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Observations on the implications of pathology induced by experimental schistosomiasis in baboons in evaluating the development of resistance to challenge infection

Published online by Cambridge University Press:  06 April 2009

R. F. Sturrock ,
B. J. Cottrell ,
S. Lucas ,
G. D. F. Reid ,
H. M. Seitz  and
R. A. Wilson
R. F. Sturrock
Affiliation:
Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, Keppel St (Gower St), London WC1E 7HT
B. J. Cottrell
Affiliation:
Department of Pathology, University of Cambridge, Tennis Court Rd, Cambridge CB2 1QP
S. Lucas
Affiliation:
Department of Medical Helminthology, London School of Hygiene and Tropical Medicine, Keppel St (Gower St), London WC1E 7HT
G. D. F. Reid
Affiliation:
Institute of Primate Research, P.O. Box 24481, Karen, Kenya
H. M. Seitz
Affiliation:
Institute of Medical Parasitology, University of Bonn, Sigmund Freud Strasse 25, D-5300 Bonn 1, FEG
R. A. Wilson
Affiliation:
Department of Biology, University of York, York YO1 5DD
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Summary

Liver samples from 10 Schistosoma mansoni-infected baboons all yielded eggs but neither their egg counts nor duration of infection (< 226 weeks) correlated with the slightly elevated liver collagen levels or minimal histological fibrosis observed. Approximately 10% of inert 9 and 15 μm diameter microspheres injected into the mesenterio veins of 2 baboons with acute, challenge S. mansoni infection reached their lungs (mainly 9 μm microspheres). Lung egg recoveries over 1000 were significantly less common among 175 baboons exposed once to S. monsoni infections than among 56 baboons exposed more than once. Among 221 S. mansoni-and S. haematobium-infected baboons, female worm, total tissue egg and lung egg recoveries were significantly correlated with each other but not with liver or (where available) spleen weights. Liver and spleen weights were strongly correlated with total body weight. Baboons did not develop significant liver fibrosis, even after prolonged schistosome infections. However, some liver ‘leakiness’ developed during acute primary and challenge infections, allowing small inert particles and eggs to pass to the lungs, but this ‘leakiness’ was not associated with resistance to challenge. In contrast to mice, such resistance in baboons cannot, therefore, be explained simply in terms of pathological changes due to previous infections.

Type
Research Article
Information
Parasitology , Volume 96 , Issue 1 , February 1988 , pp. 37 - 48
Copyright
Copyright © Cambridge University Press 1988

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