Clostridium perfringens Type A-Induced Myositis with Probable Toxemia in an Adult Walrus (Odobenus rosmarus)
Robert D. Murnane1; Michael J. Kinsel1; Michael B.
Briggs2
Abstract
An 833 kg, nine-year-old, male walrus presented with an eleven day illness. Previous medical history included an enterotomy for foreign body removal after arrival from Russia two years previously, and bilateral tusk extraction one year prior. The tusks were removed as the animal had arrived with fractured tusks, and infected tusk sulci and adjacent, sinuses. Sinusitis persisted after tusk removal. The recent episode of illness presented as depression, partial anorexia, and reluctance to move. This rapidly progressed to complete anorexia with signs of abdominal pain including alternately contracting and relaxing abdominal musculature, and vocalizing on abdominal palpation. A tentative diagnosis of partial impaction was made, as the walrus was stiff passing scant feces. Based on the current, nonspecific clinical signs and recent sinus culture results, the animal was placed on oxytetracycline SID by hand injection in the caudal musculature. Clinical condition continued to deteriorate, and because of this, history of ingesting foreign bodies, and previous enterotomy, the animal was anesthetized and an exploratory laparotomy performed. Laparotomy was unremarkable, and the animal died following surgery.
At necropsy, the animal was in good postmortem and nutritional condition. The majority of the left hamstring muscles and adjacent adipose and subcutis exhibited massive necrosis with multiple, coalescing cavitations 0.5 to 15 cm diameter. Cavitations contained large amounts of putrid, viscous, dark exudate, and frequently there was extensive gas formation. Histologically, necrosis of muscle predominated. There also was multifocal extensive suppuration with a variable granulomatous component, large areas of edema and hemorrhage, and rare early fibroplasia. Large, bacillary bacteria were occasionally observed in the exudate or necrotic debris. Anaerobic culture yielded heavy, pure growth of type A toxin producing Cloandiumper fringens, and aerobic culture was negative. Liver, brain, and heart had moderate, multifocal necrotizing and granulomatous lesions compatible with subacute, toxin-induced necrosis. There also was moderately severe, diffuse, pyogranulomatous, bronchointerstitial pneumonia, with the interstitial pattern predominating. Aerobic culture of lung isolated rare Staphylococcus epidermis which was interpreted as a contaminant Other lesions identified included a chronic, bilateral, caseous sinusitis with unilateral fistula formation associated with incomplete tusk removal, and secondary bone marrow myeloid hyperplasia, diffuse, adrenal conical hyperplasia, and multicentric reactive lymph nodes. Aerobic culture of the sinuses isolated rare to moderate growths of Escherichia coli, Streptococcus lactis, and beta-hemolytic Streptococcus sp.
Death was interpreted to be due to the cumulative effects of the clostridial myositis with toxemia induced necrosis of liver, brain, and heart, moderate respiratory compromise from the pneumonia, and the stress of anesthesia and surgery. The C. perfringens type A toxin is a lecithinase which disrupts cell membranes leading to necrosis. The pneumonia may also have been induced by toxenfia considering the diffuse distribution with a predominant interstitial pattern and lack of isolation of a bacterial pathogen, though other causes are possible. The myositis was likely caused by the trauma and contamination by C. perfringens of an intramuscular injection site. The sinusitis, though chronic and severe, was a localized lesion considered unrelated to the animals death.
Myositis, enterotoxemia, botulism, abscesses and septicemia due to various clostridial organisms have been described in a number of species of pinnipeds. However, to our knowledge this is the first case of myositis due to Clostridium perfringens type A described in a walrus.