Symptoms, prevention and treatment of porcine proliferative bowel disease
Other names include necrotizing enteritis, proliferative hemorrhagic enteropathy, porcine ileitis, terminal ileitis, and porcine intestinal adenoma. The main clinical manifestations of the disease are intermittent dysentery, loss of appetite and growth retardation. Breeding pigs and reserve sows sometimes have blood samples of dysentery and sudden death. The autopsy was characterized by thickening of small intestinal and ileal mucosa. The histopathological changes were characterized by adenomatous hyperplasia of immature intestinal cells in the ileum and colonic recess. The disease is endemic all over the world.
Pathogen
The pathogen of porcine proliferative bowel disease is intracellular Lawson, which was also known as ileal intracellular symbiosis. It is a kind of intestinal cell specific anaerobic bacteria, which can not grow in cell-free medium, but can only grow on intestinal cell lines of mice, pigs or humans. Gram staining is negative and there are no flagella and cilia.
Epidemiology
Diseased pigs and infected pigs are the source of infection of the disease.
The feces of infected pigs contain necrotic intestinal wall cells and a large number of pathogenic bacteria. The pathogen is excreted from the body with feces, pollutes the external environment, and is infected through the digestive tract with feed, drinking water and so on. Adult pigs are more susceptible, generally less than 2 months old and more than one year old pigs are not easy to get sick.
The occurrence of the disease is related to the external environment and other factors. Factors such as sudden climate change, long-distance transportation, high feeding density, stress such as conversion of feed, and or improper use of antibiotic additives can be the causes of the disease. In addition, birds and rodents also play an important role in the transmission of the disease.
pathogenesis
The pathogens mainly invaded the ileal mucosa and thickened the inner mucosa of the ileum. First of all, the site of infection is intestinal crypt cells, the epithelial cells infected with bacteria can not mature, and continue to mitosis, high proliferation, that is, the formation of porcine proliferative bowel disease.
On the basis of cell proliferation, due to the compensation and repair of the body, the lesions overlap. With the extension and in-depth development of surface fibrosis, the range of inflammatory changes condensed into necrosis, forming necrotizing enteritis. These intestinal mucosal lesions hinder the absorption of nutrients, resulting in weight loss and a decrease in feed conversion.
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