Infectious disease contributed to historical declines and extirpations of bighorn sheep (Ovis canadensis) in North America and continues to impede population restoration and management. Reports of pneumonia outbreaks in freeranging bighorn sheep following contact with domestic sheep have been validated by the results of 13 captive commingling experiments. However, ecological and etiological complexities still hinder our understanding and control of respiratory disease in wild sheep. In this paper, we review the literature and summarize recent data to present an overview of the biology and management of pneumonia in bighorn sheep. Many factors contribute to this population-limiting disease, but a bacterium (Mycoplasma ovipneumoniae) host-specific to Caprinae and commonly carried by healthy domestic sheep and goats, appears to be a primary agent necessary for initiating epizootics. All-age epizootics are usually associated with significant population declines, but mortality rates vary widely and factors influencing disease severity are not well understood. Once introduced, M. ovipneumoniae can persist in bighorn sheep populations for decades. Carrier females may transmit the pathogen to their susceptible lambs, triggering fatal pneumonia outbreaks in nursery groups, which limit recruitment and slow or prevent population recovery. The demographic costs of disease persistence can be equal to or greater than the impacts of the initial epizootic. Strain typing suggests that spillover of M. ovipneumoniae into bighorn sheep populations from domestic small ruminants is ongoing and that consequences of spillover are amplified by movements of infected bighorn sheep across populations. Therefore, current disease management strategies focus on reducing risk of spillover from reservoir populations of domestic sheep and goats and on limiting transmission among bighorn sheep.

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Mycoplasma ovipneumoniae is a primary pathogen.

ABSTRACT:Mannheimia haemolytica consistently causes severe bronchopneumonia and rapid death of bighorn sheep (Ovis canadensis) under experimental conditions. However, Bibersteinia trehalosi and Pasteurella multocida have been isolated from pneumonic bighorn lung tissues more frequently than M. haemolytica by culture-based methods. We hypothesized that assays more sensitive than culture would detect M. haemolytica in pneumonic lung tissues more accurately. Therefore, our first objective was to develop a PCR assay specific for M. haemolytica and use it to determine if this organism was present in the pneumonic lungs of bighorns during the 2009-2010 outbreaks in Montana, Nevada, and Washington, USA. Mannheimia haemolytica was detected by the species-specific PCR assay in 77% of archived pneumonic lung tissues that were negative by culture. Leukotoxin-negative M. haemolytica does not cause fatal pneumonia in bighorns. Therefore, our second objective was to determine if the leukotoxin gene was also present in the lung tissues as a means of determining the leukotoxicity of M. haemolytica that were present in the lungs. The leukotoxin-specific PCR assay detected leukotoxin gene in 91% of lung tissues that were negative for M. haemolytica by culture. Mycoplasma ovipneumoniae, an organism associated with bighorn pneumonia, was detected in 65% of pneumonic bighorn lung tissues by PCR or culture. A PCR assessment of distribution of these pathogens in the nasopharynx of healthy bighorns from populations that did not experience an all-age die-off in the past 20 yr revealed that M. ovipneumoniae was present in 31% of the animals whereas leukotoxin-positive M. haemolytica was present in only 4%. Taken together, these results indicate that culture-based methods are not reliable for detection of M. haemolytica and that leukotoxin-positive M. haemolytica was a predominant etiologic agent of the pneumonia outbreaks of 2009-2010.