Prevalence of cardiac lesions in cases of bovine clostridial myositis

Objective The aim of this retrospective study was to determine the prevalence of cardiac lesions in cases of clostridial myositis. Clostridial myositis (blackleg) is a common cause of death in cattle and is caused by the bacterium Clostridium chauvoei . The characteristic lesions include hemorrhage, necrosis, edema, and emphysema within skeletal muscle and, less commonly, the heart. Results Of the 37 cases of blackleg identified, 26 animals (70.3%) had cardiac lesions, including 4 (10.8%) which had only cardiac involvement without skeletal muscle lesions. Cardiac lesions were characterized as necrotizing myocarditis (n=21), fibrinous to fibrinosuppurative pericarditis, epicarditis, or endocarditis (n=24), or both (n=19). These data demonstrate that, in cases of bovine clostridial myositis, cardiac lesions are common, while heart involvement in the absence of skeletal muscle lesions is uncommon.


Introduction
Clostridial myositis, or blackleg, is caused by the bacterium Clostridium chauvoei. [1][2][3][4][5] Affected cattle are typically pastured and are between 6 and 24 months of age. [3] Ingested spores of C. chauvoei from contaminated soil are transported across the intestinal mucosa, presumably via M cells, and then disseminated to tissues, including striated muscle, where they are phagocytized by resident macrophages and survive intracellularly without deleterious effects. [3,6] In the face of reduced oxygen tension, usually following muscle damage, there is spore germination. [5] The now active bacteria proliferate and produce exotoxins, which result in tissue damage, systemic illness, and death. [5] A flagell um provides m obility and facilitates the spread of the organism . [2] Known toxins 3 include a pore-forming hemolysin (toxin A or CctA), a cholesterol-dependent cytolysin (chauveolysin), a neuraminidase, and others. [ 2 ,4,6] Toxins diffuse into the tissues, resulting in necrotizing myositis. [ 6 ] Although affected animals are typically found dead, some exhibit lameness or muscle swelling prior to dying. Since there are no effective treatments, [5] death typically occurs within 24-26 hours of the onset of clinical signs. [3] At necropsy, affected muscles are dark red to black (necrosis and hemorrhage) with separation of muscle fibers by emphysema and edema; they may sm ell of spoiled butter (rancid) from the production of butyric acid. [ 1− 6] Similarly, the microscopic changes are primarily necrosis and hemorrhage with edema, emphysema, and varying degrees of inflammation. [1,2,5] Associated lesions include fibrinohemorrhagic pleuritis, pericarditis, and mural or valvular endocarditis. If present, valvular endocarditis typically affects the right atrioventricular valve. [ 7] In some cases, necrotizing lesions similar to those seen in skeletal muscle occur in the heart.[1 − 3 ,5,7-10] The prevalence of cardiac lesions in cattle with blackleg in California was recently reported to be 69%. [1] This study aimed to determine the prevalence of cardiac lesions in cases of blackleg in Tennessee.

Materials And Methods
The University of Tennessee Veterinary Medical Center database was searched for cattle with a confirmed diagnosis of blackleg necropsied between 2004 and 2018. Necropsy reports were reviewed for relevant gross and microscopic findings. When available, histology slides of skeletal muscle and/or the heart were examined to confirm the presence of supportive lesions. 4

Results And Discussion
Thirty-seven cases of blackleg were identified. The presence of Clostridium chauvoei in the lesions was confirmed by immunohistochemistry [1] in 25 cases (67.6%), by culture and immunofluorescence in 11 cases (29.7%), and by polymerase chain reaction in 1 case (2.7%). In 32 cases (86.5%), affected skeletal muscle (n=6), heart (n=6), or both (n=20) were examined microscopically, and, when present, the lesions were consistent with blackleg in all of these cases. The remaining 5 cases were diagnosed based on the gross findings in conjunction with culture and immunofluorescence.
The affected muscles were grouped as limbs (any), cervical, thoracic (shoulder, pectorals),  [3] given the rarity of valvular endocarditis in cases of blackleg, the significance of this discrepancy is unclear.
The pathogenesis of clostridial myositis has been recently and thoroughly reviewed. [1,2,7] Cardiac lesions may be the result of hematogenous dissemination of the bacteria and/or toxins to the heart. In rare cases where there is only myocarditis, determining the inciting cause for the decreased oxygen tension required to cause vegetation of the spores is challenging. Some have proposed that concurrent toxicities (ionophore, gossypol) or nutritional deficiencies (Vitamin A, selenium) may precipitate cardiac hypoxia, but to date, supporting evidence of these theories is lacking. [10] Stress of handling and increased cortisol may also allow for germination of latent spores. [10] Interestingly, outbreaks of clostridial myocarditis have been associated with high rainfall in cattle [9,10] and lambs.
[7] The wet conditions may create an anaerobic environment in the soil, which favors the proliferation of C. chauvoei, or may facilitate the dissemination of spores. [2] It is unclear, however, how the wet conditions would favor activation of the spores in the heart. Given the nature of this study, it was not possible to make associations with weather conditions. Involvement of the heart in cases of blackleg is common; however, clostridial myocarditis in the absence of skeletal muscle lesions is uncommon.

Limitations
This is a retrospective study, so correlation of the data with other factors (weather conditions) was not possible.