The natural age of onset of necrotizing enteritis is from 2 weeks to 6 months of age. Most reports indicate that the onset of disease in broilers raised on litter is between 2 and 5 weeks of age. There are reports of morbidity in commercial laying hens raised on the ground between 3 and 6 months old, outbreaks of necrotizing enteritis in caged reserve layer hens aged 12 to 16 weeks, and reports of morbidity in adult commercial laying hens raised in cages. There have been reports of necrotizing enteritis outbreaks in young turkeys and turkeys aged 7 to 12 weeks.

 

Clinical Symptoms
When the disease occurs naturally, sick birds show: obvious to severe depression, loss of appetite, reluctance to move, diarrhea and disheveled feathers. The course of the disease is short, and short-lived birds often die acutely without external symptoms.



Pathological changes

gross lesions
lesions. Autopsy lesions during spontaneous onset are often limited to the small intestine, most commonly in the jejunum and ileum; however, cecal lesions have also been reported. The small intestine is brittle and full of gas. The intestinal mucosa is covered with a layer of yellow or green pseudomembranes. Some pseudomembranes are loosely combined and some are tightly combined. It is often described as having a "Turkish bath towel" appearance. Blood spots have also been reported, but bleeding is not a major feature of the disease. Thickening and dark color of the duodenum and jejunum mucosa can be seen 3 hours after experimental infection with Clostridium perfringens, and necrosis of the intestinal mucosa can be seen 5 hours later, followed by severe fibrinous necrotizing enteritis and the formation of diphtheria-like pseudomembranes in the mucosa. . When typical and subclinical necrotizing enteritis occurs, the typical manifestations of hepatitis are hepatomegaly, brown color with necrotic lesions, and cholecystitis.


Tissue lesions
The tissue lesions of natural infection are characterized by severe necrosis of the intestinal mucosa, and the necrotic lesions indicate the adhesion of large amounts of cellulose and cell debris. The lesions first occur at the tops of intestinal villi, with epithelial cells falling off and bacteria colonizing the exposed lamina propria. As the disease progresses, the necrotic area extends from the tops of microvilli to the crypts. Necrosis can extend deep into the intestinal submucosa and muscularis. Many large bacilli often adhere to the cell debris. Resistant birds showed regenerative changes, including proliferation of crypt epithelial cells and an increase in mitotic cells. The epithelial cells are mainly cuboidal epithelial cells, and cup and columnar epithelial cells are relatively reduced. Intestinal villi are relatively short and flat. In many cases, various sexual and asexual stages of coccidia are also found in the intestines.



Diagnostic

pathogen isolation and identification
The disease can be diagnosed based on typical autopsy lesions and histological lesions, as well as the isolation of Clostridium perfringens. Clinically, Clostridium perfringens can be easily isolated by sampling intestinal contents, intestinal wall scrapings or hemorrhagic Peyer's patches in cases of necrotizing enteritis, inoculating blood agar plates and culturing anaerobically at 37°C overnight. Clostridium perfringens can be identified as described in the "Etiology" section. Some commercial media are not suitable for selective culture and enumeration of C. perfringens unless combined with other specific identification tests.
A sandwich ELISA test can be used to screen diseased and healthy birds based on the amount of C. perfringens and toxins. The PCR method can be used for quantitative detection of Clostridium perfringens isolated from the chicken gastrointestinal tract, and the alpha toxin gene in Clostridium perfringens can also be detected.


Identification and diagnosis:
Pay attention to distinguishing this disease from ulcerative colitis, Eimeria brucei and Eimeria maxima infections. Ulcerative enteritis is caused by Clostridium quail infection; its characteristic autopsy lesions are multiple necrosis and ulcer lesions in the distal small intestine and cecum, as well as necrotic lesions in the liver. As mentioned previously, lesions in necrotizing enteritis are limited to the jejunum and ileum, with little or no lesions in the cecum. These characteristics distinguish necrotizing enteritis from ulcerative enteritis, and the disease can be diagnosed once the causative agent is isolated and identified. The autopsy lesions caused by Eimeria brucei infection are similar to this disease, but microscopic examination of stool smears, intestinal mucosal smears and intestinal sections can prove the presence of coccidia. A final reminder is that necrotizing enteritis and coccidiosis often infect a flock at the same time. Because, one or two pathogens need to be tested for diagnosis.