JPC SYSTEMIC PATHOLOGY
Signalment (ACVP# 75-28): 5-month-old Hereford calf
HISTORY: This animal was from a feedlot containing 42 cattle. Over a period of 2 weeks, 4 calves died. The gross lesions consisted of hemorrhagic edematous foci in the muscles with gaseous crepitation of the adjacent tissues.
HISTOPATHOLOGIC DESCRIPTION: Skeletal muscle: Affecting greater than 80% of the skeletal muscle there is marked expansion of fascial planes (epimysium, perimysium, and endomysium) up to 300um, with separation of muscle fascicles and individual myocytes by moderate to abundant amounts of fibrin, hemorrhage, and edema, admixed with degenerate neutrophils and karyorrhectic and cellular debris (necrosis). There is extensive monophasic myofiber acute necrosis characterized by hypereosinophilic, fragmented sarcoplasm and myofibrils, loss of cross striations, pyknosis, and karyolysis. Multifocally, there are fewer areas of myofiber degeneration characterized by myofiber swelling and vacuolation. Multifocally there are ectatic lymphatics, and variably sized, up to 2mm diameter, well demarcated clear spaces that compress adjacent myocytes (emphysema). Within adjacent adipose tissue, there is expansion by a neutrophilic serohemorrhagic infiltrate admixed with abundant 2-4um basophilic bacilli and beaded eosinophilic material (fibrin).
Lymph node: Expanding the subcapsular sinus, filling trabeculae, and obscuring follicular architecture, are numerous erythrocytes and fewer neutrophils.
- 1. Skeletal muscle: Myositis, necrohemorrhagic, acute, diffuse, severe, with emphysema, edema, and numerous 2-4um intralesional bacilli, Hereford, bovine.
- Lymph node: Draining hemorrhage, acute, diffuse, severe.
ETIOLOGIC DIAGNOSIS: Clostridial myositis
CAUSE: Clostridium chauvoei
SYNONYMS: Black-quarter, emphysematous gangrene
- Economically important disease of pastured ruminants that occurs in warm wet months (summer) and is most common in beef cattle 9-months to 2-years of age that are rapidly growing and on a high plane of nutrition; often affects several animals within a few days and approaches a 100% case-fatality rate
- Spore forming, gram-positive, anaerobic bacillus; spores ubiquitous in soil, highly resistant to environmental changes and disinfectants, and persist in the environment for many years
- Recent report of Clostridium chauvoei being transmitted to a fetus in utero
- Spores ingested during grazing > pass through the intestinal mucosal barrier > enter the bloodstream > spores disseminate to tissues, especially striated muscle and liver, and are dormant
- Spores germinate and multiply in low oxygen tension environments (trauma, hemorrhage, degeneration, necrosis) > toxin production > capillary damage, hemorrhage, edema > local severe necrotizing myositis and systemic toxemia
- Exotoxins include:
- Alpha toxin: Oxygen-stable hemolysin; necrotizing and hemolytic
- Beta: DNAse; hydrolyzes phosphodiester bonds in DNA
- Delta: Oxygen-labile hemolysin; forms pores in lysosomal membranes
- Gamma: Hyaluronidase; hydrolyzes hyaluronate linkages
- Neuraminidase: Removes sialic acids from glycoconjugates
TYPICAL CLINICAL FINDINGS:
- Frequently, animals are found dead without any observed clinical signs
- Typical initial signs are severe lameness, depression, anorexia, rumen stasis, fever (106oF), tachycardia (100-120 bpm), and elevated CK and AST
- Occasionally subcutaneous crepitation (emphysema) over the thigh, rump, loin, or shoulder
- Signs progress rapidly and include tremors, dyspnea (pulmonary edema) and death (circulatory collapse) in 12-36 hours; there is often a characteristic stiff extension of the affected limbs shortly after death
TYPICAL GROSS FINDINGS:
- Gross lesions vary with the age of the lesion; in earlier lesions muscles are dark red to red-black and moist at the periphery, are distended by serous/serohemorrhagic exudate, and are wet on cut surface; later lesions muscles are red-black, dry, friable, porous, and emphysematous, with a characteristic rancid butter odor (from butyric acid)
- Especially the large skeletal muscles of the pectoral and pelvic areas
- May affect any striated muscle: Heart, diaphragm and tongue
- Fibrinohemorrhagic pleuritis without pneumonia; pericarditis; rapid post-mortem autolysis of liver, kidney and endocrine glands
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Monophasic muscle necrosis
- Focally extensive areas of muscle fibers with coagulation necrosis and fragmentation; interstitial edema; hemorrhage; gas bubbles
- Gram-positive bacilli (Clostridium chauvoei) are only occasionally evident
- Clostridium septicum can proliferate rapidly after death and obscure chauvoei
ADDITIONAL DIAGNOSTIC TESTS:
- Fluorescent antibody test on tissue smears
- Culture: Gram positive (catalase negative); strict anaerobe
- One step PCR technique for wet tissue and cultures
- Peroxidase-antiperoxidase immunohistochemical technique to identify Clostridium chauvoei in formalin-fixed paraffin-embedded tissues
- Pseudoblackleg/stable blackleg (Clostridium septicum): Multiple areas of deep-seated myonecrosis and hemorrhage in widely separated muscles without a detectable wound; less severe than blackleg, only occasional small gas bubbles; bloody gelatinous exudate
- Malignant edema (gas gangrene): Ruminants, horses, and swine especially susceptible; carnivores rarely affected; caused by Clostridium septicum, Clostridium perfringens, Clostridium novyi, Clostridium sordelli and Clostridium chauvoei acting individually or in combination; serohemorrhagic myositis and cellulitis with large gaseous and/or edematous areas next to wounds; typically characterized as a cellulitis rather than myositis
- Black’s disease (big head, Clostridium novyi): In big head of sheep, penetrating wounds on head establish the initial anaerobic environment; in cattle and sheep, black disease is associated with fluke migration (Fasciola hepatica) in the liver
- White muscle disease: Young animals; associated with vitamin E and/or selenium deficiency; chalky white striations, degeneration, and necrosis of cardiac and skeletal muscle
- Ionophore toxicity (monensin): Cardiac and skeletal muscle necrosis; multifocal monophasic necrosis with regeneration (skeletal muscle) or fibrosis (cardiac muscle)
- Plant toxicity (Cassia occidentalis, coffee weed): Pale areas within skeletal and cardiac muscle; multifocal areas of necrosis with little to no mineralization
- Eosinophilic myositis: May be a hypersensitivity reaction to Sarcocystis infection; green discoloration of affected muscles because of many eosinophils; myofiber necrosis
- Trueperella (Arcanobacterium) pyogenes: Abscesses in skeletal muscles, primarily of the hind limbs, leading to swelling and lameness; encapsulated intramuscular abscess; diffuse purulent cellulitis extending down tissue planes; thick yellow-green, foul smelling pus; myonecrosis and fibrosis
- Protozoal myopathy (Sarcocystis): Common incidental finding in skeletal muscle and cardiac myofibers; no inflammatory response unless cysts rupture
Sudden death in cattle:
- Malignant edema
- Anthrax (Bacillus anthracis): Black, tarry, unclotted blood from external body orifices, no subcutaneous crepitation; large numbers of typical organisms usually identifiable on blood smears
- Bacillary hemoglobinuria (Clostridium hemolyticum): Large focal area of necrosis in the liver along with evidence of hemoglobinuria
- Dicumarol poisoning: Ingestion of moldy sweet clover (Melilotus ), or moldy sweet vernal (Anthoxanthum odoratum) hay: Multiple fresh hematomas in the carcass with absence of gross or histologic evidence of necrosis
- Other causes of sudden death: Grain overload, lightning strike
- Sheep: Occurs in all age; often secondary to wounds from shearing, tail docking, castration, or dystocia; deep, localized muscle lesions with little edema or gaseous crepitation; less common than in cattle
- Horses: Pectoral edema, stiff gait, incoordination; not well characterized
- Ratites: Paralytic disease characterized by recumbency, muscular weakness, dyspnea and death in ostriches, with isolation of Clostridium chauvoei from necrotic lesions in the liver and areas of intestinal hemorrhage
- Outbreaks of the disease have been reported in deer
- Abreu CC, Blanchard PC, Adaska JM, et al. Pathology of blackleg in cattle in California, 1991-2015. J Vet Diag Invest. 2018;30(6):894-901.
- Abreu CC, Edwards EE, Edwards JF, et al. Blackleg in cattle: A case report of fetal infection and a literature review. J Vet Diag Invest. 2017;29(5):612-621.
- Constable PD, Hinchcliff KW, Done SH, Grunberg W. Veterinary Medicine. 11th ed. St Louis, MO: Elsevier Ltd; 2017:1430-1432.
- Cooper BJ, Valentine BA. Muscle and Tendon. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. St. Louis, MO: Elsevier; 2016:230-34.
- Valentine BA. Skeletal muscle. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Elsevier Inc; 2017:926, 933, 940-941.