How to prevent and treat chicken gizzard erosion? A comprehensive analysis of its disease characteristics

Chicken gizzard erosion is a disease that occurs in young chickens, especially broiler chickens, and is similar to intestinal ulcer disease. Whether the disease occurs is closely related to the use of fishmeal in chicken feed. The occurrence of this disease often brings corresponding economic losses to @#@230@#@ production.

1. Clinical symptoms and disease characteristics

Chickens from 1 to 5 months of age can all be affected, with mortality varying, and in severe cases reaching more than 10%. Affected chickens mainly show reduced appetite, listlessness, squatting, fluffy feathers, emaciation, pale combs and wattles, anemia, and blackish-brown thin fluid as vomitus (hence the disease is also called "black vomit disease"), diarrhea, and blackish-brown soft droppings or blackish-brown thin droppings. Affected chickens grow slowly and may die suddenly. If mixed infection or concurrent infection with other diseases occurs, mortality increases.

2. Causes and pathogenesis

The fishmeal mixed into the feed contains toxic substances that cause muscle erosion, which is the root cause of the disease. In addition, long-term deficiency of essential fatty acids in the feed, which affects the body's absorption and utilization of fat-soluble vitamins, deficiency of vitamin B6 and vitamin K, and excessive use of copper sulfate are all related to the occurrence of this disease.

Toxic fish such as mackerel, carp, and chub mackerel are mixed into fishmeal during production; the amino acids contained in fish protein form various amines under the action of bacteria; during fishmeal processing, high temperature causes excessive free histidine to combine with casein to form a histidine-casein complex, thereby enhancing toxicity. This histidine-casein complex can promote increased secretion in the gizzard, and excessive secretions lead to pathological changes in the gizzard tissue. The normal lamina propria of the gizzard mucosa has arranged proventricular glands that can secrete a keratin-like substance covering the surface of epithelial cells and serve as a barrier to prevent gastric contents from damaging the mucosa. However, the histidine-casein complex can destroy this protective layer, causing disordered secretion of the gizzard glands, thereby leading to gizzard erosion and ulcers. Because the keratin-like protective layer becomes loose, brittle, and hemorrhagic, the blood that flows out turns black under the action of gastric acid and travels retrograde with mixed gastric contents to the crop, causing both the vomitus and the descending diarrheal material to appear blackish-brown.

3. Pathological autopsy changes

The body is characterized by systemic anemia. The main lesions are concentrated in the digestive tract, especially the stomach and intestines. There is rice-water-like blackish-brown thin fluid in the digestive tract; the proventriculus is dilated and empty, with mucosal shedding, and there are varying degrees of erosion and ulcers in the middle and posterior regions; the keratin-like membrane of the gizzard is dark green or black, the folds are thickened, and the surface is rough. In severe cases, there are erosive lesions, and there are few or even no sand grains in the gizzard, with residual food appearing dark green or blackish-brown; the heart, liver, proventriculus, lungs, and kidneys are pale, with bile overflow; the duodenal and cecal mucosa are hemorrhagic, with surface necrosis, and the cloacal mucosa is congested. Laboratory microscopy shows that the gizzard tissue structure is loose, the chief cells and epithelial cells of the glands under the keratin-like layer are swollen, and there are shed epithelial cells, cell fragments, and focal lesions; the tissue in the lower layer of the keratin-like substance is liquefied and eroded, the lamina propria is edematous, with scattered focal neutrophil infiltration, and the keratin-like membrane is significantly thickened and relaxed, separated from the tissue below; the duodenum has catarrhal and hemorrhagic inflammation, villi shedding, and focal lesions on the mucosal surface.

4. Clinical diagnosis

Clinical diagnosis can often be made based on the clinical symptoms of affected chickens, pathological autopsy changes (especially gizzard lesions), and combined with the use of fishmeal in the compound feed, but during the diagnostic process attention should be paid to differential diagnosis from coccidiosis.

5. Prevention and control principles and measures

1. Prevention and control principles

Because the occurrence of this disease is closely related to the quality and amount of fishmeal, the prevention and control principle for this disease should take changing the amount of fishmeal in the chicken diet as the fundamental means. In the process of preparing chicken feed, under the premise of ensuring the quality of fishmeal, other protein feed should be selected as much as possible to replace the fishmeal proportion. In addition, vitamin supplementation should be increased to enhance the chickens' resistance; hemostatic agents should be used to reduce gizzard bleeding and prevent worsening of symptoms in affected chickens.

2. Treatment methods

① For each chicken, use vitamin K1 mg and hemostatic powder 80 mg, intramuscular injection, twice daily, for 3 to 4 consecutive days, to control gastric bleeding; ② In the chicken feed, add vitamin B6 5 mg and vitamin C 40 mg per kg of feed to enhance the chickens' resistance; ③ Use cimetidine at 4 to 5 mg per kg of body weight mixed into the feed to feed the chickens, for about 7 consecutive days, to control gastric acid secretion, protect the gastric mucosa, and promote healing of gizzard erosion and ulcer surfaces.