Uropathogenic E. coli and virulence factors in UTIs

One of the main causes of many urinary tract infections, including pyelonephritis, cystitis, and disease-related complications that lead to acute renal failure, is the uropathogenic E. coli (Bien, Olga, and Przemyslaw 3). However, it is frequently found in the digestive tracts of both humans and animals, where it creates a symbiotic relationship that allows the luminal floral to continue to function at its best. In this interaction, it resides in the intestinal lumen without doing any damage but rather aids in maintaining optimal homeostasis. In some cases such as a compromised immune system of the host and destruction of the gastrointestinal wall, some strains of the E. coli become pathogenic and lead to the infections (Bien, Olga, and Przemyslaw 4). These strains become pathogenic by obtaining some virulence factors that facilitate through bacteriophages, plasmids, and pathogenicity islands and many other which improves its ability to survives and infect the host intensively. These strains are grouped two which include enteric and extraintestinal E. coli. These strains are further subdivided into other pathophytes that cause disease by colonizing host's niches such as the urinary tract and the blood that leads to infections. Urinary tract infections are the most common human infections, and their occurrence depends on the virulence of the pathogen and the state of the immune system. The UTIs are classified based on the site of their existence, for instance, pyelonephritis is when the infection occurs in the kidney while cystitis is when the UTI occurs in the bladder. Therefore Uropathogenic E. coli and its virulence capacity is a key determinant of the occurrence of the UTIs in human beings.

The E. coli is a gram-negative bacillus found in the fecal flora, and reside in the human colon. The theory of pathogenicity states that E. coli have adapted to its environment to enable it to evade host defensive attacks during the expansion of its colonic milieu. This capacity allows it to move to new niches and avoid competition with other bacteria (Subashchandrabose, and Harry 2). Virulence is the capacity that a particular organism has to cause an illness to a host. The UTI occurs in at least 12% and ten to 20% of men and women respectively in their lifetime. This has become a public health concern especially with the resistance of the antibiotics (Subashchandrabose, and Harry 3). The E. coli develop adaptation to antibiotic treatment which makes them even more virulent. They lead to both complicated and uncomplicated cases of UTIs, where the uncomplicated instances represent the case where the host has a healthy functioning urinary tract system. The uncomplicated cases are the ones commonly classified as either upper or lower UTIs. On the other end, the complicated UTIs are those cases associated with abnormalities of the urinary tract system such as immunosuppression and urine retention (Flores-Mireles, Walker, Caparon, and Hultgren 270). Some of the signs of UTIs include pain while urinating, urgency, and frequently urinating which lead to the damage of the kidneys and eventually death to the patients with this health problem.

Adherence is the virulence factor of E. coli that makes a feasible causative agent of the UTIs. E. coli uses this property to attach itself on the walls of various structures of the host to avoid being swept away from their niche as body fluids move along, for instance, the blood and intestinal content (Johnson 83). This method is utilized by many pathogens which include viruses and bacteria to facilitate their colonization of a particular niche. A study indicated that despite the presence of mannose which inhibits hemagglutination, an E. coli strain was able to agglutinate the erythrocytes of human beings. This action allows the E. coli to adhere to the uroepithelial cells making the environment suitable for it to colonize and cause UTI. The study also revealed that fimbriae were the agent that mediated this process of adherence. The fimbriae act like flagella but are longer and thicker and sometimes used by the E. coli to move to other regions and attach itself when rapid body fluid movement starts to avoid being swept away. The flagella are also vital in chemotactic movements, to detect the presence of harmful chemicals, for instance, the antimicrobial and design a response. It also enables the E. coli strains to identify regions such as the kidney which have ready nutrients to facilitate its virulence capacity. Most of the UTI cases arise from the activities of the E. coli in the periutheral area from the E. coli strains arising from the gastrointestinal regions.

Therefore it can be concluded that the E. coli strains show more chemotactic response towards urine as compared to the fecal matter. Urine provides optimum conditions as compared to fecal mediums for the growth and spread of the E. coli pathogenic characters (Subashchandrabose, and Harry 10). Additionally, the adherence effect is facilitated by the prior exposure of the microbial to the antimicrobial agents which makes them more resistant to immune attacks (Johnson 84). For instance, the exposure to nalidixic acid improve its capacity for hemagglutination and subsequently adherence to the cells. The host's properties also influence the adherence ability of the E. coli which leads to UTI. For instance, in a study that targeted to find a cure for patients who had recurrent cases of UTI, it was discovered that some parts such as the vaginal cells have a higher adherence capacity that cells of other parts of the body (Johnson 85). The results indicated that the uroepithelial cells that were collected during the center of the menstrual cycle had a higher adherence power to the E. coli and hence the ability to develop UTI during this time was higher (Siegfried, Puzova, Molokacovas And Filka 129). Additionally women who are treated with estrogen hormones improves the adherence capacity of the bacteria to the walls of the host cells. The fimbriae also have receptors to various antigens based on the first encounter which makes their ability to bind to the target sites easy. This resistance they develop improves their aggressiveness to cause UTI and is a pivotal reason to explain why various kinds of antimicrobial treatments fail to rid the problem. The fimbriae release adhesins to make their task easy in colonizing a niche. Some plasmids have an aerobactin region which contains the resistance agent in E. coli. This case is typical for patients with compromised immune system and is suffering from urosepsis. These patients develop the problem due to the overexposure the antimicrobial drugs that toughen the E. coli strain and hence improving it virulence ability to cause UTI. Other strains after prolonged exposure to these medicines develop a resistance gene that hinders the action of the microbial drugs in the presence of UTIs (Karimian, Hassan, and Mahbobe 6811). The presence of aerobactin contributes significantly to this state of events which leads to UTIs.

Another virulence factor of E. coli to improve its capacity to infect the host is by the production of colicin (Santo, Claudia and José 186). These substances hinder the activity of other microbial strains making E. coli the only element in the colony to conduct their operations which result in UTIs. This aspect helps E. coli to concentrate the magnitude of it harm on the host. The other microbial stops to reproduce and become extinct as E. coli occupies their niche which also helps it spread to different susceptible regions of the host and hence causing infections (Siegfried et al., 130). Additionally, for the E. coli to grow and spread iron is required, and, to their disadvantage, they cannot synthesize these nutrients. Also, these pathogens do not have adequate iron in their cytoplasm; therefore, they have developed systems for acquiring iron from the host. The only place these minerals are found in large quantity is the blood, and hence these systems help it to compete actively with the host for these vital elements. This virulence factor allows them to become more adapted to the host's environment and hence multiply and spread to cause more infection (Wiles, Richard, and Matthew 12 ). The E. coli uses the siderophores which are high iron affinity organisms that derains host's iron. After the siphoning, it is stored in the pathogens cytosol where it is utilized to improve the virulence nature of E. coli. Once the E. coli pathogens colonize the host, they release pathogens that attack the host cells. The toxins are leased continuously until the amount is adequate to Cause UTIs (Wiles et al., 13). This virulence feature ensures that each attack on the host cells by the E. coli yields infections that will result in the weakening of the host's immunity.

Another virulence feature is the identification of different regions that favor activity of various strains to cause infections. The cystitis strains work optimally within the bladders and hence remain there to grow and spread. On the other end, the pylenephritogenic strains rise from the bladder to the kidneys. These parts of the urinary systems have different forms of nutrients that attract the respective strains of E. coli and hence the adaptation to these sites is a useful virulence factor for the E. coli to colonize these parts.

Another virulence factor that enables the E. coli to cause infections is the ability to control the adherence versus motility capacity of its cells (Santo et al., 187). The flagella and fimbriae are responsible for the motility and adherence characteristics respectively of the E. coli. These are antagonistic forces and may inhibit the activities of E. coli in the niche that it has colonized (Subashchandrabose, and Harry 13). For instance, the presence of type 1 fimbriae hinders the motility and lowers the number flagella. Therefore the expression of this type of fimbriae may affect motility or be used by the E. coli to avoid the unnecessary movements. Similarly, if the effect of this kind of fimbriae is not controlled, it may stop E. coli motility when it is supposed to move for instance, from the bladder to the kidneys. Therefore the E. coli have mastered the skill of balancing the action of these two features to navigate in its hosts and colonize more parts of the body. The E. coli strains have become sophisticated to the extent of adhering to the leucocytes to deregulate their action. For instance, through the secreted auto-transporter toxins the movements of the leucocytes to the site with pathogens are inhibited. It also affects the inflammation actions of leucocytes against the pathogens even after reaching the colony. This virulence property ensures that all efforts by the host to counter the harmful effects of the E. coli are unsuccessful. This state of events leaves room for E. coli to rapidly grow and colonize other regions in the host's body without interference from the immune system.

Additional virulence factor is the existence of the E. coli strains as biofilm which is a multicellular and differentiated community of bacteria that are formed by various or a single species. The biofilms are sessile and highly complex which makes them tough and highly resistant to antibiotics (Subashchandrabose, and Harry 14). Some situations such as the use of urinary catheters provide surfaces for biofilms to develop which is an exposure for patients to have UTIs. The type 1 and P of fimbriae facilitate the growth of the biofilm in urine but are down-regulated by the CFT073 kind of biofilms hence their contribution is limited in this process. However, the Yad fimbrial and Auf fimbrial genes which are up-regulated result in the formation of the biofilm in the human urine. Therefore it is vital to understand the kind of fimbrial gene in urine to follow the appropriate mode of treatment for a patient.

The E. coli strains develop type two of capsules which is a form of mimicry to help in the escaping the attack by the immune system of the host (Subashchandrabose, and Harry 15). For example, the K1 types of capsule mimic the nature of the polysialic acid to avoid being detected as pathogens by the body immune system cells. These mutant genes attack the kidneys and other parts of the urinary system causing infections. They cause disease without being detected, and hence their treatment can only be accomplished by destroying the capsule so they can be compromised by the immune system cells. This virulence factor makes E. coli a formidable pathogen by causing various types of UTIs. The multiple strains of E. coli as part of enhancing their virulence capacity changes their morphology. For instance, they undergo filamentation which allows them to stop septation ring formation and the division of the cells. This status enables them to withstand the destruction by the neutrophils and eventually attacks and colonize other naïve cells of the body (Flores-Mireles, Walker, Caparon, and Hultgren 275). Furthermore, during the filamentation process, the morphology is acquired as an outcome of sensor activities by the flagella towards the urine catheter.

In conclusion, UTIs the most common infections affecting at least 12% and 10 to 20% of women around the world. The E. coli has been able to plunder on human health by causing various types of UTI for instance, cystitis by developing virulence factors which makes it a formidable pathogen. However, the E. coli natural exists symbiotically in the human and animal gastrointestinal channel without causing harm. Unfortunately, when it moves outside this region, it leads to infections. Some of the virulence factors include Adherence, development of capsule, filamentation, flagella, and mimicry of the body elements to evade attack from the immune stated. It additionally inhibits the movement and inflammation of the leucocytes which ensures they exist ad colonize further niche and cause infections.







Works cited

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