Trypanosoma brucei, the agent that causes sleeping sickness, is my new favorite protozoan. The African tsetse fly is the vector for both species of typanosoma: T. brucei gambiense, which causes sleeping sickness (Human African Trypanosomiasis, or HAT) in West and Central Africa, and T. brucei rhodesiense, which causes a different form of HAT in East and Southern Africa.
As I learned today, the best way to identify the tsetse fly is by the "hatchet cell" shape framed by wing veins 4 and 5 (seen upsidedown in upper wing in this pic), and by the characteristic way that resting fly holds its wings, folded over the abdomen in a "pair of closed scissors" formation. [Medical entomologists are a mad bunch, no?]
Both male and female tsetse flies inject the metacyclic trypanomastigote form of the parasite into the human host when taking a blood meal. In the peripheral blood, the trypanomastigotes multiply by binary fission, to form three different forms: the "short-stumpy" form, the "long-narrow" form, and the intermediate form. All of these forms look a bit like worms smimming in the blood stream, but of course they are single-celled organisms, not worms. What looks like the eye of a worm is actually a bit of mitochondrial DNA material called the kinetoplast. The tail of the worm is the flagellum, that ungelates for motility.
The clinical maifestations of HAT are as bizarre as the parasite morphology. The T. brucei gambiense form of the disease is much more insidioius and chronic than the T. brucei rhodesiense form, which progresses rapidly towards death. In both forms, the patient may present with a chancre or ulcer at the site of the tsetse bite. Multiple non-specific symptoms follow the bite, including: fever, fatigue, wasting, lymphadenopathy, rash, and itching. Once the parasite enters the central nervous system, the patient may get confused, then fall into the reverse sleep pattern of daytime somulence and nighttime agitation that gives the disease its nickname. If left untreated, the disease is uniformly fatal.
Like most diseases that occur only in poor countries, HAT has no decent treatment options. The only drugs available are toxic compounds that cause debilitating side effects (and 5% chance of mortality from the drug alone). All of the drugs were developed decades ago. There are few or no other options in the pipeline.
I was always taught that HAT is a rare disease, but our professor told us that it is actually prevalent and wide-spread. The 50,000 cases that are reported to WHO every year are probably at least a 12-fold underestimate. He believes that HAT and "nagana," which is the animal-version of the disease common in horses and livestock, are the reason that European colonists "gave up" on their conquest of Africa. The livestock ranches in the colonial era failed miserably due to illness of colonists and their herds, he says.
David Livingstone was onto the same idea way back in 1857, when he published a description of nagana in Missionary Travels, the narrative of his famous mid-century African expedition. Soon after, the colonists started calling the sleeping sickness syndrome "negro lethargy." They called HAT by this name until the white colonialists started getting sick too, at which time the Royal Society sent an expedition to investigate. In 1903, they identified the trypanosoma parasite in the blood and CSF of sick patients. They even managed to infect monkies with the agent, proving that typanosomes cause sleeping sickness disease.