Papillomaviruses (PVs) are well established to cause hyperplastic papillomas (warts) in humans and animals. In addition, due to their ability to alter cell regulation, PVs are also recognized to cause approximately 5% of human cancers and these viruses have been associated with neoplasia in a number of animal species. In contrast to other domestic species, cats have traditionally been thought to less frequently develop disease due to PV infection. However, in the last 15 years, the number of viruses and the different lesions associated with PVs in cats have greatly expanded. In this review, the PV life cycle and the subsequent immune response is briefly discussed along with methods used to investigate a PV etiology of a lesion. The seven PV types that are currently known to infect cats are reviewed. The lesions that have been associated with PV infections in cats are then discussed and the review finishes with a brief discussion on the use of vaccines to prevent PV-induced disease in domestic cats.

Pasture growth rates of ryegrass, tall fescue and phalaris were compared under combinations of 2 defoliation heights and 3 defoliation frequencies in mowing trials run in spring, summer, autumn and winter over 2 years. Lax defoliation gave on average 15%, 20% and 21% higher pasture growth rates than intense defoliation for ryegrass, tall fescue and phalaris pastures respectively over all seasons. Climate had a major influence on the response of all three pastures to defoliation management. In a dry spring, tall fescue produced most from a 15day cutting interval while for ryegrass and phalaris production was greatest from a 30day interval. In a wet spring, cutting frequency had no etfect, but a significant (P

Mammary gland tumors (MGTs) are common in dogs and show a variable clinical behavior that is difficult to predict. Currently, few immunohistochemical markers have been established to predict the prognosis of a canine MGT. However, p53 immunostaining has been variably reported to be prognostic for canine MGTs. Additionally, while p16^CDK2NA protein (p16) immunostaining has been found to be prognostic for human breast cancers, this marker has never been evaluated as a prognostic marker for canine neoplasms. In the present study, the prognostic utility of p53 and p16 was evaluated in 35 canine malignant MGTs. It was observed that 19 (54%) dogs died due to their MGTs with an overall mean survival time (MST) of 882 days. Seven MGTs showed p53 immunostaining, but this was not significantly associated with death (4 of 7 vs. 15 of 28; p = 0.6) or MST (670 vs. 934 days; p = 0.57). Five dogs had MGTs with no p16 immunostaining, 28 MGTs had intermediate p16 immunostaining, and two MGTs had increased p16 immunostaining. Neither death due to MGT (4 of 5, 14 of 28, or 1 of 2; p = 0.28) nor MST (683, 927, and 307 days; p = 0.31) were significantly associated with p16 immunostaining. Interestingly, p53 immunostaining was significantly associated with an increase or loss of p16 immunostaining. This is the first time that p16 has been evaluated as a prognostic marker for canine neoplasms. While these results suggest that a proportion of canine MGTs develop by cellular mechanisms that alter both p53 and p16 expression, there was no evidence that defects in p53 or p16 alter the behavior of a MGT. Neither p53 nor p16 was found to significantly predict prognosis, although this could reflect the limited number of MGTs included in the study.