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The pathology induced in laboratory rats by metacestodes of Taenia crassiceps and Mesocestoides corti (Cestoda)

Published online by Cambridge University Press:  06 April 2009

J. Chernin  and
Diane J. McLaren
J. Chernin
Affiliation:
Department of Biological Sciences, North East Surrey College of Technology, Reigate Road, Ewell, Epsom, Surrey KT17 3DS
Diane J. McLaren
Affiliation:
Division of Parasitology, National Institute for Medical Research, The Ridgeway, Mill Hill, LondonNW 1AA
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Summary

Sprague–Dawley rats were infected by intraperitoneal injection with either the cysticerci of Taenia crassiceps or the tetrathyridia of Mesocestoides corti. Both species of metacestodes reproduce asexually in the peritoneal cavity. The effect of T. crassiceps upon the rats was to cause chronic inflammation of the peritoneum, fibrous adhesions between the visceral organs and hyperplasia of the gut mesenteries which became extended into a large sac-like structure. Dead parasites surrounded by white calcareous material were found free in the peritoneum and attached to the inner body wall and viscera. The histopathology of the hyperplastic mesenteries and fibrous membrane is described. The tetrathyridia of M. corti were found free in the peritoneal cavity as well as in the liver (mainly the left liver-lobe), gut mesenteries and in an outgrowth of the connective tissue associated with the pancreas. The connective tissue outgrowth comprised 2 layers; an inner reticular layer and a thickened marginal layer. Metacestodes were found in collagen—fibrin capsules within the connective tissue. A layer of mucopolysaccharide material was interposed between the parasite and the capsule wall. A possible method by which the parasites gain entry into the connective tissue is described. The connective tissues of rats harbouring either M. corti or T. crassiceps had increased numbers of mast cells compared to connective tissues from control rats. Younger mast cells containing biogenic amines predominated in infected tissues whereas older heparin-containing cells dominated control tissues.

Type
Research Article
Information
Parasitology , Volume 87 , Issue 2 , October 1983 , pp. 279 - 287
Copyright
Copyright © Cambridge University Press 1983

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References

REFERENCES

Carleton, H. M. (1967). In Carleton's Histological Techniques, revised by Drury, R. A. B. and Wellington, E. A.. London: Oxford University Press.Google Scholar
Chernin, J. (1975). The maintenance of Taenia crassiceps in rats. Journal of Helminthology 49, 91–2.CrossRefGoogle Scholar
Chernin, J. (1982). The nature of antigens common to both metacestodes of Taenia crassiceps and laboratory rats. Journal of Helminthology 56, 339–44.CrossRefGoogle Scholar
Csaba, G. (1969). Mechanism of the formulation of mast cell granules. Acta biologica Academiae scientiarum Hungaricae 20, 205–10.Google Scholar
Dawes, B. & Hughes, D. L. (1964). Fascioliasis: the invasive stages of Fasciola hepatica. In Advances in Parasitology, vol. 2 (ed. Dawes, B.), pp. 97–165. London: Academic Press.Google Scholar
Folkman, J. & Cotran, R. (1976). Relation of endothelial proliferation to tumour growth. In International Review of Experimental Pathology, vol. 16 (ed. Richter, G. W. and Epstein, M. A.), pp. 207. New York: Academic Press.Google Scholar
Freeman, R. S. (1962). Studies of the biology of Taenia crassiceps. Canadian Journal of Zoology 40, 969–90.CrossRefGoogle Scholar
Freeman, R. S. (1964). Studies on responses of the intermediate host to infection with Taenia crassiceps. Canadian Journal of Zoology 42, 367–85.CrossRefGoogle Scholar
Kessler, D. A., Langer, R. S., Pless, N. A. & Folkman, J. (1976). Mast cells and tumour angiogenesis. International Journal of Cancer 36, 703–9.CrossRefGoogle Scholar
Levi-Schaffer, F. & Smolarsky, M. (1981). Schistosoma mansoni: effect of insulin and a low-molecular weight fraction of sera on schistosomula cultured in chemically defined media. Experimental Parasitology 52, 378–85.CrossRefGoogle Scholar
Lumsden, R. D. (1979). Morphological aspects of host–parasite interaction: some observations on the mammalian inflammatory response to helminth parasitism. In Host–Parasite Interfaces, (ed. Nickol, B. B.), pp. 49. New York: Academic Press.Google Scholar
Simpson, G. F. & Gleason, L. N. (1975). Lesion formation in the livers of mice caused by metabolic products of Hymenolepis microstoma. Journal of Parasitology 61, 152–4.CrossRefGoogle ScholarPubMed
Smyth, J. D. (1969). The Physiology of Cestodes. Edinburgh: Oliver & Boyd.Google Scholar
Specht, D. & Voge, M. (1965). Asexual multiplication of Mesocestoides tetrathyridia in laboratory animals. Journal of Parasitology 51, 268–72.CrossRefGoogle ScholarPubMed
Specht, D. & Widmer, E. A. (1972). Response of mouse liver to infection with tetrathyridia of Mesocestoides (Cestoda). Journal of Parasitology 56, 431–7.CrossRefGoogle Scholar
Studer, M. & Baer, J. G. (1949). Une larve de cestode bourgeonnante. Bulletin de la Société neuchâteloise des Sciences naturelles 72, 255.Google Scholar
Todd, K. S. Jr., Simon, J. & Dipietro, J. A. (1978). Pathological changes in mice infected with tetrathyridia of Mesocestoides corti. Laboratory Animals 12, 51–3.CrossRefGoogle ScholarPubMed
White, T. R., Thompson, R. C. A., Pass, O. A., Penhale, W. J. & Stephenson, J. (1981). Pathological phenomena associated with Mesocestoides corti infection in mice. Journal of Helminthology 55, 167–71.CrossRefGoogle ScholarPubMed
White, T. R., Thompson, R. C. A., Penhale, W. J., Pass, D. A. & Mills, J. N. (1982). Pathophysiology of Mesocestoides corti infection in the mouse. Journal of Helminthology 56, 145–53.CrossRefGoogle ScholarPubMed