Tsetse-transmitted Trypanosomiasis

This group of diseases caused by protozoa of the genus Trypanosoma affects all domestic animals. The major species are T congolense, T vivax, T brucei brucei, and T simiae. For the animals mainly affected by these tsetse-transmitted trypanosomes and the geographic areas where tsetse-transmitted trypanosomiasis occurs, see Blood Parasites: Tsetse-transmitted Animal Trypanosomes.

Table 2
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Tsetse-transmitted Animal Trypanosomes Trypanosoma spp Animals Mainly Affected Major Geographic Distribution T congolense Cattle, sheep, goats, dogs, pigs, camels, horses, most wild animals Tsetse region of Africa T vivax Cattle, sheep, goats, camels, horses, various wild animals Africa, Central and South America, West Indiesa T brucei brucei All domestic and various wild animals; most severe in dogs, horses, cats Tsetse region of Africa T simiae Domestic and wild pigs, camels Tsetse region of Africa a In non-tsetse areas, transmission is by biting flies.

Cattle, sheep, and goats are infected, in order of importance, by T congolense, T vivax, and T brucei brucei. In pigs, T simiae is the most important. In dogs and cats, T brucei is probably the most important. It is difficult to assign an order of importance for horses and camels. T vivax may occur outside tsetse-infested areas of sub-Saharan Africa.

The trypanosomes that cause tsetse-transmitted trypanosomiasis (sleeping sickness) in people, T brucei rhodesiense and T brucei gambiense, closely resemble T brucei brucei from animals, and suitable precautions should be taken when working with such isolates. Domestic animals may act as reservoirs of human infections.

Transmission and Epidemiology

Most tsetse transmission is cyclic and begins when blood from a trypanosome-infected animal is ingested by the fly. The trypanosome loses its surface coat, multiplies in the fly, then reacquires a surface coat and becomes infective. T brucei spp migrate from the gut to the proventriculus to the pharynx 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. The animal-infective form in the tsetse salivary gland is referred to as the metacyclic form. The life cycle in the tsetse may be as short as 1 wk with T vivax or extend to a few weeks for T brucei spp.

Tsetse flies (genus Glossina) are restricted to Africa from about latitude 15°N to 29°S. The 3 main species inhabit relatively distinct environments—G morsitans usually is found in savanna country, G palpalis prefers areas around rivers and lakes, and G fusca lives in high forest areas. All 3 species transmit trypanosomes and all feed on various mammals.

Mechanical transmission can occur through tsetse or other biting flies. In the case of T vivax, Tabanus spp and other biting flies seem to be the primary mechanical vectors outside the tsetse areas, as in Central and South America. Mechanical transmission requires only that blood containing infectious trypanosomes be transferred from one animal to another.

Pathogenesis

Infected tsetse inoculate metacyclic trypanosomes into the skin of animals, where the trypanosomes grow for a few days and cause localized swellings (chancres). They enter the lymph nodes, then the bloodstream, where they divide rapidly by binary fission. 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 the signs and lesions of the disease. Antibodies against the surface-coat glycoproteins kill the trypanosomes. However, trypanosomes have multiple genes that code for different surface-coat glycoproteins that are not vulnerable to the immune response; this antigenic variation results in persistence of the organism. The number of antigenic types of glycoprotein that can be made is unknown, but exceeds several hundred. Antigenic variation has prevented development of a vaccine and permits reinfections when animals are exposed to a new antigenic type.

Clinical Findings and Lesions

Severity of disease varies with species and age of the animal infected and the species of trypanosome involved. The incubation period is usually 1–4 wk. The primary clinical signs are intermittent fever, anemia, and weight loss. Cattle usually have a chronic course with high mortality, especially if there is poor nutrition or other stress factors. Ruminants may gradually recover if the number of infected tsetse flies is low; however, stress results in relapse.

Necropsy findings vary and are nonspecific. In acute, fatal cases, extensive petechiation of the serosal membranes, especially in the peritoneal cavity, may occur. Also, the lymph nodes and spleen are usually swollen. In chronic cases, swollen lymph nodes, serous atrophy of fat, and anemia are seen.

Diagnosis

A presumptive diagnosis 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. Other infections that cause anemia and weight loss, such as babesiosis, anaplasmosis, and haemonchosis, should be ruled out by examining a stained blood smear.

Trypanosoma vivax, bovine blood smear

Various serologic tests measure antibody to trypanosomes, but their use is more suitable for herd and area screening than for individual diagnosis. Tests for detection of circulating trypanosome species-specific antigens in peripheral blood are becoming available for both individual and herd diagnosis, although their reliability remains unproved. Molecular techniques for try-panosome detection and differentiation have been developed, but they are not generally available for routine field use.

Treatment and Control

Several drugs can be used for treatment (see Blood Parasites: Drugs Commonly Used for Trypanosomiasis in Domestic Animals). Most have a narrow therapeutic index, which makes administration of the correct dose essential. Drug resistance occurs and should be considered in refractory cases.

Table 3
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Drugs Commonly Used for Trypanosomiasis in Domestic Animals Drug Animal Trypanosoma Main Action Diminazene aceturate Cattle vivax, congolense, brucei Curative Homidium bromide Cattle vivax, congolense, brucei Curative, some prophylactic activity Homidium bromide Equids vivax Curative, some prophylactic activity Homidium chloride As for the bromide salt Isometamidium chloride Cattle vivax, congolense Curative and prophylactic Quinapyramine sulfate Horses, camels, pigs, dogs vivax, congolense, brucei, evansi, equiperdum, simiae Curative Quinapyramine dimethylsulfate Horses, camels, pigs, dogs vivax, congolense, brucei, evansi, equiperdum, simiae Prophylactic Suramin Horses, camels, dogs brucei, evansi Curative, some prophylactic activity Melarsomine dichlorhydrate Camels evansi Curative

Control can be exercised at several levels, including eradication of tsetse flies and use of prophylactic drugs. Tsetse flies can be partially controlled by frequent spraying and dipping of animals, aerial and ground spraying of insecticides on fly-breeding areas, use of insecticide-impregnated screens and targets, bush clearing, and other methods. The Sterile Insect Technique (SIT) has been used with success in Zanzibar and is expected to be used in other area-wide control operations after suppression of tsetse populations by insecticides. There is renewed international interest in large-scale tsetse eradication through the Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC) supported by the African Union. Animals can be given drugs prophylactically in areas with a high population of trypanosome-infected tsetse. Drug resistance must be carefully monitored by frequent blood examinations for trypanosomes in treated animals.

In West Africa, several breeds of cattle have been identified that show innate resistance to trypanosomiasis and play a valuable role in reducing the impact of the disease in this area. However, resistance may be lost due to poor nutrition or heavy tsetse challenge.

Control is ideally achieved by combining methods to reduce the tsetse challenge and by enhancing host resistance with prophylactic drugs.

Surra

(Trypanosoma evansi infection)

Surra is separated from the tsetse-transmitted diseases because it is usually transmitted by other biting flies that are found within and outside tsetse fly areas. It occurs in North Africa, the Middle East, Asia, the Far East, and Central and South America. The distribution of T evansi in Africa extends into the tsetse areas, where differentiation from T brucei is difficult. It is essentially a disease of camels and horses, but all domestic animals are susceptible. The disease can be fatal, particularly in camels, horses, and dogs. T evansi in other animals appears to be nonpathogenic, and these animals serve as reservoirs of infection.

Transmission is primarily by biting flies, probably resulting from interrupted feedings. A few wild animals are susceptible to infection and may serve as reservoirs.

Pathogenesis, clinical findings, lesions, diagnosis, and treatment are similar to those of the tsetse-transmitted trypanosomes (see Blood Parasites: Tsetse-transmitted Trypanosomiasis).

Dourine

Dourine is an often chronic venereal disease of horses that is transmitted during coitus and caused by T equiperdum. The disease is recognized on the Mediterranean coast of Africa and in the Middle East, southern Africa, and South America; distribution is probably wider.

Signs may develop over weeks or months. Early signs include mucopurulent discharge from the urethra in stallions and from the vagina in mares, followed by gross edema of the genitalia. Later, characteristic plaques 2–10 cm in diameter appear on the skin, and the horse becomes progressively emaciated. Mortality in untreated cases is 50–70%.

Demonstration of trypanosomes from urethral or vaginal discharges, skin plaques, or peripheral blood is difficult unless the material is centrifuged. Infected horses can be detected with the complement fixation test but only in areas where T evansi or T brucei are not found because they have common antigens. An ELISA test may become available for diagnosis.

In endemic areas, horses may be treated (see Blood Parasites: Drugs Commonly Used for Trypanosomiasis in Domestic Animals). When eradication is required, strict control of breeding and elimination of stray horses has been successful. Alternatively, infected horses may be identified using the complement fixation test; euthanasia is mandatory.

Chagas' Disease

(Trypanosoma cruzi infection)

The common transmission cycle of Chagas' disease is between opossums, armadillos, rodents, and wild carnivores, with bugs of the Reduviidae family serving as vectors. Distribution is in Central and South America and localized areas of the southern USA. Chagas' disease is important in South America. Domestic animals may become infected and introduce the trypanosome into human dwellings where the bugs are present; people then become infected by contamination of eye wounds or by eating food contaminated with insect feces that contain trypanosomes. The trypanosome is pathogenic to people and occasionally to young dogs and cats; other domestic animals act as reservoir hosts. T cruzi should be suspected in dogs in endemic areas that die acutely or have myocarditis.

Nonpathogenic Trypanosomes

Trypanosoma theileri or markedly similar trypanosomes have been detected in peripheral blood from cattle on every continent. Infection with similar trypanosomes also has been detected in domestic and wild buffalo and various other wild ungulates. In the few areas studied, transmission is by contamination after a cycle of development in species of tabanid flies. Although most parasitemias are subpatent, the trypanosomes may be seen in a blood smear being examined for pathogenic protozoa or in a hemocytometer chamber. Pathogenicity has never been proved experimentally.

T melophagium of sheep also has a worldwide distribution and is transmitted by the sheep ked. T theodori, reported in goats, may be a synonym for the same trypanosome.

Last full review/revision July 2011 by Peter H. Holmes