Salmonella Paratyphi a in Hamsters Concurrently Infected with Schistosoma Mansoni

Isis A. MikhailDepartments of Bacteriology, Immunology, and Parasitology, U.S. Naval Medical Research Unit No. 3, Al-Azhar University Faculty of Science, Cairo, Egypt

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Gene I. HigashiDepartments of Bacteriology, Immunology, and Parasitology, U.S. Naval Medical Research Unit No. 3, Al-Azhar University Faculty of Science, Cairo, Egypt

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Noshy S. MansourDepartments of Bacteriology, Immunology, and Parasitology, U.S. Naval Medical Research Unit No. 3, Al-Azhar University Faculty of Science, Cairo, Egypt

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David C. EdmanDepartments of Bacteriology, Immunology, and Parasitology, U.S. Naval Medical Research Unit No. 3, Al-Azhar University Faculty of Science, Cairo, Egypt

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Sabry H. ElwanDepartments of Bacteriology, Immunology, and Parasitology, U.S. Naval Medical Research Unit No. 3, Al-Azhar University Faculty of Science, Cairo, Egypt

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The present work deals with the development of an improved animal model to study the association of salmonellosis and schistosomiasis. The animal chosen was the hamster, Mesocricetus auratus, which can be readily infected with Schistosoma mansoni. Normal hamsters and schistosome-infected hamsters (SIH) were given approximately 2.0 × 107 Salmonella paratyphi A intracardially. It was found that S. mansoni infections enhanced and prolonged the growth of S. paratyphi A in hamsters. Animals with dual infections had increased mortality in comparison with those infected with just bacteria or parasite during the 50 days post-bacterial challenge. Further studies showed that in SIH, S. paratyphi A persisted in various organs for up to 8 weeks post infection. In contrast, concurrent Leishmania donovani infections have no effect on S. paratyphi A infections. Significant numbers of bacteria were cultured from well-washed schistosome worms recovered from SIH 6–8 weeks post-bacterial challenge. These findings suggest that a direct physical relationship between the bacteria and worms facilitates the establishment and growth of S. paratyphi A in vivo, and that a deficit in host immune response is not a major factor involved in the enhanced growth of S. paratyphi A.

Author Notes

Present address: Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, Michigan 48109.

Present address: Department of Microbiology, Royal Medical Research Institute, National Naval Medical Center, Bethesda, Maryland 20014.

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