Acute infection in C3H mice produced by the Brazil and Tulahuen strains of Trypanosoma cruzi resulted in intense parasitization of the pancreas in both strains, of the adrenals with the Brazil strain, and in parasitization of the skeletal muscle and liver with the Tulahuen strain. The extraordinary intensity of pancreatic and adrenal parasitization is noteworthy, though limited to acute infections. The Brazil strain produced approximately 11 times more circulating trypanosomes in mice than the Tulahuen strain. The number of trypanosomes of either strain required to produce a lethal infection in C.H mice resulted merely in chronic infection in Swiss mice, with slight parasitization of all tissues except skeletal muscle. This chronic infection was equivalent to that produced in C.H mice by less than half the number of trypanosomes. Since the first description of Trypanosoma cruzi Chagas (1909), lesions produced by leishmanial forms in various tissues have frequently been reported (e.g., Andrade, 1958; Del Cenget and Rojas, 1959; De Rezende, 1959; Dominguez and Gavaller, 1962; Koberle, 1959; Laranja, 1954). Pancreatic (Pizzi, 1953) and adrenal infections have been mentioned seldom or only in general terms (Cariola et al., 1950). Experiments described in this paper showed unexpected and severe lesions in both pancreas and adrenals in C3H mice with acute infection, and a remarkable difference between acute and chronic tissue parasitization and between the number of trypanosomes required to produce equivalent infections in C3H and Swiss mice. MATERIALS AND METHODS Two South American strains (Brazil and Tulahuen) of T. cruzi were used as infective material. The initial isolate of the former strain was human in origin, whereas the Tulahuen strain was isolated from Triatoma infestans. Both strains had been in culture for several years prior to these experiments; virulence was, therefore, not maximal. Virulence of the Brazil strain remained constant through 48 passages, including those in the tests. The Tulahuen strain was constant throughout the tests and was not followed further. The procedure was identical for both strains: Trypanosome counts for inoculations were done Received for publication 26 May 1965. * Supported by the University of California International Center for Medical Research and Training (Hooper Foundation, San Francisco School of Medicine) with Research Grant TW 00144 from the Office of International Research, NIH, U. S. Public Health Service. t Postgraduate student, The G. W. Hooper Foundation, University of California Medical Center, San Francisco. on plasma with a hemocytometer. To obtain acute infection, C3H mice were inoculated subcutaneously with approximately 50,000 blood trypanosomal forms and followed through passages 2 to 7. Blood for further passage and 14 tissues (Table I) were obtained when moribund mice were killed. Chronic infection resulted from subcutaneous inoculation of C3H mice with 20,000, and Swiss mice with 50,000, blood trypanosomal forms. Mice were killed 6 months after infection. All tissues were fixed in Carnoy's solution and stained with Giemsa (Bray and Garnham, 1962). Total mice infected with each of the two T. cruzi strains were the same: 20 CsH mice (mean weight 14 g) and 15 Swiss mice (mean weight 17 g) each infected with 50,000 trypanosomes; 15 C3H (mean weight 26 g) each infected with 20,000 trypanosomes. Seventyfive per cent of the mice used in each experiment were females. Since there was no marked variation in parasite counts in sections, results were pooled. Circulating trypanosomes were counted (on wet smear, field diameter 0.44 mm, 50 fields) on alternate days after inoculation. The number of leishmanias present in 50 fields was determined for each tissue examined (field diameter 0.192 mm). All sections were scanned prior to leishmanial counts; microscopic fields were distributed to allow for any unevenness in parasitization, if present.
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Apr 1, 1971
Alica Bartová + 1
Open Access