Submitted to: Journal of Parasitology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/1/2001
Publication Date: 6/1/2002
Citation: Gomez, R.E., Solana, M.E., Levander, O.A. 2002. Host selenium deficiency increases the severity of chronic inflammatory myopathy in trypanosoma cruzi-inoculated mice. Journal of Parasitology. Interpretive Summary: Chagas' disease, also known as American trypanosomiasis, is one of the most serious endemic parasitic diseases of the Americas. In Argentina alone, more than 2 million people are afflicted with this condition thereby making this disease the major tropical disease in that country. The serious public health consequences of the illness stimulated both national and international programs aimed at its control. The research presented here shows that a nutritional deficiency of the essential micromineral selenium worsens the outcome of experimental Chagas' disease in mice resulting in paralysis of the back legs, increased muscle inflammation, and replacement of skeletal muscle by fibrous tissue. In the northeastern part of Argentina where there is a high prevalence of Chagas' disease in the rural populations, selenium deficiency appears to be a practical problem in cattle. Therefore, it would be of interest to carry out a nutritional survey to characterize these populations with regard to their selenium status and determine the outcome of Chagas' disease in persons with differing selenium intakes.
Technical Abstract: Weanling C3H/HeN mice were fed either a torula yeast-based diet deficient in selenium (Se) or the same diet supplemented with 0.2 ppm Se as sodium selenite. After 4 weeks of feeding, the mice were inoculated intraperitoneally with the CA-I strain (clone K98) of Trypanosoma cruzi (TC). Prior to inoculation, mean serum Se levels were 430 vs. 61 ng/ml in adequate vs. deficient mice, respectively. During the ascending phase of parasitemia, the Se-deficient mice exhibited significantly higher levels of parasites at 22-34 days postinfection (PI). However, no differences were found in the subsequent descending phase. As judged by visual examination at 2 months PI, some Se-deficient infected mice presented clinical signs of motor dysfunction. At 3 months PI, the end of the observation period, such chronic disease became a hind limb flaccid paralysis affecting 5of 8 infected deficient mice. No signs of paralysis were seen in non-infected mice fed either diet nor in infected mice fed the Se-adequate diet. At the histological level, both Se-adequate and Se- deficient infected mice showed mild myocarditis and moderate to severe myositis with increasing intensity from one to 3 months PI in both groups. However, the severity of myositis was always more intense in the Se- deficient mice so that prominent areas of skeletal muscle replaced by fibrotic tissue were frequently observed. Thus, it can be concluded that Se deficiency in the murine host increases the severity of TC-induced myositis.