Newcastle disease (ND) is an endemic disease in Oman’s poultry industry and impacts negatively on food security. However, little is known regarding the potential risks of the disease in backyard poultry. The objectives of this study were to determine the seroprevalence of Newcastle disease virus (NDV) in backyard chickens and the herd-level risk factors in Oman. In total, 1383 serum samples were collected from chickens in 139 flocks from nine governorates. Information on associated risk factors was assessed using a semi-structured questionnaire. The samples were tested using commercial indirect ELISA kits.A logistic regression model was applied to assess the associated risk factors. The bird and flock-level NDV seroprevalence was 33.8% (95% Confidence Interval (CI): 12.8–38.6%) and 57.1% (95% CI: 35.7–71.4%), respectively. The highest seroprevalence of antibody to NDV at bird and flock levels was recorded in North Ash Sharqiyah (38.6%) and Al Buraimi (71.4%), respectively. Also, the lowest seroprevalence at bird and flock levels was recorded in Musandam (12.8%) and South Al Batinah (35.7%), respectively. A significant difference in NDV seroprevalence at flock and bird levels was only recorded in Ad Dakhliyah. Factors associated with higher seroprevalence to NDV included absence of a veterinarian in the farm (OR = 5.3; 95% CI: 2.1, 11.7), usage of dead ND vaccine (OR = 2.3; 95% CI: 1.2–4.2), employment of non-permanent staff (OR = 3.9; 95% CI: 1.5, 10.6) and free entry of visitors (OR = 6.2; 95% CI: 2.0, 20.3). In conclusion, the results of this study revealed a high exposure of backyard chickens to NDV and the identified risk factors could be vital in the prevention and control of the disease in Oman.

Milk producers in Malaysia make extensive use of crossbred Sahiwal Friesian dairy cattle. These animals have, however, been found susceptible to lactation failure. A survey of cows in an experimental herd of F1 Sahiwal Friesian animals indicated that, in 30% of animals, milk yield decreased to negligible levels within the first 8 weeks post partum. Lactation failure was associated with a progressive increase in the amount of residual milk left in the udder after normal milking. By week 3 of lactation, residual milk volume was significantly greater than that in animals that, based on previous lactation history, were not susceptible to lactation failure, and accounted for up to 30% of milk available at the morning milking. The cellular consequences of residual milk accumulation were evident in the activities of acetyl-CoA carboxylase, fatty acid synthetase and galactosyltransferase, key enzyme markers of cellular differentiation, which decreased in glands undergoing lactation failure and were lower than values measured in tissue of control cows. Mammary cell number, estimated by tissue DNA content, was also reduced in animals undergoing lactation failure. These indices of mammary development indicate that lactation failure is the result of premature involution in susceptible animals. Premature involution is a predictable consequence of progressive milk stasis in failing lactation, and attributable to an increase in autocrine feedback by inhibitory milk constituents. The progressive increase in residual milk is, on the other hand, unlikely to be attributable to impaired mammary development. Measurements of milk storage during milk accumulation showed no differences between control and lactation failure cows in the distribution of milk between alveolar and cisternal storage compartments. We conclude that lactation failure in Sahiwal Friesian cows is due to a failure of milk removal, and probably the result of an impaired milk ejection reflex rather than to the glands' milk storage characteristics.