Sleeping sickness is caused by a protozoa transmitted by the tsetse fly.
- Outline the life cycle of Trypanosoma brucei and its route of transmission that causes African trypanosomiasis
- The disease is caused by protozoa of the species Trypanosoma brucei, which in a mammalian blood system become a trypomastigote and travels throughout the host mammalian and infects spinal fluid and lymph nodes.
- The protozoa Trypanosoma brucei infects the tsetse fly when it feeds on the blood of an infected mammal. Once infected a tsetse fly can transmit the disease to other mammals.
- Initially, sleeping sickness has many symptoms of other viral infections, but if left untreated it will affect the nervous system, causing lethargy.
- trypomastigote: A stage in unicellular life-cycle, typically trypanosomes, where the flagellum is posterior of the nucleus, and connected to the cell body by a long undulating membrane.
- epimastigotes: A stage in unicellular life-cycle, typically trypanosomes, where the flagellum is anterior of the nucleus, and attached the cell body by a short membrane.
Human African trypanosomiasis, sleeping sickness, African lethargy, or Congo trypanosomiasis is a parasitic disease of people and animals, caused by protozoa of the species Trypanosoma brucei and transmitted by the tsetse fly. The disease is endemic in some regions of sub-Saharan Africa, covering areas in about 37 countries containing more than 60 million people. An estimated 50-70 thousand people are currently infected, the number having declined somewhat in recent years. The number of reported cases was below ten thousand in 2009, the first time in 50 years. Many cases are believed to go unreported. About 48 thousand people died of it in 2008. Four major epidemics have occurred in recent history: one from 1896-1906, primarily in Uganda and the Congo Basin, two epidemics in 1920 and 1970 in several African countries, and a recent 2008 epidemic in Uganda.
The tsetse fly (genus Glossina) is a large, brown, biting fly that serves as both a host and vector for the trypanosome parasites. While taking blood from a mammalian host, an infected tsetse fly injects metacyclic trypomastigotes into skin tissue. From the bite, parasites first enter the lymphatic system and then pass into the bloodstream. Inside the mammalian host, they transform into bloodstream trypomastigotes, and are carried to other sites throughout the body, reach other body fluids (e.g., lymph, spinal fluid), and continue to replicate by binary fission. The entire life cycle of African trypanosomes is represented by extracellular stages. A tsetse fly becomes infected with bloodstream trypomastigotes when taking a blood meal on an infected mammalian host. In the fly’s midgut, the parasites transform into procyclic trypomastigotes, multiply by binary fission, leave the midgut, and transform into epimastigotes. The epimastigotes reach the fly’s salivary glands and continue multiplication by binary fission.The entire life cycle of the fly takes about three weeks.
In addition to the bite of the tsetse fly, the disease can be transmitted by, mother-to-child infection; the trypanosome can sometimes cross the placenta and infect the fetus. Transmission can also occur in laboratories by accidental infections; for example, through the handling of blood of an infected person and organ transplantation, though this is uncommon. Blood transfusions and possibly sexual contact, are two other causes.
African trypanosomiasis symptoms occur in two stages. The first stage, known as the haemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. If left untreated, the disease overcomes the host’s defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac, and kidney dysfunctions. The second phase, the neurological phase, begins when the parasite invades the central nervous system by passing through the blood–brain barrier. The term “sleeping sickness” comes from the symptoms of the neurological phase. The symptoms include confusion, reduced coordination, and disruption of the sleep cycle, with bouts of fatigue punctuated with manic periods, leading to daytime slumber and night-time insomnia. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma and death. Damage caused in the neurological phase is irreversible.