Pets may contract foodborne pathogens, including Salmonella, Listeria monocytogenes, and Shiga toxin-producing Escherichia coli (STEC), from their diet, environment, and infected humans and animals. 17,18,20 A 2014 study reported Salmonella, L. monocytogenes, and STEC in 7.7%, 16.3%, and 4.1%, respectively, of 196 samples of commercial raw pet foods tested. 18 In addition, a 2017 multi-laboratory study of Salmonella prevalence in pets demonstrated that dogs testing positive for Salmonella were more likely to have consumed raw food than cooked food. 20 The U.S. Food and Drug Administration (FDA; https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm403350.htm) and the Centers for Disease Control and Prevention (https://www.cdc.gov/ salmonella/schwarzengrund_faq.html) have issued statements to consumers that feeding raw meat diets to pets may pose a public health risk. Despite the public health risk, previous surveys on pet feeding practices in the United States, Canada, and Australia indicate that 16-30% of dogs and 9.6% of cats may receive raw diets or bones. 5,14 Infected animals, however, may not show clinical signs, complicating the diagnosis of pet foodborne illness. 20 Because of the potential for human exposure, identifying and diagnosing pet foodborne illness is crucial to protecting animal and human health. 18 We report the results of 2 case investigations involving 3 breeders, each with pet illness associated with consumption of raw pet food. For each case investigation, FDA received consumer complaints either through the FDA Safety Reporting Portal (https://www.safetyreporting.hhs.gov/) or through a FDA District Office. The FDA Center for Veterinary Medicine evaluated the complaints (https://www.fda.gov/Safety/ ReportaProblem/QuestionsandAnswersProblemReporting/ ucm056069.htm), and the FDA Veterinary Laboratory Investigation and Response Network (Vet-LIRN; https://www.fda. gov/AnimalVeterinary/ScienceResearch/ucm247334.htm) requested medical records and conducted dietary and environmental exposure interviews to obtain signalment and significant clinical histories from both case investigations (Table 1). Clinical samples, leftover open products, and closed unopened products were tested for foodborne pathogens, primarily Salmonella and Listeria in case 1, with the addition of E. coli in case 2. In both cases, product pathogen testing was 823046V DIXXX10.1177/1040638718823046Whole genome sequencing to confirm pet foodborne illnessJones et al.

Spinal cord glioma is uncommonly reported in dogs. We describe the clinicopathologic and diagnostic features of 7 cases of canine spinal cord glioma and briefly review the veterinary literature on this topic. The median age at presentation was 7.2 y. Six females and 1 male were affected and 4 dogs were brachycephalic. The clinical course lasted from 3 d to 12 wk, and clinical signs were progressive and associated with multiple suspected neuroanatomic locations in the spinal cord. Magnetic resonance imaging of 6 cases revealed T2-weighted hyperintense lesions with variable contrast enhancement in the spinal cord. All dogs had a presumptive clinical diagnosis of intraparenchymal neoplasia or myelitis based on history, advanced imaging, and cerebrospinal fluid analysis. Euthanasia was elected in all cases because of poor outcome despite anti-inflammatory or immunosuppressive treatment or because of poor prognosis at the time of diagnosis. Tumor location during autopsy ranged from C1 to L6, with no clear predilection for a specific spinal cord segment. The diagnosis was based on histopathology and the immunohistochemistry expression of glial fibrillary acidic protein, oligodendrocyte lineage transcription factor 2, 2',3'-cyclic-nucleotide 3'-phosphodiesterase, neuron-specific enolase, synaptophysin, and Ki-67. Diagnoses consisted of 4 cases of oligodendroglioma, 2 cases of gliomatosis cerebri, and 1 astrocytoma. This case series further defines the clinicopathologic features of canine spinal glioma and highlights the need for comprehensive immunohistochemistry in addition to routine histopathology to confirm the diagnosis of these tumors.

A 23-yr-old female spayed bobcat (Lynx rufus) presented with a 1-wk history of hypersalivation. On examination, the right mandible was markedly thickened, the right mandibular dental arcade was missing, and the oral mucosa over the right mandible was ulcerated and thickened. Skull radiographs and fine needle aspirate cytology were supportive of squamous cell carcinoma. The bobcat was euthanized as a result of its poor prognosis. Necropsy confirmed a diagnosis of oral squamous cell carcinoma of the mandible. To the authors' knowledge, this is the first report of oral squamous cell carcinoma in a bobcat.