsy.

ALTERED REFLEXES INCLUDING SENSORY AND MOTOR DISTURBANCES

Beriberi.—It is usually stated that the tendon reflexes of the lower extremity, especially the patellar reflex, are absent. While this is generally true they may at first show an exaggeration and some cases do not seem to show any decided change. There may be striking variation from day to day in the reflexes. The superficial reflexes, especially the cremasteric, are as a rule more active than normally.

The sensory changes in beriberi are less marked than those of the motor side. There is rarely complete anaesthesia but rather a blunting of sensation. Hyperaesthesia, particularly of the muscles of the calf of the leg, is well marked when the muscles are grasped with the hand.

The anaesthesia is earliest noted over the shin bone and dorsum of the foot. A loss of tactile sense is often noted about finger tips making it difficult for the patient to button his coat.

The most striking motor phenomena are the foot and wrist-drop, especially the former. The extensor muscles are more markedly involved than the flexors. There is marked muscular weakness of foot as well as hands. The weakness of the muscles of the leg is often the first symptom to be complained of. The type of palsy in beriberi is mainly paraplegic although hemiplegic and monoplegic types have been reported. The paralysis of the diaphragm is the most serious of the muscle palsies.

Contractures of the muscles of the foot or calf of the leg may occur. Contractures of the muscles of the upper extremity are more rare. Muscular atrophy of the leg muscles is often marked. In the upper extremity the muscles of the hand are most frequently atrophied.

Pellagra.—There is considerable variation from time to time in the reflexes. Some authorities attach diagnostic value to the appearance of an exaggerated reflex on one side and a diminution or absence of the corresponding reflex on the other side. Ankle clonus may be present.

Paraesthesias and in particular a burning sensation of the erythematous areas are often noted. Hyperaesthesia of the dorsal and lumbar regions is often noted. Pruritus is at times complained of in the region of the perineum. We have muscular weakness.

Sleeping Sickness.—The deep reflexes are usually exaggerated and the superficial ones diminished or absent.

There is no distinct alteration of motor or sensory function except that of deep hyperaesthesia (Kérandel’s sign). There is usually marked weakness of muscles of locomotion.

Leprosy.—The usual statement is that there is an exaggeration of the deep reflexes. Ankle clonus has been rarely reported.

Anaesthesia is the most important symptom in the diagnosis of leprosy. This loss of sensation is often for pain and temperature with retention of tactile sense (dissociation of sensation—a prominent symptom of syringomyelia). The anaesthesia is not only found in the spots but associated with the leprous neuritis which chiefly involves the ulnar, facial and peroneal nerves. Muscle palsies and atrophies are common and the main-en-griffe appearance of the hand is seen.

In lathryism we have spasticity and an exaggeration of the reflexes.

A very remarkable disease called kubisagari or paralytic vertigo has been observed in Japan. This disease is thought to affect those living in stables. The attacks only last a few minutes and at other times the patient seems normal. An attack shows ptosis and diplopia, speech disturbances and palsy of muscles of back of neck, causing the head to fall forward. There may also be some paresis of muscles of extremities. The disease is not fatal. Cases have been observed in Switzerland.

THE GAIT

There are no gaits in tropical diseases which can strictly speaking be regarded as special types of gait. In beriberi we often note the designation tripod gait of beriberi. This simply refers to the manner in which a case of the paraplegic type of beriberi uses a stick held by his hands to assist him in dragging along his atrophied and enfeebled legs. The legs are widely separated and the stick placed in front makes the two legs and stick resemble a tripod.

It is true that beriberics show the steppage gait of multiple neuritis as, owing to more or less foot-drop and lack of power to extend the toes, the patient lifts his foot high from the ground to avoid scraping the toes, and bends to the other side. It is as if a man were walking through a mire.

When other groups of muscles than the foot extensor ones become involved the gait is that of extreme weakness—a shuffling one.

In sleeping sickness it is a shuffling gait. It is as if one were dragging the feet along from pure muscular weakness.

In pellagra we may see a gait in which the patient separates his legs rather widely and uses a stick in front, shuffling his feet along with knees slightly bent and soles of the feet scarcely raised from the ground.

Some cases show a typical spastic paralytic gait.

We often note under dengue the designation dandyfied gait. This refers to the stilted, mincing gait of a dandy and is probably the explanation of the derivation of the word dengue. The pains about the site of the insertions of muscles with the slightest movement make these patients walk in a stiff, self-conscious manner.

PSYCHIC AND NEURASTHENIC STATES

A very remarkable fact is that in many tropical and subtropical regions where syphilis is rampant among the natives there is slight or absent incidence of general paresis and locomotor ataxia.

Jefferys and Maxwell state that the parasyphilitic manifestations were absent in thousands of cases observed by them in Formosa. In the Philippines one sees occasionally typical cases of these parasyphilitic diseases but of course standard methods of treatment of syphilis have been employed there for many years.

In China, where there is practically no treatment for syphilis, luetic ulcerations are exceedingly common and it has been suggested that insufficient treatment cures the skin lesions but adds to the effects on the nervous system. It will be remembered that skin and nerve tissue arise from similar embryological layers (epiblast) hence a suppression of toxic effect on one tissue may add to the burden on the other. It has been suggested that if the surface lesions are allowed to develop to maturity, the skin, which is the great elaborating center for antibodies, will produce enough adequately to protect the whole body; whereas, if the surface lesions are aborted, there is a diminished stimulus with consequent diminished elaboration of protective bodies. The brain is then liable to parenchymal invasion, since chemicals, owing to difference in their physical properties, cannot replace natural antibodies in controlling the disease in this location. This theory takes no reckoning of differences exhibited by variant strains of treponema in their tendencies toward selective localization. It has been noted that the form of syphilis endemic in certain regions is much less virulent than is the cosmopolitan form.

Pellagra.—Very important in diagnosis is a more or less prolonged prodromal period of neurasthenia which is apt to be more marked in the winter at a time when the skin and alimentary tract manifestations are in abeyance. Along with the anxiety and unrest of this neurasthenia we have lack of mental concentration and depression of spirits.

A melancholic state is almost always present in the psychosis of pellagra. There is not the indifferent, satisfied, more or less happy mental state of the case of general paresis. Some consider the pellagrous psychosis to belong to the toxic group, as from alcohol or cocaine, while others place it in the group of infective psychoses, as the post-influenzal one. Gregor regards it as belonging to the infective-exhaustive group. The insanity of pellagra is that of an acute confusional one.

In the final cachexia there is a dementia.

Sleeping Sickness.—It may be many months or even years before the mental changes follow the trypanosome fever stage. At first a change in disposition is noted, the patient becoming listless and apathetic.

There is great impairment of mental concentration and memory. There may be later on catatonic manifestations as echolalia, mutism or flexibilitas cerea. There may at times be paranoid manifestations to be succeeded by states of profound melancholia. In the terminal stage a comatose state overshadows the psychical manifestations.

Malaria.—Leaving out of account the acute delirious states which accompany cerebral malaria there have been reported cases showing various manifestations of psychic disturbances even to maniacal or melancholic forms of insanity.

It is a common practice to attribute the irritability and lack of mental concentration of those who have lived for a long time in the tropics to the damage done the cerebral cortex by the malarial parasite. It is certainly more reasonable to attribute these minor psychic disturbances to malaria rather than to actinic rays of the sun.

There is no doubt but that quinine, given either for treatment or prophylaxis of malaria, is a cause as potent as alcohol and tobacco in tropical neurasthenia.

Insolation.—It is popular to assign neurasthenic manifestations to the actinic rays of the sun or the tropical heat, as these influences operate on every resident of the tropics. It is very necessary to exclude derangements of the digestion due to errors in diet with resulting exhaustion of the pancreatic and hepatic functions.

Alcohol is a potent factor for tropical neurasthenia as the tendency is for excess in this direction in those who in temperate climates are only moderate drinkers.

Hookworm Disease.—The patients with this disease are apt to become hypochondriacal and even melancholic.

There is a correspondence between the physical and mental backwardness of children with this disease, a child of twelve, who by the Binet-Simon test will only be rated at 7 will also not seem larger or better developed physically than a child of seven years would be.

Malta Fever.—Owing to the neuralgic pains and insomnia patients with this disease are apt to become neurasthenic. They are peculiarly liable to form the morphine habit if this drug be placed in their hands for the relief of pain.

The victims of leprosy not only may show an indifference to their condition but may also exhibit a moral apathy.

Dengue often shows a rather marked neurasthenia during convalescence and this may be protracted if the patient tries to resume his active duties before his complete recovery.

In latah there is echolalia and echopraxia, the patient repeating words he hears and mimicking movements he sees. The mind is usually clear. As a matter of fact the symptoms show similarity to those of the catatonic form of dementia praecox. The disease is more common in that part of the world centering in the Malay peninsula. Suggestion is an important factor in this neurosis.

In amok, a sort of epileptiform seizure in which the patient is obsessed with a desire to kill, there may be no recollection of the running amok. After the attack the patient may be stuporous.

LUNACY IN THE TROPICS

Van Loon, having examined over 200 cases from among 1100 insane patients in Java, found the most common types of mental disease to be dementia praecox, general paresis, various manifestations of cerebral syphilis and acute maniacal or confusional states. Not only were all forms of mental disorder known in European countries represented, but their comparative frequency and the types of conduct exhibited were, on the whole, what might be expected in the study of a group of similar cases encountered in any other part of the world.

Overbeck-Wright in his book—“Lunacy in India”—notes that 44% of cases were under treatment for various types of mania, 15.9% for melancholia, 4.8% for delusional insanity, 5.2% for idiocy, 5.7% for dementia and 6.6% for insanity following the use of Cannabis indica. It is noted that dementia praecox is not included in the statistical returns, but the author states that in his experience hebephrenia and katatonia account for a much larger proportion of cases than melancholia.

Overbeck-Wright is of the opinion that general paresis is quite common in India notwithstanding the fact that for many years the opinion has obtained that syphilis of the central nervous system and the parasyphilitic diseases were exceedingly rare among tropical natives. He regards the incidence of cerebral disease in syphilitic natives as less than with Europeans, attributing this fact to the existence of an immunity acquired through the prevalence of syphilis among these people during a period of several centuries. Cases of general paresis are generally reported under the diagnosis of chronic mania.

Van Loon also notes the mistake made in most books on tropical medicine as to the rarity of general paresis. General paresis being a disease in which we have such characteristic laboratory diagnostic tests, especially the colloidal gold test, there should be little difficulty in settling this question of its absence or relative infrequency among natives of tropical regions.

INDEX

Acanthocheilonema perstans, 339

Acidosis, 525 in blackwater, 58 in cholera, 236 in heat stroke, 468 in kala-azar, 131

Aedes calopus, 105, 433

Agglutination tests, 517 in blood transfusion, 521 in cholera, 230 in dysentery, 184 in Malta fever, 244

Ainhum, 471, 595

Alastrim, 486

Albumin tests, 570

Albuminuria, 574 in blackwater, 61 in malaria, 39 in yellow fever, 110, 574

Alcohol, and neuritis, 270, 287 and liver abscess, 167

Alimentary tract, 586

American leishmaniasis, 138

Amoebae, 148, 158, 159

Amoebic dysentery, 147

Amok, 610

Anaemia, 553

Ancylostomiasis, 319, 493, 546, 548, 554, 563, 567, 609 ancylostoma in, 320 diagnosis in, 329 epidemiology of, 323 geographical distribution of, 320 ground itch in, 328 history of, 319 life history of hookworm, 321 pathology of, 324 prognosis in, 331 prophylaxis in, 331 symptomatology of, 326

Ancylostomiasis, symptoms in detail of, 328 treatment of, 332

Anopheline mosquitoes, 18, 20, 24

Antimony, administration of, 134

Arsenic and beriberi, 270

Arsphenamine, administration of, 96

Arthritis, infectious, 592 noninfectious, 592

Aspergillus fumigatus, 474

Atriplicism, 556

Aural myiasis, 568

Bacillus alkaligines faecalis, infection with, 485 dysenteriae, 175 icteroides, 101 leprae, 248 pestis, 190

Bacterium tularense, 214

Balch’s staining method, 513

Basal metabolism, 489

Benign malaria, 29

Beriberi, 268, 492, 547, 555, 596 acute pernicious, 282 and scurvy, 286 asylum, 279 atrophic, 280 definition of, 268 diagnosis in, 285 endocrine gland disturbances and, 274 epidemic dropsy, 278 epidemiology of, 276 etiology of, 269 food deficiency, 270 geographical distribution of, 269 history of, 268 infantile, 279, 287, 547 paraplegic, 282 pathology of, 277

Beriberi, polyneuritis gallinarum and, 275 prognosis in, 288 prophylaxis in, 288 rice in, 272 rudimentary, 280, 282 ship, 285, 547 symptomatology of, 278 symptoms in detail of, 284 synonyms for, 268 treatment of, 290 types of, 280 vitamines in, 271, 275 wet, 280

Berne, 421

Big heel, 595

Bilharziasis, 357, 360

Bilious remittent malaria, 34

Bilious typhoid of Egypt, 92, 111

Black death, 188

Blackwater fever, 55, 498, 541, 547, 553, 557, 560, 572, 574, 579 complications in, 60 definition of, 55 diagnosis in, 61 epidemiology of, 58 etiology of, 57 geographical distribution of, 56 history of, 55 pathology of, 59 prognosis in, 64 prophylaxis in, 64 symptomatology of, 59 symptoms in detail of, 61 synonyms for, 55 treatment of, 64

Blastomycosis, 474

Blood, chemical analysis of, 530, 576 groups of, 521 specific gravity of, 538 transfusion of, 521

Blood examinations, 504 acidosis in, 525 coagulation rate in, 537 counting cells in, 507, 508 culturing in, 516 differential count in, 514

Blood examinations, dried smears, 509 fresh preparations in, 509 haemoglobin in, 519 in blackwater, 541 in malaria, 39, 539 in kala-azar, 131, 543 staining films, 509, 512 thick films in, 511 wet preparations in, 509

Blood in tropical diseases, 504, 538 blackwater fever, 541 filariasis, 544 kala-azar, 543 liver abscess, 542 malaria, 539 Malta fever, 541 plague, 542 relapsing fever, 544 trypanosomiasis, 543 typhus fever, 546 Weil’s disease, 544

Boils, tropical, 420

Bone affections, 595

Brazilian trypanosomiasis, 80, 501, 548 diagnosis of, 84 epidemiology of, 81 etiology of, 80 prophylaxis in, 84 symptomatology of, 83 transmission of, 81 treatment of, 84 types of, 83

Bronchial spirochaetosis, 550

Bronchomoniliasis, 474 pulmonary tuberculosis and, 474

Bubas, 138, 564

Calabar swellings, 354, 556

Carriers, in cholera, 225 in dysentery, 153, 178 in malaria, 24, 47

Cephalalgia, 604

Cerebro-spinal fluid, 598

Chaulmoogra oil, 266

Chenopodium, 163, 334

Cholera, 218, 492, 547, 579, 597 agglutination in, 230

Cholera, autopsy findings in, 227 blood transfusion, 235 carriers in, 225 definition of, 218 diagnosis in, 230 disinfection in, 233 epidemiology of, 222 etiology of, 220 geographical distribution of, 219 history of, 218 pathology of, 226 prognosis in, 232 prophylaxis in, 233 sequelae in, 229 serum in, 236 symptomatology of, 227 symptoms in detail of, 229 treatment of, 235 vaccination in, 234 water transmission, 223

Cholera red reaction, 232

Cholerine, 229

Chrysomyia macellaria, 422, 551, 568

Chyluria, 346, 575

Circulatory system, 547

Climatic bubo, 469, 552 diagnosis in, 470 symptomatology of, 470

Climatic fevers, 501

Clonorchiosis, 371 symptomatology of, 372

Clonorchis endemicus, 372

Coagulation rate, 537

Coccidioidal granuloma, 474 pulmonary tuberculosis and, 474

Coccidioides immitis, 474

Cochin China diarrhoea, 312, 374

Colloidal gold test, 600

Colon bacillus infection, 484

Color index, 520

Coma, 602

Conorhinus rubrifasciatus, 123 megistus, 80

Convulsions, 605

Cosmopolitan diseases, 480

Craw-craw, 424

Creeping eruption, 422

Cryptococcus gilchristi, 474

Culex fatigans, 432, 342

Culicine mosquitoes, 20

Culturing blood, 516

Cutaneous system, 561

Cyclops, 356

Danysz’s virus, 210

Delirium, 602

Dengue, 431, 495, 545, 563, 593, 608, 609 clinical types, 435 definition of, 431 diagnosis in, 436 epidemiology of, 432 etiology of, 432 geographical distribution of, 432 history of, 431 mosquitoes in, 432 pathology of, 434 prophylaxis in, 438 spirochaetes in, 432 symptomatology of, 434 symptoms in detail of, 436 synonyms for, 431 treatment of, 438

Dengue-like fevers, 438

Dermatobia cyaniventris, 421

Dermatophiliasis, 418

Dhobie itch, 414

Diagnosis in tropics, 477

Diarrhoea, 589

Diphtheria, 487

Dracunculus medinensis, 339, 355

Dysentery, 141 bacterial, 145, 174 ciliate, 143 definition of, 141 etiology of, 142, 148, 175 flagellate, 142 from animal parasites, 142 from poisons, 146 helminthic, 145 protozoal, 142

Dysentery, (amoebic), 147, 492, 554, 596 Charcot-Leyden crystals in, 157 complications in, 155 diagnosis in, 156 epidemiology of, 153 etiology of, 148 geographical distribution of, 148 history of, 147 pathology of, 154 prophylaxis in, 160 symptomatology of, 154 transmission of, 153 treatment of, 160

Dysentery (bacillary), 145, 174, 501, 545, 548, 567, 594, 603 chronic, 182 collapse types, 181 complications in, 181 diagnosis in, 182 epidemiology of, 177 etiology of, 175 gangrenous, 181 geographical distribution of, 174 history of, 174 pathology of, 179 prophylaxis in, 185 symptomatology of, 180 treatment in, 186 vaccination against, 185

Ear diseases, 568

Ekiri, 145

Elephantiasis, 347 of scrotum, 348

Emetine, 160, 171, 318

Endemic haematuria, 363

Endocrine disturbances, 489

Entamoeba coli, 149, 150 histolytica, 142, 148, 164 tetragena, 149

Eosinophilia, 533

Epidemic dropsy, 278 gangrenous rectitis, 589

Epistaxis, 569

Espundia, 138, 564

Eye diseases, 565

Faeces, 581 intestinal parasites, 583 occult blood in, 582 ova in, 583

Fasciolopsis buski, 373

Fever-free diseases, 491

Filaria bancrofti, 337, 341

Filariasis, 336, 493, 544, 550, 552, 564, 566, 575, 594, 597 abscesses in, 346 and chylous hydrocele, 351 chyluria, 346, 575 clinical types, 344 diagnosis in, 351 elephantiasis, 347 elephantoid fever, 345, 493 etiology of, 337 history of, 339 life history of F. bancrofti, 342 mosquitoes in, 342 orchitis in, 347 pathology of, 343 scrotum in, 345 varicose groin glands in, 345

Flagellate dysentery, 142

Flagellated body, 8

Fleas in leishmaniasis, 124 in plague, 192

Focal infections, 490

Framboesia, 384

Funiculitis, endemic, 346, 580

Gaits, 607

Gametes in malaria, 8

Gangosa, 395, 550, 569 and yaws, 395 diagnosis in, 398 epidemiology of, 397 etiology of, 395 geographical distribution of, 395 history of, 395 pathology of, 397 symptomatology of, 397 treatment of, 398

Genito-urinary system, 570, 579

Giardia, 142

Giemsa’s stain, 514

Glanders, 487

Glandular fever, 536 involvements, 551

Globulin increase, 600

Glossina morsitans, 67, 71 palpalis, 66, 69

Goundou, 472, 569, 595

Granuloma venereum, 404 diagnosis in, 406 etiology of, 404 history of, 404 pathology of, 404 symptomatology of, 405

Guha, 551

Guinea worm, 339, 340, 355, 595

Haemacytometry, 505

Haematoxylin staining, 514

Haematuria, 575

Haemoglobin estimations, 519

Haemoglobinuria, 574 haemoglobinuric fever, 55 paroxysmal, 61, 574

Haemolysis, test for, 521

Haemorrhages, 554

Haemosporidia, 4

Haffkine’s plague prophylactic, 211 cholera vaccine, 234

Heat prostration, 464, 467, 494 cramps, 467, 597 stroke, 464, 501, 550, 573, 603 etiology of, 464 susceptibility to, 466 symptomatology of, 466 treatment of, 467

Hill diarrhoea, 316

Hirudiniasis, 559

Hosts, 9

Impetigo, 419

Index of malaria, 9

Infantile beriberi, 279 scurvy, 287

Influenza, 488

Insolation, 464, 609

Insomnia, 603

Intestinal bacteria, 177 parasites, 503, 583 tract, 589

Jansky’s blood grouping, 515

Jaundice, 557 epidemic, 114

Jaundice, infectious, 114, 503, 544, 558 cultivation of Leptospira icterohaemorrhagiae, 115 definition of, 114 diagnosis in, 117 epidemiology of, 116 etiology of, 115 geographical distribution of, 114 history of, 114 pathology of, 116 prophylaxis in, 117 symptomatology of, 116 synonyms for, 114 treatment of, 117

Joint involvement in tropical diseases, 592

Juxta-articular nodules, 472, 564

Kaffir milk-pox, 486

Kala-azar, 121, 127, 498, 543, 552, 554, 558, 560, 563 diagnosis in, 131 epidemiology of, 127 etiology of, 123 history of, 121 pathology of, 128 prognosis in, 133 prophylaxis in, 133 symptomatology of, 128 symptoms in detail of, 130 synonyms for, 121 treatment of, 133

Katayama disease, 364, 550, 556

Kidney function and its determination, 575

Kubisagari, 607

Lamblia, 142

Lamus megistus, 81

Large mononuclear increase, 536

Latah, 610

Latent malaria, 35

Lathyrism, 288, 607

Laverania, 5

Leishmania donovani, 123, 127 infantum, 123, 127 tropica, 123

Leishmaniases, 121 American, 138, 553, 564 canine, 123 cutaneous, 135, 564 infantile, 130 post-antimonial, 564 relationship, 126 visceral, 127

Leishmanoid, dermal, 564

Leishman’s staining method, 513

Leprosy, 246, 492, 539, 555, 562, 565, 569, 580, 595, 596, 605, 607, 609 bible and, 247 cultivation of bacillus, 249 definition of, 246 diagnosis in, 261 epidemiology of, 249 etiology of, 248 geographical distribution of, 247 history of, 246 lepra cells in, 253 nerve, 257 nodular, 255 of rats, 252 pathology of, 252 prognosis in, 264 prophylaxis in, 264 symptomatology of, 254 symptoms in detail of, 260 synonyms for, 246 transmission of, 251 treatment of, 265 Wasserman reaction in, 262

Leptospira icteroides, 98 icterohaemorrhagiae, 115 morsus-muris, 118

Leucocytosis, 534

Leukopenia, 533

Liver, alterations in size of, 558 pains of, 559 tropical, 166

Liver abscess, 164, 501, 542, 550, 557, 558, 559

Liver abscess, complications in, 166, 168 diagnosis of, 169 emetine in, 171 etiology of, 164 geographical distribution of, 164 history of, 164 operation for, 172 pathology of, 165 prophylaxis in, 171 rupture of, 166 symptomatology of, 166 symptoms in detail of, 168 treatment of, 171

Liver fluke disease, 371

Loa loa, 337, 352, 566

Lunacy in the tropics, 610

Lymphatic glands, in trypanosomiasis 76, 551 system, 551

Lymphocytosis, 536

Lymph scrotum, 345

Lyon blood tube, 516

Maize in pellagra, 296

Malaria, 1, 493, 494, 495, 496, 539, 548, 553, 560, 562, 566, 574, 579, 602, 605, 609 algid, 34 anaphylaxis and the paroxysm in, 18 cachexia, 36 cerebral, 33 cultivation of parasite, 16 definition of, 1 diagnosis in, 40 discovery of parasite, 2 epidemiology of, 24 etiology of, 4 geographical distribution of, 4 heredity in, 16 history of, 1 immunity in, 17 in animals, 5 index of, 9 latent, 35, 493 life history of parasite, 7 malignant tertian, 28, 30 masked, 36 mosquitoes in, 6, 18 pathology of, 25 perniciousness in, 31 prognosis in, 42 prophylaxis in, 42 provocative measures in, 41 quinine-affected parasites, 16, 17 relapses in, 35 sequelae of, 37 symptomatology of, 27 symptoms in detail of, 37 synonyms for, 1 toxin in, 7, 16 transmission of, 7 treatment of, 47 variations in cycle, 27

Malignant tumors, 488

Malta fever, 237, 497, 541, 550, 554, 560, 579, 580, 593, 603, 604, 609 clinical types of, 242 complications in, 242 definition of, 237 diagnosis in, 243 epidemiology of, 239 etiology of, 238 geographical distribution of, 238 goat milk in, 239 history of, 237 pathology of, 240 prognosis in, 244 prophylaxis in, 245 sequelae in, 242 symptomatology of, 241 symptoms in detail of, 242 synonyms for, 237 treatment of, 245

Marris atropin test for fevers, 484

Mastic test, 601

Media, Aronson’s, 232 Teague, 582

Methylene blue, in malaria, 53

Mexican typhus, 452

Micrococcus melitensis, 238

Monilia Candida, 474 tropicalis, 474

Mosquito, anatomy of, 20 Anopheline, 18 destruction, 43 hibernation of, 21 in dengue, 432 in filariasis, 342 in yellow fever, 105 malaria transmitters, 6

Moss’ blood grouping, 521

Mouth, 586

Mumps, 487

Muscle involvement in tropical diseases, 592, 596

Mycetoma, 399, 595 diagnosis in, 402 epidemiology of, 400 etiology of, 400 geographical distribution of, 399 history of, 399 pathology of, 401 prognosis in, 403 symptomatology of, 401 treatment of, 403

Mycoses, visceral, 473

Myiasis, cutaneous, 421 intestinal, 590 larval characteristics, 590

Myositis purulenta tropica, 597

Nasal myiasis, 551, 568

Nausea, 588

Necator americanus, 320

Neo-arsphenamine, administration of, 95

Neurasthenia, 608

Neurological manifestations, 598

Night blindness, 567

N. N. N. medium, 517

Nocardia pseudotuberculosis, 474

Nose, diseases of, 568

Occult blood, 523, 571, 582

Oedema, 555

Oesophagus, 587

Onchocerca volvulus, 339, 341, 354, 552

Onyalai, 587

Opisthorchis felineus, 372

Oriental sore, 137, 564 diagnosis in, 139 epidemiology of, 136 etiology of, 123 geographical distribution of, 136 history of, 135 pathology of, 137 prophylaxis in, 140 symptomatology of, 137 synonyms for, 121 treatment, 140

Ornithodorus moubata, 89 talaje, 91

Oroya fever, 425, 541, 553, 595, 603 etiology of, 426 pathology of, 426 prophylaxis in, 428 symptomatology of, 427 treatment of, 428

Pappataci fever, 438, 545

Paragonimiasis, 368, 549, 555 diagnosis in, 371 etiology of, 368 history of, 368 symptomatology of, 369

Paragonimus westermanni, 368 life history, 368

Paralytic vertigo, 607

Paratyphoid fever, 484, 503, 545

Pediculi, 454

Pellagra, 291, 492, 539, 561, 572, 586, 588, 589, 603, 605, 606, 608 amino-acid deficiency in, 294 animal experimentation in, 298 blood in, 308 corn in, 296 definition of, 291 diagnosis in, 308 diagnostic triad in, 302 epidemiology of, 298 eruption of, 300, 303 etiology of, 292 experimental, 295 geographical distribution of, 292 history of, 291 moulds and, 296

Pellagra, mouth in, 586 pathology of, 299 periodic recurrences of, 302 prognosis in, 309 prophylaxis in, 309 protein deficiency in, 294 Simulium in, 298 stages in, 302 symptomatology of, 300 symptoms in detail of, 308 synonyms for, 291 treatment of, 310 urine in, 308, 572

Penicillium crustaceum, 474

Pernicious malaria, 31

Phenolsulphonephthalein test, 577

Phlebotomus fever, 438, 545 pappatassii, 439

Piedra, 420

Pinta, 416

Piroplasms, 58

Plague, 188, 499, 542, 547, 549, 551, 559, 575, 602, 604, 605 bubonic, 199 confusing organisms in suspected, 191 cutaneous, 200 definition of, 188 diagnosis in, 205 epidemiology of, 192 etiology of, 190 Flugges droplet method, 197 geographical distribution of, 189 guinea pig test, 207 Haffkine’s prophylactic, 211 history of, 188 pathology of, 198 pneumonic, 197, 201, 549 prognosis in, 208 prophylaxis in, 208 rat and, 191, 196 septicaemic, 203 symptomatology of, 199 symptoms in detail of, 203 synonyms for, 188 tokens in, 200 treatment of, 211 Yersin’s serum, 211

Plasmodium falciparum, 12 malariae, 11 vivax, 10

Pneumonia, 488

Polyneuritis gallinarum, 275, 277

Prickly heat, 561

Proteosoma, 4

Psychoses, 608

Quinine, 45, 47 administration of, 49 in blackwater, 64 idiosyncrasy to, 47 prophylaxis, 45 toxic effects, 47

Rachialgia, 604

Rand scurvy, 286

Rat bite fever, 118, 502, 552, 563, 602 definition of, 118 epidemiology of, 118 etiology of, 118 pathology of, 119 symptomatology of, 120 treatment of, 120

Rats and leprosy, 252 and plague, 191, 196

Reflexes, 606

Relapsing fever, 86, 494, 495, 544, 550, 558, 560, 596, 604 definition of, 86 diagnosis in, 93 epidemiology of, 89 etiology of, 87 geographical distribution of, 87 history of, 86 Panama and, 91 pathology of, 91 prognosis in, 94 prophylaxis in, 94 symptomatology of, 91 symptoms in detail of, 92 synonyms for, 86 transmission of, 87 by the louse, 88 by the tick, 87 treatment of, 94

Remittent fever, 28

Respiratory system, 548

Rheumatic fever, 482

Rhino-pharyngitis mutilans, 395

Rhizomucor parasiticum, 474

Rice and beriberi, 272

Ringworm infections, 561

Rocky Mountain spotted fever, 446, 502, 546, 558, 560, 563, 580, 602, 605 definition of, 446 diagnosis in, 449 epidemiology of, 447 etiology of, 447 history of, 446 pathology of, 448 prophylaxis in, 449 symptomatology of, 448 synonyms for, 446 treatment of, 450

Romanowsky stains, 513

Saline enemata, 65 infusions in blackwater, 65 in cholera, 235 in heat stroke, 468

Sand-fly fever, 441

Sarcopsylla penetrans, 418

Scarlet fever, 482

Schilling-Torgau’s differential count, 514

Schistosoma haematobium, 363 japonicum, 364 mansoni, 364

Schistosomiasis, 357, 493, 546, 555, 560, 563, 575, 579, 589, 590, 606 diagnosis in, 366 etiology of, 357 geographical distribution of, 363, 364 history of, 360 infection in, 357 Japanese type, 364 pathology of, 362 prophylaxis in, 367 rectal type, 364 symptomatology of, 363 treatment of, 367 urticarial fever in, 366 vesical type, 363

Schizogony, 7

Schizotrypanum cruzi, 81

Screw worm, 422, 568

Scurvy, 286

Seven-day fever, 440

Ship beriberi, 285

Simulium reptans, 292

Six-day fever, 441

Skin diseases, 561 eruptions, 561

Sleeping sickness, 66

Smallpox, 486

Somnolence, 603

Spinal fluid, 598

Spirillum cholerae asiaticae, 220

Spironema duttoni, 87 recurrentis, 86

Spleen, enlargements of, 559 pains of, 559 puncture in kala-azar, 132, 559

Sporogony, 8

Sporotrichosis, 474

Sporozoites, 8

Spotted fever of the Rocky Mountains, 446

Sprue, 312, 492, 538, 553, 559, 572, 586, 588, 589 and hill diarrhoea, 316 and pellagra, 316 diagnosis in, 316 etiology of, 313 history of, 312 pathology of, 314 stools in, 316, 589 symptomatology of, 314 symptoms in detail of, 315 tongue, 315, 586 treatment of, 317

Sputum examination, 548

Statistics of cosmopolitan diseases, 481 of intestinal parasites, 584

Stegomyia calopus, 105, 433

Stomach, 587

Strongyloides stercoralis, 374

Strongyloides stercoralis, life history of, 375 symptoms of infestation, 374, 590 treatment of infestation, 376

Syphilis and liver abscess, 170 and yaws, 392 and tropical ulcer, 407 in tropics, 488, 598

Tabardillo, 451

Table of arthropodan diseases, 382 cosmopolitan diseases, 481 filarial worms, 338 helminthic diseases, 379 intestinal bacteria, 177 malarial parasites, 14 protozoal diseases, 377

Tartar emetic, 53, 80, 134, 140

Temperature chart in blackwater fever, 498 dengue, 495 kala-azar, 498 liver abscess, 501 malaria, 493, 494, 495 Malta fever, 497 Oroya fever, 502 plague, 499 relapsing fever, 495 trypanosomiasis, 500 typhus fever, 500 yellow fever, 498

Tetanus, 488

Thick film smears, 511

Three-day fever, 441

Thymol treatment, 332

Ticks, 89, 447

Tinea cruris, 414 etiology of, 414 symptomatology of, 414 treatment of, 415

Tinea imbricata, 411 etiology of, 411 symptomatology of, 412 treatment of, 413

Trachoma, 565

Transfusion of blood, 521

Trematode diseases, 357, 368, 379

Tremors, 605

Trench fever, 460, 503, 596, 605 definition of, 460 diagnosis in, 462 epidemiology of, 461 etiology of, 461 geographical distribution of, 461 history of, 460 pathology of, 462 prognosis in, 463 prophylaxis in, 463 symptomatology of, 462 synonyms for, 460 treatment of, 463

Treponema pertenue, 384

Trichinosis, 534, 597

Tropical liver, 166 and syphilis, 170 etiology of, 166 symptomatology of, 166 treatment of, 167 ulcer, 407

Trypanosoma brucei, 68, 84 gambiense, 66, 68, 69 nigeriense, 68 rhodesiense, 67, 69

Trypanosomes in animals, 84

Trypanosomiasis, 66, 500, 543, 548, 551, 556, 563, 566, 603, 604, 605, 607, 608 Brazilian, 80 definition of, 66 diagnosis in, 77 epidemiology of, 70 etiology of, 67 geographical distribution of, 67 history of, 66 Kérandel’s sign in, 74 pathology of, 72 prognosis in, 78 prophylaxis in, 78 symptomatology of, 72 symptoms in detail of, 76 synonyms for, 66 treatment of, 79

Tsetse flies, 70

Tsutsugamushi, 442 diagnosis in, 445 epidemiology of, 443 etiology of, 443 symptomatology of, 443

Tuberculosis, 485

Tularaemia, 213, 503, 552, 563 definition of, 213 diagnosis in, 217 epidemiology of, 214 etiology of, 214 geographical distribution of, 213 history of, 213 pathology of, 215 prognosis in, 217 prophylaxis in, 217 symptomatology of, 216 synonyms for, 213 treatment of, 217

Tumbu fly disease, 423

Typhoid fever, 483, 545 Marris atropin test in, 484

Typhus fever, 451, 500, 546, 548, 555, 558, 560, 565, 568, 587, 602 definition of, 451 diagnosis of, 457 epidemiology of, 453 etiology of, 452 history of, 451 louse in, 454 pathology of, 454 prophylaxis in, 458 symptomatology of, 455 synonyms of, 451 treatment of, 459

Urine, 570 amount of, 573 bacteriology of, 580 bile pigment in, 572 blood in, 571 Erlich’s aldehyde test, 573

Urobilinuria, 572 in blackwater, 572

Urticarial fever, 364, 493, 546, 563

Uta, 138, 564

Varicella, 487

Veld sore, 408

Venereal diseases, 488

Ver macaque, 421

Verruga, 425, 428, 494 pathology of, 428 symptomatology of, 429 treatment of, 430

Viscerel mycoses, 474

Vincent’s angina, 487

Virus, filterable, in dengue, 432

Vitamines, 271, 275, 288, 290, 293, 567

Vomiting, 588 sickness, 588

Weil’s disease, 114, 544, 558, 559

Wright’s staining method, 513

Xerophthalmia, 567

Yaws, 384, 494, 539, 553, 593 and syphilis, 392 diagnosis in, 391 epidemiology of, 385 etiology of, 384 geographical distribution of, 384 history of, 384 inoculation experiments, 385 pathology of, 386 prognosis in, 393 prophylaxis in, 393 symptomatology of, 387

Yaws, tertiary, 389 treatment of, 393

Yellow fever, 97, 498, 539, 547, 554, 557, 560, 566, 569, 573, 574, 575, 602, 604 Bacillus icteroides, 101 black vomit in, 109, 110 Commission reports, 103 definition of, 97 diagnosis in, 111 epidemiology of, 105 etiology of, 98 experimental work, 99, 103 Faget’s law, 108 geographical distribution of, 98 history of, 97 immune sera, use of, 113 immunity in, 105 Leptospira icteroides, 98 pathology of, 107 prognosis in, 112 prophylaxis in, 112 Stegomyia in, 101, 105 symptomatology of, 108 symptoms in detail of, 109 synonyms for, 97 treatment of, 112 vaccination against, 112

Yersin’s plague serum, 211

Zygote, 9

TRANSCRIBER’S NOTE

Obvious typographical errors and punctuation errors have been corrected after careful comparison with other occurrences within the text and consultation of external sources.

For consistency four occurrences of P^2O^5 (superscripts) have been changed to P_{2}O_{5} (subscripts).

For consistency a few occurrences of the ligatures æ and œ have been replaced by ae and oe.

Some hyphens in words have been silently removed, some added, when a predominant preference was found in the original book.

The wide table on page 159 has been split into two parts; the first column has been duplicated in the second part. The wide table on page 532 has been slightly restructured with no loss of text; the first column has been put into CAPS for readability.

Except for those changes noted below, all misspellings in the text, and inconsistent or archaic usage, have been retained.

Pg xii: ‘CHAPTER LI ... 392.’ replaced by ‘CHAPTER LI ... 592.’. Frontispiece: ‘MALARIAL PARASITIES’ replaced by ‘MALARIAL PARASITES’. Pg 17: ‘become chilled’ replaced by ‘becomes chilled’. Pg 21: ‘completely convered’ replaced by ‘completely covered’. Pg 26: ‘matter fo fact’ replaced by ‘matter of fact’. Pg 44: ‘part salcohol)’ replaced by ‘parts alcohol),’. Pg 50: ‘must be sterlie’ replaced by ‘must be sterile’. Pg 58: ‘apearances may not’ replaced by ‘appearances may not’. Pg 100: ‘about the infecton’ replaced by ‘about the infection’. Pg 102: ‘it would negative’ replaced by ‘it would negate’. Pg 102: ‘could t have been’ replaced by ‘could not have been’. Pg 122: ‘bodies, Lavaran’ replaced by ‘bodies, Laveran’. Pg 128: ‘spleen, parcicularly’ replaced by ‘spleen, particularly’. Pg 128: ‘pulp tords’ replaced by ‘pulp cords’. Pg 128: For consistency the heading ‘Symptomatology’ has been changed from =bold= to an ALLCAPS heading.<br> Pg 133: ‘place in diaganosis’ replaced by ‘place in diagnosis’. Pg 137: For consistency the heading ‘Symptomatology’ has been changed from =bold= to an ALLCAPS heading.<br> Pg 152: ‘magnesium oxdie’ replaced by ‘magnesium oxide’. Pg 172: ‘dressing froceps’ replaced by ‘dressing forceps’. Pg 177: ‘B. enteritidis’ replaced by ‘B. enteriditis’. Pg 185: ‘than prophylatic’ replaced by ‘than prophylactic’. Pg 187: ‘praise yaghurt’ replaced by ‘praise yoghurt’. Pg 223: ‘district and among’ replaced by ‘districts and among’. Pg 233: ‘The most scrupuous’ replaced by ‘The most scrupulous’. Pg 235: ‘was striken by’ replaced by ‘was stricken by’. Pg 249: ‘that of Kedrowski’ replaced by ‘that of Kedrowsky’. Pg 256: ‘cernea and iris’ replaced by ‘cornea and iris’. Pg 262: ‘nodular ases’ replaced by ‘nodular cases’. Pg 262: ‘of mixed lepcosy’ replaced by ‘of mixed leprosy’. Pg 265: ‘and very rarley’ replaced by ‘and very rarely’. Pg 269: ‘of Berberi’ replaced by ‘of Beriberi’. Pg 279: ‘formicaton of the’ replaced by ‘formication of the’. Pg 291: ‘exacerabtions but’ replaced by ‘exacerbations but’. Pg 309: ‘do not parallel’ replaced by ‘does not parallel’. Pg 314: ‘mind. sprue patient’ replaced by ‘mind. The sprue patient’. Pg 316: ‘Hill Diarrhea’ replaced by ‘Hill Diarrhoea’. Pg 331: ‘phenolphthalin test’ replaced by ‘phenolphthalein test’. Pg 332: ‘and chenopodiun’ replaced by ‘and chenopodium’. Pg 334: ‘Carbon tetrachlorid’ replaced by ‘Carbon tetrachloride’. Pg 350: ‘dose not involve’ replaced by ‘does not involve’. Pg 381: ‘Broad Rusian’ replaced by ‘Broad Russian’. Pg 393: ‘or with Giemas’ replaced by ‘or with Giemsa’. Pg 436: ‘cases occuring in’ replaced by ‘cases occurring in’. Pg 452: ‘eradicted from’ replaced by ‘eradicated from’. Pg 466: For consistency the heading ‘Pathology’ has been changed from italic to a separate ALLCAPS heading.<br> Pg 469: ‘peculiarly o affect’ replaced by ‘peculiarly to affect’. Pg 481: ‘Diarrhea and’ replaced by ‘Diarrhoea and’ (twice). Pg 484: ‘a broncho-penumonia’ replaced by ‘a broncho-pneumonia’. Pg 486: ‘is responsibile for’ replaced by ‘is responsible for’. Pg 494: ‘with manifestaitons’ replaced by ‘with manifestations’. Pg 501: ‘amoebic dystentery’ replaced by ‘amoebic dysentery’. Pg 501: ‘that liver abcess’ replaced by ‘that liver abscess’. Pg 507: ‘mixing throughly’ replaced by ‘mixing thoroughly’. Pg 510: ‘Erhlich’s method’ replaced by ‘Ehrlich’s method’. Pg 517: ‘ring of vsaeline’ replaced by ‘ring of vaseline’. Pg 522: ‘pippette off the’ replaced by ‘pipette off the’. Pg 527: ‘ension of alveolar’ replaced by ‘tension of alveolar’. Pg 529: ‘are not synonomous’ replaced by ‘are not synonymous’. Pg 530: ‘by bl d chemistry’ replaced by ‘by blood chemistry’. Pg 532: ‘the ura ic, and’ replaced by ‘the uraemic, and’. Pg 539: ‘febrile accesssions’ replaced by ‘febrile accessions’. Pg 557: ‘liquor formaldehydi’ replaced by ‘liquor formaldehyde’. Pg 573: ‘aldehyd reaction’ replaced by ‘aldehyde reaction’. Pg 574: ‘adminstration of’ replaced by ‘administration of’. Pg 590: ‘For more detailed’ replaced by ‘For a more detailed’. Pg 596: ‘and multilation are’ replaced by ‘and mutilation are’. Pg 598: ‘howevert, unless’ replaced by ‘however, unless’. Pg 605: ‘endo- and perineurium’ replaced by ‘endoneurium and perineurium’.

Spotted a typo or a problem in this chapter? Tell us