A 3-mo-old, female Boer goat was presented because of respiratory difficulties. Tachypnea and inspiratory dyspnea were noted during physical examination. Thoracic radiographs were unremarkable; however, upper airway and nasal passage radiographs revealed a soft tissue mass within the nasal passages. The patient underwent cardiorespiratory arrest and did not respond to resuscitation efforts during endoscopy. A large, pedunculated, semi-firm mass originated from the soft palate and obstructed 90% of the nasopharynx on autopsy. Histologically, the mass was composed of primitive cells that multifocally formed tubules and glomeruloid structures intermingled with areas of fusiform and blastemal cells. The neoplastic cells were positive for cytokeratin (tubular and glomeruloid cells), vimentin (fusiform population and blastemal cells), and Wilms tumor 1 protein (glomeruloid structures) on immunohistochemistry, consistent with a triphasic nephroblastoma. To our knowledge, nasopharyngeal nephroblastoma has not been reported previously in any species.

Canine thyroid carcinomas are relatively common malignant endocrine neoplasms in dogs derived from either thyroid follicular cells (forming follicular thyroid carcinomas) or medullary cells (parafollicular, C-cells; forming medullary thyroid carcinomas). Older and recent clinical studies often fail to discriminate between compact cellular (solid) follicular thyroid carcinomas and medullary thyroid carcinomas, which may skew conclusions. The compact subtype of follicular thyroid carcinomas appears to be the least differentiated subtype of follicular thyroid carcinomas and needs to be differentiated from medullary thyroid carcinomas. This review includes information on the signalment, presentation, etiopathogenesis, classification, histologic and immunohistochemical diagnosis, clinical management, and biochemical and genetic derangements of canine follicular and medullary carcinomas, and their correlates with human medicine.

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Case summary A 2-year-old castrated male domestic longhair cat presented for acute, diffuse, flaccid paralysis. Thoracic and abdominal radiographs, biochemistry panel and complete blood count were unremarkable. Titers to Toxoplasma gondii, myasthenia gravis radioimmunoassay testing and creatinine kinase levels were within normal limits. The most likely differentials included acute toxicity (coral snake envenomation, organophosphate toxicity), botulism and, less likely, acute polyradiculoneuritis. A thorough physical examination revealed a single engorged tick attached to the ventral neck of the cat, which was later identified as an adult female Ixodes species. Topical fipronil and (S)-methoprene was administered. Over the next 48 h, the cat recovered full motor function and at 5 days post-tick removal the cat had resumed all normal activities. Relevance and novel information Tick paralysis is considered endemic in Australia by bites from, most commonly, the Ixodes holocyclus tick. However, this phenomenon is rarely reported in the USA. This is the first report of a domestic cat suffering from acute tick paralysis in North America.