Fig 1; Tse-Tse fly (Genus Glossina)
1.0 OVERVIEW AND CAUSES
Animal trypanosomiasis, also known as nagana or sleeping sickness, is a disease of vertebrates which mostly affects ruminant animals. The disease is caused by the protozoan parasite trypanosomes of different species of the genus Trypanosoma.
Though found in other parts of the world, its prevalence is mainly seen in West Africa. The causative agents which are the trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which leads to weight loss and anemia, in some animals the disease is fatal unless treated. The trypanosomes are mainly transmitted by tse-tse flies
African animal trypanosomiasis can be caused by several species of trypanosomes such as;
Trypanosoma congolense is found in most domestic mammals: cattle, sheep, goats, horses, pigs, camels and dogs; and also in many wild animals.
T. vivax is a parasite of domestic and wild ruminants and of horses.
T. simiae is found mainly in domestic and wild pigs.
T. brucei is a parasite very close to T. gambiense and T. rhodesiense, which are the causes of human sleeping sickness. It can be found in practically all domestic and wild animals.
T. evansi is found in Africa only in the Saharan and Sahelian regions where it is primarily a camel parasite, but it may be a parasite of horses, cattle and dogs as well. It also occurs in Asia — where it commonly causes disease in camels and horses, and less commonly in cattle, water buffaloes, elephants and dogs — and in Central and South America. Thus it has a very wide distribution.
T. equiperdum is the causal agent of dourine, a contagious equine disease transmitted by coitus, which in Africa occurs only in the north African region and in South Africa. As control of dourine is an entirely different problem from that presented by other forms of trypanosomiasis, it will not be discussed in the present review, which deals only with the African trypanosomiasis transmitted by insects
2.0 EPIDEMIOLOGY AND TRANSMISSION
Transmission can either be cyclical or non cyclical. In cyclical transmission, the trypanosome undergoes multiplication and morphology in its host and there are two major groups namely;
Salivaria group e.g T. vivax
Stercoraria group e.g T. theileria
In the non-cyclical transmission, there is no multiplication or morphological transformation of the trypanosomes.
The transmission of trypanosomes is mostly cyclic and begins when blood from a trypanosome-infected animal is ingested by the fly. The trypanosome alters its surface coat by undergoing morphological changes and multiplies in the fly before becoming infective. The predilection sites for species of trypanosomes varies, T brucei migrate within the tsetse from the gut and eventually to the salivary glands, the cycle for T congolense stops at the hypopharynx, and the salivary glands are not invaded, the entire cycle for T vivax occurs in the proboscis. Therefore, the location of the protozoa within the tse-tse fly can be useful in identifying the specific specie of the trypanosome. The animal-infective form in the tse-tse fly salivary gland is referred to as the metacyclic form. The life cycle in the tse-tse fly may be as short as 1 week with T vivax or extend to a few weeks for T brucei .
Mechanical transmission can also occur through tse-tse flies or other biting flies such as the stomoxys and tabanids flies. Mechanical transmission requires only that blood containing infectious trypanosomes be transferred by bite from one animal to another.
Fig 2; Trypanosoma sp
3.0 PATHOGENESIS OF TRYPANOSOMIASIS
Infected tse-tse flies inoculate metacyclic trypanosomes into the skin of animals, where the trypanosomes resides for a few days and causes localized inflammation . They enter the lymph and lymph nodes, then the bloodstream, where they divide rapidly by binary fission (multiplication). In T congolense infection, the organisms attach to endothelial cells and localize in capillaries and small blood vessels. T brucei species and T vivax invade tissues and cause tissue damage in several organs.
The immune response is vigorous, and immune complexes cause inflammation, which contributes to fever and other signs and lesions of the disease. Antibodies against the surface-coat glycoproteins kill the trypanosomes. However, trypanosomes have a large family of genes that code for variable surface-coat glycoproteins that are switched in response to the antibody response, evading immunity (morphological changes). This antigenic variation results in persistence of the organism. Antigenic variation has prevented development of a protective vaccine and permits reinfections when animals are exposed to a new antigenic type.
Fig 3; Life cycle of trypanosome in the intermediate host and mammalian host
4.0 CLINICAL SIGNS AND DIAGNOSIS
The infection leads to significant weight loss and anemia and various symptoms observed are; fever, oedema, adenitis, dermatitis and nervous disorders among several others.
The disease cannot be diagnosed with certainty except physically detecting parasites by blood microscopic examination or various serological reactions
A presumptive diagnosis of trypanosomiasis is based on finding an anemic animal in poor condition in an endemic area. Confirmation depends on demonstrating trypanosomes in stained blood smears or wet mounts. The most sensitive rapid method is to examine a wet mount of the buffy coat area of a PCV tube after centrifugation, looking for motile parasites. Other infections that cause anemia and weight loss, such as babesiosis, anaplasmosis, theileriosis, and haemonchosis, should be excluded by examining a stained blood smear.
Various serologic tests measure antibody to trypanosomes, but their use is more suitable for herd and area screening than for individual diagnosis. Rapid agglutination tests to detect circulating trypanosome species-specific antigens in peripheral blood are available for both individual and herd diagnosis, although their reliability remains varied.
Molecular techniques for trypanosome detection and differentiation have been developed, but they are not generally available for routine field use.
5.0 TREATMENT AND CONTROL
Due to their hazardous effect, it is important to know how to treat the disease and control the prevalence of its vector and this can be done by;
ACTION ON PARASITES
This consists of the use of trypano-dal drugs on infected animals. The method aims first at limiting losses caused by the disease, and second at eliminating trypanosome reservoirs. Thus, detection and treatment of infected animals can be considered to be both a curative and a prophylactic procedure.
ACTION ON HOST ANIMALS
Although immunological responses occur in trypanosomiasis, it has not yet been possible to develop a practical method for immunization. Short of such a method, the use of prophylactic trypanocidal drugs makes it possible in certain conditions to protect animals for several months. Another method can be done by raising animals showing natural resistance to trypanosomiasis such as the humpless cattle of West Africa.
ACTION ON VECTORS
This method applies primarily to Glossina sp. Attempts may be made to;
destroy the insects, particularly through the use of insecticides
make the environment unsuitable as a habitat, either by altering the vegetation or by eliminating the animal species which constitute the preferred hosts of these insects
reduce their reproductive capacity by the release of sterile males
limit their number by using biological control methods.
The two latter techniques are still only in the research stage and have not been used so far as a practical control method for Glossina sp.
REFERENCES
https://www.msdvetmanual.com/circulatory-system/blood-parasites/trypanosomiasis-in-animals
https://www.cfsph.iastate.edu/Factsheets/pdfs/trypanosomiasis_african.pdf
https://www.galvmed.org/livestock-and-diseases/livestock-diseases/animal-african-trypanosomosis/
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