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dc.contributor.authorRoss, Brian J.
dc.date.accessioned2021-02-22T15:08:13Z
dc.date.available2021-02-22T15:08:13Z
dc.date.issued2008-05
dc.identifier.urihttp://digital.library.wisc.edu/1793/81296
dc.description.abstractLeyogonimus polyoon (Plagiorchiformes: Lecithodendriidae) is a flatworm digenean trematode parasite that causes the death of thousands of American coots (Fulica americana) in Wisconsin each fall. As adults, L. polyoon are about one millimeter in size and inhabit the intestine of the coot. Within the intestine, adult L. polyoon worms produce eggs which are expelled in feces of the coot. These eggs must then be ingested by the snail intermediate host, Bithynia tentaculata. Once inside the snail, L. polyoon larvae produce sporocysts, which in turn asexually produce tailed cercariae. The cercariae leave the snail and encyst as metacercariae in a variety of aquatic insects. When coots ingest insects infected with metacercariae, the life cycle is completed, and adult L. polyoon develop to sexual maturity within the coot intestine. Leyogonimus polyoon appears to have been introduced to North America during the introduction of its snail host, Bithynia tentaculata, and it has been reported to also cause coot mortality in Europe. Because knowledge of how the pathology is engendered in coots may provide insight into treatment and methods of disease control, I used standard histopathological techniques to examine how L. polyoon engenders intestinal pathology in infected coots. Five coots from Shawano Lake, WI, were shot in November, 2006 and the intestines from each bird were removed and preserved in Gendre's solution. Intestines were subsequently cut into 2 cm lengths, dehydrated in alcohol and xylene, infiltrated with paraffin under vacuum, and sectioned at thicknesses ranging from 5 - 11μ. Whole worm voucher specimens were recovered from several intestines, and these were stained, mounted, and identified as Leyogonimus polyoon. Intestinal sections were stained variously with Hematoxylin and Eosin, Alcian blue pH 2.5, Mercuric Bromphenol Blue, and PAS with a salivary amylase control. Stained sections were examined for presence and location of L. polyoon in the intestine (lumen or mucosa), depth of penetration into mucosa, evidence of inflammation, necrotic tissue, vascular leakage, and plasma cell infiltration. Most sections of intestine harbored at least one worm, and in some sections over ten L. polyoon were visible in sections. While some worms were observed in the lumen of the intestine, most were associated with mucosal layers, and many penetrated deeply into the muscularis mucosae. Significant damage to mucosae, muscularis mucosae, and smooth muscle was evident in many sections, with necrotic host tissue commonly found near worms. In terms of acute immune response, infiltrating plasma cells were observed near worms and worm eggs. Concomitantly however, there was no evidence of granuloma formation or other typical chronic immune reactions. The observable pathology induced by a single worm was generally restricted to the nearby mucosae and penetration of smooth muscle. However, cumulative pathology induced in an infected coot is intensity dependent, and infections of several thousand L. polyoon result in lethal disruption and destruction of mucosae and muscle tissues. The ecological conditions at Shawano Lake, WI are conducive to transmission of high intensity and lethal infections to American coots.en_US
dc.language.isoen_USen_US
dc.publisherUniversity of Wisconsin-Stevens Point, College of Natural Resourcesen_US
dc.titleA Histopathological Study of Leyogonimus Polyoon in Shawano Lake, WI Cootsen_US
dc.typeThesisen_US


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