Gangrenous dermatitis: Guarding against a costly disease

In recent years, gangrenous dermatitis (GD) has been on the increase among commercial broiler operations in the US, resulting in significant economic losses.[1] This serious bacterial disease of poultry tends to occur in fast-growing broilers between 4 and 8 weeks of age.
calendar icon 5 February 2018
clock icon 8 minute read

by Tom Tabler, PhD
Extension Professor
Mississippi State University Extension Service, Poultry Science Department
Mississippi State, Mississippi

GD is often fatal within 24 hours. Death losses ranging from 50 to 400 birds per house per day due to GD aren’t uncommon.[2] I’ve witnessed losses in excess of 200 birds per house per day.

For years, it was thought that for GD to occur, there needed to be an initial skin wound that set the bird up for GD, followed by a secondary bacterial infection with Clostridium prefringens type A, Clostridium septicum or Staphylococcus aureus.

We now realise that although the bacteria involved with the occurrence of GD usually aren’t able to penetrate intact skin, they can be ingested if live birds peck at infected dead birds or if litter and faeces are contaminated with large numbers of these disease-causing bacteria.

Theories about the cause

It’s been suggested that for GD to occur and affect large numbers of birds, these three things are generally required:[3] Some type of injury to the skin, a pathogen such as Clostridium or other species present in sufficient numbers to cause disease and some type of immune suppression. Both Clostridia and Staphylococci are present everywhere. They’re in the poultry house, in the intestines of birds and on the skin of birds.

Birds with a strong or even competent immune system generally aren’t affected by GD. That’s why it’s often believed that other diseases that trigger immunosuppression may play a role in the occurrence of GD. These diseases would include infectious bursal disease, inclusion body hepatitis, reovirus, reticuloendotheliosis, Marek’s disease and chick infectious anaemia (CIA).[4] In the past, I’ve seen GD in flocks diagnosed with CIA.

More recently, I saw a case of GD on a farm with a history of the disease, but the current flock had no sign of immunosuppression. However, feed for that flock had run out, and several birds had evidence of skin scratches. It’s possible the repeat case of GD may have resulted from large numbers of disease-causing bacteria left behind from the previous flock, along with the stress caused by the absence of feed.

Oftentimes, farms with a history of GD will experience repeat outbreaks unless corrective action is taken, which I’ll address later in this article.

Role of coccidiosis control

Currently, some veterinarians and production managers believe late coccidial cycling that results from ionophore “leakage” can trigger GD outbreaks. While leakage of coccidial organisms can help stimulate flock immunity to coccidiosis, too much may open the door for GD infection.

In recent years, another theory about the cause of GD has emerged that’s supported by a growing body of field observations. For years, in-feed administration of ionophores has provided reliable coccidiosis control in broilers; however, ionophores are also antibiotics that affect Gram-positive organisms. As such, they alter the balance of good and bad gut microbiota, allowing certain subpopulations to proliferate at the expense of others.

Clostridium septicum and, to a lesser extent, Clostridium perfringens as well as Staphylococcus aureus are able to thrive in the presence of ionophores, thereby allowing them to penetrate the intestinal wall, become systemic and eventually travel to the skin where they set up conditions favourable for GD. There doesn’t have to be a skin injury. Many details for this pathway have yet to be elucidated, but removing ionophores from feed from the fourth week of growout onward quite consistently reduces the incidence of GD in commercial flocks.

Many producers raising broilers without antibiotics or with reduced use of antibiotics are vaccinating to control coccidiosis. In my experience, flocks vaccinated against coccidiosis tend not to develop GD or do so less often. Coccidiosis vaccines aren’t effective against GD, but when administered correctly, they have been shown to provide lifelong immunity against coccidiosis and tend to prevent late coccidial cycling.

What to watch for

Whatever the cause of GD, it’s important to recognize the characteristic lesions of the disease. Initially, there are small pimples on the skin that soon progress to involve larger areas. Watch for spots on top of the wings that look like a raw sore or bloody spot. In the early stages, these will be small — perhaps the size of a dime or a nickel. The top of the wing is easily seen as you walk through the flock, and these spots will indicate that something isn’t right.

Birds with GD die rapidly and, as noted before, generally within 24 hours. Decomposure occurs extremely rapidly, and birds appear to have been dead several days even though they may have died less than 1 hour ago.

The lesions on birds that have died consist of dark reddish to purple to green areas on the skin. These are most often on the abdomen, breast, wings and/or legs. There may be gas or gelatinous fluid accumulated under the skin. To the touch, the skin may feel “spongy” because the numbers of bacteria are increasing, causing a gas buildup between the muscle and skin. Birds that are still alive may have these lesions, but they usually die before the lesions are noted.

Muscle tissue is also affected and may appear as raw, moist areas where skin has deteriorated.

Outbreak measures

Remember that live, healthy birds can contract GD from pecking at dead birds or ingesting their faeces. The causative organism also can be picked up from feeders if litter and faeces are scratched into feed pans. It’s therefore imperative for producers to pick up dead birds several times daily.

GD can also be tracked from house to house, so take precautions and practice sound biosecurity. If you have an outbreak in one house, work that house last to avoid tracking the disease into other buildings.

Corrective action at the farm level generally means a total cleanout of old litter, followed by washing down and disinfecting the premises.

As an alternative, some field reports indicate varying degrees of success when litter amendments are used to induce a dramatic shift downward in litter pH, which may reduce microbial growth. Aluminium sulfate, sodium bisulfate, salt and other treatments have been tried in an attempt to reduce the occurrence of GD. However, here’s an important note of caution: Contract growers should not apply any product to the litter until they first consult with the producer’s service technician to ensure these litter amendments are approved for use in their system.

Another alternative is windrowing litter between flocks in an effort to reduce the pathogen load. When done correctly, in-house windrowing can eliminate most pathogens present in litter, including Clostridium.[5] Windrowing primarily takes advantage of heat to kill microorganisms, although high ammonia levels and competitive exclusion (“good” bacteria overwhelming “bad” bacteria) may also play a role in reducing pathogen numbers.

GD prevention

Good management is imperative if GD is to be prevented or, in case of an outbreak, controlled.

Poor general farm management — including unsanitary conditions as well as stressful conditions such as wet litter and high humidity — can predispose flocks to GD. Reports of GD outbreaks seem to be greater in summer and fall, so these are months when producers need to be especially watchful for the disease. Cool cells that run throughout much of the summer and fall to keep birds comfortable during hot weather can often times lead to wet litter, high humidity and unsanitary conditions even in systems with otherwise good management.

I advise producers to do whatever they can to prevent situations that can agitate birds and increase their activity and the risk for skin injuries and GD. For instance, don’t allow birds to run out of feed because their activity level increases if they’re hungry when they’re fed. Be sure migration fences are in place on time to prevent overcrowding. Avoid subjecting flocks to loud, disturbing noises, and use a lighting program that helps birds stay calm.

Control of immunosuppressive diseases at the complex level through monitoring and a sound vaccination program to prevent immunosuppressive diseases is imperative when GD is a problem. If you’re using ionophores for coccidiosis control, evaluate the protocol to determine if it needs to be adjusted. Do whatever you can to provide a less stressful environment for birds and minimise the risk of skin injuries. These are all steps that may help reduce the risk of a GD outbreak.


1. Waneck CR. Preventive measures to control clostridial outbreaks of gangrenous dermatitis in commercial broiler operations. MS Thesis. Texas A&M University. 2010

2. Tabler T, et al. Gangrenous dermatitis in broilers. Mississippi State University Extension. Publication 2990. 2016

3. Clark FD, et al. Understanding and control of gangrenous dermatitis in poultry houses. FSA7048. University of Arkansas Cooperative Extension Service. 2008 July.

4. Jensen EL. Overview of gangrenous dermatitis in broilers and strategies for prevention. Ross Tech Newsletter. Ross Breeders. 1998 April.

5. Macklin K, et al. Windrow composting of litter to control disease-causing pathogens. Poultry Engineering, Economics, and Management Newsletter. Auburn University, Auburn, AL. No. 47. 2007 May.

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