Trypanosoma evansi

Trypanosoma evansi (Steel, 1885) Balbiani, 1888

(Figure 1-31)

 

ETYMOLOGY: This parasite is named after Dr. Griffith Evans, the British veterinarian who discovered the parasite.

SYNONYMS:Spirochaete evansi Steel, 1885; Trypanosoma elmassiani Lignières, 1902; Trypanosoma soudanense Laveran, 1907; Trypanosoma hiipicum Darling, 1910; Trypanosoma venezuelense Mesnil, 1910; Trypanosoma annamense Laveran, 1911; Trypanosoma cameli Pricolo & Ferror, 1914; Trypanosoma macracanum Sergent, Lhéritier & Belleval, 1915; Trypanosoma ninae kohl-yakimov Yakimoff, 1921.

HISTORY: This was the first pathogenic trypanosome to be discovered. Dr. Griffith Evans discovered the organisms in 1880 in the blood of horses and camels in India that were suffering from a disease called Surra. Mechanical transmission by biting flies was first shown by Rogers (1901).

GEOGRAPHIC DISTRIBUTION: The organism is found in Africa north of the Sahara, Asia, and Central and South America.

LOCATION IN THE HOST: These parasites are parasites of the blood stream and tissue fluids. In the cat, organisms have only been observed in the blood.

IDENTIFICATION OF THE PARASITE: The morphology of this parasite (Fig 1-31) is indistinguishable from that of Trypanosoma brucei.

LIFE CYCLE: This parasite is transmitted between hosts by mechanical transmission by biting flies (Rogers, 1901). In South America, transmission has also been shown to be possible through the bite of vampire bats (Desmodus rotundus) (Dunn, 1932).

CLINICAL PRESENTATION AND PATHOGENESIS: Typically, this parasite is thought of as causing disease in horses, camels, and elephants, and dogs wherein there is emaciation and edema. There have been few reports in cats.

A naturally infected cat presented with lethargy and inappetence, sunken eyes, and incoordination (Paikne and Dhake, 1974). Poisoning was the expected etiology. The animal died and a necropsy was performed. Blood smears revealed numerous Trypanosoma evansi organisms. There was perivascular cuffing around vessels in the brain.

At least two studies have been performed in which cats have been experimentally infected (Choudhury and Misra, 1972; Scheidle, 1982). In the earlier report, cats were inoculated intraperitoneally. The trypanosomes appeared in the circulation 14 to 15 days after infection. Young cats could succumb during the first peak parasitemia, but if they survived, 4-day-long peaks of parasitemia appeared every two weeks. During the peak parasitemias, the cats showed signs (Dwight, what signs??) of infection. In the later report, three cats were inoculated with 1,500 trypanosomes. Two days after infection, parasites were detectable in the blood; after two weeks of infection, there were 70,000 trypanosomes observed per cubic millimeter of blood. The body temperature of the infected cats seldom exceeded 40• C. After nine days of infection, the cats were severely anemic with, which was the major observation at necropsy.

TREATMENT: Two experimentally infected cats were treated with Berenil, 4-4'-diamidino-diazoamino-benzol-diaceturat (dose??) (Scheidle, 1982). A second treatment was given 2 days later because the cats still had low parasitemias one day after the first treatment. After the second treatment, trypanosomes were not observed for 8 to 20 days, but they then appeared and rose to near the pretreatment levels of 70,000 trypanosomes per l.

EPIZOOTIOLOGY:Trypanosoma evansi is considered to use cattle and buffalo as the reservoir host. Transmission to horses and dogs is not uncommon, but it is unclear how often cats may be infected.

HAZARDS TO OTHER ANIMALS: Unknown.

HAZARDS TO HUMANS:Trypanosoma evansi is not considered to be a human pathogen. However, precautions should be taken to reduce potential hazards to humans 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 prevalence, control, or prevention of the disease in cats. The biology of the parasite would suggest that cats should be protected from fly bites.

REFERENCES:

Choudhury A, Misra KK. 1972. Experimental infection of T. evansi in the cat. Trans Roy Soc Trop Med Hyg 66:672-673.

Dunn LH. 1932. Experiments in the transmission of Trypanosomahippicum Darling with the vampire bat, Desmodusrotundusmurinus Wagner, as a vector in Panama. J Prevent Med 6:415-424.

Paikne DL, Dhake PR. 1974. Trypanosomiasis in a deomestic cat (Feliscatus). Ind Vet J 51:10

Rogers L. 1901. The transmisison of Trypanosomaevansi by horseflies and other experiments pointing to the probable identity of Surra and Nagana or Tsetse-fly disease in Africa. Proc Roy Soc Ser B 68:163-170.

Scheidle G. 1982. Das Infektionsverhalten von Trypanosomaevansi (Stamm Manila) in vershiedenen Tierarten. Dissertation, Ludwig-Maximillians-Universität München. 53 pages

FIGURE 1-31.Trypanosomaevansi in the blood of a horse. Giemsa stain. As in Fig 1-16, trypomastigotes in this preparation can be observed to be undergoing cellular division.

Comments are closed.