Dermatology Made Easy is based on the most popular topics from DermNet NZ's vast array of material. The book combines the essential focus of the ‘Made Easy’ book series with the authority and knowledge base of DermNet NZ's unparalleled resources.
Author: Marie Hartley, Staff Writer, 2009.
The protozoa Trypanosoma is responsible for two distinct diseases in humans. T. brucei causes Human African trypanosomiasis, also known as sleeping sickness, in Africa (described on this page). T. cruzi causes American trypanosomiasis, also known as Chagas disease, and is found predominantly in the tropical Americas (described elsewhere).
African trypanosomiasis (sleeping sickness) is a potentially fatal disease caused by the protozoan parasite Trypanosoma brucei. The parasites are transmitted to humans via the bite of tsetse flies (Glossina species), which become infected by ingesting blood of infected mammalian hosts. There are more than 30,000 documented infections and more than 5000 deaths annually, although the majority of cases likely go undetected.
|T. brucei gambiense (Gambian sleeping sickness)||T. brucei rhodesiense (Rhodesian sleeping sickness)|
|Mammalian species affected||
*The differences between Gambian and Rhodesian sleeping sickness are not absolute and the opposite can also occur.
There are two distinct phases of clinical illness.
T. brucei initially multiplies in subcutaneous tissues, blood, and lymph within a few weeks of the tsetse fly bite. This is called the haemolymphatic phase and may be associated with bouts of general malaise, fever, headaches, joint pain, itchiness, swelling of the hands, face, and feet, enlarged lymph nodes, and anaemia. Myocardial (heart muscle) and pericardial (sac around the heart) inflammation, disseminated intravascular coagulation, and renal insufficiency (kidney disease) may also occur.
In time, the parasites cross the blood-brain barrier to infect the central nervous system (the meningoencephalitic phase). Early findings include insomnia, loss of appetite, behavioural changes, mood disorders, apathy, and headaches. A variety of muscle disorders may follow, including tremors and disturbances of speech, gait, and reflexes. Pain, paralysis, and seizures may also occur. Severe, delayed pain when soft tissues are compressed (Kerandel sign) may be present. Somnolence is the classic symptom of the disease; however it is preceded by a period of nighttime insomnia and daytime somnolence. Deep somnolence appears late and is progressively difficult to overcome.
The skin signs of trypanosomiasis include chancre, trypanids, itching and petechiae.
A trypanosomal chancre may appear around 48 hours after the tsetse bite. This is an itchy, painful, inflammatory reaction at the site of the bite. The chancre is an indurated (hardened) red or purple nodule, 2 to 5 cm in diameter, which is accompanied by enlarged lymph nodes. A central necrotic eschar (dark-coloured crust) may form before the chancre desquamates (peels off in scales) within 2 to 3 weeks, leaving no trace.
Trypanids are transient rashes that occur 6 to 8 weeks after the onset of illness in approximately 50% of light-skinned patients. Trypanids are found on the trunk and may have the following characteristics:
Petechiae are small red, purple, or brown spots due to bleeding into the skin. They are a rare complication that may be accompanied by generalised flushing.
Diagnosis of T. brucei requires identification of the parasite in the bite lesion, blood, lymph node, or cerebrospinal fluid. Various concentration methods and stains can make identification easier.
All patients should have a lumbar puncture before and after treatment to determine whether there is central nervous system involvement. An elevated level of IgM in the cerebrospinal fluid is the most sensitive indicator of the meningoencephalitic phase.
Immunodiagnostic blood tests have also been developed to detect T. brucei antigens and antibodies.
If the disease is diagnosed before the meningoencephalitic phase, suramin (not registered in New Zealand) is the drug of choice. Pentamidine is an alternative drug for the treatment of early disease. These drugs do not cross the blood-brain barrier.
The drug of choice for patients who have entered the meningoencephalitic phase, is melarsoprol (not registered in New Zealand), which is an arsenic-containing drug. Nitrofurazone or eflornithine are alternatives (neither are registered in New Zealand).
Most patients recover if treatment is started in the haemolymphatic phase or early meningoencephalitic phase. Early identification is critical because irreversible brain damage or death will occur if therapy is started late.
No vaccine or drug for prophylaxis is available for trypanosomiasis.
Preventive measures are aimed at reducing contact with tsetse flies – avoid travel to areas of heavy infestation with tsetse flies.
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