The epidemiological, clinical, and anatomopathological aspects of an outbreak of congenital caprine goiter are described in this article. The cause of the congenital goiter and neonatal deaths was attributed to the absence of mineral supplementation with iodine to the pregnant dams. Clinically, all neonatal dead goats presented with marked swelling on the cranioventral cervical area and diffuse body alopecia. One of the dead kids was submitted to necropsy, and changes consisted of marked, symmetrical enlargement of both thyroid lobes, which were also firm, compact, and dark red. Histologically, changes were characteristic of diffuse hyperplastic goiter and consisted of: 1) marked follicular thyroid hyperplasia and hypertrophy; 2) formation of heterogeneous thyroid follicles due to the variable amounts of luminal colloid; and 3) presence of endocytic vacuoles, which represent colloid endocytosis and demonstrate activity of the thyroid gland
diseases of goats; hyperplastic goiter; iodine deficiency; congenital anomalies
