Babesia felis

Babesia felis Davis, 1929

ETYMOLOGY:Babesia for Dr. Babès and felis (cat)

SYNONYMS:Babesiella felis (Davis, 1929) Carpano, 1934; Nuttallia felis (Davis, 1929) Krylov, 1974; Nuttallia felis var domestica Jackson and Dunning, 1937; Nicollia felis (Davis, 1929) Krylov, 1981.

HISTORY:Babesia felis was first described as a parasite of the domestic cat by Jackson and Dunning in 1937; these authors gave it the name Nuttallia (a synonym of Babesia) felis of the variety domestica. The variety designation was to separate it on the basis of its pathogenicity from a previously described, but morphologically, indistinguishable Babesia felis described by Davis in 1929 from a Sudanese wild cat (Felis ochreata) that was not pathogenic when inoculated into domestic cats.

GEOGRAPHICAL DISTRIBUTION: Reports of feline babesiosis due to Babesia felis are restricted almost exclusively to Zimbabwe and South Africa (Futter and Belonje, 1980a). The original isolate from a sudanese wild cat was established experimentally in domestic cats (Davis, 1929).

LOCATION IN HOST: The only cell in the body parasitized by merozoites of Babesia spp. are the red blood cells.

PARASITE IDENTIFICATION: The merozoites of Babesia felis that occur within the red cell are small, faintly blue staining organisms that have a dense chromatin granule. Many forms have a large central vacuole which gives them the appearance of being ring shaped. Single organisms measure less than 1 m to 2.5 m in diameter. Division of the organisms produces pairs and cross-shaped tetrads of organisms. The ultrastructure of Babesia felis was described by Dennig and Hebel (1969).

LIFE CYCLE: The life cycle of Babesia felis has not been elucidated, but it is believed that ixodid ticks serve as the biological vector of the parasite. In 1937, Dr. McNeil reported that he reared larval and nymphal ticks from an adult female Haemaphysalis leachi that was removed from a cat with babesiosis. Neither the eggs nor the nymphs that developed transmitted the disease to cats upon which they were fed. The bottle containing the imago ticks was then broken and the ticks escaped, and Dr. McNeil without evidence or proof was convinced that they were the source of babesiosis that developed in his own household cat. There have been no other studies on the transmission of feline babesiosis.

If, as suspected, the life cycle utilizes ixodid ticks that have fed on cats, sporozoites will develop within the salivary glands of the tick. Within the tick there is the possibility that the different stages, larvae, nymphs, and adults, may differ in their ability to transmit the infections, and further work is needed to clarify this in the case of Babesia felis.

Once in a cat, the merozoites infect blood cells, dividing and multiplying to form stages infecting new blood cells. In cats that have been inoculated with blood from other cats, parasites are evident within the peripheral blood within 1 to 2 days after inoculation (Futter and Belonje, 1980b). It is not known how long after the appearance of organisms in the blood that infectivity for the tick vector might develop.

CLINICAL PRESENTATION AND PATHOGENESIS: Cats are typically admitted with a history of inappetence, lethargy, and weakness or morobund. Mucous membranes may be pale, and tachycardia and tachypnea (perhaps dyspnea) consistent with profound anemia may be noted. Icterus is seldom seen and fever does not seem to typically accompany the disease. (Futter and Belonje, 1980b). In experimentally infected animals, anemia is most severe about 3 weeks after inoculation, and there are significantly lowered hematocrits, hemoglobin levels, and erythrocyte numbers (Futter et al., 1980). Erythrocytes tend to be macrocytic and hypochromic. There are no significant changes in total leukocyte counts initially. In most cases liver function, renal function, and venous blood pH will remain normal (Futter et al., 1981). Without treatment, cats are very likely to die of severe anemia. Of 70 naturally infected cats, 50 recovered, 7 died, 7 were euthanatized (3 were strays, 1 for chronic respiratory disease, 1 for aplastic anemia, and 2 for unstated reasons) and 6 were lost to follow up (Futter and Belonje, 1980b).

TREATMENT: Treatment with primaquine phosphate will often lead to a rapid and successful recovery. In cases of severe anemia and prostration, it may be necessary to also give a blood transfusion followed by primaquine therapy. However, the current effective dose (0.5mg/kg, IM, once) is very close to the lethal dose in cats (1 mg/kg).

EPIZOOTIOLOGY: It would appear that Babesia felis is a parasite of the cat. There may have been some initial African source of this parasite, but the parasite now seems mainly to affect its domestic host.

HAZARD TO OTHER ANIMALS: Specimens of Babesia considered to be Babesia felis by some workers (Dennig and Brocklesby, 1972) have been found in the blood of a puma, Felix concolor, that had been housed in a zoo in Egypt (Carpano, 1934) and in a blood smear from an Indian leopard, Panthera pardus fusca (Shortt, 1940). As stated above, Babesia felis was first noted in the blood of a Sudanese wild cat (Felis Ocreata). It would appear that the has been little spread of this parasite between cats and wildlife.

HAZARDS TO HUMANS: Although humans have been infected with species of Babesia these have been felt to be mainly of bovine and murine types. None have been considered as being due to Babesia felis.

CONTROL/PREVENTION: The disease can be controlled by preventing tick infestations and by treatment of cats that have circulating stages in their bloodstream.

REFERENCES:

Carpano M. 1934. Sur les piroplasmoses des carnassiers et wur un noveau piroplasme des félins (Babesiella felis) chez le puma: Felis concor. Bull Min Agr Egypt Tech Sci Ser No 136, 20 pp.

Davis LJ. 1929. On a piroplasm of the Sudanese Wild Cat (Felix ocreata). Trans Roy Soc Trop Med Hyg 22:523-534.

Dennig HK, Brocklesby DW. 1972. Babesia pantherae sp. nov. a piroplasm of the leopard (Panthera pardus). Parasitology 64:525-532.

Dennig HK, Hebel R. 1969. Licht- und elektronenmikroskopische Untersuchungen an zwei Babesia-Arten der Feliden. Ztschr Parasitenk 32:95-111.

Futter GJ, Belonje PC. 1980a. Studies on feline babesiosis. 1. Historical review. J S Af Vet Assoc 50:105-106.

Futter GJ, Belonje PC. 1980b. Studies on feline babesiosis. 2. Clinical observations. J S Af Vet Assoc 51:143-146.

Futter GJ, Belonje PC, Van Den Berg A. 1980. Studies on feline babesiosis. 3. Haematological findings. J S Af Vet Assoc 51:272-280.

Futter GJ, Belonje PC, Van Den Berg A, Van Rijswijk AW. 1981. Studies on feline babesiosis. 4. Chemical pathology; macroscopic and microscopic post mortem findings. J S Af Vet Assoc 52:5-14.

Jackson C, Dunning FJ. 1937. Biliary fever (Nuttalliosis) of the ct: a case in the Stellenbosch district. J S Af Vet Med Assoc 8:83-87.

McNeil J. 1937. Piroplasmosis of the domestic cat. J S Af Vet Med Assoc 8:88-90.

Shortt HE. 1940. Babesia sp in the Indian leopard, Panthera pardus fusca (Meyer). Ind J Med Res 28:277-278.

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