Trypanosoma cruzi Chagas, 1909

(Figures 1-33 through 1-35)

ETYMOLOGY: This parasite is named after Dr. Cruzi, the director of the Institute in which Dr. chagas worked.

SYNONYMS:Schizotrypanum cruzi Chagas, 1909; Trypanosoma triatomae Kofoid and McCulloch, 1916.

HISTORY: This parasite and the life cycle in which triatomid bugs serve as the vectors were described by Chagas in 1909. Chagas was also the first to observe this trypanosome in the blood of domestic cats.

GEOGRAPHIC DISTRIBUTION: This organism is found in the southern United States, and throughout Mexico, Central America, and South America down into Argentina.

LOCATION IN THE HOST: In the mammalian host, the trypomastigote stage of the parasite is found within the peripheral blood. The amastigote stage is found in reticuloendothelial cells at the site of the initial insect bite, and later, throughout the body. Other cells that may contain the amastigote stage includes striated and cardiac muscle cells.

DIAGNOSIS: Although not well described in the cat, similar methods used in other species are likely to be successful. Blood smears stained with Giemsa stain may be effective in showing organisms during the first 1 to 2 weeks of infectionAfter this time the parasitemia becomes subpatent requiring a concentration technique to identify organisms, or blood culture. Examining the region just above the buffy coat in a microhematocrit tube may show the presence of trypomastigote forms. Serum (1:10 dilution) may be cultured in LIT (liver infusion tryptose broth) at room temperture for 6 weeks after which the broth may be examined for epimastigote forms. Serum may also be inoculated onto Vero cell cultures and maintained at 37C for 4 to 6 weeks to identify trypomastigote forms. Inoculation of infected cat blood into weanling laboratory inbred mice (C3H) will usually develop parasitemias 10 to 10 days later. There are currently no immunologic serology tests for cats, although tissue stage organisms could be identified using immunohistochemistry. Polymerase chain reaction tests used for man or dogs should also work in cats.

IDENTIFICATION OF THE PARASITE: The trypomastigote stage of Trypanosoma cruzi that is present in peripheral blood is never seen to be dividing, is about 20 m long, tends to be fixed in a "C" shape on prepared slides, has one to two undulations of the undulating membrane, and has a relatively large kinetoplast at the posterior end that appears to bulbously expand the cell body (Fig. 1-33). The free flagellum of Trypanosoma cruzi that extends from the anterior end is about one-half to two-thirds of the length of the cell body.

The amastigote stage of Trypanosoma cruzi is indistinguishable morphologically from that of the Leishmania spp. (see below), although if present in muscle cells, the location is diagnostic (Fig. 1-34), because the leishmanial amastigotes are found only in reticuloendothelial cells. 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: This parasite is transmitted between hosts by triatomid bugs (Chagas, 1909); genera that have been shown to serve as vectors include Rhodnius, Panstrongylus, and Triatoma. Within bugs that have ingested blood containing trypomastigotes, the parasites undergo development from the trypomastigote through various stages (Fig. 1-35) to become an infective metacyclic trypomastigote form that is shed in the feces of the bug. Hosts become infected when they rub the feces into the bite wound after the bug has fed. Hosts can also become infected by the ingestion of the bugs with the parasites penetrating the mucosa of the mouth. It is also known that the parasite can be transmitted from a mother to her foetus transplacentally. Cats have been experimentally infected by feeding them infected mice (Baretto et al., 1978)

In the vertebrate host, the parasites multiply initially within macrophages and histiocytes at the location of the bite wound. There is next the development trypomastigotes within the blood and the development of additional amastigotes in other tissues. Ultimately, the blood forms become less common, and the amastigote stages are found within the reticuloendothelial cells of the spleen and liver and within muscle cells, especially the myocardium.

CLINICAL PRESENTATION AND PATHOGENESIS: Only a single cat has been described as having signs due to Trypanosoma cruzi (Talice, 1938). This cat in Montevideo, Uruguay, had signs that included convulsions and transient posterior paralysis.

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

EPIZOOTIOLOGY: Cats are commonly found to be infected when examined as part of surveys in Latin America, e.g., 3.3% of cats in Chile (Rojas et al., 1973), 2.9% of cats in Costa Rica (Zeledón et al, 1975), 28.6% of cats in northeastern Brazil (Mott et al., 1978), 26.9% of cats in Bolivia (Balderama et al., 1981), 7% to 8.5% of cats in Venezuela (Tonn et al., 1983), 63.6% of cats in Argentina (Wisnivesky-Colli et al, 1985), and 50% of cats in Oaxaca, Mexico (Salazar Schettino, et al., 1987). The role of cats in the perpetuation of the parasite would thus appear to be a real one, although studies in which the blood meals within the triatomid bugs have been identified as to host by immunologic methods have shown that in some areas cats are seldom fed on by the bugs (Wisnivesky-Colli, 1982) while others have shown that cats are routinely fed on by the vector (Deane, 1964).

HAZARDS TO OTHER ANIMALS:Trypanosoma cruzi is capable of infecting most vertebrates. Also, if introduced into a poorly maintained facility that might have infestations with the vector, transmission could occur.

HAZARDS TO HUMANS:Trypanosoma cruzi is a serious human pathogen. Also, the prevalence data would suggest that it should often be considered as a potential pathogen in cats that are being treated in Mexico and Central and South America. Precautions must 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: Control and prevention of the disease in cats would, in part, be similar to that for humans, i.e., removing the domesticated triatomid vectors from the living quarters. However, the nature of cats to hunt on their own in the wilds will continue to place them at great risk of acquiring infections from this parasite either from the bite of the bugs or the ingestion of infected rodents.


Balderama F, romero A, Garcia JA, BErmudez h, Serrano R, LaFuente C, Romero F. 1981. Estudio epidemiologico de la enfermedad de Chagas en el Trigal dpto. de Santa Cruz - Bolivia. Bol Inf Cenetrop 3:16-22.

Barreto MP, Ribeiro RS, Neto FMB. 1978. Estudos sobre reservatórios e vectores silvestres do Trypanosomacruzi. LXCVIII: Infecção de mamíferos pela via oral. Rev Brazil Biol 38:455-459.

Chagas C. 1909. Nova tripanozomiaze humana. Estudo sobre a morfologia e o ciclo evolutivo do Schizotrypanumcruzi, n. gen. n. sp., agent etiológico de nova entidade morbida do homen. Mem Inst Osw Cruz 1:159-218.

Deane LM. 1964. Animal reservoirs of Trypanosomacruzi in Brazil. Brasil Malario Doenças Trop 16:27-48.

Mott KE, Mota EA, Sherlock I, Hoff R, Muniz TM, Oliveira TS, Draper CC. 1978. Trypanosomacruzi infection in dogs and cats and household seorreactivity to T. cruzi in a rural community in northeast Brazil. Am J Trop Med Hyg 27:1123-1127.

Rojas A, Sotelo JM, Villarroel F, Contrerar MC. 1973. La importancia del perro y el gato en la epideiologia de la enfermedad de Chagas. Bol Chile Parasit 28:42-43. 1973

Salazar Schettino PM, Bucio Torres MI, De Haro Arteaga I, Tay Zavalka J, Alonso Guerrero T. 1987. Reservorios y transmisores de Trypanosomacruzi en el estado de Ozxaca. Sal Publ Mex 29:26-32.

Talice RV. 1938. Primeras observaciones en el Uruguay de gatos espontáneamente infectados por el Trypanosomacruzi. Arch Urug med, chir, espesiald 13:61-65.

Tonn RJ, Cedillos RA, Ortegon A, Gonzalez JJ, Carrasquero B. 1983. Reservorios domésticos de Trypanosomacruzi y Trypanosomarangeli en Venezuela. Bol Dir Malariol Saneam Ambient 23:18-26.

Wisnivesky-Colli C, Gürtler RE, Solarz ND, Lauricella MA, Segura EL. 1982. Epidemiological role of humans, dogs, and cats in the transmission of Trypanosomacruzi in a central area of Argentina. Rev Inst Med trop São Paulo 27:346-352.

Zeledon R, Solano G, Burstin L, Schwartzwelder JC. 1975. Epidemiological pattern of Chagas’ disease in an endemic area of Costa Rica. Am J Trop Med Hyg 24:214-225.

FIGURE 1-33.Trypanosomacruzi trypomastigotes in the blood of a mouse, stained with Giemsa (Preparation courtes of Dr. L Leiva, School of Medicine, Lousiana State University). Note the “C” shape of the trypomastigote and the very large kinetoplast at the posterior end of the cell.

FIGURE 1-34.Trypanosomacruzi amastigotes in the heart muscle of an experimentally infected mouse (Preparation courtes of Dr. L Leiva, School of Medicine, Lousiana State University). Note that in some of the amastigotes present within this cell can be seen the small round nucleus and the smaller bar-shaped kinetoplast.

FIGURE 1-35.Trypanosomacruzi epimastigote culture forms representative of stages that would be ovserved in the invertebrate vector (Preparation courtes of Dr. L Leiva, School of Medicine, Lousiana State University).