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The objectives of these studies were to identify associations between udder half defects (hard or lump) and bacteria isolated from milk or mammary tissue swabs, to compare with samples from normal udder halves at different physiological time points and to compare bacterial species isolated via milk and swabs of mammary tissue from within the same udder halves. A total of 1054 samples were aseptically collected from each udder half of 199 non-dairy breed (Romney) ewes from three different studies (Study A, n = 77; Study B, n = 74; and Study C, n = 48). Conventional bacterial culture and MALDI-ToF mass spectrometry were used for bacterial identification. Of the 225 samples from which bacteria were isolated, Mannheimia haemolytica and Streptococcus uberis were the dominantly identified species from defective udder halves, whereas coagulase-negative staphylococcus (CNS) species, mostly Staphylococcus simulans and Staphylococcus chromogenes, were more frequently isolated from normal udder halves. The ongoing presence of bacterial species over time was variable, although less frequently identified species showed less stability over time. A very high agreement (91.5%) of bacterial species identified was observed between the mammary tissue swab and udder half milk samples during post-weaning. In summary, palpable udder half defects were associated with bacterial positivity, and the ongoing presence of the bacteria over time was dependent on the species involved. Hence, culling ewes with palpable udder half defects that had more stable bacterial species could contribute to reducing the recurrence of palpable defects or mastitis.

A total of 1039 non-dairy breed (Romney) ewes were enrolled in two studies to assess the changes in udder half defect status (hard, lump, or normal) over time and to predict the risk of future udder half defect occurrence. In the first study (study A), udder halves of 991 ewes were assessed utilizing a standardized udder palpation method and scored four times a year, for two successive years (pre-mating, pre-lambing, docking, and weaning). The second study (study B) assessed the udder halves at pre-mating, and at six weekly intervals in the first six weeks of lactation in 46 ewes that had defective and normal udder halves. Udder half defect change over time was visualized via lasagna plots, and multinomial logistic regression was used to predict the risk or probability of udder half defect occurrence. In the first study, the highest occurrence of udder halves categorised as hard was observed at either pre-mating or docking. Udder halves categorised as lump had their highest occurrence at either docking or weaning. Udder halves detected with a defect (hard or lump) at pre-mating were more likely (RRR: 6.8 to 1444) to be defective (hard or lump) at future examinations (pre-lambing, docking, or weaning) within the same year or pre-mating the following year, compared to udder halves categorised as normal. In the second study, the change of udder half defect type over the first six weeks of lactation was variable. However, it was observed that the udder half defects, particularly udder halves categorised as hard, decreased during lactation. Failure to express milk in udder halves in early lactation was associated with a higher occurrence and persistency of udder half defects. In conclusion, the occurrence of diffuse hardness or lumps in an udder half changed over time, and the risk of future occurrence of a defect was higher in udder halves previously categorised as either hard or lump. Hence, it is recommended that farmers identify and cull ewes with udder halves categorised as hard and lump.

In non-dairy ewes, udder defects hinder the survival and weight gain of their pre-weaned lambs. The objectives of this study were to determine the effects of palpable udder defects on milk yield, somatic cell count (SCC), and milk composition in non-dairy Romney ewes. Ewes with a history of udder defects or normal udders were selected for the study. Of a total of 48 ewes that lambed, 30 ewes reared at least one lamb, and were milked six times, once weekly, for the first six weeks of lactation. Udder halves were palpated and scored at each milking event. Multivariate linear mixed models examined the impacts of udder defects on udder-half and whole-udder milk yield, SCC, and milk composition (fat, protein, lactose, total solids, and solids non-fat (SNF)). Across the six examinations, 24.7% of the total 352 udder-half examinations were observed to be defective. Udder halves that were defective at least once produced on average 57.9% less (p < 0.05) milk than normal udder halves, while normal udder halves with a contralateral defective half yielded 33.5% more (p < 0.05) milk than normal udder halves. Successive occurrence of both hard and lump udder defect categories in an udder-half, udder defect detection early in lactation, and a high frequency of udder defect detection were all associated with udder-half milk yield loss (p < 0.05). At the whole-udder level, no differences in milk yield (p > 0.05) were observed between those with one udder-half defective and both normal udder-halves. However, udders in which one udder half was categorised as hard but progressed to lump and remained as lump until 42 days of lactation produced less (p < 0.05) milk compared with normal udders. With the exception of SNF, there were no significant associations (p > 0.05) between milk composition parameters and udder defect. Overall, these findings emphasise the importance of udder health in non-dairy ewes and the potential effect of udder defects on their lambs.

Papillomaviruses (PVs) cause around 5% of all human cancers, including most cervical cancers and around a quarter of all oral cancers. Additionally, some studies have suggested that PVs could cause a proportion of human lung, breast, and bladder cancers. As PVs have been associated with skin cancer in cats and, more rarely, dogs, it was hypothesized that these viruses could also contribute to epithelial cancers of the lung, mammary gland, and bladder of dogs and cats. Formalin-fixed paraffin-embedded samples of 47 canine and 25 feline cancers were examined histologically for evidence of PV infection. Additionally, three sets of consensus PCR primers were used to amplify PV DNA from the samples. No histological evidence of PV infection was visible in any of the cancers. DNA from a bovine PV type was amplified from one sample, while two different samples were found to contain human PV DNA. However, these were considered to be contaminants, and no canine or feline PV types were amplified from any of the cancers. These results suggest that PVs do not frequently infect the lung, mammary gland, or bladder of dogs and cats and therefore are unlikely to be significant factors in the development of cancers in these tissues.