TRYPANOSOMIASIS

TRYPANOSOMIASIS

African trypanosomiasis (Sleeping sickness)

Etiology
There are two clinical forms of African trypanosomiasis: 1) a slowly developing disease caused by Trypanosoma brucei gambiense and 2) a rapidly progressing disease caused by T. brucei rhodesiense.

Epidemiology
T. b. gambiense is predominant in the western and central regions of Africa, whereas T. b. rhodesiense is restricted to the eastern third of the continent (figure 2E). 6,000 to 10,000 human cases are documented annually. 35 million people and 25 million cattle are at risk. Regional epidemics of the disease are cause of major health and economic disasters.

Morphology
T. b. gambiense and T. b. rhodesiense are similar in appearance: The organism measures 10 - 30 micrometers x 1-3 micrometers. It has a single central nucleus and a single flagellum originating at the kinetoplast and joined to the body by an undulating membrane (Figure 2A-D). The outer surface of the organism is densely coated with a layer of glycoprotein, the variable surface glycoprotein (VSG).
Life cycle
The infective, metacyclic form of the trypanosome is injected into the primary host during a bite by the vector, the tsetse fly (figure 3). The organism transforms into a dividing trypanosomal (trypomastigote) blood form (figure 1B) as it enters the draining lymphatic and blood stream. The trypanosomal form enters the vector during the blood meal and travels through the alimentary canal to the salivary gland where it proliferates as the crithidial form (epimastigote) and matures to infectious metacyclic forms (Figure 1B). Trypomastigotes can traverse the walls of blood and lymph capillaries into the connective tissues and, at a later stage, cross the choroid plexus into the brain and cerebrospinal fluid. The organism can be transmitted through blood transfusion.
Symptoms
The clinical features of Gambian and Rhodesian disease are the same, however they vary in severity and duration. Rhodesian disease progresses more rapidly and the symptoms are often more pronounced. The symptoms of the two diseases are also more pronounced in Caucasians than in the local African population. Classically, the progression of African trypanosomiasis can be divided into three stages: the bite reaction (chancre), parasitemia (blood and lymphoid tissues), and CNS stage.

Bite reaction: A non-pustular, painful, itchy chancre (Figure 4 A and B) forms 1-3 weeks after the bite and lasts 1-2 weeks. It leaves no scar.

Parasitemia: Parasitemia and lymph node invasion is marked by attacks of fever which starts 2-3 weeks after the bite and is accompanied by malaise, lassitude, insomnia headache and lymphadenopathy and edema (figure 4E). Painful sensitivity of palms and ulnar region to pressure (Kerandel's sign) may develop in some Caucasians. Very characteristic of Gambian disease is visible enlargement of the glands of the posterior cervical region (Winterbottom's sign) (Figure 4C). Febrile episodes may last few months as in Rhodesian disease or several years as in Gambian disease. Parasitemia is more prominent during the acute stage than during the recurrence episodes.

CNS Stage: The late or CNS stage is marked by changes in character and personality. They include lack of interest and disinclination to work, avoidance of acquaintances, morose and melancholic attitude alternating with exaltation, mental retardation and lethargy, low and tremulous speech, tremors of tongue and limbs, slow and shuffling gait, altered reflexes, etc. Males become impotent. There is a slow progressive involvement of cardiac tissue. The later stages are characterized by drowsiness and uncontrollable urge to sleep. The terminal stage is marked by wasting and emaciation. Death results from coma, intercurrent infection or cardiac failure (figure 5).