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Am. J. Trop. Med. Hyg., 30(5), 1981, pp. 1043-1052
Copyright © 1981 by The American Society of Tropical Medicine and Hygiene

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Characteristics of the Larval Echinococcus vogeli Rausch and Bernstein, 1972 in the Natural Intermediate Host, the Paca, Cuniculus Paca L. (Rodentia: Dasyproctidae)*

R. L. Rausch, A. D'Alessandro AND V. R. Rausch
Division of Animal Medicine, SB-42, and Department of Pathobiology, University of Washington, Seattle, Washington 98195, and Tulane University—International Center for Medical Research, Apartado Aereo 5390, Cali, Colombia

In Colombia, the natural intermediate host of Echinococcus vogeli Rausch and Bernstein, 1972 is the paca, Cuniculus paca L. (Rodentia: Dasyproctidae). The larval cestode develops in the liver of the host, where it usually is situated superficially, partly exposed beneath Glisson's capsule. The infective larva consists of a subspherical to asymmetrical, fluid-filled vesicle, up to 30 mm in diameter, enclosed by a thick laminated membrane. It typically contains numerous chambers, often interconnected, produced by endogenous proliferation of germinal and laminated tissue, within which brood capsules arise in an irregular pattern from the germinal layer. Invasive growth by means of exogenous proliferation, typical of infections in man, was not observed in the natural intermediate host. The development of the larval cestode is described on the basis of material from pacas, supplemented by observations on early-stage lesions in experimentally infected nutrias, Myocastor coypus (Molina) (Rodentia: Capromyidae). The tissue response is characterized for early-stage, mature (infective), and degenerating larvae in the comparatively long-lived intermediate host. In addition to previously reported differences in size and form of rostellar hooks, other morphologic characteristics are defined by which the larval stage of E. vogeli is distinguished from that of E. oligarthrus (Diesing, 1863). Pathogenesis by the larval E. vogeli in man, like that by the larval E. multilocularis Leuckart, 1863, is the consequence of atypical proliferation of vesicles attributable to parasite-host incompatibility.

Accepted for publication February 21, 1981.


* Supported in part by the Tulane University-COLCIENCIAS International Center for Medical Research, and by Grants AI-10050 and AI-15172 from the National Institute of Allergy and Infectious Diseases, National Institutes of Health, U.S. Public Health Service.




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Copyright © 1981 by the American Society of Tropical Medicine and Hygiene.