MMR_2025v15n1

Molecular Microbiology Research, 2025, Vol.15, No.1, 18-27 http://microbescipublisher.com/index.php/mmr 20 3 Pathogenic Strains of E. coli 3.1 Classification of pathogenic E. coli strains Some E. coli can make people sick, and this type of bacteria is called "pathogenic E. coli". Depending on the virulence factors they carry and the disease they cause, these bacteria can be divided into several categories. There are three common types: enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), and uropathogenic E. coli (UPEC). EPEC is one of the common causes of diarrhea in young babies in developing countries. This bacteria attaches to the intestinal wall and destroys intestinal surface cells (Hazen et al., 2017). EHEC is also well known, especially the O157 strain in it, because it produces Shiga toxin. This toxin can cause severe hemorrhagic enteritis and even hemolytic uremic syndrome. UPEC is the main bacteria that causes urinary tract infection. It can stick to the urethra and escape the attacks of the human immune system (Russo and Johnson, 2000). 3.2 Genetic determinants of virulence in pathogenic strains The reason why these pathogenic bacteria are powerful is that they carry some special genetic fragments. These fragments come from pathogenic islands, plasmids and bacteriophages, and contain many "discomfortable" genes, such as toxins or other harmful substances. EPEC has a gene region called LEE, which encodes the type III secretion system (T3SS) and some proteins that can attack host cells (Donnenberg and Whittam, 2001; Hazen et al., 2017). EHEC carries the genes of Shiga toxin, which are "bringed" through lyogenic phages. Shiga toxin is the key to its severe illness. UPEC has more types of “weapons”. It carries the fimH protein that helps it attach, and it also carries a variety of toxins and a system that helps absorb iron. Most of these genes are hidden in its plasmids and pathogenic islands (Khairy et al., 2019). They will also "teach" these genes to each other, and this process is called horizontal gene transfer. This also explains why these strains change quickly and are adaptable. 3.3 Comparison of pathogenic E. coli with commensal strains Compared with symbiotic E. coli, there are many differences in pathogenicity. Symbiobiosis generally does not make people sick and is a "good partner" in our intestines; but pathogenic bacteria are different. They carry special virulence factors and can cause various infections. For example, EPEC has a T3SS secretion system, EHEC has Shiga toxin, UPEC has adhesions that help it stick to cells, and toxins. These are all that symbiotics do not have (Russo and Johnson, 2000). In addition, the "workability" of pathogenic strains is also stronger. They often obtain or lose virulence factors through gene transfer, and these changes are relatively rare in symbiotic bacteria (Halaji et al., 2022). This “flexibility” allows pathogens to adapt to different environments or human parts more quickly, causing more types of diseases (Khairy et al., 2019). 4 Mechanisms of Pathogenesis 4.1 Adhesion and invasion mechanisms Pathogenic E. coli enters the human body through various methods and causes infection. For example, UPEC, which causes urinary tract infection, will stick to urethral cells with some "little hook-like" structures. These structures include type 1 pilates, type P pilates, type S pilates, and an adhesion protein called Dr (Mulvey, 2002). Once they stick, they can get into the cells and reproduce there. In this way, they can avoid the human immune system and are not easily removed. Shiga toxin-producing E. coli (STEC) will also stick to intestin cells through a protein called "integrin". This is their first step in settlement in the gut and beginning to release toxins (Farfán and Torres, 2011). In addition, there are STEC strains that do not have LEE regions (enter cell erosion sites) that use a gene called tia to help them enter intestinal cells (Bondíet al., 2017). These examples show that E. coli has many different ways to adhere and enter human tissue. 4.2 Toxin production and its role in disease manifestation Toxins of E. coli are their important "weapons" for their disease. For example, STEC releases Shiga toxins (Stxs), which can interfere with the process of cell making proteins, resulting in cell death, damage to the intestines, causing severe hemorrhagic colitis, and even hemolytic uremic syndrome (HUS) (Farfán and Torres, 2011). In addition, there is a toxin called Sat, which not only directly destroys cells, but also affects the body's immune response. It weakens the immune system by lying complement proteins, makes it easier for bacteria to "escape",

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