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Findings from polymerase chain reaction-based methods have suggested a role of Felis catus papillomavirus 2 (FcaPV-2) in the development of feline cutaneous squamous cell carcinoma (SCC). However, because polymerase chain reaction cannot localize deoxyribonucleic acid or ribonucleic acid within the lesion, it is difficult to differentiate a coincidental FcaPV-2 infection and a causative association. Given that a key event in the pathogenesis of human papillomavirus-induced cancer is the expression of viral E6 and E7 oncogenes, localization of FcaPV-2 E6 and E7 transcription within neoplastic cells in feline SCCs would support a causative role for this papillomavirus. Therefore, RNAscope in situ hybridization was used to localize FcaPV-2 E6 and E7 transcripts in 18 formalin-fixed paraffin-embedded samples of cutaneous SCC. Positive signals were present within 5 of 9 samples (56%) from ultraviolet-protected sites and 0 of 9 samples from ultraviolet-exposed sites. In the 4 in situ hybridization-positive samples that contained adjacent hyperplastic skin, hybridization patterns in these regions were characterized by intense nuclear signals within the superficial epidermis and punctate signals within the basal epithelial layers. However, within the 5 SCCs, punctate signals were present within all layers of the epidermis, with progressive loss of intense nuclear signals within the superficial epidermis. This hybridization pattern is consistent with unregulated E6 and E7 transcription and decreased viral replication and is similar to the pattern observed in human papillomavirus-induced cancers as they progress from hyperplastic lesions containing productive infections to nonproductive neoplasms. These findings support a causative role for FcaPV-2 in the pathogenesis of feline SCC.

Histiocytic proliferative diseases are uncommon in cats, although recently a progressive histiocytosis of the skin with terminal involvement of internal organs has been described in cats. Here we describe 3 cats (2 males and 1 female) with pulmonary Langerhans cell histiocytosis (PLCH). The cats were euthanized due to progressive respiratory clinical symptoms and deterioration. Macroscopically, extensive, multifocal to confluent, pulmonary masses were evident. Infiltration of pancreas (2 cats), kidneys (1 cat), liver (1 cat), as well as tracheobronchial, hepatosplenic, or mesenteric lymph nodes (2 cats) was observed by gross or microscopic examination. The infiltrating cells had histiocytic morphology with cytologic atypia characterized by anisokaryosis and hyperchromasia regionally within infiltrated tissues. Lesional histiocytes expressed vimentin, CD18, and E-cadherin. Expression of E-cadherin was usually markedly reduced in extra-pulmonary lesions, which is consistent with possible down-regulation of E-cadherin associated with distant migration from the lung. Transmission electron microscopy demonstrated intracytoplasmic organelles consistent with Birbeck's granules of Langerhans cells in the lesional histiocytes in all cats, except in the pancreas of one cat. These findings were compatible PLCH with limited organ involvement of humans. It remains unproven whether feline PLCH represents a reactive or neoplastic cell proliferation.

The study objective was to describe the underlying diseases, predisposing factors, clinical signs and clinicopathologic abnormalities associated with thromboembolic disease of non-cardiogenic origin in cats. Necropsy-based retrospective study (1991–2002) Forty-eight cats with thromboemboli that were not associated with significant structural heart disease were identified in a retrospective study using case records from the small animal necropsy service of the University of Pennsylvania, from 1991 to 2002. Thirty-five cats presented for non-specific signs such as lethargy and anorexia while others presented for signs such as paresis (10) or dyspnea (10) that were referable to the location of the thromboemboli. Thromboembolic disease was suspected clinically in 12 of 48 cats. In cases where a single predisposing factor could be identified, thromboemboli were associated with neoplastic (9), infectious (7) and inflammatory (3) disease. Thirteen cats had multiple predisposing factors and no obvious predisposing factor could be identified in 16 cats. The thromboemboli were found in the systemic arteries (12), systemic veins (9), both systemic arteries and veins (7), pulmonary vasculature (7) and in both the pulmonary and systemic circulation (13). Eleven cats either died at home, presented in respiratory or cardiac arrest, or arrested shortly after presentation to the emergency service. Two cats arrested later during hospitalization and the remainder were euthanized (35). No sex or breed disposition was found. There were no significant differences in serum biochemistries, coagulation profiles, lactate, Doppler blood pressure or rectal temperature when groups were compared by primary disorder. Cats with neoplasia as the underlying disorder were significantly older (median 13.5 years, p=0.04). Cats with infectious disease had statistically significant higher white blood cell counts (median 35,000/μl, p=0.03) and cats with inflammatory disease had significantly longer hospital stays (median 3 days, p=0.006). These results suggest that most cats with non-cardiac related thromboemboli often have multiple predisposing factors, non-specific signs and non-specific changes on laboratory parameters. More sensitive tests for hypercoagulability may aid in diagnosing thromboemboli in cats. [ABSTRACT FROM AUTHOR]