Department of Pathobiology, Ontario Veterinary College, University of Guelph, Guelph, ON, Canada.
Vaccine and Infectious Disease Organization, 120 Veterinary Road, Saskatoon, SK, Canada.
Vet Microbiol. 2024 Oct;297:110203. doi: 10.1016/j.vetmic.2024.110203. Epub 2024 Jul 30.
Many cattle infected with Mycoplasma bovis remain healthy while others develop severe chronic respiratory disease. We hypothesized that inflammatory stimuli such as co-pathogens worsen disease outcomes in M. bovis-infected calves. Calves (n=24) were intrabronchially inoculated with M. bovis and either killed bacterial lysate, transient M. haemolytica infection, or saline. Caseonecrotic lesions developed in 7/7 animals given M. haemolytica and M. bovis compared to 2/8 given M. bovis with no inflammatory stimulus, and 6/9 animals given bacterial lysate and M. bovis (P=0.01). Animals receiving M. haemolytica and M. bovis had more caseonecrotic foci in lungs than those receiving M. bovis with no inflammatory stimulus (median = 21 vs 0; P = 0.01), with an intermediate response (median = 5) in animals given bacterial lysate. In addition to caseonecrotic foci, infected animals developed neutrophilic bronchiolitis that appeared to develop into caseonecrotic foci, peribronchiolar lymphocytic cuffs that were not associated with the other lesions, and 4 animals with bronchiolitis obliterans. The data showed that transient lung inflammation at the time of M. bovis infection provoked the development of caseonecrotic bronchopneumonia, and the severity of inflammation influenced the number of caseonecrotic foci that developed. In contrast, caseonecrotic lesions were few or absent in M. bovis-infected calves without a concurrent inflammatory stimulus. These studies provide insight into how caseonecrotic lesions develop within the lung of M. bovis-infected calves. This and other studies suggest that controlling co-pathogens and harmful inflammatory responses in animals infected with M. bovis could potentially minimize development of M. bovis caseonecrotic bronchopneumonia.
许多感染牛支原体的牛仍然保持健康，而其他牛则发展为严重的慢性呼吸道疾病。我们假设，炎症刺激物（如共生病原体）会使感染牛支原体的小牛的疾病结果恶化。将小牛（n=24）经支气管内接种牛支原体，并给予细菌裂解物、短暂性溶血性巴氏杆菌感染或生理盐水。与给予牛支原体而未给予炎症刺激物的 2/8 只动物相比，给予溶血性巴氏杆菌和牛支原体的 7/7 只动物出现了坏死性病变，而给予细菌裂解物和牛支原体的 6/9 只动物（P=0.01）。接受溶血性巴氏杆菌和牛支原体的动物肺部坏死性病变焦点比接受无炎症刺激物的牛支原体的动物更多（中位数=21 对 0；P=0.01），给予细菌裂解物的动物呈中间反应（中位数=5）。除坏死性病变焦点外，感染动物还出现中性粒细胞性细支气管炎，这些细支气管炎似乎发展为坏死性病变焦点，支气管周围淋巴细胞袖套与其他病变无关，4 只动物出现细支气管炎性闭塞。数据表明，在感染牛支原体时短暂的肺部炎症会引发坏死性支气管肺炎的发展，炎症的严重程度会影响发展为坏死性病变焦点的数量。相比之下，在没有同时发生炎症刺激的感染牛支原体的小牛中，坏死性病变很少或不存在。这些研究深入了解了坏死性病变在感染牛支原体的小牛肺部内的发展方式。这些研究和其他研究表明，控制感染牛支原体的动物中的共生病原体和有害炎症反应可能会最大限度地减少牛支原体坏死性支气管肺炎的发生。
