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and Early Death in C57BL/6 Mice1
Departments of
*
Microbiology and Immunology and
Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853
To address the question of how the murine host responds to a
prototypic type 1 cytokine inducer while concurrently undergoing a
helminth-induced type 2 cytokine response, C57BL/6 strain animals with
patent schistosomiasis mansoni were orally infected with the cystogenic
Toxoplasma gondii strain ME49. Schistosoma
mansoni infection resulted in a significantly higher mortality
rate when mice were subsequently orally infected with ME49, and these
animals displayed a defective IFN-
and NO response relative to
animals infected with T. gondii alone. Plasma levels of
TNF-
and aspartate transaminase in double-infected mice were greatly
elevated relative to mice infected with either parasite alone.
Consistent with the latter observation, these animals exhibited severe
liver pathology, with regions of coagulative necrosis and hepatocyte
vacuolization unapparent in mice carrying either infection alone.
Interestingly, mean egg granuloma size was 
50% of that in mice with
S. mansoni infection alone. The exacerbated liver
pathology in coinfected mice did not appear to be a result of
uncontrolled tachyzoite replication, because both parasite-specific
RT-PCR analysis and immunohistochemical staining demonstrated a low
number of tachyzoites in the liver. We hypothesize that mortality in
these animals results from the high level of systemic TNF-, which
mediates a severe liver pathology culminating in death of the
animal.
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