GD is also called cellulitis and blue wing disease, in turkeys and chickens, respectively, and it is characterized by congestion, hemorrhage, and necrosis of the skin and subcutaneous tissue, although sometimes these lesions can extend into the underlying musculature. Breast, back, abdomen, thighs, tail, and wings are the most frequently affected areas.
The primary causes of GD are Clostridium septicum and C perfringens type A; these microorganisms may act singly or in combination.
Several other anaerobic and aerobic bacteria may also cause GD. Amongst those are C sordellii, C novyi, Staphylococcus aureus, S epidermidis, S xylosus, Escherichia coli, Enterococcus faecalis, Pasteurella multocida, Gallibacterium anatis biovar haemolytica, Proteus spp, Pseudomonas aeruginosa, Bacillus spp, and Erysipelothrix rhusiopathiae.
The great majority of the microorganisms that can cause GD are ubiquitous in the environment, in the intestine, and on the skin of birds. Therefore, the sole detection of these microorganisms does not confirm a diagnosis of GD. Contributing factors thought to play a major role in development of clinical signs of gangrenous dermatitis within a flock include immunosuppressive diseases such as:
inclusion body hepatitis Inclusion Body Hepatitis and Hepatitis Hydropericardium Syndrome in Poultry Inclusion body hepatitis and hepatitis hydropericardium syndrome are diseases of young broilers caused by fowl adenoviruses. Clinical signs are nonspecific but often include a sudden increase... read more
Environmental conditions associated with poor litter conditions may also predispose flocks to GD, especially when present in conjunction with immunosuppressive viruses. Failing to remove moribund or dead birds may increase the 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, irregular meal times, and bird migration in tunnel-ventilated houses, may increase the incidence of infection.
Affected farms tend to have repeated outbreaks if the environment is not treated. The incidence and severity of the disease depend on the bacterial species and strains involved in the infection, their ability to produce toxins, and the specific toxins produced.
Clinical Findings of Gangrenous Dermatitis in Poultry
The incubation period of gangrenous dermatitis is usually less than 24 hours. Most affected birds are well-fleshed. The main clinical signs are fever, listlessness, anorexia, ataxia, and recumbency.
The lower parts of the body and inner thighs frequently have an accumulation of subcutaneous edema. The skin of affected areas is usually devoid of feathers and shows dark reddish, purple, green, or green-blue discoloration. The most frequently affected areas of the body are breast, abdomen, back, thighs, legs, and wings. Cases of GD may also occur without clinical signs being observed.
A predominant feature of GD is rapid autolysis, which is more prevalent in cases of sudden death. Severe edema mixed with gas and hemorrhages in the subcutaneous tissue are present. Abrasions are frequently found on the skin. The muscle under skin lesions may show gray or tan discoloration, hemorrhages, edema, and emphysema. The feathers are easily removed from the affected skin areas.
Diagnosis of Gangrenous Dermatitis in Poultry
Detection of bacteria
The presumptive diagnosis of gangrenous dermatitis is based on clinical signs (fever, listlessness, anorexia, ataxia, and recumbency) and gross (skin and subcutaneous necrosis, edema, emphysema, and hemorrhage) and microscopic (necrotizing dermatitis and cellulitis, with hemorrhage and emphysema) postmortem findings. Confirmation should rely on detection of the agents involved, associated with the clinical signs and gross and microscopic findings. This may be achieved by aerobic and anaerobic culture, fluorescent antibodies, immunohistochemistry, and/or PCR assay.
It is important to remember that isolation of any of the agents of GD without clinical signs and/or lesions of the disease is not diagnostic.
Treatment and Control of Gangrenous Dermatitis in Poultry
Cleaning and disinfection of houses
Appropriate litter management
Prevention of trauma
Vaccination against immunosuppressive viral diseases
Total cleanout and disinfection of affected houses has decreased or eliminated gangrenous dermatitis infection on farms with historical problems. Salting of floors has also decreased bacterial challenge in subsequent flocks. Minimizing trauma by avoiding overcrowding is another way to prevent cases of GD.
In those cases in which GD is secondary to immunosuppressive viral infections, vaccination against those diseases helps in the control of GD.
Gangrenous dermatitis can be effectively treated with many broad-spectrum antibiotics. Water acidifiers have been used in cases to decrease, but not eliminate, mortality where these rates are low or antibiotic efficacy has been poor.
Zoonotic Risk of Gangrenous Dermatitis in Poultry
The zoonotic potential and public health importance of gangrenous dermatitis has not been well documented, although it is thought to be minimal. However, several of the agents responsible for the disease can also cause human disease (eg, C perfringens is the main cause of human gas gangrene), and therefore adequate personal protective equipment Introduction to Toxicologic Hazards in the Veterinary Workplace Veterinarians are potentially exposed to myriad potent pharmaceuticals and other hazardous materials as part of their work environment, and particularly during patient decontamination procedures... read more (PPE) should be worn when dealing with birds affected with GD.
GD in poultry is caused by Clostridium spp but also by other common pathogens, including E coli and Pasteurella.
Prevention includes vaccination and avoidance of skin trauma related to overcrowding.
GD is characterized by acute death and necrosis of the skin, including gas and severe edema.
For More Information
Abdul-Aziz T, Barnes HJ. Miscellaneous and sporadic bacterial infections. In: Swayne DE, ed. Glisson JR, McDougald LR, Nolan LK, Suarez DL, Nair VL, associate eds. Diseases of Poultry. 13th ed. Wiley-Blackwell, 2013:1017-1027.
Clark S, Porter R, McComb B, et al. Clostridial dermatitis and cellulitis: an emerging disease of turkeys. Avian Dis. 2010;54(2):788-794. doi:10.1637/9147-111309-Review.1
Dinev I. Enzootic outbreak of necrotic gastritis associated with Clostridium perfringens in broiler chickens. Avian Pathol. 2010;39(1):7-10. doi:10.1080/03079450903431382
Fancher CA, Zhang L, Kiess AS, Adhikari PA, Dinh TTN, Sukumaran AT. Avian pathogenic Escherichia coli and Clostridium perfringens: challenges in no antibiotics ever broiler production and potential solutions. Microorganisms. 2020;8(10):1533. https://doi.org/10.3390/microorganisms8101533
Gornatti-Churria CD, Crispo M, Shivaprasad HL, Uzal FA. Gangrenous dermatitis in chickens and turkeys. J Vet Diagn Invest. 2018;30(2):188-196. doi:10.1177/1040638717742435
Li G, Lillehoj HS, Lee KW, et al. An outbreak of gangrenous dermatitis in commercial broiler chickens. Avian Pathol. 2010;39(4):247-253. doi:10.1080/03079457.2010.487517
Lighty, ME, Elvinger F, Evans RD, Sriranganathan N, Leroith T, Pierson FW. Incidence of clostridial dermatitis (cellulitis) and factors for development of the disease in turkeys. J Appl Poult Res. 2015;25(1):104-112. https://doi.org/10.3382/japr/pfv065
Shivaprasad HL. Gangrenous dermatitis in poultry. In: Uzal FA, Songer JG, Prescott JF, Popoff MR, eds. Clostridial Diseases of Animals. Wiley-Blackwell. 2016:255-264.
Tellez G, Pumford NR, Morgan MJ, Wolfenden AD, Hargis BM. Evidence for Clostridium septicum as a primary cause of cellulitis in commercial turkeys. J Vet Diagn Invest. 2009;21(3):374-377. doi:10.1177/104063870902100313
Thachil AJ, McComb B, Andersen MM, Shaw DP, Halvorson DA, Nagaraja KV. Role of Clostridium perfringens and Clostridium septicum in causing turkey cellulitis. Avian Dis. 2010;54(2):795-801. doi:10.1637/9009-080309-Reg.1