AVIAN/FUR/EXOTIC SPECIES

Identification of focal duodenal necrosis in several Ontario table-egg laying flocks  

Marina Brash, Mike Petrik

Focal duodenal necrosis (FDN) was first reported in a Pennsylvania cage-free layer flock in 1997.  Since then, FDN has been reported in pullet and laying flocks, including organic, caged and cage-free flocks composed of all the major breeds throughout the United States.  This report documents the identification of the first cases of FDN in several Ontario table-egg layer flocks.

The disease is typically associated with flocks in early lay with the most remarkable clinical finding being the production of smaller eggs.  In addition, there can be a 0.5 to 1.0% decline in egg production or failure to reach peak production.  Pale combs are sometimes reported, but elevated mortality is not.

Diagnosis is based on the identification of characteristic 0.5 to 1.5 cm single to multiple dark flat to slightly raised foci within the mucosa of the duodenal loop of recently euthanized birds (Figure 1) with the dark discoloration also visible through the serosa.  Upon opening the affected duodenum, the odor of hydrogen sulfide has been described.  Gross lesions can be few and subtle, so postmortems of birds dying naturally are less useful because of rapid autolysis of the intestine.

Histologically, the dark mucosal lesions are composed of small foci of acute superficial necrosis of the villus tips with luminal effusion of proteinaceous fluid and large numbers of heterophils accompanied by proliferation of large numbers of slender filamentous gram-positive bacteria that do not morphologically resemble Clostridium perfringens (Figures 2 & 3).  Numerous heterophils also aggregate within the underlying superficial lamina propria

Presently, Clostridium colinum is considered to be the etiologic agent, however Koch’s postulates have not been proven.  Clostridium perfringens may also be involved.  Research groups in the US continue to pursue identification of the etiologic agent and future plans include vaccine development.

The pathogenesis is not known but, because the duodenum is not a site of high nutrient absorption, it is likely that nutrient digestion and iron absorption are impacted.

Treatment includes extended in-feed administration of antibiotics known to be effective against gram-positive anaerobic bacteria until production and egg size have returned to normal.  Following the removal of the antibiotics, recurrence of the disease is possible.  The effectiveness of prebiotics and probiotics and organic acids in prevention of FDN is being investigated.

Because focal duodenal necrosis cannot be reliably identified by postmortems of the daily mortality, periodic monitoring of flocks is required.  Based on one of the authors’ (MP) clinical experience with FDN, this condition can be difficult to identify as not all hens will have well-developed lesions, entailing the examination of several freshly euthanized hens at each session.  Other management, nutritional, and infectious causes of reduced egg size and production must be considered.   

Figure 1: Diagnosis of FDN is based on the diagnosis of multiple small flat to slightly raised dark foci on the mucosa of the duodenal loop of a recently euthanized laying hen. Examination of duodenal loops of several hens is necessary.	Figure 2: Histology of FDN.  Focal necrosis of villus tips with luminal effusion of proteinaceous fluid and heterophils accompanied by large numbers of slender filamentous bacteria.	Figure 3: The slender filamentous bacteria are gram-positive and do not morphologically resemble Clostridium perfringens.