Two-year-old female bovine (Bos taurus), breed unknownThis producer had lost 10 head of young cattle (6-18 months of age) over a period
of approximately 10 days. Most cattle were simply found dead; this one was seen staggering, depressed, and died before attending veterinarian could get to the premises.
The animal was in good nutritional and post-mortem condition.Â Age was estimated at approximately 1 year.Â There were multifocal variably sized and irregular shaped purplish-black areas of discoloration of skeletal muscle occurring with random distribution in the caudal neck, brisket, and quadriceps muscles; these were bilateral distribution on both sides of the animal.Â Lesions were present both on the surfaces of the muscles, and deeper into musculature.Â These lesions were quite dry and there was crepitus on palpation.
Skeletal muscle fibers were in varying stages of necrosis, varying from early coagulation necrosis to complete fragmentation and collapse.Â There were large zones of hemorrhage with some aggregates of neutrophils and macrophages were found between muscle fibers, as well as edema fluid.Â Multifocal pockets of emphysema were also seen, primarily in fascial planes.Â Occasional rectangular bacterial organisms were seen, again primarily in fascial planes.
Myositis, necrotizing, due to Clostridium chauvoei (blackleg)
Bacteriology Clostridium chauvoei was detected via both fluorescent antibody and anaerobic culture methods.
The lesions are virtually pathognomonic grossly, and bacterial FA techniques can verify a diagnosis quite rapidly.Â Differential diagnoses would include other clostridial disease (i.e., C.Â septicum or pseudo-blackleg) (3); however, C.Â chauvoe is the only disease that consistently produces gas pockets in the muscles in freshly dead animals, coupled with the prominent areas of discoloration (due to hemolyzed erythrocytes).Â Microscopic lesions are typical, but relatively moderate in severity.Â Death is caused by the production and absorption of a potent exotoxin by the organism, thus causing a toxemia with subsequent muscular hemorrhages and edema.(2,3) The progress of the disease is extremely rapid, thus in some cases it may produce only moderate histologic lesions associated with the toxemia, or they may be widespread and severe, as with this one.Â
This case was submitted because this condition is not commonly seen anymore due to better herd management practices and good vaccines being available and in use in most cattle operations.Â
However, in the Southwestern United States, we do see blackleg occasionally due to some management issues that are unique to our geography and climate.Â In a desert environment, large acreages are required to range (i.e., pasture) cattle; yearling cattle such as these would require a minimum of 40-60 acres per animal, depending upon availability of forage, drought, etc.Â Requirements for cow/calf pairs commonly range from 60-100 acres per animal; hence, a 200 cow herd would require 12,000-20,000 acres (20-30 sections).Â Many operations leave the bulls out with the cows all year, thus having year round calving and calves of many different sizes and weights.Â Thus, these large ranges (often in very rugged and inaccessible country, except by horseback) make doing a gather for any reason difficult, very labor intensive, time consuming, and requires experienced and savvy cowboys.Â As a result, cattle are often only gathered up once a year, usually to select and market heavier calves.Â Obviously, with these types of management problems, installation of a comprehensive herd health (including vaccinations) program is often a hit-and-miss proposition, as was the case with these animals.Â This particular animal had not been vaccinated (nor had any of the others).Â
Skeletal muscle: Myocyte degeneration and necrosis, multifocal, moderate, with hemorrhage, emphysema, and few intralesional bacteria (Fig.Â 4-1)
The pathogenesis of blackleg involves ingestion and passage of spores across the intestinal mucosa, and distribution to tissues where they are stored for long periods in the phagocytic cells.Â The latent spores germinate when there is muscle damage or low oxygen tension.(3) The large muscles of the pelvic and pectoral girdles are most often affected, but any striated muscle is susceptible including the tongue, heart and diaphragm.(3) Grossly, the peripheral tissue is dark red and edematous, while the center is red-black, dry, friable and emphysematous.Â Additional findings include a rancid-butter odor, rapid autolysis of tissues, and fibrinohemorrhagic pleuritis (without corresponding severe pneumonia).Â Histologically, leukocytes are sparse since they are destroyed by the exotoxins.(3)
Differentiating blackleg from pseudo-blackleg, gas gangrene and malignant edema has important management implications.Â Pseudo-blackleg is caused by the activation of latent spores of C.Â septicum in the muscle.Â C.Â septicum proliferates rapidly after death, unlike C.Â chauvoei, so the carcass must be examined immediately after death.Â Pseudo-blackleg lesions are often multiple and are much less emphysematous.Â C.Â septicum also causes hemorrhagic abomasitis (Braxy) in ruminants.(3) Blackleg results from activation of latent spores in muscle, whereas gas gangrene and malignant edema results from contamination of an open wound.(3) Gas gangrene and malignant edema can be caused by a single or mixed infection of C.Â chauvoei, C.Â septicum, C.Â perfringens and C.Â novyi.Â The most common cause of malignant edema is C.Â septicum.Â Ruminants, horses and swine are most susceptible.(3) Malignant edema causes primarily a cellulitis, rather than a myositis as in gas gangrene.Â Also, the gas characteristic of gas gangrene is not a feature of malignant edema.(3) C.Â novyi also causes swelled head in rams, resulting from the infected head wounds received during fighting.(3) C.Â novyi is also the cause of necrotic hepatitis (Black disease) in sheep, and C.Â haemolyticum causes bacillary hemoglobinuria in cattle and sheep.Â In both diseases, clostridial spores are ingested, cross the intestinal mucosam, and remain latent within Kupffer cells.Â Migrating larvae of the common liver fluke, Fasciola hepatica, cause necrosis which leads to activation of the latent clostridial spores.Â The spores release beta toxin, a necrotizing and hemolytic lecithinase (phospholipase C), that causes necrosis of the surrounding tissue and hemolysis in bacillary hemoglobinuria.Â Grossly, there are large pale areas of necrosis surrounded by broad zones of hyperemia.Â The necrotic area in bacillary hemoglobinuria is usually focal and larger than in Black disease.Â Bacillary hemoglobinuria causes intravascular hemolysis with anemia and hemoglobinuria.(2)
1.Â Jones TC, Hunt RD: Veterinary Pathology, 5th ed., pp.Â 579-580.Â Lea Febiger, Philadeplphia, PA, 1983
2.Â Stalker MJ, Hayes MA: Liver and biliary system.Â In: Pathology of Domestic Animals, ed.Â Maxie MG, 5th ed., vol.Â 2, pp.Â 355-356.Â Saunders Elsevier, London, UK, 2007
3.Â Van Vleet JF, Valentine BA: Muscle and tendon.Â In: Pathology of Domestic Animals, ed.Â Maxie MG, 5th ed., vol.Â 1, pp.Â 259-264.Â Saunders Elsevier, London, UK, 2007