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Elsheikha HM, Hussein HS, Rahbar MH: Clinico-pathological effects of Schistosoma mansoni infection associated with simultaneous exposure to malathion in Swiss outbred albino mice. Acta Trop. 2008 Oct;108(1):11-9. Epub 2008 Aug 3.
To investigate whether infection of Swiss outbred mice with the digenetic fluke Schistosoma mansoni is influenced by exposure to environmental pollutants, experimentally infected mice were exposed to 200 and 400 mg/kg of malathion. Pathology of liver and spleen, worm burden and levels of key hematological, biochemical and liver enzymes parameters of these mice were evaluated and were compared with data from infected, unexposed mice, uninfected, exposed mice as well as with data from uninfected, unexposed mice. Oral administration of malathion to mice infected with 20, 40 or 60 S. mansoni cercariae adversely affect architecture of liver and spleen and critically alter hematological, biochemical, histological and hepatic enzymes parameters significantly more than the controls. Alterations observed in infected, exposed mice included (i) higher mortality rate; (ii) severe pathologies in liver and spleen; (iii) increased serum level of bilirubin and alanine aminotransferase/aspartate aminotransferase (ALT/AST) enzymes; (iv) decreased serum level of albumin and total proteins; and (v) decreased red blood cell count (RBC), lymphocytes, leucocytic count, and hemoglobin content. The number of recovered adult worms of S. mansoni or their oviposition capacity did not seem to be affected with malathion treatment. Statistical analysis revealed that the increase alteration in hepatic functions is correlated with increasing the number of S. mansoni cercariae and malathion doses. Such alterations were more significant in mice treated with the higher dose of malathion or infected with the largest numbers of S. mansoni cercariae. These data indicate that schistosomiasis can be exacerbated by simultaneous malathion exposure, which in turn adversely impact the clinical and pathological outcome of the disease. |
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