Trypanosoma brucei Plimmer and Bradford, 1899
Trypanosoma brucei is morphologically indistinguishable from Trypanosoma gambiense and Trypanosoma rhodesiense. Together, these three parasites are considered to form a tsetse transmitted complex (see Hoare, 1967), of which T. gambiense is almost exclusively human wherein chronic disease is produced, T. rhodesiense is a zoonosis from African ungulates producing fulminant disease in humans, and T. brucei occurs mainly in animals and may or may not cause human disease. Hill (1955) summarizes the reports of these three species in the cat including several personal communications with workers in the field, but in most cases only very minor notes have been presented by those cited by Hill. Thus, there seems to be little or no literature concerning the infection of cats with T. rhodesiense. Experimental infections of cats with Trypanosoma gambiense has been examined on at least one occasion.
ETYMOLOGY: The parasite is named after Major David Bruce.
SYNONYMS:Trypanosoma pecaudi Laveran, 1907; Trypanosoma togolense Mesnil & Brimont, 1909; Trypanosoma ugandae Stephens & Blacklock, 1913; Trypanosoma multiforme Kinghorn et al., 1913; Trypanosoma anceps Bruce et al., 1914; Trypanosoma dukei Knuth & duToit, 1921.
HISTORY: The parasite was found to be the causative agent of Nagana in cattle by Sir David Bruce in 1894 who recognized the trypanosome in the blood of cattle and showed that it could be transmitted by inoculation into horses and dogs where it caused acute disease (Hoare, 1967). Bruce also showed that naturally infected Tsetse flies were involved in the transmission of the parasite, but it was not until the work of Kleine (1909 a&b) that it was shown that a period of development within the Tsetse was required for transmission to occur.
GEOGRAPHICAL DISTRIBUTION: This parasite is distributed throughout the range of the tsetse fly vector in western Africa. The mammalian reservoirs of infection are considered to be various forms of African antelope.
LOCATION IN THE HOST: The parasite is considered to be a parasite of blood and tissue fluids. Although in cats, the parasite has only been observed in the blood.
IDENTIFICATION OF THE PARASITE:Trypanosoma brucei is the type of trypanosome that has two stages present in the blood, a short and stumpy form with no free flagellum and a long and slender form with a free flagellum. The short form has a length of around 18 m (range: 12-26 m) while the long form has a length of 29 m (range: 23-42 m).
In Giemsa-stained blood films, the trypanosomes can be examined, and dividing forms can be seen. The slender forms will typically be S-shaped with 3 to 5 undulations of the undulating membrane throughout the length of the cell body. The free flagellum will be about one-half to one-third of the length of the cell. The nucleus will be near midbody, and the rather small kinetoplast will be near the posterior end of the cell body. In the stumpy forms of the parasite, the cell often takes on more of a C-shape or L-shape, the nucleus will be near the end of the cell body, and there will be no free flagellum. There will still be around three undulations of the membrane along the cell surface.
LIFE CYCLE: The transmission of Trypanosoma brucei typically requires the development within a Tsetse fly (genus Glossina) wherein development of infective stages occur within the gut and salivary glands (Kleine 1909 a&b). The trypano somes are transmitted to the next host through the bite of the fly. Transmission of the parasite can also be caused by inoculation of blood containing the organisms as might occur with a dirty needle, the contaminated mouthparts of a horse fly (tabanid), or by transfusion. In cats, it has been shown that they can also be transmitted by feeding on the meat of an infected goat with parasites in circulation; 3 of 17 cats became infected in this manner (Moloo et al., 1973).
In cats inoculated with blood, trypanosomes will appear in the blood stream beginning 5 days after inoculation (Kanthack et al., 1899). When cats were fed goat meat, trypanosomes first appeared in the blood 31 to 38 days after they had been fed the infected meat; these cats were killed soon after the infection was detected in the blood. In cats fed an infected mouse or an infected guinea pig, the prepatent periods were 44 and 25 days, respectively (Laveran and Mesnil, 1912). In general, it is considered that the infected cat seldom lives long enough to play a major role in transmis sion.
CLINICAL PRESENTATION AND PATHOGENESIS: Cats that have been experimentally infected die within 22 to 26 days after infection (Kanthack et al., 1899). These cats were noted to develop pyrexia and changes in the eyes including an aqueous flare and conjunctivitis, and edema of the face and eyelids. At necropsy, these cats were found to have pronounce wasting with generalized lymphadenopathy, splenomegaly, hepatomegaly, and pleura and pericardium hemorrhage.
A naturally infected cat (Hill, 1955) was noted to be listless and off its food with a dry rough hair coat and pale mucous membranes. There was edema and erythema of the head region. In this cat, both eyes were acutely affected with photophobia, lacrimation, conjunctivitis and keratitis; in the right eye there was pannus, hypopyon, and hypertony. Within 6 days of the initial presentation, the cat became blind and too weak to stand.
TREATMENT: Treatment of only one infected cat has been reported in the literature (Hill, 1955). This cat was treated with antycide methyl-sulphate (6.0 mg/kg body weight) subcutaneously. It began to eat again by the third day after treatment, and the hypopyon began to disappear. Both eyes appeared normal 8 days after treatment. This cat did relapse a few weeks later, again with ophthalmologic signs, and was again treated. Relapse developed again several months later, and following treatment and another relapse, the cat was euthanatized.
EPIZOOTIOLOGY:Trypanosoma brucei is considered a parasite of African ungulates that can get into domestic cats by the bite of a tsetse fly.
HAZARDS TO OTHER ANIMALS: As noted above, cats seldom live long enough after infection to serve as major sources of infection to other animals.
HAZARDS TO HUMANS: The hazard to humans would be in the veterinary clinic where an accident with a contaminated needle could serve to introduce the parasite into someone supplying veterinary care.
CONTROL/PREVENTION: There is currently very little known about the control and prevention of the disease in cats. The biology of the parasite would suggest that cats should be protected from Tsetse bites and not fed meat of wild game that might be infected.
REFERENCES:
Hoare, 1967 NEED REFERENCE
Hill DH. 1955. Trypanosoma brucei in the cat. Brit Vet J 111:77-80.
Kanthack AA, Durham HE, Blandford WFH. 1899. On Nagana, or TseTse Fly disease. Proc Roy Soc 64:100-118.
Kleine FC. 1909a. Positive Infektiens versuche mit Trypanosomabrucei durch Glossinapalpalis. Dtsch Med Wochenschr 35:469-470
Kleine FC. 1909b. Weitere Beobachtungen über Tsetsefliegenu nd Trypanosomen. Dtsch Med Wochenschr 35:1956-1958.
Laveran A, Mesnil F. In Masson’s Trypanosomas et Trypanosomiases. Paris, France.
Moloo SK, Losos GJ, Kutuza SB. 1973. Transmission of Trypanosoma brucei to cats and dogs by feeding on infected goats. Ann Trop Med Parasitol 67:331-334.