|Subramaniam, R -|
|Herndon, C -|
|Shanthalingam, S -|
|Dassanayake, R -|
|Bavananthasivam, J -|
|Potter, K -|
|Foreyt, W -|
|Srikumaran, S -|
Submitted to: Veterinary Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 15, 2011
Publication Date: June 22, 2011
Repository URL: http://dx.doi.org/10.1016/j.vetmic.2011.06.008
Citation: Subramaniam, R., Herndon, C.N., Shanthalingam, S., Dassanayake, R.P., Bavananthasivam, J., Potter, K.A., Knowles Jr, D.P., Foreyt, W.J., Srikumaran, S. 2011. Defective bacterial clearance is responsible for the enhanced lung pathology characteristic of Mannheimia haemolytica pneumonia in bighorn sheep. Veterinary Microbiology. 153(3-4):332-8. Interpretive Summary: Pneumonia in bighorn sheep is a population limiting disease and an issue for multiple uses of Western rangelands. The data in this manuscript shows that bighorn compared to domestic sheep are less efficient in removing bacteria from their lungs. This lower efficiency is one likely factor contributing to the severity of bacterial pneumonia in bighorn sheep.
Technical Abstract: The molecular and cellular basis for the enhanced lung pathology and mortality caused by Mannheimia haemolytica in bighorn sheep (BHS, Ovis canadenesis), in comparison to domestic sheep (DS, Ovis aries), is not clear. Polymorphonuclear leukocytes (PMNs) of BHS are four- to eight-fold more susceptible to M. haemolytica leukotoxin-induced cytolysis, which is likely to reduce the number of functional phagocytes in the lung. We hypothesized that enhanced lung pathology is due to defective clearance of M. haemolytica from the lungs of BHS. To test this hypothesis, M. haemolytica (1x107 colony forming units [cfu]) were inoculated intra-tracheally into three groups each of BHS and DS, which were euthanized and necropsied at 4, 12, and 18 h post-inoculation (hpi). Bacterial and leukocyte counts were performed on broncho-alveolar lavage fluid (BALF) collected at necropsy. BALF from BHS euthanized at 4 and 12 hpi contained a significantly higher number of M. haemolytica than that from DS. More importantly, DS did not have any bacteria in BALF at 18 hpi, while the BHS still had significant numbers. As expected, the BHS did exhibit more extensive lung lesions at 12 and 18 hpi when compared to DS. At 18 hpi, necrotic PMNs were observed in the lesional lung tissues of BHS, but not DS. Furthermore, BALF from BHS had significantly lower titers of antibodies to Lkt and surface antigens of M. haemolytica, than that of DS. These findings suggest that the enhanced pathology in BHS lungs is due to defective clearance of M. haemolytica from the lungs.