Introduction

Trypanosomes are protozoan parasites belonging to the subphylum Mastigophora. The trypanosomaes of medical importance are

1. Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense which cause African Trypanosomiasis in humans. The disease is also known as sleeping sickness. The parasites are closely related and belong to the Trypanosoma brucei group, or complex. T. brucei belongs to the salivarian group of trypanosomes which develop mid gut in the vector and transmission is by inoculation when the vector feeds. The vector is the Tse-Tse fly.

2. Trypanosoma cruzi  which causes American trypanosomiasis, or Chagas disease (Carlos Chagas 1907). T. cruzi belongs to the stercorarian group of trypanosomes which develop in the hindgut of the vector and transmission is by faecal contamination after the vector bites. The vector is the Reduvid bug.

A trypomastigote of Trypanosoma cruzi

 African Trypanosomiasis

Lifecycle

Metacyclic (infective) trypomastigotes are inoculated through the skin when a tsetse fly takes a blood meal. The parasites develop into long slender trypomastigotes which multiply at the site of inoculation and later in the blood, lymphatic system and tissue fluid. The trypomastigotes are carried to the heart and various organs and in later stages of infection invade the CNS. Trypomastigotes are taken up by the tsetse fly when it sucks blood (male and female). The parasites develop in the midgut of the fly and multiply. From about 2-3 weeks the trypomastigotes move to the salivary glands transforming through epimastigotes into metacyclic trypomastigotes. The tsetse fly remains infective for life - about 3 months. T. b. rhodesiense infects many animals as well as humans whereas T. b. gambiense is infective to fewer animals.In Africa the disease causes a lot of cattle wasting because of the infection rate.

Clinical Disease

African trypanosomiasis is a wasting disease which is usually fatal unless treated. In the early stages of the disease there is a high irregular fever with shivering, sweating and an increased pulse rate. The lymph glands near the bite often become swollen, gambiense the glands at the back of the neck and rhodesiense usually the glands under the jaw are affected. Enlarged spleen oedema of the eyelids, face and sleeplessness are features as the disease progresses.

In the late stages of the disease the trypanosomes invade the CNS giving symptoms of meningoencephalitis, mental dullness, apathy, excessive sleeping and incontinence. The CSF usually contains mononuclear cells and a few trypanosomes may be detected. CSF protein is raised. If untreated, coma develops and finally death. Such signs are more commonly seen with gambiense than in rhodesiense in which patients often die before these symptoms develop fully.

Laboratory Diagnosis

a. Examination of blood for trypanosomes (thick/thin) and Buffy coat

b. Aspirates from enlarged lymph glands - trypanosomes.

c. CSF for trypanosomes, cells (Morula), raised protein , IgM and motile trypanosomes.

d. Serum for anti trypanosomal antibodies - tests available for T. b. gambiense (IFAT, ELISA CFT).

 South American Trypanosomiasis

Life cycle

Metacyclic trypomastigotes are deposited in faeces on the skin as the triatomine bug (Reduvid)feeds. The bug usually bites round the edges of the mouth and eyes. The trypomastigotes are either rubbed into the skin by scratching the irritated area or penetrate the conjunctiva or membranes of the nose and mouth. Trypomastigotes become amastigotes in localised RE cells and multiply. The amastigotes develop into trypomastigotes which are released into the blood when the cell ruptures. No multiplication of the parasite takes place in the blood in its trypomastigote stage. By way of the blood and lymphatic system the trypomastigotes reach tissue cells especially heart muscle, nerves, skeletal muscle and smooth muscle of the gastrointestinal system. The trypomastigotes become amastigotes and multiply forming pseudocysts. One trypomastigote may produce 500 amastigotes within a single pseudocyst in as little as 5 days. Within the pseudocyst some amastigotes become elongated and develop first into epimastigotes and then trypomastigotes. When the cell ruptures the trypomastigotes are released into the blood and continue to circulate whilst others invade further tissue cells. The life cycle completes when a triatomine bug vector ingests circulating trypomastigotes. In the vector the trypomastigotes transform and develop into epimastigotes, multiply by binary fission in the gut of the bug. After about 10 - 15 days, metacyclic trypomastigotes are formed and can be found in the hindgut of the bug.

Clinical features

Many people infected with T. cruzi remain asymptomatic and free from Chagas disease or experience only an acute infection without progressing to the chronic stage.Multiplication of T. cruzi at the site of infection can produce an inflamed swelling (chagoma) - persists for weeks. If in the eye then the conjunctiva becomes inflamed (Romana's sign). In the acute stage of infection trypomastigotes can be found in the blood. Symptoms may pass unnoticed, there may be fever, malaise increased pulse rate and enlargement of lymph glands, liver and possibly spleen. Blood films often resemble glandular fever. The acute form is most often seen in young children and occasionally can cause serious damage to the heart and other complications leading to death.Chronic manifestations include signs of cardiac muscle damage with a weak and irregular heartbeat, oedema and heart enlargement leading to heart failure. About 10% of persons infected with T. cruzi develop chronic Chagas cardiopathy.

Laboratory Diagnosis

a. Trypanosomes of T. cruzi in blood (early acute)

1) careful examination of fresh blood for motile trypanosomes as wet prep.

2) Capillary tube (microhaematocrit) concentration technique. Rapid and sensitive.

(1) IFAT indirect fluorescence antibody test

(2) CFT complement fixation test

(3) IHAT indirect haemaglutination test

(4) ELISA enzyme linked immunoabsorbent assay