RUMINANTS

Perinatal mortality secondary to goiter in goat kids

Andrew Vince, Brent Hoff

 

Two 1-day-old goat kids presented to the AHL had been delivered with difficulty approximately 24 h prior to presentation after difficult and prolonged labor.  Noted by the clinician were large masses on the ventral aspect of each of their necks, just caudal to the jaw.  The dam herself had notable hair loss and scabs on her udder.

Each goat kid was submitted in entirety for postmortem, and both had similar lesions: elongate, finger-like masses ranging from 7-10 cm in length and up to 2 cm in diameter that replaced the normal thyroid tissue (Figure 1).  A tentative diagnosis of perinatal mortality secondary to hyperplastic goiter was made, and tissues were submitted for histopathology.  Under the microscope, the thyroid follicular cells were columnar (rather than normal cuboidal) with large quantities of foamy-to-vacuolated cytoplasm, and frequently surrounded diminished quantities of colloid, confirming the diagnosis of hyperplastic goiter.  Airways in the lungs contained occasional anucleate squamous cells, a common finding in neonates at postmortem as a result of aspiration of amniotic fluid with distress in utero.

Concurrent with postmortem assessment of the goat kids, maternal serum was submitted for assessment of iodine levels.  Maternal serum contained 40.6 ppb iodine (reference range 100-400 ppb, with defined deficiency below 50 ppb), implicating a maternal iodine deficiency. Investigation on-farm found that multiple mineral sources were provided but that inappropriate mineral was provided to pregnant does; no unusual goitrogenic plants were found within feed samples.

Goiter can, in general, be attributable to one of two imbalances: a deficiency in bioavailable iodine, or a profound excess of bioavailable iodine.  Deficiency can be related to either an absolute dietary deficiency in iodine, or to the concurrent consumption of antithyroid compounds (or goitrogens), such as low-level exposure to white clover, couch grass, linseed meal, and Brassica spp. (including broccoli, Brussels sprouts, cabbages, kale, turnip, rutabaga, rape, kohlrabi).  Excessive iodine exposure paradoxically results in goiter as a result of serum iodide-mediated inhibition of fusion of thyroidal colloid and lysosomes, disrupting the proteolysis of colloid and release of thyroid hormones T4 and T3.

Congenital goiter is typically associated with hyperplastic goiter and the dam often shows no obvious signs of thyroid dysfunction. Gestation is often prolonged and complicated by dystocia, placental retention, and fetal weakness progressing to mortality within a few days of labor.  Kids, lambs, and piglets are most susceptible, while calves and carnivores are resistant.  Common findings in susceptible species are thyroid enlargement, alopecia, and myxedema; a proportion of animals may die as a result of asphyxiation secondary to tracheal compression by the enlarged thyroids.

Diagnosis of iodine deficiency disorders (IDD) has been based on morphological, histological and biochemical indices of iodine status. The evaluation of iodine status is important because of the large potential for dietary deficiency, the possibility of toxicity, and also because of the transfer of iodine to human food products, especially dairy products. While initial diagnosis of goiter-related periparturient mortality may at first seem simple, adequate clinical assessment of the underlying cause typically requires two additional steps beyond post-mortem assessment of the goat kids: serum sampling from the dam (to identify whether goiter relates to iodine deficiency or excess), and then assessment of maternal diet for points of exposure to excessive or deficient iodine levels, or to potential goitrogens.   AHL

Figure 1. Ventral neck of one goat kid at postmortem.  There are two roughly symmetrical 7 cm x 2 cm x 2 cm masses (representing enlarged thyroid glands) at the caudal angle of the mandible and extending over 50% of the length of the neck.