Sleeping Sickness

Sleeping sickness

Sleeping sickness (trypanosomiasis) is a protozoan infection passed to humans through the bite of the tsetse fly. It progresses to death within months or years if left untreated. Near-control of trypanosomiasis was achieved in the 1960s, but the disease has since re-emerged in Sub-Saharan Africa, where political instability and war have hampered public health efforts. As of 2002, the World Health Organization , in conjunction with Médicines Sans Frontièrs (Doctors Without Borders) and major pharmaceutical companies were in the midst of a five-year major effort to halt the spread of trypanosomiasis and treat its victims.

Protozoa are single-celled organisms considered to be the simplest animal life form. The protozoa responsible for sleeping sickness are a flagellated variety (flagella are hair-like projections from the cell which aid in mobility) which exist only in Africa. The type of protozoa causing sleeping sickness in humans is referred to as the Trypanosoma brucei complex. It is divided further into Rhodesian (Central and East Africa) and Gambian (Central and West Africa) subspecies.

The Rhodesian variety live within antelopes in savanna and woodland areas, causing no disruption to the antelope's health. (While the protozoa cause no illness in antelopes, they are lethal to cattle who may become infected.) The protozoa are acquired by tsetse flies who bite and suck the blood of an infected antelope or cow. Within the tsetse fly, the protozoa cycle through several different life forms, ultimately migrating to the salivary glands of the tsetse fly. Once the protozoa are harbored in the salivary glands, they can be deposited into the bloodstream of the fly's next blood meal.

Humans most likely to become infected by Rhodesian trypanosomes are game wardens or visitors to game parks in East Africa. The Rhodesian variety of sleeping sickness causes a much more severe illness with a greater likelihood of eventual death. The Gambian variety of Trypanosoma thrives in tropical rain forests throughout Central and West Africa, does not infect game or cattle, and is primarily a threat to people dwelling in such areas. It rarely infects visitors.

The first sign of sleeping sickness may be a sore appearing at the tsetse fly bite spot about two to three days after having been bitten. Redness, pain, and swelling occur. Two to three weeks later, Stage I disease develops as a result of the protozoa being carried through the blood and lymphatic circulations. This systemic (meaning that symptoms affect the whole body) phase of the illness is characterized by a high fever that falls to normal then re-spikes. A rash with intense itching may be present, and headache and mental confusion may occur. The Gambian form includes extreme swelling of lymph tissue, enlargement of the spleen and liver, and swollen lymph nodes. Winterbottom's sign is classic of Gambian sleeping sickness; it consists of a visibly swollen area of lymph nodes located behind the ear and just above the base of the neck. During this stage, the heart may be affected by a severe inflammatory reaction, particularly when the infection is caused by the Rhodesian form.

Many of the symptoms of sleeping sickness are actually the result of attempts by the patient's immune system to get rid of the invading organism. The overly exuberant cells of the immune system damage the patient's organs, causing anemia and leaky blood vessels. These leaky blood vessels help to spread the protozoa throughout the patient's body.

One reason for the immune system's intense reaction to the Trypanosomes is also the reason why the Trypanosomes survive so effectively. The protozoa are able to change rapidly specific markers on their outer coats. These kinds of markers usually stimulate the host's immune system to produce immune cells specifically to target the markers and allow quick destruction of these invading cells. Trypanosomes are able to express new markers at such a high rate of change that the host's immune system cannot catch up.

Stage II sleeping sickness involves the nervous system. The Gambian strain has a clearly delineated phase in which the predominant symptomatology involves the brain. The patient's speech becomes slurred, mental processes slow, and he or she sits and stares or sleeps for long periods of time. Other symptoms resemble Parkinson's disease: imbalance when walking, slow and shuffling gait, trembling of the limbs, involuntary movement, muscle tightness, and increasing mental confusion. These symptoms culminate in coma, then death.

Diagnosis of sleeping sickness can be made by microscopic examination of fluid from the site of the tsetse fly bite or swollen lymph nodes for examination. A method to diagnose Rhodesian trypanosome involves culturing blood, bone marrow, or spinal fluid. These cultures are injected into rats to promote the development of blood-borne protozoan infection. This infection can be detected in blood smears within one to two weeks.

Medications effective against the Trypanosoma brucei complex protozoa have significant potential for side effects. Suramin, eflornithine, pentamidine, and several drugs which contain arsenic (a chemical which is potentially poisonous) are effective anti-trypanosomal agents. Each of these drugs requires careful monitoring to ensure that they do not cause serious complications such as a fatal hypersensitivity reaction, kidney or liver damage, or inflammation of the brain. Trials are underway to monitor the effectiveness of new medications for treatment of trypanosomiasis.

Prevention of sleeping sickness requires avoiding contact with the tsetse fly; insect repellents , mosquito netting, and clothing that covers the limbs to the wrists and ankles are mainstays. There are currently no immunizations available to prevent sleeping sickness.

See also Protists