Leishmania donovani (Laveran & Mesnil, 1903) Ross, 1903

(Figures 1-36 and 1-37)

ETYMOLOGY: This parasite is named after William Leishman who discovered the organisms in spleen smears and Charles Donovan who found the organisms in a splenic puncture biopsy.

SYNONYMS:Piroplasma donovani Laveran & Mesnil, 1903; Leishmania chagasi Chagas et al, 1937.

HISTORY: In 1900, William Leishman found organisms in spleen smears of a soldier who died from a fever known as kala-azar (Leishman, 1904), and in 1903 Donovan found the same organisms in a splenic biopsy. Rogers (1904) showed that flagellate forms developed in cultures, and Adler & Ber (1941) showed promastigotes would develop in sandflies and transmit the disease. Nicolle and Compte found Leishmania donovani in dogs in Tunisia in 1908.

GEOGRAPHIC DISTRIBUTION: This organism is found in North Africa, Southern Europe, and the Middle East through India into western China. The disease was brought to the America after Columbus and is now endemic in parts of South and Central America. There have been reports of visceral leishmaniasis in cats around the Mediterranean [Spain (Gimeno Ondovilla, 1933), Italy (Giordano, 1933), Algeria (Sergent et al, 1912; Bosselut, 1948), Jordan (Morsy et al., 1980), and France (Bergeon, 1927)) and in Brazil (Mello, 1940)].

LOCATION IN THE HOST: In the mammalian host, the only stage that is present is the amastigote that is found within histiocytes, monocytes, and other cells of the reticuloendothelial system. Typically, Leishmania donovani is found within the spleen, liver, bone marrow, intestinal mucosa, and mesenteric lymph nodes. Other Leishmania spp. tend to be confined to ulcers on the skin.

DIAGNOSIS: Serologic tests exist for the cat, but are unreliable as cats are rarely clinically affected even when they are serologically positive. The cutaneous form, the most common, may be diagnosed by identifying organisms within cells on aspirate cytology (Wright’s or Giemsa stain) or histopathology of excised lesions. Although not reported in cats, PCR tests on infected tissues should be very sensitive and specific.

IDENTIFICATION OF THE PARASITE: The amastigote stage of Leishmania donovani is indistinguishable morphologically from that of the Trypanosoma cruzi and other Leishmania spp. (Fig. 1-36). The amastigote stage is round to oval, is 1.5 to 4.0 m in diameter, and contains a large nucleus and a smaller kinetoplast. The amastigotes appear slightly larger in impression smears than in histologic sections due to flattening and the different methods of fixation.

LIFE CYCLE: Within the mammalian host the parasite grows and multiplies within cells of the reticuloendothelial system by simple binary division. Leishmania donovani is transmitted between hosts by the bite of infected sandflies (genera: Phlebotomus in Europe and Asia, and Lutzomyia in the Americas). Within the sandfly are found the flagellated promastigote forms of the parasite that are similar to the stage found in cell-free cultures (Fig. 1-37).

CLINICAL PRESENTATION AND PATHOGENESIS: Very few of the reports dealing with cats have described clinical signs other than to say that the cats were thin and may have had cutaneous manifestations of the visceral disease. In one case, organisms were found in the spleen (Bergeon, 1927) and in another case amastigotes were seen in bone marrow (Sergent et al., 1912).

The course of infection of has been followed in cats with experimentally induced visceral leishmaniasis (Kirkpatrick et al, 1984). Cats inoculated intravenously with amastigotes developed large numbers of organisms in the liver, spleen, and bone marrow. On the other hand, cats inoculated intradermally with promastigotes from culture developed transient (of 3 days duration) palpable nodules at the site of inoculation but no parasites were recovered from the internal organs of these cats. Of those infected cats that were maintained up to 16 weeks after infection, none developed signs of leishmaniasis or cutaneous lesions. At necropsy, there was no apparent hepatomegaly or splenomegaly. These results describing the failure of the inoculation of promastigotes are not surprising in light of recent work showing the importance that the saliva of the sandfly plays in the development of visceral infection with this parasite (NEED REFERENCE).

TREATMENT: There are no reports of attempted treatment of infected cats.

EPIZOOTIOLOGY: Overall, very few cats have been examined for the presence of Leishmania donovani. It has been considered that they do not play a major role as mammalian hosts of this parasite, but at this time, there role is actually not known.

HAZARDS TO OTHER ANIMALS: Transmission to other animals could occur, but at this time, the significance of the role of the cat in the wild is not known.

HAZARDS TO HUMANS: Cats could serve as sources of human infection, but they are not considered to be major reservoirs of this parasite. However, personnel need to be protected from possible accidents that could introduce the organisms into their skin.

CONTROL/PREVENTION: To control and prevent this disease in cats it would be necessary to prevent cats from being bitten by the sandfly vec tor.


Adler S, Ber M. 1941. Transmission of Leishmaniatropica by the bite of Phlebotomuspapatasii. Ind J Med Tes 29:803.

Bergeron PVA. 1927. Un cas de leishmaniose chez le chat. Bull Soc Sci Vet Lyon 30:92-93.

Bosselut H. 1948. Un cas de leishmaniose générale du chat. Arch Inst Pasteur d’Alg 26:14.

Gimeno Ondovilla A. 1933. Contribución a la epidemiología del kala azar. Trabajos Madrid 2:26-27.

Giordano A. 1933. Le chat dans la transmission de la leishmaniose viscérale de la médittéranée. bull Sez Ital Soc Intern Microbiol 5:330-332.

Kirpatrick CE, Farrell JP, Goldschmidt MH. 1984. Leishmaniachagasi and Ldonovani: Experimental infections in domestic cats. Exp Parasitol 58:125-131.

Leishman WB. 1904. Note on the nature of the parasitic bodies found in tropical splenomegaly Brit Med J (2249) 1:303

Mello GB. 1940. Verificão de infecção natural do gato (Felixdomesticus) por um protozoario do genero Leishmania. Bras Med 54:180.

Morsy TA, Michael SA, El Disi AM. 1980. Cats as reservoir hosts of human parasites in Amman, Jordan. J Egypt Soc Parasitol 10:5-18.

Nicolle c, Comte C. 1908. Origine canine du Kala-azar. Compt Rend Acad Sci 146:789-791.

Rogers L. 1904. Preliminary note on the development of Trypanosoma in cultures of the Cunningham-Leishman-DOnovan bodies of cachexial fever and kala-azar. Lanct (4221) 167:215-216.

Sergent EE, Lombard J, Quilichini M. 1912. La leishmaniose â Alger. Infection simultanée d’un enfant, d’un chien et d’un chat dans la même habitation. Bull Soc Pathol Exot 5:93-98.

FIGURE 1-36.Leishmaniadonovani in impression smear of experimentally infected hamster that was stained with Giemsa stain (Preparion courtesy of Dr. J Farrell, College of Veterinary Medicine, University of Pennsylvania). Note the large host-cell nucleus in the middle that is surrounded by the amastigotes that have a small round nucleus and the bar-shaped kinetoplast.

FIGURE 1-37.Leishmaniadonovani culture form showing the elongate shape and the presence of the free, anteriorly directed flagellum.