title: Evaluation of hyperplastic goiter in a colony of Syrian hamsters (Mesocricetus auratus).
abstract: Hyperplastic goiter was diagnosed during routine health monitoring of a closed Syrian hamster colony (SG). Adult and juvenile hamsters were affected at a prevalence of 45%. Histologic examination of the enlarged thyroid gland revealed marked follicular cell hyperplasia. Because prevalence of thyroid hyperplasia in this colony exceeded the 6 to 7% prevalence expected in aged hamsters, additional studies were performed to investigate the pathogenesis of this condition. Juvenile male SG hamsters and age- and sex-matched Syrian hamsters that did not have increased prevalence of goiter were obtained from an unrelated source (Fredrick Cancer Research and Development Center [FCRDC]). The thyroid glands of hamsters were evaluated by 123I radionuclide imaging. Eight of 18 SG hamsters and none of the FCRDC hamsters had a diagnosis of enlarged thyroid gland. Serum baseline and post-thyrotropin thyroxine concentrations in SG hamsters were not statistically different from those in FCRDC hamsters. To investigate whether diet played a role in development of hyperplastic goiter, for 6 months 15 FCRDC hamsters were fed the diet that had been fed to SG hamsters (mouse breeder diet), and five were fed a control diet. To determine whether dietary change would result in resolution of goiter, affected SG hamsters were fed a control diet for 3 months. At the end of each feeding trial, thyroid gland uptake of 123I was reevaluated. The amount of 123I taken up by the thyroid glands of FCRDC hamsters fed the mouse breeder diet was not significantly different from that of controls. In contrast, thyroid gland uptake of 123I remained high for all affected SG hamsters fed the control diet. On the basis of results of these investigations, diet was ruled out as the cause of goiter. Also, a diagnosis of euthyroid hyperplastic goiter was made for the SG hamsters. A genetic cause is suspected to play a role in the increased prevalence of goiter in SG hamsters.
authors.affiliation: Department of Veterinary Pathobiology, University of Missouri, Columbia 65211, USA.
authors.forename: R S
authors.initials: RS
authors.lastname: Livingston
authors.forename: C L
authors.initials: CL
authors.lastname: Franklin
authors.forename: J C
authors.initials: JC
authors.lastname: Lattimer
authors.forename: R S
authors.initials: RS
authors.lastname: Dixon
authors.forename: L K
authors.initials: LK
authors.lastname: Riley
authors.forename: R R
authors.initials: RR
authors.lastname: Hook
authors.forename: C L
authors.initials: CL
authors.lastname: Besch-Williford
mesh_terms: D000818:Animals; D006224:Cricetinae; D004032:Diet; D006042:Goiter / Q000235:genetics / Q000473:pathology / Q000662:veterinary*; D008297:Male; D008647:Mesocricetus; D015995:Prevalence; D011877:Radionuclide Imaging; D012376:Rodent Diseases / Q000235:genetics / Q000473:pathology*; D013961:Thyroid Gland / Q000000981:diagnostic imaging / Q000473:pathology; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood
chemical_list: D013972:Thyrotropin; D013974:Thyroxine