Although this blog focus mostly on bacteria, I do occasionally dip out of my comfort zone into other infectious elements such as viruses, prions and fungi. One topic that I haven’t covered nearly enough is the protozoan pathogens; the unicellular organisms that are not bacterial, but are responsible for some of the deadliest diseases in the world including malaria, sleeping sickness and toxoplasmosis.
Although some of these protozoa can be taken up directly through contact with fecal matter or infected water, many of them rely on animal vectors for part of their life-cycle. As a result, the study and control of these vectors plays a major part in the fight against the disease. Recently, PLoS Neglected Tropical Diseases put together a whole collection of articles and editorials about the Tsetse fly: the vector for the protozoa that causes sleeping sickness.
Sleeping sickness is caused by a parasite called Trypanosoma brucei. T. brucei is made up of a single eukaryotic cell, and therefore contains all the internal features of such a cell: nucleus, mitochondria, Golgi apparatus and internal membrane systems. It also has a tail, or flagellum, for most of its life-cycle. The life-cycle is complex and involves several changes in form for the protozoa. After being injected into the human blood stream by the tsetse fly, the parasite can swim to various sites in the body and multiply in bodily fluids including lymph and spinal fluid. Parasites in the blood are then picked up by another tsetse fly taking a meal. They are taken into the fly gut and then make their way to the salivary glands ready to be injected into another human.
The symptoms of sleeping sickness include joint pain, headaches and fever along with a drowsiness that gives the disease its name. Unfortunately T. brucei is able to cross the blood-brain barrier and once inside the central nervous system is causes the patient to become lethargic or insane followed by a coma and death. There are two main varieties of sleeping sickness caused by two different subspecies of T. brucei. One is a longer term chronic disease which can persist for several years with only mild symptoms before it gets into the central nervous system. The other is far more severe and acute – causing death within 3-12 months of infection. There is also a related disease which causes sleeping sickness in cattle and livestock.
One of the difficulties in eradicating sleeping sickness is that because T. brucei can change its outer protein coat there are no effective vaccines against it. There are also no existing natural cures, such as quinine for treating malaria. The most successful approaches to the disease are therefore those that rely on controlling the vector: the tsetse fly. The use of traps and insecticides to remove the insect vector leads to a decrease in the incidence of the disease. Very recently the complete genome sequence of the fly has been released which, along with research into its immune, digestive and reproductive systems should improve efforts to effectively remove it from areas where sleeping sickness is endemic.
Aksoy S, Attardo G, Berriman M, Christoffels A, Lehane M, et al. (2014) Human African Trypanosomiasis Research Gets a Boost: Unraveling the Tsetse Genome. PLoS Negl Trop Dis 8(4): e2624.
Headrick DR (2014) Sleeping Sickness Epidemics and Colonial Responses in East and Central Africa, 1900–1940. PLoS Negl Trop Dis 8(4): e2772.
International Glossina Genome Initiative. Genome sequence of the tsetse fly (Glossina morsitans): vector of African trypanosomiasis. Science. 2014 Apr 25;344(6182):380-6 [behind paywall]
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