PROTOZOA.

INTRODUCTION.

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

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

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

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

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

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

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

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

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tried in many parasitic diseases can be found in the Sleeping Sickness Bulletin and Kala-azar Bulletin, both now superseded and greatly extended in scope in the Tropical Diseases Bulletin, published by the Tropical Diseases Bureau, Imperial Institute, London, S.W.

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

I.—AMŒBIC DYSENTERY.

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

Walker and Sellards429 (1913) conducted important experiments with amœbæ on prisoners in the Philippine Islands. They showed experimentally that cultural amœbæ are non-pathogenic. As regards experiments with Entamœba coli, after feeding to twenty individuals they concluded that E. coli is a parasite of the human intestine but non-pathogenic and non-culturable. In a third series of experiments, after feeding with motile Entamœba histolytica, tetragena cysts were found in the stools later; when tetragena cysts were administered, motile E. histolytica were present in the subsequent stools. Some of the histolytica cases developed dysentery after a time. They lay stress on the necessity for the frequent examination of stools in order to detect carriers. The incubation period of entamœbic dysentery is usually long.

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

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

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

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

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

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

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

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

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

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

Recently (July, 1914), Dr. W. E. Deeks430 has given an account of his successful procedure in dealing with the dysenteries in the Ancon Hospital, Panama Canal Zone, of which medical clinic he is the chief. With regard to amœbic dysentery he advocates: (1) Rest, to increase the patient’s resistance; (2) a generous milk diet, which is practically all absorbed before it reaches the large bowel; (3) saline or plain water irrigations, one to three daily; (4) the administration of bismuth sub-nitrate in heroic doses; 180 gr. is given mechanically suspended in about a tumbler of plain or effervescent water every three hours, day and night in severe cases, only lessening the amount when improvement takes place. Mechanical suspension in a large quantity of water is essential. When the stools begin to decrease in number and the tongue becomes clean, the number of doses is reduced to three or four daily. In very chronic cases one or two doses daily for a month after convalescence are recommended.

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

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

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

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

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

Rogers431 (1915) recommends a combined treatment of emetine and streptococcal vaccines for pyorrhœa alveolaris.

II.—TRYPANOSOMIASES.

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

African Sleeping Sickness.

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

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

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

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

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

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

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

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

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

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

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

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

Large doses of atoxyl were often said to cause distressing results such as optic atrophy, and when the onset of such occurred the drug was usually discontinued. However, Daniels432 (July, 1915) points out that eye troubles, such as iridocyclitis, are symptoms of trypanosomiasis.

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

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

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

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

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

South American Trypanosomiasis.

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

III.—FLAGELLATE DIARRHŒA AND DYSENTERY.

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

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

(i) Mello-Leitao433 (1913), writing from Rio de Janeiro, states that there is a primary flagellate dysentery, due to Trichomonas intestinalis (Leuckart) and to Lamblia intestinalis (Lambl), either separately or in combination. He considers it a benign disease, and the most frequent form of dysentery in young children. Trichomonas and Lamblia were found to be pathogenic to children under 3 years of age.

Escomel434 (1913) collected 152 cases of dysentery in Peru due solely to Trichomonas. Examination of the reservoirs containing the water used for drinking purposes showed the presence of Trichomonas. After the reservoirs were cleaned no more Trichomonas was found and the cases of dysentery ceased.

Brumpt435 (1912) described a colitis due to Trichomonas intestinalis in a patient returned from Tonkin.

Cases of infection by Chilomastix (Tetramitus) mesnili, with colitis or dysenteric symptoms, are recorded by Brumpt (1912) from France, and by Nattan-Larrier436 (1912) from the Ivory Coast respectively.

Marques da Cunha and Torres437 (1914) describe five cases of chronic diarrhœa in Brazilian children due to the Chilomastix (Tetramitus).

Gäbel438 (1914) described a case of seasonal diarrhœa contracted in Tunis and caused by a Tetramitid parasite which he named Difämus tunensis, as the discoverer considered that it lacked an undulating membrane in its large cytostome.

Derrieu and Raynaud439 (1914) record a case of chronic dysentery in Algeria due to a Trichomonad possessing an undulating membrane and five free flagella. The parasite was named Hexamastix ardindelteili, but the generic name Hexamastix is pre-occupied. Chatterjee’s Pentatrichomonas bengalensis (1915) is possibly the same organism.

Treatment.—Escomel (1913), finding ipecacuanha and calomel useless, recommends turpentine for Trichomonad dysentery. Two to 4 gr of essence of turpentine in an emulsion are given by the mouth, and enemata containing 15 to 20 drops of turpentine emulsified in the yolk of an egg to which is added a little water and tincture of opium. Derrieu and Raynaud found this treatment effective in Algeria. Smithies440 (1912) reports two cures of cases of severe dyspepsia, in which Trichomonads were found in the stomach contents, after administration of a single dose of 50 to 60 gr. of thymol, given at bed-time, together with 2 gr. of calomel, and followed by an ounce of Carlsbad salts in the morning. The patients came from the Southern United States, and had been in the habit of drinking unfiltered surface water in the localities in which they lived. Mello-Leitao441 used magnesium sulphate and water or milk diet. Sometimes enemata of collargol (1 per cent.) or electrargol were required. Rosenfeld recommended calomel. Methylene blue has also been tried. Recently, Escomel442 (1914) recommends enemata of an aqueous solution of iodine (1 per 1,000) and farinaceous diet. Lynch443 (1915), working in South Carolina, recommends a mouth wash of saturated solution of bicarbonate of soda three times daily in oral infections. A similar solution was used as a douche in vaginal trichomoniasis.

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

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

Mathis444 (1914) gives an interesting account of cases in Tonkin. In a child, aged 3, the stools were at first glairy and blood-stained, containing many encysted Lamblia. The child’s home was infested with mice. In another case, the house of the patient harboured numerous rats.

According to Mathis, prognosis is favourable, but emetine hydrochloride is without action on Lamblia. Prowazek and Werner445 (1914), however, state that emetine will act upon the flagellates, but not upon the cysts. They recommend uzara (two tablets, three times daily) and extract of male fern as useful in certain cases. Martin Mayer (1914) found emetine hydrochloride successful in a case in the Hamburg Seamen’s Hospital, but Assmy (1914) points out that a suitable diet and daily doses of magnesium sulphate are sufficient, in his experience, to effect an improvement, and he doubts the specific action of emetine. Escomel (1914) recommends milk diet, then calomel succeeded by castor oil.

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

IV.—LEISHMANIASES.

A. Kala-azar.

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

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

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

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

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

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

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

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

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

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

B. Oriental Sore, due to Leishmania tropica.

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

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

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

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

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

This form of Leishmaniasis has been reported from South America and recently by Christopherson448 (1914) from the Sudan. In South America it is often called Espundia, also Buba and Forestal Leishmaniasis. The primary lesion is found usually on the forearms, legs, chest or trunk. This ulcer is of the Oriental sore type, and after some months, or even as long as two years, heals up, leaving a thick scar. While the ulcer is open, or more often after it has healed, lesions appear on the mucosa of the mouth and nose. The hard and soft palate, gums and lips all may be attacked. The mucosa of the nose is usually attacked and the cartilages become destroyed, producing great deformity. In bad cases the pharynx and larynx may become infected.

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

In 1913 Vianna, working in Brazil, introduced treatment by tartar emetic, which is now becoming more widely known and proving efficacious. Carini449 (1914) applies it thus. Tartar emetic (that is, potassium antimonyl tartrate) in 1 per cent. aqueous solution is introduced slowly into a vein, such as the vein at the bend of the elbow, in doses of 5 to 10 c.c. daily or on alternate days according to the tolerance of the patient to the drug. Eighteen to forty injections have been used. In some of the memoirs on the subject, the drug is referred to as antimony tartrate.

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

At present the actual transmitter of Espundia is not known with certainty. Various sand-flies (Simulidæ) have been suspected of transmitting the disease, though so far proof is wanting. It has also been suggested that the natural food sources of some Simulidæ known to bite man, namely, certain snakes450 and lizards,451 are possible reservoirs of the disease.

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

V.—SPIROCHÆTOSES.

A. Relapsing Fevers.

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

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

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

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

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

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

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

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

In North Africa (Algeria, Tunis, Tripoli, Egypt), and sometimes in the Anglo-Egyptian Sudan, a spirochætosis due to S. berbera occurs. According to Castellani and Chalmers, the incubation period varies somewhat. The fever reaches its height during the first twenty-four hours, and afterwards shows a morning remission. Jaundice is often absent, but there may be hepatic tenderness and splenic enlargement. One or two relapses usually occur. The treatment is on the same lines as for the other spirochætal fevers. Sergent and Gillot452 (1911), working at the Institut Pasteur of Algeria, have had good results by using injections of salvarsan in doses of 0·75 to 1·0 cg. per kilogramme weight of the patient. The prophylactic measures are directed against lice and other biting insects. Personal cleanliness is most necessary.

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

B. Yaws or Frambœsia tropica.

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

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

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

C. Syphilis.

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

D. Bronchial Spirochætosis.

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

Chalmers and O’Farrell453 (1913), writing from Khartoum, recommended rest in bed, good food and ventilation, coupled with treatment by arsenic in some form, preferably associated with glycerophosphates. These may be given by the mouth, or intramuscularly as an injection of:—