Cutaneous viral plaques and bowenoid in situ carcinomas (BISCs) in cats are thought to be caused by papillomavirus (PV) infection. There is evidence that PVs may also cause some feline invasive squamous cell carcinomas (ISCCs). Human oncogenic PVs degrade retinoblastoma (RB) protein, impairing cell cycle control. Loss of RB function also increases p16(CDKN2A) protein (p16), and increased p16 immunoreactivity within a human oral ISCC indicates that the neoplasm was caused by PV infection. In the present study, p16 immunoreactivity was evaluated in 14 feline viral plaques, 14 BISCs, 7 non-solar-induced ISCCs, 11 solar-induced ISCCs, and 14 trichoblastomas. Increased p16 was present within all viral plaques, BISCs, and non-solar-induced ISCCs. In contrast, little p16 immunoreactivity was visible in the solar-induced ISCCs or trichoblastomas. PV DNA was consistently amplified from viral plaques, BISCs, and non-solar-induced ISCCs. However, just 5 solar-induced ISCCs and 1 trichoblastoma contained PV DNA. Given that both increased p16 immunoreactivity and PV DNA were present within viral plaques, BISCs, and non-solar-induced ISCCs, all 3 may be caused by PV infection. This suggests that feline non-solar-induced ISCCs may develop as a result of neoplastic progression from viral plaques and BISCs. Whether PVs promote this progression is unknown; however, evidence from this study suggests the PV that is associated with viral plaques and BISCs is able to disrupt the p16-RB pathway and therefore could have oncogenic potential. Immunohistochemical detection of p16 appears to be a useful technique to investigate the role of PVs in feline skin disease.

Treatment using thalidomide may improve survival of dogs with splenic haemangiosarcoma and should be considered a possible adjuvant therapy.

Solitary and multiple cutaneous and mucocutaneous masses were identified in 5 of 24 captive African lions (Panthera leo) over a 6-month-period. All masses were surgically excised, and all were histologically similar to equine and feline sarcoids. DNA was extracted from formalin-fixed, paraffin-embedded tissue. Polymerase chain reaction amplified DNA sequences that had been previously detected in feline sarcoids and clinically normal bovine skin. All lions had been fed a diet that included bovine carcasses that had not been skinned. Since the cessation of feeding bovine carcasses with cutaneous lesions, no additional skin lesions have been observed within any of the lions. Herein is described the clinical, gross, and histopathological findings of sarcoids in 5 captive lions. As the causative papillomavirus most likely has a bovine definitive host, it is hypothesized that the lions were exposed to the virus by feeding on bovine carcasses with skin still attached.

The results provide additional evidence that BISCs develop at a younger age in Devon Rex cats and that BISCs in Devon Rex cats have a more aggressive behaviour than BISCs in other cat breeds. These unusual features should be considered when evaluating and treating skin disease in Devon Rex cats. The detection of FcaPV-2 gene expression in the lung neoplasms suggests a potential role of FcaPV-2 in the development of metastatic disease. However, the absence of FcaPV-2 gene expression in two cutaneous SCCs suggests that other factors could have also promoted cancer development.

Abstract. A 7-year-old dairy cow presented with clinical signs of neurologic disease. Despite treatment with penicillin, the cow died 36 hours after initial presentation. Necropsy examination revealed multiple foci of hemorrhage within the cerebrum and thickened meninges. Additionally, endometritis and consolidation of approximately 30% of both lungs was observed. Histology revealed necrotizing vasculitis, infarction, and hemorrhage within sections of the brain, uterus, and lung. Large numbers of intralesional fungal hyphae were visible. Because only formalin-fixed tissue was available, polymerase chain reaction was used to make an etiologic diagnosis of Mortierella wolfii.