Broiler enterotoxemia is a disease commonly found in commercial broilers, with the following characteristics:
I. Incidence and clinical symptoms:
Large numbers of chickens develop diarrhea. Their droppings are loose and do not form piles, cover a larger area than normal droppings, and are pale yellow, with large amounts of undigested feed particles. Feed intake drops rapidly. In the early stages, some affected chickens show abnormally high excitement, head and neck tremors, running and crashing about, and screaming. After becoming excited, they die from weakness and exhaustion, and sudden deaths before dawn become more frequent.
II. Postmortem changes:
In early cases, swelling of the duodenal and jejunal walls can be seen, along with thickening of the intestinal mucosa, which becomes pale grayish-white. Pinpoint to mung-bean-sized red hemorrhagic spots appear on the serosal surface of the small intestine; in dead chickens, the intestinal wall becomes thin and the mucosa sloughs off. The intestinal contents may be pus-like, fish-intestine-like, or tomato-like. In a few severe cases, the intestinal mucosa almost completely sloughs off and disintegrates.
III. Causes and mechanisms:
1, Severe coccidial infection: Small-intestinal coccidia multiply extensively beneath the intestinal mucosa, causing lesions such as mucosal thickening, hemorrhage, and sloughing. This reduces the intestine’s ability to absorb nutrients from feed and decreases water absorption, causing dehydration in chickens. This is an important reason for the loose droppings containing undigested feed.
2, changes in the intestinal environment: Coccidia reproduce rapidly inside intestinal mucosal cells and consume oxygen, causing the small intestinal mucosal tissue to produce large amounts of lactic acid. Intestinal pH drops sharply, the intestinal flora changes, beneficial bacteria decrease and harmful bacteria multiply in large numbers. Digestive enzyme activity declines, intestinal peristalsis accelerates, and more digestive fluids are excreted. Feed remains in the digestive tract for less time and is digested for a shorter period, resulting in incomplete digestion.
3, effects of vitamins, energy, and protein in feed: In mixed infections involving coccidia and bacteria, the abundant energy, protein, and vitamins in high-quality feed can promote the proliferation of both, aggravating the disease. Therefore, the better the nutritional quality of the feed, the higher the incidence and the more severe the symptoms.
4, substantial electrolyte loss: The extensive proliferation of coccidia and bacteria causes indigestion and impaired absorption, reducing electrolyte absorption. At the same time, the breakdown of large numbers of cells causes substantial electrolyte loss. In particular, significant loss of potassium ions can lead to excessive cardiac excitation and sudden death in broiler chickens.
5, autointoxication: During the disease, large numbers of intestinal epithelial cells rupture and decompose through putrefaction. In addition, after the host absorbs the large quantities of toxic substances released by the breakdown of dead parasites and bacteria, autointoxication occurs. Clinically, this first causes restlessness and agitation, followed by weakness, coma, and death from exhaustion.
Five. Epidemic characteristics:
In recent years, commercial broiler chickens can become ill at any time during the entire rearing cycle, and the disease can occur in all seasons. Inadequate coccidiosis prevention is the main cause. The disease is more likely to occur and symptoms are more severe in environments with poor sanitation, high stocking density, high humidity, and inadequate ventilation. Coccidia can complete their life cycle repeatedly in the internal and external environments of the host, and the large number of oocysts in feces can lead to repeated coccidial infections.
Six. Treatment measures:
1, treatment should be based on antibacterial and anti-inflammatory treatment, heat-clearing and detoxification, anticoccidial treatment, and strengthening the animal's constitution. If the disease has not yet occurred, anticoccidial drugs such as sulfaquinoxaline sodium soluble powder or diclazuril can be administered in drinking water; anticoccidial drugs can also be added to feed for prevention. For mild symptoms, intestinal anti-inflammatory drugs such as colistin sulfate soluble powder can be used. For more severe symptoms, administer orally absorbed drugs such as amoxicillin soluble powder by gavage, together with anemarrhena powder mixed into feed, and also provide anticoccidial treatment. For flocks with severe autointoxication, add glucose and vitamin C separately to aid detoxification.
2, preventing necrotic enteritis in broiler chickens requires strengthening farm management, including maintaining suitable temperature and humidity in the poultry house, ensuring good ventilation, disinfecting regularly, promptly cleaning up manure and treating it harmlessly, and cutting off routes of transmission; arranging preventive medication appropriately to reduce stress; and ensuring feed is safe and free of mold.
3, during treatment, take care to avoid certain misconceptions. For example, do not forcibly stop diarrhea, as this may worsen autointoxication; avoid using potent drugs in the early stages, to prevent large numbers of Gram-negative bacteria from dying and releasing excessive endotoxins, which can disrupt the body's regulatory systems; do not use large amounts or overdoses of multivitamins, to avoid increasing the nutrient content of the intestinal contents and encouraging the proliferation of harmful bacteria; and avoid administering medication through feed where possible, because sick chickens eat less and may therefore not receive an effective overall treatment dose.
At the same time, strengthen daily management, hygiene, and disease prevention and control at the chicken farm to reduce the risk of disease.