Blackleg (Clostridium chauvoei)

Blackleg is an acute, highly fatal infectious disease of cattle and occasionally sheep caused by the anaerobic, spore-forming bacterium Clostridium chauvoei. This devastating condition typically affects young, well-nourished cattle between six months and two years of age, causing rapid death often before any clinical signs are observed. The disease is characterized by gas gangrene of the large skeletal muscles, producing the distinctive crepitant swelling that gives the condition its common name. Blackleg represents one of the most economically significant clostridial diseases of cattle worldwide and remains an important cause of mortality despite the availability of effective vaccines.

This disease primarily affects cattle, with the highest incidence in young, rapidly growing animals in excellent body condition. The age distribution shows peak susceptibility between six months and two years, with calves under four months partially protected by maternal antibodies and older cattle developing natural immunity through subclinical exposure. Sheep can also be affected by Clostridium chauvoei, though the disease in sheep typically follows wound contamination rather than the endogenous activation seen in cattle. The geographic distribution is worldwide, with the disease endemic in many cattle-raising regions where the organism persists in soil for extended periods. Environmental factors including soil type, previous contamination, and weather patterns influence local disease occurrence.

The economic and welfare impact of blackleg is substantial despite its relatively low overall prevalence due to vaccination programs. When the disease occurs in unvaccinated herds, multiple deaths can occur within days, causing significant financial losses. The acute nature of the disease means that affected animals typically die before treatment can be instituted, and those that are treated rarely survive. Beyond direct mortality, blackleg impacts include vaccination costs, diagnostic expenses, and the psychological impact on producers who lose animals suddenly. The disease also represents a significant welfare concern, as affected animals experience severe pain during the brief clinical course before death.

Prevention through vaccination is highly effective and represents the cornerstone of blackleg control. The clostridial vaccines available for cattle provide excellent protection when administered according to recommended protocols. Despite vaccine availability, blackleg continues to occur due to vaccination failures, inadequate protocols, or failure to vaccinate altogether. Understanding the epidemiology and pathogenesis of the disease enables producers and veterinarians to implement effective prevention programs. Recognition of clinical signs, though rarely leading to successful treatment, allows for rapid diagnosis and implementation of herd-level interventions to prevent additional cases.

The primary cause of blackleg is infection with Clostridium chauvoei, a gram-positive, anaerobic, spore-forming bacterium that inhabits soil and the gastrointestinal tract of cattle. The organism produces highly resistant spores that can survive in soil for many years, maintaining environmental contamination that serves as the source of infection. Cattle ingest spores during grazing, and these spores traverse the intestinal wall to enter the bloodstream. Circulating spores are phagocytosed by macrophages and deposited in various tissues, particularly muscle, where they remain dormant as latent infections. The transition from dormant spores to active, toxin-producing vegetative bacteria requires specific conditions that reduce oxygen tension in tissues.

Genetic and breed predisposition to blackleg relates primarily to factors affecting tissue oxygen levels rather than true genetic susceptibility. Well-muscled, rapidly growing cattle appear more susceptible, possibly due to the metabolic demands of muscle tissue creating lower oxygen tensions. Some anecdotal breed associations may reflect differences in growth rates and muscle mass rather than inherent susceptibility. Certain bloodlines within breeds that produce exceptionally well-conditioned young cattle may see higher blackleg rates simply due to their rapid growth characteristics. There is no evidence for genetic resistance or susceptibility to Clostridium chauvoei infection independent of these physiological factors.

Environmental and management factors play critical roles in blackleg occurrence. Soil type and contamination level influence spore exposure, with alkaline and calcium-rich soils particularly supportive of spore survival. Flooding or soil disturbance can bring buried spores to the surface where cattle are exposed during grazing. Seasonal patterns show increased cases in late summer and fall in many regions, possibly related to forage quality and animal condition. High nutritional planes that promote rapid growth increase tissue susceptibility to infection. Bruising or muscle damage from handling, transportation, or strenuous exercise may provide the anaerobic microenvironment necessary for spore germination. Failure to vaccinate or improper vaccination protocols leave animals susceptible.

Risk factors for developing clinical blackleg include age, body condition, vaccination status, and environmental exposure. Young cattle between six months and two years represent the highest-risk group, with the disease rare outside this age range. Animals in excellent body condition with well-developed musculature are preferentially affected. Unvaccinated animals or those with inadequate vaccination are clearly at elevated risk. Grazing on historically contaminated pastures increases exposure. Recent muscle trauma from any cause may trigger disease in animals harboring latent spores. Nutritional programs promoting rapid weight gain may increase susceptibility. Environmental events such as flooding that redistribute soil and spores can precipitate outbreaks.

The pathophysiology of blackleg involves a unique mechanism of endogenous infection from latent spores. Following ingestion and systemic dissemination, Clostridium chauvoei spores lodge in well-perfused tissues, particularly skeletal muscle, where they remain dormant. Tissue damage or reduced oxygenation from any cause creates conditions favoring spore germination. The vegetative bacteria multiply rapidly in the anaerobic environment, producing potent toxins that cause further tissue necrosis. The principal toxin is alpha toxin, a lethal and necrotizing cytolytic agent that destroys muscle cells and damages blood vessels. Gas production by bacterial fermentation causes the characteristic crepitant swelling of affected muscles. Toxemia from absorbed bacterial toxins produces systemic effects leading to cardiovascular collapse and death, typically within twelve to forty-eight hours of clinical onset.

Early warning signs of blackleg are often absent or so brief that they go unnoticed, with many cases discovered only as sudden death in previously healthy animals. When observed, the earliest signs may include mild depression, reduced appetite, and reluctance to move. Slight fever may be present in the very early stages before toxemia develops. A subtle change in posture or gait may indicate developing muscle involvement. Affected animals may separate from the group and appear uncomfortable. Unfortunately, the rapid progression of the disease means that these early signs often progress to severe illness within hours, and many animals are found dead without any premonitory signs having been observed.

Common symptoms of established blackleg include severe lameness if a limb muscle is affected, with the animal showing marked reluctance or inability to bear weight. High fever, often exceeding one hundred six degrees Fahrenheit, accompanies systemic toxemia. Depression becomes profound, with the animal appearing dull and unresponsive to stimuli. Affected muscles become swollen, initially with a doughy consistency that rapidly progresses to characteristic crepitant swelling from gas accumulation. The skin over affected areas may become tense and warm initially, then progress to cold and discolored as tissue dies. Respiratory rate increases as toxemia and pain worsen. Affected animals may grind their teeth and display other signs of severe pain.

Behavioral changes in cattle with blackleg reflect the severe systemic illness and local tissue destruction. Affected animals isolate from the herd and show no interest in feed or water. They may stand with their head lowered and back arched, or become recumbent and unable to rise. Movement is avoided due to pain, and when forced to move, severe lameness is evident if limb muscles are involved. Affected animals may vocalize or show other signs of distress. The rapid deterioration of condition is striking, with animals progressing from apparently normal to moribund within hours. Terminal animals show collapse, labored breathing, and loss of consciousness before death.

Physical signs of blackleg on examination reveal characteristic findings that aid diagnosis. Affected muscle masses show swelling that is initially firm but becomes crepitant as gas accumulates, producing a crackling sensation on palpation. The skin overlying affected areas may be hot initially but becomes cold, dry, and discolored (dark red to black) as tissue necrosis progresses. Subcutaneous emphysema may extend beyond the primary muscle involvement. The affected area typically has a sweet, rancid odor from bacterial fermentation products. Common sites of involvement include the heavy muscles of the hindquarter, shoulder, and back, but any large muscle mass can be affected. Multiple sites may be involved simultaneously.

Symptom progression in blackleg is extremely rapid, with death typically occurring within twelve to forty-eight hours of the first observable signs. Initial signs of depression and fever progress over hours to severe systemic illness with recumbency. Local lesions evolve from firm swelling to crepitant gas gangrene. Toxemia causes progressive cardiovascular deterioration with rapid, weak pulse and cold extremities. Respiratory distress develops as the animal weakens. Terminal stages include collapse, recumbency, coma, and death. The brevity of the clinical course means that most cases are found either dead or in terminal stages, with opportunities for intervention extremely limited.

Emergency symptoms in blackleg essentially describe the typical presentation, as the disease is inherently an emergency from the time clinical signs are observed. Any young, well-conditioned bovine showing acute severe lameness, high fever, and muscle swelling should be considered a blackleg emergency. Crepitant swelling of large muscles is pathognomonic and demands immediate action. Signs of shock including rapid weak pulse, pale mucous membranes, and cold extremities indicate terminal toxemia. Recumbency with inability to rise represents a grave prognostic sign. Any sudden death in young cattle should prompt consideration of blackleg and immediate examination of additional at-risk animals.

Clinical examination of suspected blackleg cases focuses on identifying the characteristic lesions and ruling out other causes of sudden death or acute illness. Physical examination of acutely affected animals reveals high fever, depression, and localized muscle swelling with crepitus. Palpation of large muscle masses identifies areas of gas accumulation that feel crackly or bubbly under the skin. The affected area may be warm initially but becomes cool as tissue dies. A characteristic sweet, rancid odor may be detected. Careful examination of the entire animal helps identify all affected sites, as multiple locations may be involved. In animals found dead, carcass examination reveals typical postmortem changes.

Diagnostic tests for blackleg include both rapid field tests and laboratory confirmation. Impression smears from affected muscle tissue stained with Gram stain reveal large, gram-positive rods with characteristic morphology. Fluorescent antibody testing on tissue samples can specifically identify Clostridium chauvoei and distinguish it from other clostridia. Bacterial culture from affected tissues grows the organism under anaerobic conditions, though this takes several days. Postmortem examination reveals characteristic findings including dark red to black muscle tissue with gas bubbles and a distinctive odor. The affected muscles cut easily and appear dry and spongy. Blood samples for serology are rarely useful in acute cases due to rapid progression.

Differential diagnosis of blackleg must consider other causes of sudden death and acute muscle disease in cattle. Other clostridial diseases including malignant edema (Clostridium septicum) and Clostridium perfringens infections can cause similar presentations; mixed infections occur, and polyvalent vaccines address multiple clostridia. Anthrax causes sudden death but typically produces bloody discharges and lacks the crepitant muscle involvement. Lightning strike may cause sudden death in cattle on pasture but shows characteristic postmortem findings. Bloat causes sudden death with obvious ruminal distension. Trauma with gas-forming bacterial contamination can mimic blackleg. Hardware disease and other acute abdominal emergencies may cause rapid death. Careful examination and appropriate diagnostic testing distinguishes these conditions.

Herd-level diagnostics become essential when blackleg is confirmed to prevent additional cases. Review of vaccination records identifies gaps in protection that allowed disease occurrence. Assessment of vaccination protocols evaluates timing, products used, and administration technique. Examination of other animals in the group identifies any showing early signs requiring treatment. Environmental assessment notes recent activities that might have distributed soil spores or caused muscle trauma. Analysis of the age and condition of affected animals confirms the typical epidemiology. Feed and mineral records are reviewed to ensure no factors promoting excessive growth or muscle damage. Implementation of emergency vaccination for at-risk animals follows diagnosis confirmation.

Emergency and immediate treatment of blackleg must be instituted at the first recognition of clinical signs, though prognosis remains extremely guarded. High-dose penicillin therapy is the treatment of choice, with procaine penicillin G administered intramuscularly at high doses. The initial dose should be given immediately upon suspicion of blackleg, with withdrawal time considerations secondary to the life-threatening nature of the condition. Oxytetracycline may be used as an alternative antibiotic. Anti-inflammatory therapy with flunixin meglumine or dexamethasone may help counter toxemic effects. Aggressive fluid therapy addresses cardiovascular collapse from toxemia. The affected animal should be moved to comfortable, shaded housing with easy access to feed and water. Pain management is important for animal welfare during the clinical course.

Medical management beyond emergency treatment has limited additional options given the rapid progression of blackleg. Antibiotic therapy should continue for several days in any animal that survives initial treatment. Some practitioners advocate surgical drainage or debridement of gas gangrenous lesions, though this is rarely practical in field situations and benefit is uncertain. Supportive care including nutritional support and prevention of secondary complications continues as long as the animal survives. Hyperimmune serum against Clostridium chauvoei was historically used but is rarely available currently. The reality is that most animals with clinical blackleg die despite treatment, making prevention the only effective approach to this disease.

Surgical options for blackleg are extremely limited and rarely successful. Theoretically, wide surgical excision of affected muscle tissue before toxemia becomes overwhelming might save some animals, but the practical challenges are immense. The rapid progression of disease means that by the time diagnosis is made, toxemia is usually too advanced for surgical intervention to succeed. Fasciotomy to release pressure from gas accumulation has been attempted. Amputation might be considered for distal limb involvement, but blackleg rarely affects these areas. In practice, surgical treatment of blackleg is rarely attempted in the field, and treatment efforts focus on medical management with recognition of poor prognosis.

Supportive care during blackleg treatment addresses both the systemic illness and local lesion effects. Housing in a comfortable, quiet area reduces stress and allows close monitoring. Soft bedding protects recumbent animals from pressure sores. Ensuring adequate hydration through intravenous fluids when possible and offering water when the animal can drink supports cardiovascular function. Pain management through anti-inflammatories provides comfort even when prognosis is poor. Prevention of secondary complications including aspiration pneumonia in recumbent animals requires attention to positioning and nursing care. Humane considerations should guide decisions about treatment continuation versus euthanasia.

Herd treatment protocols for blackleg focus exclusively on prevention of additional cases, as the disease is not directly contagious. Upon confirmation of a blackleg case, immediate vaccination of all susceptible animals in the group should be undertaken. Cattle that have been recently vaccinated may receive a booster. Moving cattle to alternative pastures that are less contaminated may reduce exposure, though the widespread distribution of spores limits this strategy. Prophylactic antibiotic treatment of at-risk animals has been used during outbreaks, providing temporary protection while vaccine immunity develops. Any cattle showing early signs of illness should be treated aggressively even though prognosis is poor.

Treatment decision factors for individual blackleg cases center on the realistic assessment of survival probability. By the time clinical signs are recognized, the disease has usually progressed beyond the point where treatment can be successful. Animals found early with minimal lesions and no signs of toxemia may warrant aggressive treatment efforts. Advanced cases with extensive lesions, profound depression, and cardiovascular collapse have essentially no chance of survival, and humane euthanasia should be considered. The welfare of the animal must be paramount in decisions about treatment versus euthanasia. Economic factors are largely irrelevant given the poor prognosis regardless of treatment investment. Focus of resources should be on protecting remaining animals rather than futile treatment of advanced cases.

Recovery timeline for blackleg survivors, in the rare cases where survival occurs, is prolonged and complicated. The initial critical period extends through the first seventy-two hours, during which most fatalities occur. Animals surviving beyond this point face weeks of recovery from muscle necrosis and systemic toxemia. Affected muscles may slough extensively, requiring prolonged wound management. Muscle function may be permanently impaired depending on the extent and location of necrosis. Full recovery, if achieved, typically requires two to three months or longer. The rarity of survivors makes systematic documentation of recovery timelines limited, but expectations should be for prolonged convalescence with uncertain outcomes.

Post-treatment care and monitoring for blackleg survivors involves intensive nursing care and wound management. Affected muscle tissue may slough and require debridement. Open wounds from tissue loss need cleaning and protection from contamination. Antibiotic therapy may continue for extended periods to prevent secondary infection. Nutritional support helps meet the metabolic demands of healing. Physical therapy and assisted exercise may help prevent muscle contracture and maintain function in affected limbs. Monitoring for complications including secondary infections, pressure sores, and sequelae of prolonged recumbency continues throughout recovery. Regular veterinary reassessment guides ongoing management decisions.

Prognosis factors for blackleg are heavily weighted toward poor outcomes. The overwhelming majority of clinical cases die despite treatment. Factors associated with any chance of survival include very early recognition and treatment, limited extent of muscle involvement, and young healthy animals with good prior immune status. Animals showing signs of advanced toxemia at presentation have essentially no survival probability. Involvement of multiple muscle sites or massive swelling indicates advanced disease with grave prognosis. Even survivors may have permanent muscle loss and disability. The prognosis for blackleg should be communicated honestly as extremely poor, with emphasis on prevention as the only reliable approach.

Return to production considerations for blackleg survivors are largely theoretical given the rarity of survival. Animals that do survive may have permanent muscle damage affecting function and appearance. The market value of survivors is likely reduced due to scarring and muscle loss. Breeding function may be impaired if pelvic or limb muscles are affected. Dairy production would likely be compromised during the extended recovery period. Whether survivors develop lasting immunity is uncertain; vaccination should be continued. The decision to retain survivors versus cull depends on extent of permanent damage and individual animal value. Most survivors would be expected to have significantly reduced productive capacity.

Vaccination protocols represent the cornerstone of blackleg prevention and are highly effective when properly implemented. Clostridial vaccines containing Clostridium chauvoei antigen, typically combined with other clostridial species in multivalent products, provide excellent protection. Initial vaccination of calves should occur at two to four months of age, with a booster dose administered four to six weeks later. Annual revaccination maintains immunity. In herds with history of blackleg or in highly endemic areas, more frequent vaccination may be warranted. Proper vaccine handling, including cold chain maintenance and attention to expiration dates, ensures product efficacy. Administration technique should follow label directions for route, dosage, and injection site.

Biosecurity measures for blackleg prevention focus on reducing environmental contamination and animal exposure. While spores persist in soil for years, avoiding heavy grazing of historically contaminated pastures may reduce exposure. Avoiding activities that disturb contaminated soil, such as excavation or flooding irrigation, limits spore dispersal. Proper disposal of carcasses from blackleg deaths prevents focal environmental contamination; burning or deep burial is recommended. Avoiding introduction of soil from unknown sources reduces risk of importing spores. General hygiene measures in handling and processing cattle prevent wounds that could serve as entry points. Quarantine is not applicable as the disease is not directly transmitted between animals.

Nutritional prevention of blackleg involves managing growth rates and body condition to reduce tissue susceptibility. Avoiding excessively rapid growth in young cattle may reduce the metabolic conditions favoring spore germination. Monitoring body condition and adjusting nutrition to prevent excessive conditioning is prudent, particularly in high-risk age groups. Adequate mineral nutrition supports immune function and tissue health. Avoiding abrupt dietary changes that might cause metabolic upset is generally good practice. However, nutritional management alone is not sufficient for blackleg prevention and should be considered adjunctive to vaccination.

Management practices for blackleg prevention extend beyond vaccination and nutrition. Avoiding unnecessary handling or transportation stress that might cause muscle bruising reduces risk. Facilities should be designed to minimize traumatic injuries during handling. Timing vaccinations to provide protection before high-risk periods is important. Maintaining awareness of disease occurrence in the region allows appropriate vigilance. Training personnel to recognize early signs of blackleg enables rapid response when cases occur. Having treatment supplies on hand allows immediate intervention when disease is suspected. Working with a veterinarian to develop a comprehensive prevention program ensures systematic protection.

Quarantine and testing protocols are less applicable to blackleg than to contagious diseases, but some considerations apply. New animals entering the herd should have documented vaccination history and receive boosters upon arrival if status is uncertain. Animals from herds with recent blackleg history should be carefully vaccinated before mixing with resident cattle. No practical testing identifies subclinical carriers of latent spores, so vaccination remains the only reliable preventive measure. Soil testing for clostridial spores is technically possible but not practical for routine prevention decisions. The focus of prevention efforts should remain on systematic vaccination programs rather than testing or quarantine approaches.

Daily management and monitoring of cattle in blackleg-endemic areas requires consistent attention to herd health and vaccination status. Regular observation of young cattle in the high-risk age group enables early detection of any illness. Cattle should be observed at least daily, with particular attention during periods of known increased risk. Any animal showing depression, reluctance to move, or apparent stiffness warrants close examination. Documentation of observations helps identify patterns or concerns. Training all personnel who observe cattle to recognize abnormal behavior and appearance improves surveillance. Rapid reporting of any suspicious findings to appropriate management or veterinary support enables timely response.

Housing and environmental management for blackleg prevention focuses on reducing exposure and injury risk. Pasture management should consider historical contamination when allocating grazing areas. Avoiding overgrazing that forces cattle to consume soil-contaminated forage may reduce spore ingestion. Proper drainage prevents standing water that can harbor and distribute spores. Facility design should minimize crowding and injury risk during handling. Providing adequate space and appropriate flooring reduces traumatic muscle injuries that might trigger disease in animals harboring latent infections. General attention to clean, safe housing environments supports overall herd health.

Herd health programs should integrate blackleg prevention with broader vaccination and management protocols. Vaccination schedules should be established and maintained as routine herd procedures. Records of vaccination dates, products used, and animals vaccinated provide documentation of protection status. Timing of vaccinations should provide protection during known high-risk periods. Review of any disease occurrences identifies gaps in protection that need addressing. Veterinary involvement ensures appropriate product selection and administration protocols. Integration with other clostridial disease prevention creates comprehensive protection against this family of pathogens.

Record keeping and monitoring systems support effective blackleg prevention programs. Individual animal vaccination records document protection status. Herd vaccination compliance can be tracked and reported. Any disease occurrences should be documented with details including affected animals, presenting signs, and outcomes. Environmental conditions or events that might affect risk should be noted. Analysis of records over time identifies patterns or risk factors specific to the operation. Benchmarking against regional disease incidence provides context for program evaluation. Sharing records with veterinary advisors enables collaborative program refinement.

Economic considerations for blackleg management heavily favor prevention over treatment. Vaccination costs are modest compared to the value of cattle protected. A basic clostridial vaccination program costs a few dollars per animal annually. The cost of a single blackleg death typically exceeds many times the annual vaccination cost for the entire herd. Treatment costs, while significant, are largely irrelevant since treatment rarely succeeds. The economic analysis strongly supports investment in comprehensive vaccination programs. Even in areas with no recent disease occurrence, the potential for losses from introduced or activated infection justifies continued prevention efforts.

High-risk breeds and species for blackleg include cattle of all breeds, with susceptibility related more to physiological factors than genetic background. Well-muscled beef breeds in excellent condition may appear predisposed, though this likely reflects the tissue conditions favoring spore germination rather than breed-specific susceptibility. British beef breeds including Angus, Hereford, and their crosses are frequently affected, possibly due to their prevalence in grazing systems where exposure occurs. Continental breeds with heavy muscling may also be susceptible. Dairy breeds experience blackleg less frequently, possibly due to different management systems and body composition, but are not immune. Sheep can be affected by Clostridium chauvoei but typically only following wound contamination.

Production type considerations influence blackleg risk through effects on age structure, body condition, and management. Beef cattle operations maintaining young growing cattle in excellent condition represent the highest-risk production type. Cow-calf operations see cases primarily in calves and yearlings. Stocker and backgrounder operations with cattle in the susceptible age range face significant risk. Feedlots may experience blackleg, particularly in cattle recently arriving that may not have been adequately vaccinated. Dairy operations typically have lower risk due to different management, but replacement heifers in good condition can be affected. Any operation with cattle in the six-month to two-year age range should implement vaccination programs.

Genetic selection and testing do not play significant roles in blackleg prevention, as the disease is not influenced by heritable susceptibility factors. No genetic markers or tests identify animals at increased risk. Selection for extreme muscling or rapid growth might theoretically increase susceptibility by creating tissue conditions favoring spore germination, but this association is not well documented. Breeding decisions should not be influenced by blackleg considerations beyond general selection for healthy, sound animals. The focus of prevention efforts should remain on vaccination and management rather than genetic approaches.

Commonly co-occurring conditions with blackleg include other clostridial diseases that share similar epidemiology and prevention strategies. Malignant edema, caused by Clostridium septicum, produces similar gas gangrene lesions following wound contamination. Mixed clostridial infections can occur, with multiple species contributing to disease. Enterotoxemia from Clostridium perfringens affects cattle of various ages and shares vaccine formulations with blackleg prevention. Tetanus from Clostridium tetani may occur in the same environments. Botulism from Clostridium botulinum represents another clostridial threat in some regions. The polyvalent clostridial vaccines commonly used address multiple species simultaneously, providing comprehensive protection against this family of diseases.

Conditions with similar symptoms to blackleg require careful differentiation for accurate diagnosis. Anthrax causes sudden death and may produce swelling but lacks the crepitant gas gangrene characteristic of blackleg. Lightning strike can cause sudden death in pastured cattle but typically shows distinctive postmortem findings. Trauma with secondary bacterial contamination may produce localized swelling with gas production. Injection site reactions can cause localized swelling that might initially be confused with early blackleg. Acute bloat causes sudden death with obvious ruminal distension. Malignant edema produces similar gas gangrene but typically follows visible wound contamination. Laboratory diagnosis may be needed to distinguish these conditions definitively.

Complications and sequelae of blackleg relate primarily to the extremely high case fatality rate. Death is the most common outcome, occurring in the vast majority of clinical cases. Survivors face prolonged recovery with extensive tissue loss and potential permanent disability. Secondary infections of necrotic tissue may complicate recovery. Muscle scarring and dysfunction may persist indefinitely. In herds experiencing outbreaks, the psychological impact on producers observing sudden deaths in valuable animals can be significant. The demonstration of vaccine failure in individual cases may prompt review and modification of prevention programs. Confirmation of blackleg in a herd should trigger immediate protective vaccination of remaining susceptible animals.