In recent years, E. coli disease has become a major disease constraining the rapid development of the poultry industry, with high morbidity and mortality, threatening the poultry industry and causing serious economic losses.
For the current domestic specific situation, the causes of E. coli disease are mainly primary, induced, and secondary.
According to tests, feces samples of 1 g of healthy chickens are randomly taken and calculated by microbiological methods, often containing 1 million E. coli. Although most of them are non-pathogenic, they also have considerable pathogenicity. Their serotype is O1. , O2, O35, O78 and so on. These E. coli strains, floating out of the chicken droppings and drifting with the air, can easily fall on the mucosa of the respiratory tract as they drift with the air. With the help of pilus adhesion, they can â€œsettleâ€ in the epithelium and gain access to the â€œchannelâ€. . When the chickens have poor feeding conditions and their resistance decreases, the pathogenic E. coli enters the chicken through the â€œchannelâ€ and presents acute septicemia or subacute pericarditis, pericarditis, and balloon inflammation.
We often say that "slow calls," that is, mycoplasma is a recognized E. coli causative disease. Mycoplasma and E. coli diseases are often inseparable in the case of chicken farms. U.S. poultry experts have said this in describing this situation. Once mycoplasmosis and E. coli are combined, this will become a chronic problem. Therefore, purifying the cause of E. coli disease has a very important practical significance. Or take the example of mycoplasma. If the ancestral chicken farm purifies the mycoplasma and the parent chicken farm has strict measures for the eradication of mycoplasma, then the chances of E. coli infection in chicken farms will be much less.
Escherichia coli causes are Bacillus mildew disease, hemorrhagic enteritis and so on.
When viruses in breeding environments, such as Newcastle disease, bird flu, infectious bronchitis, and infectious bursal disease virus, accumulate to a certain extent, they will develop morbidity; virulent viruses first attack the chicken body and cause chicken body damage. Decline in resistance; followed by virulent attack in chickens, typical symptoms. At this time, the E. coli in the environment enters the chicken body after virulent poisoning, or enters the chicken body after the chicken body becomes weak. This kind of E. coli disease that enters the chicken body after virulent poisoning is called secondary E. coli disease.
E. coli has many serotypes and the antigen structure is complex. At present, there are 173 O antigens, 74 K antigens, 53 H antigens and 17 F antigens (pilus antigens). According to reports from foreign countries, the serotypes of infected poultry are mainly O, O, O, and O; while studies of sorghum in China indicate that the main serotypes of poultry infecting my country are O, O, O, O, O, and O; Researches in China, etc. are based on O, O, O, O, O, O, O. These findings not only indicate that the main serotype of E. coli that infects our country's poultry is different from that of other countries, but also indicate that the main serotypes in different parts of China are also different. Most strains of serotypes isolated from birds are only pathogenic to poultry. However, in recent years, the emergence of O:H strains that contaminate poultry meat has caused haemorrhagic enteritis in humans, making it difficult for people to taste delicious food. I have a lot of heart. Therefore, controlling E. coli disease in poultry also has important public health significance.
Colonization factors (CF); also known as Adhesin, the pilus of E. coli. The pathogenic E. coli must first adhere to the intestinal wall of the host in order to avoid clearance by intestinal peristalsis and intestinal secretions. The colonization factors that cause human diarrhea are CFAI and CTAII (Colonization factorantigen I, II). The colonization factor has strong immunogenicity and can stimulate the body to produce specific antibodies.
Enterotoxin: It is an exotoxin released from the enterotoxigenic Escherichia coli during growth and reproduction. It is classified into heat-resistant and heat-resistant.
Heatlabile enterotoxin (LT): Instable to heat, inactivated at 65Â°C for 30 minutes. For protein, it has a large molecular weight and is immunogenic. It consists of two subunits, A and B. A is divided into A1 and A2, where A1 is the active part of the toxin. After the B subunit binds to the GM1 ganglioside receptor on the surface of the intestinal mucosal epithelial cell membrane, the A subunit passes through the cell membrane and acts on adenylyl cyclase, converting intracellular ATP into cAMP. When cAMP is increased, it causes excessive secretion of intestinal fluid, which exceeds the intestinal absorption capacity and causes diarrhea. The immunogenicity of LT is similar to that of Vibrio cholerae enterotoxin, and the antisera of the two are cross-neutralizing.
Heatstable enterotoxin (ST): It is heat-stable, and it is not destroyed at 100Â° C. for 20 minutes. Its molecular weight is small and the immunogenicity is weak. ST activates guanylate cyclase in intestinal epithelial cells, increases intracellular cGMP, alters the flow of fluid in the open field, and causes diarrhea in the intestinal effusion. There is no common antigenic relationship between ST and cholera toxin.
Some strains of enterotoxigenic E. coli produce only one enterotoxin, LT or ST, and some produce both. Some pathogenic E. coli can also produce verotoxins.
Lipid A of other cell wall lipopolysaccharides is toxic, and O-specific polysaccharides have a role in resisting the host defense barrier. E. coli K antigen has phagocytosis. In addition, enteroadhesive E. coli (EAEC) can also cause diarrhea, but its pathogenesis and serotype are still unknown. EAEC does not invade intestinal epithelial cells, does not produce LT or ST, and does not have VT toxins. Its unique feature is its ability to adhere to Hep-2 cells (human laryngeal epithelial cell line) and is also called Hep-2 cell-adherent E. coli.
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