Necrotic enteritis is an acute enterotoxemia. The clinical illness is usually very short, and often the only signs are a severe depression followed quickly by a sudden increase in flock mortality. The disease primarily affects broiler chickens (2–5 wk old) and turkeys (7–12 wk old) raised on litter but can also affect commercial layer pullets raised in cages. Early mortality is often related to coccidiosis vaccination programs, with Eimeria cycling in these flocks.
Etiology and Pathogenesis:
The causative agent is the gram-positive, obligate, anaerobic bacteria Clostridium perfringens. It is usually isolated on blood agar, incubated anaerobically at 37°C (98.6°F), on which it produces a double zone of hemolysis. There are two primary C perfringens types, A and C, associated with necrotic enteritis in poultry. Toxins produced by the bacteria cause damage to the small intestine, liver lesions, and mortality.
C perfringens is a nearly ubiquitous bacteria readily found in soil, dust, feces, feed, and used poultry litter. It is also a normal inhabitant of the intestines of healthy chickens and turkeys. The enterotoxemia that results in clinical disease most often occurs either after a change in the intestinal microflora or from a condition that results in damage to the intestinal mucosa (eg, coccidiosis, mycotoxicosis, salmonellosis, ascarid larvae). High dietary levels of animal byproducts (eg, fishmeal), wheat, barley, oats, or rye predispose birds to the disease. Anything that promotes excessive bacterial growth and toxin production or slows feed passage rate in the small intestine could promote the occurrence of necrotic enteritis. In many cases, concurrent coccidiosis (especially Eimeria maxima, and E acervulina to a lesser extent) is associated with outbreaks in commercial broilers, although recent investigations with NetB-positive isolates have reportedly caused disease without predisposition from Eimeria infections.
Clinical Findings and Lesions:
Most often the only sign of necrotic enteritis in a flock is a sudden increase in mortality. However, birds with depression, ruffled feathers, and diarrhea may also be seen. The gross lesions are primarily found in the small intestine (jejunum/ileum), which may be ballooned, friable, and contain a foul-smelling, brown fluid. The mucosa is usually covered with a tan to yellow pseudomembrane often referred to as a “Turkish towel” in appearance. This pseudomembrane may extend throughout the small intestine or be localized. The disease usually persists in a flock for 5–10 days, and mortality is 2%–50%.
A presumptive diagnosis is based on gross lesions and a gram-stained smear of a mucosal scraping that exhibits large, gram-positive rods. Histologic findings consist of coagulative necrosis of one-third to one-half the thickness of the intestinal mucosa and masses of short, thick bacterial rods in the fibrinonecrotic debris. Isolation of large numbers of C perfringens, from intestinal contents that produce the double zone of hemolysis as described above, can confirm the diagnosis. Double zone hemolysis should not be used as the sole criterion for identification of C perfringens, because some strains do not produce both toxins responsible for the hemolysis characteristics. Differential media specifically designed for isolation of C perfringens is available and may be useful for diagnosis.
Necrotic enteritis must be differentiated from lesions produced by Eimeria brunetti and also from ulcerative enteritis. Uncomplicated coccidiosis rarely produces lesions as acute or severe as those seen with necrotic enteritis. Ulcerative enteritis caused by C colinum usually produces focal lesions from the distal portion of the small intestine (ileum) to the ceca and is almost always accompanied by hepatic necrosis.
Prevention, Control, and Treatment:
Because C perfringens is nearly ubiquitous, it is important to prevent coccidiosis, especially E acervulina and E maxima infections, as well as changes in the intestinal microflora that would promote its growth. This has traditionally been accomplished by adding antibiotics in the feed such as virginiamycin (20 g/ton feed), bacitracin (50 g/ton feed), and lincomycin (2 g/ton feed), as well as ionophore-class anticoccidial treatments. The move to antibiotic-free feeds has also been associated with markedly increased use of coccidiosis vaccines, resulting in early circulation of mixed Eimeria infections that are associated with the resurgence in incidence of necrotic enteritis. Avoiding drastic changes in feed and minimizing the level of fishmeal, wheat, barley, or rye in the diet can also help prevent necrotic enteritis. When higher amounts of wheat, barley, or rye are necessary, use of enzymes for nonstarch polysaccharides in the feed has reduced the level of necrotic enteritis in flocks fed these cereals. Administration of selected probiotics or competitive exclusion cultures has been used successfully to both prevent and treat clinical necrotic enteritis (presumably by preventing proliferation of C perfringens).
Treatment for necrotic enteritis is most commonly administered in the drinking water, with bacitracin (200–400 mg/gal. for 5–7 days), penicillin (1,500,000 u/gal. for 5 days), and lincomycin (64 mg/gal. for 7 days) most often used. In each case, the medicated drinking water should be the sole source of water. Moribund birds should be removed promptly, because they can serve as a source of toxicosis or infection due to cannibalism.