Economic effect of pneumonia and pleurisy in lambs in New Zealand.

AIM: To estimate the cost of pneumonia and pleurisy in lambs to the sheep industry in New Zealand, in order to provide a reference for future cost-benefit calculations for control programmes to reduce the incidence of pneumonia. METHODS: An estimate of the economic cost of pneumonia and pleurisy in lambs was based on: cohort studies of the association between growth rate and the extent of pneumonic lesions at slaughter (n=14 flocks), the prevalence of moderate to severe (MS) pneumonia (> or =10% lung surface area affected) and pleurisy (n=1,719 flocks), the correlation between the prevalence of MS pneumonia and economic loss at the flock level, and data on annual slaughter statistics and carcass value in New Zealand. A stochastic spreadsheet model was developed and run with 1,000 iterations. Input variables represented by probability distributions were growth rate, average cost of loss according to the prevalence of pneumonia per month, carcass value, prevalence of pleurisy, and carcasses downgraded for pleurisy, and annual national slaughter statistics. The output was a posterior distribution of the annual cost of disease. RESULTS: The cost of pneumonia only included the loss associated with reduced growth rate, while mortality due to pneumonia was assumed to be low and was ignored. The cost of pleurisy included the loss associated with downgraded or condemned carcasses. Thus, the simulated annual average cost of pneumonia was NZ$28.1 (95% CI=NZ$15.0-42.0) million, and that of pleurisy NZ$25.1 (95% CI=NZ$10.2-48.1) million. The combined cost of pneumonia and pleurisy averaged NZ$53.2 (95% CI=NZ$32.4-78.9) million. The parameters with the greatest impact on the combined cost of pneumonia and pleurisy were prevalence of pleurisy between March and May, and cost of reduced growth due to pneumonia for lambs slaughtered in June. CONCLUSIONS: The average cost of pneumonia and pleurisy to the sheep industry in New Zealand due to reduced lamb growth and decreased carcass value is likely to be between NZ$32.4 and $78.9 million. This is a conservative estimate, omitting mortalities, indicating that pneumonia and pleurisy have substantial economic impact on sheep farming in New Zealand. Considering that 23,833,000 lambs were slaughtered in 2003/2004 (average value $65.56/lamb), this cost would equate to NZ$1.36-3.31 per lamb. CLINICAL RELEVANCE: Pneumonia and pleurisy are common diseases in lambs in New Zealand, leading to substantial economic loss to producers.

Flock-level case-control study of slaughter-lamb pneumonia in New Zealand.

Subclinical pneumonia is common in production lambs, and causes reductions in growth rate. We selected farms from meat-inspection records of three New Zealand abattoirs from December 2000 to May 2001 to study risk factors for flocks having >or=3% of their lambs with >or=10% of the lung surface with lesions, compared to flocks with a zero lamb-level prevalence of such pneumonia. A questionnaire of management practices was mailed to participating managers of case and control farms and we received responses from 132/192 (69%) cases and 181/300 (60%) in control farms. Risk factors for case farms were shearing lambs on the day of weaning (OR 6.4), breeding ewe replacements on-farm (OR 4.0), and the percentage of lambs sold between March and May (OR 1.0 for <23% sold (reference category), OR 3.9 for 23-42% sold, OR 2.7 for 43-64% sold, OR 4.3 for >64% sold). Protective factors included: grazing lambs at a fixed stocking rate after weaning (OR 0.4), injecting lambs with vitamin B12 at the time of docking (OR 0.4), and at the time of weaning (OR 0.3). Path analysis was used to show important associations between risk and protective factors differentiated according to time (e.g. before and after birth, at weaning and during growth on pasture). Flocks breeding their own ewe replacements were more likely to shear lambs at weaning, were less likely to buy lambs post-weaning and more likely to have ill-thrift present in >5% of lambs post-weaning. The purchase of lambs post-weaning was indirectly associated with greater odds of pneumonia at slaughter.

Effect of vaccinating lambs against pneumonic pasteurellosis under New Zealand field conditions on their weight gain and pneumonic lung lesions at slaughter.

In a field trial, 9174 lambs from seven commercial sheep flocks with a history of subclinical pneumonia were either vaccinated with Ovipast Plus (Intervet) or given a placebo by systematic random allocation; they were vaccinated twice at an interval of four to six weeks and grazed on pasture in the same paddocks. They were weighed at the first vaccination, 11 and 23 weeks later, and one to three days before they were slaughtered. The extent of the pneumonic lesions in their lungs was scored visually postmortem. A subset of pneumonic lung samples was examined bacteriologically and histopathologically. There were no statistically significant differences between the pneumonic lesions at slaughter or the mean average daily weight gains of the vaccinated and placebo-treated lambs between 11 and 23 weeks or between first vaccination and slaughter. The vaccinated lambs had a lower mean daily gain between first vaccination and 11 weeks. The extent of pneumonic lesions at slaughter was negatively correlated with the mean daily gain between first vaccination and slaughter. There were no significant differences between the frequency of isolation of Mannheimia (Pasteurella) haemolytica and Pasteurella trehalosi or the histopathological classification of disease between pneumonic lung samples from the placebo-treated and vaccinated lambs.

Hierarchical and spatial analyses of pneumonia-lesion prevalence at slaughter in New Zealand lambs.

We recorded lesions of moderate-to-severe pneumonia (>or=10% lung surface area affected; "pneumonia") in 1,899,556 lambs submitted to three New Zealand abbatoirs between December 2000 and September 2001. The average prevalence of pneumonia ranged between 7 and 13%, by abbatoir. We ran a two-level mixed-effects binomial logistic-regression model with the prevalence of pneumonia as the outcome, and adjusting for abbatoir and month. The intracluster correlations for batch (slaughter lambs from the same farm sent at the same time) and farm were 31.3 and 12.4%, respectively. (We also noted threefold differences in odds across abbatoirs, and >30-fold differences among slaughter months.) Case flocks (those in the upper quintile of pneumonia prevalence) generally were not clustered in the spatial incidence-risk analysis (after adjusting for flock-level and batch level effects, and as compared to flocks in the lower two quintiles). We therefore concluded that the risk of moderate-to-severe pneumonia-lesion prevalence detectable at slaughter of lambs was determined at the flock and batch level, rather than at the spatial level.

Characterization of the in vivo function of TNF-alpha-related apoptosis-inducing ligand, TRAIL/Apo2L, using TRAIL/Apo2L gene-deficient mice.

To define the normal physiological role for the TRAIL/Apo2L in vivo, we generated TRAIL/Apo2L gene-targeted mice. These mice develop normally and show no defects in lymphoid or myeloid cell homeostasis or function. Although TRAIL/Apo2L kills transformed cells in vitro, TRAIL/Apo2L(-/-) mice do not spontaneously develop overt tumors at an early age. However, in the A20 B cell lymphoma-transferred tumor model, TRAIL/Apo2L(-/-) mice are clearly more susceptible to death from overwhelming tumor burden, due to increased lymphoma load in the liver. A20 tumors are susceptible to TRAIL/Apo2L killing in vitro, indicating that TRAIL/Apo2L may act directly to control A20 cells in vivo. Despite the fact that TRAIL binds osteoprotegerin and osteoprotegerin-transgenic mice are osteopetrotic, TRAIL/Apo2L(-/-) mice show no evidence of altered gross bone density, and no alterations in frequency or in vitro differentiation of bone marrow precursor osteoclasts. Moreover, leucine zipper TRAIL has no toxicity when repeatedly administered to osteoprotegerin(-/-) mice. Thus, TRAIL/Apo2L is important in controlling tumors in vivo, but is not an essential regulator of osteoprotegerin-mediated biology, under normal physiological conditions.