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  • Title: Small strongyles. Recent advances.
    Author: Reinemeyer CR.
    Journal: Vet Clin North Am Equine Pract; 1986 Aug; 2(2):281-312. PubMed ID: 3527374.
    Abstract:
    The recent increased interest in cyathostomes can be traced to simplification of their taxonomy, improved knowledge of pathogenicity, and failures of practical control due to anthelmintic resistance. Cyathostome ova develop to infective third-stage larvae (L3) at a rate that is directly proportional to environmental temperature. Equine feces serve as a reservoir for L3, which are liberated by moderate amounts of rainfall. Third-stage larvae persist for longer periods at low temperatures, easily surviving over-winter on pastures to provide a source of infection during the following grazing season. Third-stage larvae exsheath within the host and enter the mucosa and submucosa of the cecum and large colon. Larvae develop within mucosal cysts, molt to the fourth stage, and may persist within the tissues for up to 2 1/2 years. Larvae ultimately emerge from the mucosa to become adults in the lumen. Adult populations are replenished by recently ingested larvae and by immature worms newly emerged from arrested development. The magnitude of larval and adult populations within the host displays seasonal variations, with peak numbers occurring in early spring and autumn in the United States. In typical natural infections, a small number of species comprise the majority of the cyathostome populations. Cyathostome infection may result in anorexia, weight loss, diarrhea, colic, and death. Cyathostome ova are easily detected in feces, but ova may not be present during larval cyathostomiasis. Increased concentrations of beta-globulins, hypoalbuminemia, anemia, and leukocytosis occur inconsistently. Two major problems in the treatment of cyathostome infections are anthelmintic resistance and the insusceptibility of encysted larvae to recommended dosages of most anthelmintics. The major goal of cyathostome control is prevention of environmental contamination with nematode ova. Host resistance appears to protect against cyathostome disease rather than cyathostome infection, and one manifestation of this resistance appears to be prolongation of the prepatent period.
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