21 H. L. Shivaprasad Gangrenous dermatitis (GD) is a common disease of broiler chickens and turkeys caused by various species of anaerobic and aerobic bacteria, including several clostridial species. The disease is characterized by a sudden increase in mortality and lesions in the skin, subcutaneous tissue, and the underlying muscles, usually over the keel, abdomen, thigh, and wings. GD is a disease of considerable economic significance in poultry and occurs throughout the world. GD has also been called cellulitis and clostridial dermatitis, especially in turkeys, as well as gangrenous dermatomyositis, blue wing disease, and avian malignant edema, amongst others, in broiler chickens. The disease is most common in commercial broiler chickens and turkeys raised on re-used deep-litter production systems. GD can result in increased condemnation rates and downgrading of the carcasses at processing plants. GD should be distinguished from cellulitis in broiler chickens caused by Escherichia coli, which is characterized by fibrinonecrotic inflammation of the subcutaneous tissue. Various anaerobic and aerobic bacteria have been associated with GD. These include mainly Clostridium septicum and Clostridium perfringens type A, and, occasionally Clostridium sordellii, Staphylococcus aureus, E. coli, Pseudomonas aeruginosa, and others. However, most of the outbreaks of GD have been associated with C. septicum and C. perfringens, either alone or in combination with some of the aerobic bacteria mentioned above acting as secondary contaminants. There is experimental evidence that C. septicum is more significant than C. perfringens in causing GD based on subcutaneous inoculation in turkeys. C. septicum and C. perfringens are found in the environment, especially in the soil and litter. C. perfringens is part of the normal flora of the intestines of many animals, including chickens and turkeys. C. septicum has also been isolated from the intestine of normal animals including chickens. C. septicum produces at least four major toxins, namely alpha, beta, delta, and gamma (Chapter 4). Alpha toxin, a cytolysin, is a lethal toxin which is considered the critical virulence factor for GD. Multilocus sequence typing (MLST) analysis of numerous isolates of C. septicum from poultry has revealed a highly conserved core genome. All strains of C. perfringens produce alpha toxin (CPA), while some of them may also produce other toxins, including NetB (Chapter 5). The role of the individual toxins of C. perfringens type A in the pathogenesis of GD is not known although it is thought that, as is the case for all the diseases produced by this microorganism, GD is mediated by one or more of the toxins produced by C. perfringens, with CPA likely playing the most critical role. GD occurs most commonly in market-age broiler chickens (> 35 days) and turkeys (> 13–16 weeks). GD has been known to occur in the same farms in successive flocks. The mode of transmission is not well understood but it is thought that the bacteria are transmitted through a break in the skin or ingestion of contaminated feed and/or water. Breaks in the skin of chickens and turkeys are common due to scratching by toe nails and biting by pen mates, and may be exacerbated by aggression between the birds. Factors such as overcrowding, poor and wet litter conditions, increased humidity, reduced resting of buildings between broods of birds, poor hygienic conditions, contaminated equipment, use of contaminated animal byproducts in the feed, multi-age birds on the ranch/farm, failure to remove dead birds in a timely manner, and contaminated feed and water can all predispose GD, likely because of the build-up of clostridial pathogens in the environment. Administration of dexamethasone, an immunosuppressive drug, has been shown to promote high incidence of GD in turkeys, and supports the notion that “stress” may be a further predisposing factor. GD has also been known to occur more often in males than in females, perhaps because they are larger or more aggressive, and to be more prevalent in certain strains or breeds; the disease is seen more often in spring. GD can also occur secondarily to various immunosuppressive diseases such as infectious bursal disease caused by Birnavirus and chicken infectious anemia caused by Circovirus, both in chickens, and hemorrhagic enteritis caused by group II Adenovirus in turkeys. Feeds containing growth-promoting antibiotics have also been known to be associated with outbreaks of GD. There is also anecdotal evidence that the use of ionophores to control coccidia can predispose the birds to GD. It is speculated that ionophores disturb the normal intestinal flora, resulting in overgrowth of C. septicum and C. perfringens, which are then absorbed into the bloodstream and reach the skin, where they cause GD. The pathogenesis of GD is poorly understood. The so-called “outside-in” theory suggests that a break in the skin of birds provides an optimal environment for colonization from the contaminated environment of C. septicum and/or C. perfringens of the skin, with subsequent invasion of the subcutis and underlying muscles, causing the typical lesions of the disease. It is assumed that the disease is mediated by one or more toxins produced by these bacteria which, as noted, may act synergistically. Another theory, called “inside-out”, suggests that pathogenic bacteria and/or their toxins enter the circulation though a damaged intestinal wall and localize in the skin, resulting in the lesions of GD, but this theory seems far less likely. It has been demonstrated that chickens with GD have lower T-cell and B-cell mitogen-stimulated lymphoproliferation, higher levels of nitric oxide and α-1-acid glycoprotein, a greater number of MHC class II intradermal and intraepithelial lymphocytes, and increased levels of mRNAs encoding pro-inflammatory cytokines and chemokines in skin compared to GD-free chickens.
Gangrenous Dermatitis in Poultry
Introduction
Etiology
Epidemiology
Pathogenesis
Clinical signs
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