Human African Trypanosomiasis Quiz

Human African Trypanosomiasis (HAT), also known as sleeping sickness, is a parasitic disease caused by protozoans of the genus Trypanosoma.

It is transmitted through the bite of the tsetse fly.

The Trypanosoma brucei species are responsible for the infection. There are two main subtypes: T. brucei gambiense and T. brucei rhodesiense, each with a distinct geographical range and mode of transmission.

T. brucei gambiense primarily affects West and Central Africa, whereas T. brucei rhodesiense is prevalent in East and Southern Africa.

T. brucei gambiense is primarily transmitted through infected humans, with humans acting as the main reservoir. In contrast, T. brucei rhodesiense transmission occurs through infected wild animals as the primary reservoir.

The bite of the tsetse fly, a species of Glossina found only in Africa, is the primary mode of transmission. The flies are found in specific geographical regions within Africa.

The trypanosomes go through different stages of development within the tsetse fly and the human host. These stages are important for understanding the lifecycle of the trypanosome and how it spreads.

The first stage of the disease, the haemolymphatic stage (Stage 1), involves the parasite multiplying in the bloodstream and lymphatic system. It leads to widespread lymphadenopathy (swollen lymph nodes), histiocytic infiltration, and fibrosis.

The trypanosomes can cross the blood-brain barrier and enter the central nervous system, leading to the second stage of the disease, the neurological stage (Stage 2). This stage is characterized by severe neurological symptoms and can be fatal if left untreated.

Antigenic variation in the surface antigens of trypanosomes leads to incomplete immune control, resulting in multiple waves of parasitaemia.

The first stage of African trypanosomiasis, marked by a painless sore at the site of the tsetse fly bite.

A symptom of African trypanosomiasis characterized by swollen lymph nodes in the back of the neck.

A severe form of African trypanosomiasis where the parasite enters the central nervous system (CNS).

A change in the parasite's protein coat that helps it evade the immune system.

The second stage of African trypanosomiasis, characterized by neurological symptoms like headache, sleep disturbances, and behavioral changes.

A type of African trypanosomiasis that is zoonotic, meaning it can be transmitted from animals to humans.

Trypanosoma brucei gambiense is the main cause of human African trypanosomiasis and is characterized by a long incubation period and a more gradual progression of symptoms.

The most common form of African trypanosomiasis, characterized by a slower progression and less severe symptoms than Rhodesian trypanosomiasis.

A more aggressive form of African trypanosomiasis with a rapid progression and severe symptoms.

A sign of advanced African trypanosomiasis, where the body's response to a light touch is delayed.

A diagnostic method for African trypanosomiasis that involves examining a blood sample for the parasite.

A diagnostic test for African trypanosomiasis that uses a blood sample to detect antibodies against the parasite.

A sign of advanced neurological involvement in African trypanosomiasis, observed when the toes extend upward instead of curling downward when the sole of the foot is stroked.

A symptom of African trypanosomiasis, often characterized by a buildup of fluid in the chest or around the heart.

A symptom of African trypanosomiasis associated with liver inflammation and jaundice.

Suramin is administered intravenously, typically in a test dose on day 1 followed by larger doses on days 3, 10, 17, 24, and 31. It's generally well-tolerated but can cause fever, nausea, and proteinuria.

Pentamidine is given either intramuscularly or intravenously, the latter being preferred to avoid painful injections. The usual dose is 4 mg/kg/day for 7-10 days. It can cause side effects like syncope and hypotension.

Melarsoprol is administered intravenously and is effective against trypanosomes found in the blood, tissues, and CNS. It's often given after a preliminary course of Suramin to clear parasites from the blood and tissues.

Melarsoprol's main side effect is reactive arsenical encephalopathy, a serious neurological condition affecting the brain. This risk is reduced by giving prophylactic corticosteroids, especially for T.b.gambiense infections.

Eflornithine is administered intravenously for late-stage T.b.gambiense infections. The dose is 400 mg/kg/day for 14 days. It is relatively expensive but less toxic than Melarsoprol.

Treatment success is measured by observing symptom resolution, a decrease in CSF cell count below 5/mL, and normal CSF protein levels. These parameters may take months to normalize. A 2-year follow-up is crucial to ensure a cure.

If treatment for CNS involvement is delayed, neurological defects, particularly intellectual impairment, may persist despite successful treatment.

Relapses in T.b.gambiense infections are rare. The probability of relapse is much higher in T.b.rhodesiense.