The primary area of endemic infection with T. brucei gambiense (West African trypanosomiasis) coincides with the vector tsetse fly belt through the heart of Africa, where 300,000 to 500,000 people may be infected in Western and Central Africa. T. brucei rhodesiense (which causes Rhodesian trypanosomiasis or East African sleeping sickness) is more limited in distribution than T. brucei gambiense, being found only in central East Africa, where the disease has been responsible for some of the most serious obstacles to economic and social development of Africa. Within this area, the tsetse flies prefer animal blood, which therefore limits the raising of livestock. The infection in humans has a greater morbidity and mortality than does T. brucei gambiense infection, and game animals, such as the bushbuck, and cattle are natural reservoir hosts.

A unique feature of African trypanosomes is their ability to change the antigenic surface coat of the outer membrane of the trypomastigote, helping to evade the host immune response. The trypomastigote surface is covered with a dense coat of variant surface glycoprotein (VSG). There are approximately 100 to 1000 genes in the genome, responsible for encoding as many as 1000 different VSGs. More than 100 serotypes have been detected in a single infection. It is postulated that the trypomastigote changes its antigenic coat about every 5 to 7 days (antigenic variation). This change is responsible for successive waves of parasitemia every 7 to 14 days and allows the parasite to evade the host humoral immune response. Each time the antigenic coat changes, the host does not recognize the organism and must mount a new immunologic response. The sustained high immunoglobulin M (IgM) levels are a result of the parasite producing variable antigen types, and in an immunocompetent host, the absence of elevated IgM levels in serum rules out trypanosomiasis.

General Characteristics

 Trypanosomal forms are ingested by the tsetse fly (Glossina spp.) when a blood meal is taken. The organisms multiply in the lumen of the midgut and hindgut of the fly. After approximately 2 weeks, the organisms migrate back to salivary glands where the organisms attach to the epithelial cells of the salivary ducts and then transform to their epimastigote forms. Multiplication continues within the salivary gland, and metacyclic (infective) forms develop from the epimastigotes in 2 to 5 days. While feeding, the fly introduces the metacyclic trypanosomal forms into the next victim in saliva injected into the puncture wound. The entire developmental cycle in the fly takes about 3 weeks, and once infected, the tsetse fly remains infected for life.

In fresh blood, the trypanosomes move rapidly among the red blood cells. An undulating membrane and flagellum may be seen with slower moving organisms. The trypomastigote forms are 14 to 33 µm long and 1.5 to 3.5 µm wide (see Table 1, Figure 1). With a blood stain, the granular cytoplasm stains pale blue. The centrally located nucleus stains reddish. At the posterior end of the organism is the kinetoplast, which also stains reddish, and the remaining intracytoplasmic flagellum (axoneme), which may not be noticeable. The flagellum arises from the kinetoplast, as does the undulating mem brane. The flagellum runs along the edge of the undulating membrane until the undulating membrane merges with the trypanosome body at the anterior end of the organism. At this point, the flagellum becomes free to extend beyond the body.

Table1. Characteristics of American Trypanosomiasis

Fig1. Characteristic stages of species of Leishmania and  Trypanosoma in human and insect hosts. (Illustration by Nobuko  Kitamura.)

Pathogenesis and Spectrum of Disease

 Trypanosoma brucei gambiense. African trypanosomiasis caused by T. brucei gambiense (West African sleeping sick ness) has a long, mild, chronic course that ends in death with central nervous system (CNS) involvement after several years’ duration. This is unlike the disease caused by T. brucei rhodesiense (East African sleeping sickness), which has a short course and ends fatally within 1 year.

After the host has been bitten by an infected tsetse fly, a nodule or chancre at the site may develop after a few days. Usually, this primary lesion will resolve spontaneously within 1 to 2 weeks, and is rarely seen in patients living in an endemic area. Trypomastigotes may be detected in fluid aspirated from the ulcer. The trypomastigotes enter the bloodstream, causing a low-grade parasitemia that may continue for months with the patient remaining asymptomatic. This is considered stage I disease, where the patient can have systemic trypanosomiasis without CNS involvement. During this time, the parasites may be difficult to detect, even by thick blood film examinations. The infection may self-cure during this period without development of symptoms or lymph node invasion.

Symptoms may occur months to years after infection. When the lymph nodes are invaded, the first symptoms appear and include remittent, irregular fevers with night sweats. Headaches, malaise, and anorexia may also be present. The febrile periods of up to 1 week alternate with afebrile periods of variable duration. Many trypomastigotes may be found in the circulating blood during fevers, but few are seen during afebrile periods. Lymph adenopathy is a consistent feature of Gambian trypanosomiasis, and the enlarged lymph nodes are soft and painless. In addition to lymph node involvement, the spleen and liver become enlarged. With Gambian try panosomiasis, the blood lymphatic stage may last for years before the sleeping sickness syndrome occurs.

When the organisms finally invade the CNS, the sleeping sickness stage of the infection is initiated (stage II disease). Behavioral and personality changes are seen during CNS invasion. This stage of the disease is characterized by steady progressive meningoencephalitis, apathy, confusion, fatigue, loss of coordination, and somnolence (state of drowsiness). In the terminal phase of the disease, the patient becomes emaciated and progresses to profound coma and death, usually from secondary infection. Thus, the typical signs of true sleeping sickness are seen in patients with Gambian disease.

Trypanosoma brucei rhodesiense. T. brucei rhodesiense produces a more rapid, fulminating disease than does T. brucei gambiense. Fever, severe headaches, irritability, extreme fatigue, swollen lymph nodes, and aching muscles and joints are typical symptoms. Progressive con fusion, personality changes, slurred speech, seizures, and difficulty in walking and talking occur as the organisms invade the CNS. The early stages of the infection are like those of T. brucei gambiense infections. However, CNS invasion occurs early, the disease progresses more rapidly, and death may occur before there is extensive CNS involvement. The incubation period is short, often within 1 to 4 weeks, with trypomastigotes being more numerous and appearing earlier in the blood. Lymph node involvement is less pronounced. Febrile episodes are more frequent, and the patients are more anemic and more likely to develop myocarditis or jaundice. Some patients may develop persistent tachycardia, and death may result from arrhythmia and congestive heart failure. Myocarditis may develop in patients with Gambian trypanosomiasis but is more common and severe with the Rhodesian form.

Laboratory Diagnosis (All Species)

Routine Methods. Blood can be collected from either finger stick or venipuncture (use EDTA anticoagulant). Multiple thick and thin blood films should be made for examination, and multiple blood examinations should be done before trypanosomiasis is ruled out. Parasites will be found in large numbers in the blood during the febrile period and in small numbers when the patient is afebrile. In addition to thin and thick blood films, a buffy coat concentration method is recommended to detect the parasites. Parasites can be detected on thin blood films with a detection limit at approximately 1 parasite/200 microscopic fields (high dry power magnification, ×400) and thick blood smears when the numbers are greater than 2000/mL, and when they are greater than 100/mL with hematocrit capillary tube concentration.

Antigen Detection. A simple and rapid test, the card indirect agglutination trypanosomiasis test (TrypTect CIATT), is available, primarily in areas of endemic infection, for the detection of circulating antigens in persons with African trypanosomiasis. The sensitivity of the test (95.8% for T. brucei gambiense and 97.7% for T. brucei rhodesiense) is significantly higher than those for lymph node puncture, micro hematocrit centrifugation, and cerebrospinal fluid examination (CSF) after single and double centrifugation. Its specificity is excellent, and it has a high positive predictive value.

Antibody Detection. Serologic techniques that have been widely used for epidemiologic screening include indirect fluorescent antibody assays (enzyme-linked immunosorbent assay [ELISA]), the indirect hemagglutination test, and the card agglutination trypanosomiasis test. A major problem in endemic areas is that individuals have elevated antibody levels attributable to exposure to animal trypanosomes that are noninfectious to humans. Serum and CSF IgM concentrations are of diagnostic value. However, CSF antibody titers should be interpreted with caution because of the lack of reference values and the possibility that the CSF will contain serum as the result of a traumatic tap.

Molecular Diagnostics. Referral laboratories have used molecular methods to detect infections and differentiate species, but these methods are not routinely used in the field. The PCR-based methods have not been standardized and validation studies have not been performed. There have been few studies where the various PCR methods used for diagnostic purposes have been compared. In general, these tests are not available in the routine laboratory.

Therapy

All drugs used in the therapy of African trypanosomiasis are toxic and require prolonged administration. Treatment should be started as soon as possible, and the antiparasitic drug selected depends on whether the CNS is infected. Suramin or pentamidine isethionate can be used when the CNS is not infected. Melarsoprol, a toxic trivalent arsenic derivative, is effective for both blood and CNS stages but is recommended for treatment of late-stage sleeping sickness. Eflornithine (dl-α difluoromethylornithine; DFMO) has been used for more than 10 years for melarsoprol-resistant T. brucei gambiense infection with or without CNS involvement. Any individual treated for African trypanosomiasis should be monitored for 2 years after completion of therapy.

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