Clostridium septicum dermatitis, cellulitis, and myositis (malignant edema) in swine

Josepha DeLay, Margaret Stalker, Đurđa Slavić, Clint Lichty, Greg Wideman

Animal Health Laboratory, University of Guelph, Guelph, ON (DeLay, Stalker, Slavić); South West Ontario Veterinary Services, Stratford, ON (Lichty, Wideman).

AHL Newsletter 2019;23(3):10.

Sudden (unexpected) death was reported in several grow-finisher pigs from 2 unrelated herds. Most of the affected pigs had well-demarcated 30-50 cm diameter raised purple skin lesions involving mainly the ears, neck, and ventral trunk. Subcutaneous emphysema was palpable in some lesions. Similar skin lesions in a few live pigs expanded rapidly and the pigs’ clinical condition deteriorated, culminating in death or euthanasia. Those pigs treated very early in the disease course, with clinical signs of lethargy and ≤5 cm skin lesions, did survive.

A range of tissue samples, including samples from the margin of affected and non-affected skin and underlying skeletal muscle, were examined histologically, and significant lesions were confined to skin. Epidermis was necrotic (infarcted); dermis and subcutis were expanded by edema, fibrin, and neutrophils; and myocyte bundles were degenerate and surrounded by fibrin and neutrophils. Many long bacilli compatible with Clostridium spp. were visible among the inflammatory debris. Clostridium septicum was cultured in low-to-moderate numbers from skin swabs from each of 4 sampled pigs. Malignant edema caused by C. septicum was confirmed based on the combination of clinical history, gross appearance of skin lesions, histologic lesions, and isolation of the causative bacterium from lesions.

Infection with the anaerobic bacillus C. septicum is an uncommon cause of disease and death in swine, and literature reports of this condition are sparse. C. septicum cellulitis and myositis is known as malignant edema, gas gangrene, or ‘pseudo-blackleg’ due to the clinical and pathologic similarity of the condition to blackleg (clostridial myositis, C. chauvoei) in ruminants. Clostridial exotoxins, particularly alpha toxin (ATX), cause localized tissue necrosis and inflammation, and systemic toxemia results in death. Fibrinohemorrhagic peritonitis and pulmonary edema are present in some animals. Wound infection is considered the main portal of entry for bacteria, although activation of dormant intramuscular clostridia and bacteremia secondary to gastrointestinal mucosal injury are also possible. Concentration of lesions in the head and neck area of these pigs supports contamination of fighting wounds in this case. Lesions may also be associated with injection sites. Both histopathology and bacterial culture are important for confirmation of a diagnosis of C. septicum cellulitis and myositis, because the organism may also be present in tissues as a postmortem invader unassociated with lesions. Penicillin is the antibiotic of choice for treatment of animals with suspected C. septicum-associated disease.   AHL

References

Cooper BJ, Valentine BA. Muscle and tendon. In: Maxie MG, ed. Jubb, Kennedy and Palmer’s Pathology of Domestic Animals. 2016. St. Louis, MO: Elsevier, 2016;Vol 1:232-233.

Uzal FA, Songer JG. Clostridial diseases. In: JJ Zimmerman et al, ed. Diseases of Swine. 2019:799-801.

Animal Health Laboratory – Toxicology section, University of Guelph, Guelph, ON

AHL Newsletter 2019;23(3):11-12.

Acute deaths were reported in a pig farm after feeding a new diet for 12-24 hours. A non-specified number of animals weighing 35-60 kg died within 24 hours, while sublethally affected animals showed clinical signs consisting of incoordination, stumbling, hind-end weakness, and ataxia. Some tail biting and ear tip necrosis were also noted. Most animals improved upon removal of the diet; however, some were euthanized because of welfare reasons.

Blood work on 1 severely affected animal showed the following biochemical changes: CK: 217,940 U/L (RI: 50 – 3,531), AST: 4,561 U/L (RI: 16 – 65), K: 9.9 mmol/L (RI: 2.1 – 7.1) and P: 3.74 mmol/L (RI: 1.16 - 2.97). Of 7 blood samples tested, 4 consistently showed elevated serum CK and AST activities, compatible with ongoing muscle injury (rhabdomyolysis). Considering clinical presentation, laboratory test results, and history of recent diet change, feed samples were submitted to the Toxicology section of the Animal Health Laboratory (AHL) for ionophore quantification. Samples from 2 different bins contained salinomycin at 320 and 390 µg/g (ppm), respectively; monensin and narasin concentrations were below the limit of quantitation (< 1.0 ppm). The target dose of salinomycin in the feed was 25 ppm, as recommended,¹ however, a mistake was made on the prescription and the final concentration was high enough to cause acute toxicity (reported lethal doses in pigs: 166-720 ppm of feed^2,3). Most survivors had recovered one week after the incident; however, a few animals still showed hind-end weakness and lameness.

Ionophores are feed additives used as coccidiostats or to improve feed efficiency; however, overdose or inadvertent exposure of non-target species can cause toxicity. Clinical signs of salinomycin toxicosis in pigs are typically related to the gastrointestinal and muscular (skeletal more than cardiac) systems. Affected animals commonly have anorexia, lethargy, stiffness, tremors, recumbency, and may be reluctant to move. They may also have diarrhea. Clinicopathologic changes are related to degenerative myopathy consisting of elevated serum CK and AST activities, as well as some electrolyte changes, in particular hyperkalemia. Rhabdomyolysis can also cause myoglobinuria and possibly renal disease as a result of acute tubular damage. Clinical signs may appear within 24 hours, and some animals will continue to show problems after several days or weeks. Prognosis is guarded when the intoxication has caused significant heart damage. Animals surviving the acute phase may recover but weight gain and other parameters might be compromised.

       Table 1. Cases of ionophore toxicosis confirmed at the AHL in recent years.

References

1. (http://www.inspection.gc.ca/animals/feeds/medicating-ingredients/mib/salinomycin-sodium-sal-/eng/1331066179898/1331066230292#a2)

2. Feed-associated toxicants. In: Plumlee KH. Clinical Veterinary Toxicology. Mosby, 2004.

3. Plumlee KH, et al. Acute salinomycin toxicosis in pigs. J Vet Diagn Invest 1995;7:419-420.