Akshit Tyagi1, Himanshu Gautam2, Shivang Madhyan3, Shivam Nigam4
1M.V.Sc. Scholar, Department of Veterinary Pathology
2M.V.Sc. Scholar, Department of Veterinary Medicine
College of Veterinary Science & Animal Husbandry, A.N.D.U.A.T., Kumarganj, Ayodhya
3M.V.Sc. Scholar, Department of Veterinary Medicine
4B.V.Sc. and A.H.
College of Veterinary and Animal Sciences, S.V.P.U.A.T., Meerut
Introduction
Gangrenous dermatitis (GD) is a disease that mainly affects fast growing broiler chickens of age between 4 to 8 weeks and causes severe economical loss to poultry industry worldwide. The disease is also known by other names like necrotic dermatitis, gangrenous cellulitis, gangrenous dermatomyositis, poultry gangrene, avian malignant edema, gas edema disease, subcutaneous emphysema, blue wing disease, and wing rot.The disease is characterized by congestion, hemorrhage, and necrosis of the skin and subcutaneous tissue, associated with edema or emphysema, which sometimes extends into the underlying musculature. The affected areas mostly include breast, back, abdomen, thighs, tail and wings of chicks.
Etiology
A wound to the skin usually starts disease which is quickly followed by a secondary bacterial infection.Secondary bacterial infection is mainly caused by Clostridium perfringens type A, Clostridium septicum or Staphylococcus aureus.Genus Clostridium is composed of anaerobic, mostly gram-positive, spore-forming rods whereas Genus Staphylococcus is composed of gram-positive, coccoid-shaped, aerobic bacteria, which are commonly seen as clusters when grown in solid media and short chains when cultured in liquid media. C. perfringens type A isolates produce alpha toxin (CPA); some strains may also produce one or more additional toxins including necrotic enteritis B–like toxin (NetB) and enterotoxin (CPE).Alpha toxin (ATX), a necrotizing pore-forming toxin (PFT) that is distinct from C. perfringens’ alpha toxin, is the primary virulence component of C. septicum. ATX induces increased membrane permeability, which leads to cell necrosis. S. aureus can produce several toxins, including hyaluronidase, deoxy ribonuclease, fibrinolysin, lipase, protease, leucocidin, hemolysins, epidermolytic toxin, and dermonecrotic toxin. These bacteria can act alone or along with combination of different anaerobic and aerobic bacteria including Clostridium sordellii, Clostridium novyi, Staphylococcus aureus, Staphylococcus epidermidis, Staphylococcus xylosus, Escherichia coli, Enterococcus faecalis, Pasteurella multocida, Proteus spp., Pseudomonas aeruginosa, Bacillus spp., and Erysipelothrix rhusiopathiae. These bacteria are usually not able to penetrate intact skin. They infectious agents can be ingested if healthy birds peck at dead birds that have died with the disease or if litter and feces are contaminated with large numbers of disease-causing organisms.
Pathogenesis
Pathogenesis of disease is due to many predisposing factors in which immunosuppression may be the key predisposing factor for GD in chickens.In natural settings, a variety of pathogenic agents and environmental elements can cause immunosuppression in flocks of hen.Immunosuppressive viral agents that may predispose to GD in chicken include Marek’s disease virus, infectious bursal disease virus, chicken anemia virus, several reoviruses, and inclusion body hepatitis virusin chickens.
Environmental factors that can predispose chickens to GD are traumatic lesions of the skin associated with cannibalism or fighting, Overcrowding, feed outages, deficient diets, wet and poor litter conditions, contaminated feed, water, equipment, and vaccines, high ammonia levels and mycotoxins in feed. GD is mostly caused by traumatic skin damage in broiler chickens, which is typically linked to cannibalism and the population explosion. Bacteria can enter the body through these types of skin sores.Chaotic multiplication of the intestinal flora followed by absorption into the bloodstream promoted bacteremia, which is also the origin for some of the GD lesions. Outbreaks appear to be more prevalent throughout the summer and autumn seasons compared to winter and spring.
Clinical signs
The disease may manifest in the absence of observable clinical manifestations. Nevertheless, it is common to observe symptoms such as elevated body temperature, depressive symptoms, loss of appetite, lack of coordination, weakness in the legs, and lateral recumbency. The formation of subcutaneous oedema commonly affects the lower belly and inner thighs. The skin in affected regions typically lacks feathers and may exhibit discoloration in shades of dark-red, purple, green, or green-blue.The most frequently affected areas of the body are breast, abdomen, back, thighs, legs, and wings of chicken.
Microscopic lesions are characterized by edema, emphysema, hyperemia, hemorrhages and necrosis in the subcutaneous tissues.
Gross Lesions
Rapid autolysis is a prominent characteristic of GD, particularly in instances of unexpected death. The subcutaneous tissue exhibits a combination of severe oedema, gas, and haemorrhages. The skin often exhibits abrasions. Grey or tan discolouration, haemorrhages, oedema, and emphysema may be observed in the muscle beneath skin lesions. The feathers can be easily removed from the affected skin areas.
Diagnosis
Presumptive diagnosis of GD can be based on clinical signs (fever, listlessness, anorexia, ataxia, and recumbency), Microscopic finding, Detection of bacteria, Gross findings,Epidemiology and post mortem changes. Detection of bacteria can be achieved by aerobic and anaerobic culture, fluorescent antibodies, immunohistochemistry, and PCR assay.Microscopic findings like gram-positive rods on smears of the serosanguinous exudate, collected from affected skin or subcutaneous tissue, adds certainty to the presumptive diagnosis. Inspection ought to be based on the recognition of the agents implicated, linked to the clinical manifestations and observable observations at both the macroscopic and microscopic levels. It is crucial to bear in mind that the absence of clinical indications and/or lesions of the disease does not establish the diagnosis of any of the agents of GD.
Prevention
Following are key management strategies that poultry producers can implement to help with disease prevention:
- Ensure a robust immune status.
- Decrease the concentration of clostridium in the surroundings.
- Minimize injury to the skin and intestinal tract, which are the two main route of infection.
To help reduce immunosuppression in poultry flocks, proper vaccination against Infectious bursal disease, Marek’s, chick anemia virus and reovirus is important for protecting the broiler’s immune system. An environment that promotes poor litter conditions may also predispose flocks to GD. Good litter management, immediately addressing water leaks, and regular pickup and proper disposal of affected dead multiple times a day are necessary to keep barn clostridium at low levels. Affected poultry farms are likely to have repeat outbreaks if the environment if not treated properly. It is recommended to do a full litter clean-out between flocks along with reduced stocking density. The use of a pH-lowering chemical to the barn floor has the potential to mitigate the occurrence of recurrent breaks in succeeding flocks.
Intestinal Integrity provided by an effective anticoccidial program, as well as pro and prebiotics, helps maintain a healthy intestinal micro flora and a tight intestinal barrier that keeps clostridium or other disease-causing bacteria found in the intestine from passing into the blood and causing infection. Products have the potential to restore equilibrium to the bacteria present in the digestive system, hence potentially mitigating the occurrence and mortality rates. Nevertheless, due to the crucial role of Clostridial in the disease, a robust microflora does not consistently diminish the sickness.
Growers should closely monitor feeding status and schedule. Do not let your birds run out of feed.An abundance of hungry chickens leads to intensified bird activity, which in turn increases the occurrence of cuts, scratches, and skin damage. Additionally, it is crucial to promptly establish migration fences to prevent overcrowding in certain areas of the house that may heighten the risk of GD. It is advisable to avoid loud noises that could disturb the birds and increase the likelihood of cuts, scratches, and skin damage. Implementing a lighting programme that aids in calming the birds and regulating their activity level is also recommended. A proper management will reduce the stress for the birds and reduces the possibility of a skin injury will reduce the risk of a GD outbreak.
Treatment
- Antibiotics in starter feed to reduce bacteria.
Effective antibiotics against gangrenous dermatitis include penicillin, erythromycin and tetracycline group of antibiotics.