A naturally occurring disease involving hyperplasia of the thyroid gland and a consistent pattern of musculoskeletal deformities of newborn foals in western Canada was first described in 1981. This disease was an important cause of foal mortality and, therefore, reproductive loss throughout western Canada during the 1990s and has since been recognized in western Ontario and the northwestern United States. A series of investigations were conducted to describe, characterize, and attempt to determine the pathogenesis and cause of this syndrome. Affected foals were typically born after a long gestation (x = 360 days, range = 340 to 400 days), were diagnosed as hypothyroid based on a poor response to the administration of thyroid-stimulating hormone, and had various musculoskeletal lesions of which mandibular prognathism, flexural deformities and rupture of tendons of the limbs, and incomplete ossification of the carpal and tarsal bones were present most commonly. In spite of the normal to long gestation, foals had signs of immaturity, were usually weak and unable to stand, became septic, and died or were euthanatised. Similar histories, clinical findings, and lesions were present in surgically created hypothyroid foals that were thyroidectomized in utero at about 210 days gestation. These findings supported the conclusion that foals which naturally developed these lesions were also hypothyroid in utero and that all the lesions present in affected foals were the result of the hypothyroidism and not of an underlying concurrent disease process. A case-control study was conducted to identify risk factors for naturally occurring congenital hypothyroidism. Information from congenitally hypothyroid foals concerning foal and dam signalment, farm environment, and dam management was compared with that from normal foals. Pregnant mares fed greenfeed, not supplemented with mineral, that left their "home farm" during gestation, or grazed irrigated pasture, had a 13.1 (<i>P</i>=0.0068), 5.6 (<i>P</i>=0.0472), 4.3 (<i>P</i>=0.0076) and approximately 15.3 (<i>P</i>=0.0245) times greater odds, respectively, of producing a congenitally hypothyroid foal than mares not exposed to these factors. Greenfeed often contains high levels of nitrate (NO<sub>3</sub><sup>-</sup>) which is known to impair thyroid gland function. In light of this, forage samples from participating farms were analysed for nitrate levels. The odds of one or more congenitally hypothyroid foal being born on a farm feeding forage with at least a trace of nitrate was 8.0 times greater (<i>P</i>=0.0873) than the odds of the disease occurring a farm that fed forage free of nitrate. Further, the odds of a mare producing an affected foal when fed forage containing at least a trace of nitrate was 5.9 times greater (<i>P</i>=0.0007) than a mare fed nitrate-free forage.This study suggests that congenital hypothyroidism in foals may result from diets containing nitrate or low in iodine being fed to pregnant mares. These results need to be confirmed through further field investigations and controlled experiments. However, if they are accurate, there is cause for concern that other livestock raised in areas where congenitally hypothyroid foals occur may be exposed to the same dietary risk factors and may suffer similar disease.
Identifer | oai:union.ndltd.org:USASK/oai:usask.ca:etd-10212004-000356 |
Date | 01 January 1997 |
Creators | Allen, Andrew Lyndon |
Contributors | Riddell, Craigmyle, Fretz, Peter B. |
Publisher | University of Saskatchewan |
Source Sets | University of Saskatchewan Library |
Language | English |
Detected Language | English |
Type | text |
Format | application/pdf |
Source | http://library.usask.ca/theses/available/etd-10212004-000356 |
Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to University of Saskatchewan or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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