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Trans R Soc Trop Med Hyg. 1988;82(1):90-3.

Trypanosoma cruzi infection in diabetic mice.

Author information

1
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461.

Abstract

The course of infection due to Trypanosoma cruzi (Brazil strain) was examined in mutant and streptozotocin (STZ)-induced diabetic mice. Mutant diabetic mice (+db/+db) are obese, have elevated blood glucose levels, normal insulin levels and impaired cell mediated immunity (CMI). Their littermates (m+/m+, m+/+db) are of normal weight, normoglycaemic and immunocompetent. Infected +db/+db mice died within 20-25 d after infection (AI) with a mean peak parasitaemia of 6 X 10(6) trypomastigotes/ml accompanied by heavy tissue parasitism. The nondiabetic littermates had low, transient, parasitaemia, no tissue parasitism, and 100% survival. Immune mouse serum (IMS) was given to infected +db/+db mice thrice weekly beginning on day 1 AI. During IMS treatment, parasitaemia remained significantly lower than in untreated mice. However, when IMS treatment was discontinued parasitaemia rose and mortality ensued. To examine the effects of hyperglycaemia in the absence of other variables such as genetics or CMI, T. cruzi infection was studied in STZ-induced diabetic mice. Normal C57BL/6 mice, resistant to infection with the Brazil strain, exhibited low transient parasitaemia and no mortality. In contrast, STZ-induced hyperglycaemic C57BL/6 mice developed high parasitaemia and 100% mortality by day 40 AI. When these hyperglycaemic mice were treated with insulin continuously by pump, their blood glucose levels returned to normal but parasitaemia and mortality were unchanged. These data indicate that hyperglycaemia significantly increases parasitaemia and mortality in mice infected with T. cruzi.

PMID:
3140447
[Indexed for MEDLINE]

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