THE MERCK VETERINARY MANUAL
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Overview of Gangrenous Dermatitis in Poultry

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Gangrenous dermatitis is a disease of turkeys and chickens caused by Clostridium septicum, C perfringens type A, and Staphylococcus aureus, either singly or in combination. The condition is characterized by rapid onset of acute mortality. Birds succumbing to the infection have necrosis of the skin and subcutaneous tissue, usually involving the breast, abdomen, wing, or thigh.

Both clostridia and staphylococci are ubiquitous in the poultry house environment and in (intestine) or on (skin) the birds. The presence of these organisms, however, does not necessarily indicate a disease challenge. Other contributing factors are thought to play a major role in development of clinical disease within a flock. For example, gangrenous dermatitis often is believed to occur as a sequela of other diseases that produce immunosuppressive effects such as infectious bursal disease, chicken infectious anemia, reticuloendotheliosis, reovirus, and inclusion body hepatitis. Environmental conditions that promote poor litter conditions may also predispose flocks to gangrenous dermatitis, especially when present in conjunction with challenges from immunosuppressive viruses. Failing to remove moribund or dead birds may increase incidence of the disease, because such birds serve as a reservoir for the causative agent(s). Management practices that lead to scratching, such as overcrowding, feed outages, meal time feeding, and bird migration in tunnel-ventilated houses may increase incidence of infection. Affected farms tend to have repeat outbreaks if the environment is not treated. Incidence and severity of the disease depend on the bacterial strains involved in the infection, their ability to produce toxins, and the specific toxins produced.

The incubation period is relatively short (12–24 hr), with death occurring in well-fleshed birds. Other clinical findings are general in nature and include depression, incoordination, inappetence, leg weakness, ataxia, and high fever.

Lesions:

Gross lesions consist of dark reddish purple to green, weepy areas of the skin. Affected areas usually include abdomen, breast, wings, or legs. Areas of affected dermis and subcutis are characterized by extensive blood-tinged edema, with or without gas (crepitus). Infection may extend into underlying musculature, which may be discolored and contain edema and gas. Lesions in turkeys may be seen around the tail head, with blisters and tissue edema present around the tail.

Presumptive diagnosis may be assigned based on an acute increase in mortality and characteristic gross lesions. Diagnostic confirmation is based on the presence of lesions and isolation of the causative agent(s) from affected tissue. Diagnosis of an underlying etiology is often necessary to fully understand the complexity of gangrenous dermatitis, because manifestation of the disease may be preceded by other immune-compromising infectious agents.

Total cleanout and disinfection of affected houses has reduced or eliminated gangrenous dermatitis infection on farms with historical problems. Salting of floors has also reduced bacterial challenge in subsequent flocks. Reducing excessive moisture and microbial levels in poultry house litter and minimizing trauma are useful adjuncts to other prevention and control measures. Where infection is secondary to predisposing viral infection, modification of vaccine programs directed at immunosuppressive agents may be used to control widespread gangrenous dermatitis.

Gangrenous dermatitis has historically been treated effectively with administration of many broad-spectrum and gram-positive antibiotics. Water acidifiers have been used in cases to reduce, but not eliminate, mortality where mortality rates are low or antibiotic efficacy has been poor.

The zoonotic potential and public health significance of gangrenous dermatitis is thought to be minimal, because nearly all affected birds succumb quickly to infection and do not survive to processing age.

Last full review/revision January 2014 by Kenneth Opengart, MS, DVM, PhD, DACPV

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