Focal Duodenal Necrosis (FDN) in table egg flocks

Focal duodenal necrosis (FDN) is an intestinal disease of table egg flocks first described by Dr. Patricia Dunn of the Diagnostic Laboratory at Pennsylvania State University in a cage-free layer flock in 1997.

Since that description, FDN has been observed by poultry health workers in most of the states in the United States. Layers of all ages are susceptible but FDN has not been observed in pullets prior to maturity. FDN has also been found in organic flocks.

Various names have been used to describe the disease such as "gray gut," "MUD" (multifocal ulcerative duodenitis), and FND which is the original acronym which is most commonly used.

FDN impacts production goals

The condition is characteristically associated with an inability of a flock to attain standard egg weight or egg production goals or a combination of these parameters. Egg weight lags behind normal by up to two pounds per case in young flocks. Peak egg production may be 2% or 3% below standard or flocks may show a post-peak drop of 1% to 10%.

The only clinical sign reported is that some of the birds show pale combs.

Financial loss depends on the severity of the disease but will be at least 1 to 2 cents per hen for each outbreak if only egg size is affected for a three week period, and an additional 3 cents per hen for each 1% drop in egg production, assuming a depression of three weeks in duration.

Duodenal lesions indicate FDN

Diagnosis is based on observations made when performing post mortem examinations of freshly euthanized birds. Necropsy of birds that have died naturally is not appropriate as the duodenum, the site of FDN lesions, decomposes quite rapidly after death.

Active surveillance for FDN is performed in one major egg production operation by sacrificing six birds from flocks every two weeks for necropsy to ascertain the presence of FDN lesions. The duodenal loop is the site of FDN lesions which consist of single to multiple, dark, irregularly shaped, 5- to 15-mm diameter areas in the mucosa that can be seen from the serosal surface. Upon opening the duodenum, the grey areas can be visualized on the surface.

A "rotten-egg smell" due to the evolution of hydrogen sulfide from the lesions is noted emanating from the surface of the intestine. Histologically, a heterophilic infiltration of the duodenal villus tips is observed with numerous bacteria visualized on the surface.

Cause not confirmed

Originally the condition was ascribed to recycled feed ingredients such as bakery waste, animal byproducts or certain sources of calcium carbonate but this was disproved by finding FDN at the same incidence rate in flocks irrespective of being fed these ingredients. The presence of tapeworms was also considered to be a factor but flocks both with and without cestode infestation appear to be equally affected.

The cause of FDN is currently attributed to the Gram positive bacterium Clostridium colinum which is responsible for ulcerative enteritis in quail and is frequently isolated from cases of necrotic enteritis in broilers and breeders.

At this time the specific cause has not been confirmed as it is not possible to satisfy Koch's postulates by reproducing FDN with pure isolates of Cl. colinum. This finding is not unusual for clostridial enteropathies which require predisposing nutritional, environmental, managemental or as yet non-defined factors. The current theory is that the microenvironment of the intestinal lumen may undergo changes which lead to proliferation of Cl. colinum which produces toxins. This may be stimulated by suboptimal numbers of beneficial competitive bacteria which occur naturally in the intestinal flora. Studies have been conducted by Agtech Products Inc. in cooperation with a Pennsylvania egg producer using PCR technology to examine samples of duodenal tissue from both affected and normal flocks.

Antibiotics are effective

Antibiotics that are effective against Gram positive bacteria are able to suppress clinical FDN. Compounds such as bacitracin, tylosin or oxytetracycline can be added in accordance with label instructions and restrictions.

Preventive measures include the addition of an antibacterial agent in the feed with or without a probiotic.

Since FDN usually affects egg weight early in production, an antibiotic is normally fed until a target egg weight is reached followed by withdrawal of medication.

A recurrence of FDN is normally seen six to eight weeks after termination of administering an antibiotic. A decision is made at that time whether or not to treat depending on the production parameters of the flock.

Bacitracin at 25 grams per ton in feed, is the most commonly used product for prevention with or without a probiotic supplement. Probiotics, such as Primalac (Star-Labs) or Avicor (AgTech), and prebiotics, such as Bio-Mos (Alltech) or Diamond V XPC, or botanical products, including Apex (BFI) or Regano Poultry (Ralco Nutrition), are used alone or in combination but have not been thoroughly tested for their effect on FDN.

Organic or antibiotic-free egg producers must, however, rely on NOP-approved products for prevention.

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