Sleeping Sickness (Trypanosomiasis).—To the group of diseases
caused by Trypanosomes must now be added sleeping sickness.
This disease is due to the presence and action in the human body
of a form known as T. gambiense (Dutton).
In order to demonstrate the parasite in the blood of a case of sleeping sickness, where they are very scanty and difficult to find, the best method is repeated centrifugalization of the blood (Bruce), 10 c.c. being treated at a time; then the sediment in a number of these tubes is collected and again centrifugalized. The living trypanosome may, as a rule, be distinguished in this final sediment, even under a low power of the microscope. The organism may be found in greater numbers in the cerebro-spinal fluid of a case in which the symptoms of sleeping sickness have been developed, though centrifugalization of from 10 to 15 c.c. of the cerebro-spinal fluid for half an hour may be necessary before they can be demonstrated. Greig and Gray, at Mott’s suggestion, were able to find the organism in the fluid removed by means of a hypodermic syringe from the swollen lymph glands that appear as one of the earliest signs of infection. Examined fresh and in its native fluid or in normal saline solution it is seen as an actively motile, highly refractile, somewhat spindle-shaped organism (see Plate I., fig. 9). The anterior end is prolonged into a pointed flagellum, the posterior end being slightly blunted or rounded. This organism darts about rapidly between the red blood corpuscles or other corpuscles or particles, and shows rapid undulations, the flagellum beating quickly and the body following the flagellum. In this body a couple of very bright points may be seen. On staining by Leishman’s stain (see under Kála-ázar) the general protoplasm of the body is stained blue and is somewhat granular. This trypanosome is from 15 to 25μ in length (without the flagellum, which is from 5 to 6μ) and from 1·5 to 2·5μ broad. In the centre of the spindle-shaped mass is a very distinct reddish purple oval corpuscle corresponding to the larger of the two bright points seen in the unstained specimen; this, the nucleus or macronucleus, is slightly granular. Near the posterior or blunt end of the organism is a second, but much smaller, deeply stained reddish purple point, the second of the bright spots seen in the unstained specimen; this is known as the micro-nucleus or centrosome. Around the micro-nucleus is a kind of court or area of less deeply stained protoplasm, arising from or near which and running along the margin of the body is a narrow band with a very sharply defined wavy free margin. This thin band of protoplasm seems to be continuous with the large spindle-shaped body of the trypanosome, but at the free margin it takes on the red tint of the micro-nucleus instead of the blue tint of the protoplasm. The undulatory membrane, as this band is called, is narrowest at the posterior end, getting broader and broader until the micro-nucleus is reached, beyond which it tapers off irregularly until finally it merges in the flagellum. In sleeping sickness the presence of this organism is usually associated with distinct anaemia, the red cells being diminished in number and the haemoglobin in quantity. Along with this there is an increase in the number of mononuclear leucocytes.
The trypanosome is carried to the human patient by the Glossina palpalis, in the proboscis of which the organisms may be seen for some short time after the insect has sucked blood from an infected patient. These trypanosomes have been found living and active in the stomach of this insect up to 118 hours, but after 140 hours no living parasites can be demonstrated. They undergo no metamorphoses in this intermediate host and are simply discharged in the intestinal excreta. It may be readily understood that the trypanosome under these conditions soon loses its virulence, and an animal cannot be infected through the bite of the Glossina for more than 48 hours after the infected blood has been ingested by the fly. The organism may remain latent in the human body for a considerable period. It certainly sets up very tardily any changes by which its presence can be detected. The first symptoms of its presence and activity are enlargement of the lymphatic glands, especially those behind the neck, a condition often accompanied by irregular, and intermittent fever.
After a time, in from three months to three years, according to Bruce, the organism gains access to the fluid in the cerebrospinal canal. Accompanying this latter migration are languor, lassitude, a gradually increasing apathy, and finally profound somnolence.
The incubation period, or that between the time of infection and the appearance of the symptoms associated with trypanosomiasis may be as short as four weeks, or it may extend over several years. The inhabitants of the island of Senegal who have lived in Casamance do not consider themselves safe from the disease until at least seven years after they have left an infected area. At first, amongst negroes, according to Dutton and Todd, there is no external clinical sign of disease except glandular enlargement; in mulattoes and whites an irregular and intermittent fever may be the chief sign of infection, “the temperature being raised for two to four days, then falling to normal or below normal for four or five days.” In other cases the fever is of the septic type, the temperature being normal in the morning but rising in the evening to 101·3° or 102·2° F., rarely to 104° F., the curve differing from that characteristic of malaria in which the rise usually takes place in the morning. Moreover, in sleeping sickness there are no rigors before the rise of temperature and but slight sweating, such as there is usually occurring at the end of the rise. Here again we have a distinction between the malarial condition and that of sleeping sickness. The respiration and the pulse rate are increased both during the febrile and the non-febrile attacks; the respiration is from 29 to 30 a minute, and the pulse rises to 90, and even up to 140, a minute, according to the degree of cardiac excitability which appears to be constantly present. The localized swelling and redness are seen as puffiness of the face, oedema of the eyelids and ankles and feet, congested erythematous patches on the face, trunk or limbs. Anaemia, general weakness and wasting, at first very slightly marked, gradually become prominent features, and headache is often present. The enlargement of the spleen appears to go on concurrently with enlargement of the lymphatic glands. Manson points out that trypanosomiasis may terminate fatally without the appearance of any characteristic symptoms of sleeping sickness, but as a rule the “sleeping” or second stage supervenes. The temperature now becomes of the hectic type, rising to 102·2° F. in the evening and falling to 98·6° F. in the morning. Here again there are no rigors or sweating. During the last stages of the disease the rectal temperature may fall as low as 95° and for the last day or two to 92° F., the pulse and respiration falling with the temperature. The irritability of the heart is still marked. Headache in the supraorbital region, and pain in the back, and even in the feet, have been described. Activity and intelligence give place to laziness, apathy and dullness; the face loses its brightness, the eyelids approximate, and the muscles around the mouth and nose become flabby and flaccid, the patient becomes drowsy, and when questioned replies only after a marked interval. Fibrillary tremors of the tongue and shaking of the hands and arms, distinct even during rest, become increased when any voluntary movement is attempted. These tremors may extend to the lower limbs and trunk. Epileptiform convulsions, general weakness and progressive emaciation come on, and shortly before death there is incontinence of urine and faeces. “The intellectual faculties gradually become impaired, the patient has a certain amount of difficulty in understanding what is said to him, and becomes emotional, often crying for no reason whatever; delirium is usually absent, the drowsiness increases and the patient’s attitude becomes characteristic, the head falls forward on the chest and the eyelids are closed. At first the patient is easily aroused from this drowsy condition, but soon he reaches a stage in which he falls sound asleep almost in any attitude and under any conditions, especially after meals. These periods of sleep, which become gradually longer and more profound, lead eventually to a comatose condition from which the patient can be aroused only with the greatest difficulty. It is at this stage that the temperature becomes normal and death occurs.” Nabarro points out, however, that this condition of drowsiness and sleep, leading eventually to coma, is by no means invariably present.
