Escherichia Coli 131
Escherichia coli sequence type 131 (also known as ST131) is regarded as a clone. It is a recent discovery in the scientific field. The clone was first identified in 2008. The group is regarded as a colonial and pathogenic type of bacteria (Giuffre et al. 8). It causes serious health problems that include gastroenteritis and urinary tract infections. The pathogens are extraintestinal. It is noted that in many cases, strains of E. coli colonize the gut.
However, they are also known to thrive in other regions of the body, such as the peritoneal cavity. They are also found in the urinary tract, the kidney, as well as in bloodstream. The ST131 clone is mainly known for its tendency to attack the urinary tract. The resulting condition is referred to as urinary tract infection (UTI). The organisms belonging to this clone are known for their resistance to antimicrobial agents, such as fluoroquinolone.
ST131 and Antimicrobial Resistance
The ST131 clone is responsible for over 50 percent of known cases of resistance to antimicrobials. Such a figure makes it a significant group with regard to scientific studies. A case in point is the study conducted in an Italian neonatal intensive care unit to determine the spread of the pathogen. The objective of the study was to improve healthcare services provided to the population (Giuffre et al. 8). In addition, this clone makes up approximately half of E. coli strains that produce ESBL. The development has attracted the attention of many scholars. The ST131 clone is also associated with the production of CTX-M-15, a type of ESBL.
Studies in this field have identified additional subclones under the E. coli ST131 group. The new additions include H30 and H30-R subclones. The two are more common compared to other variants of ST131. Scholars have given a number of reasons to explain this prevalence. However, in spite of these varying explanations, the exact reason for the increased occurrence of these two variants is not well known.
The H30 subclone gets its name from its allele (Skold 54). It contains allele 30 of the type 1 fimbrial adhesin gene. The gene is present in the genome of a large percentage of E. coli ST131 resistant to fluoroquinolone. Both H30 and H30-RX trace their roots to a common ancestor. Their originator carries the allele fimH30 that is often characterized by multi-drug resistance (Ogura 180).
Expansion of ST131
A number of subclones are known to multiply at a very high rate. Research has shown that H30-R is the most rapidly expanding subclone. It is also the most resistant subgroup among the isolates of the ST131 clone (Vaidya 37). To this end, the group makes up 91 percent of CTX-M-15 producing subclones. As such, it is regarded as a virulent subgroup. Consequently, it has come to be referred to as the H30-RX subclone. It is also known that the group has two of the most antimicrobial-resistant ST131 sublineages. The two are aac(6’)-lb-cr and blaCTX-M-15 (Vaidya 37). They are commonly detected in blood samples than in other cultures. The subclone is also prevalent in urinary samples. They thrive and multiply in these regions since there are no medical remedies to control them or check their development.
The H30-RX subclone has the capability to horizontally transfer antimicrobial resistance to other bacteria (Skold 22). As a result, some strains of the bacteria that were previously susceptible to antimicrobial agents are no longer controllable using the same antibiotic. A number of factors explain the development of resistance among these organisms. In most cases, bacteria lose susceptibility to multiple antimicrobial agents based on the quality of the gene transferred to them (Ogura 180). As such, it is believed that resistance is acquired through gene transfer. Horizontal transfer of these elements is the basis of bacterial evolution in nature.
When virulent bacterial strains acquire genes from the E. coli ST131 H30-RX, their nature is altered. They become widespread and colonial. Given the fact that they cannot be controlled through the application of antimicrobial agents, they easily gain local and global predominance over other bacteria. ST131 clones are also known to acquire drug resistance through independent mutation (Martinez 44).
As stated earlier in this paper, there is no exact reason known for the proliferation of H30-RX. A number of scientists speculate that its widespread nature and high prevalence are a result of its antimicrobial resistance. Under normal circumstances, the gut and the urinary tract are colonized by microflora (Skold 75). However, the existence of these organisms poses no danger to the host. The safety is sustained as long as the required balance is maintained (Skold 88).
The administration of antimicrobial agents is normally aimed at wiping out the population of pathogenic species. Due to the production of ESBLs, the ST131 clone is able to metabolize the antimicrobial agent. However, the bacteria that lack the enzymes are eliminated from the host. According to Martinez, the elimination of these microbes helps in bringing down competition for resources (44). As a result, the environment created in these regions becomes conducive for colonisation by ST131.
Transmission of E. Coli
Just like other E. coli bacteria, ST131 is transmitted through the faecal-oral route. Once released to the environment, the H30-RX and the H30 subclones survive for a considerable duration of time. They remain dormant until they are ingested by another host. Given that they are not destroyed by antimicrobial agents, they are able to grow and reproduce without any disruptions. As a result, their population is always on the rise. They are passed on from one host to the other. For this reason, their spread across the population cannot be controlled unless new interventions are devised.
The ability of ST131 H30-RX and H30 bacteria to acquire antimicrobial resistance genes from other bacterial strains poses significant health problems to the population. The two subclones are capable of acquiring virulent genes. The transfer of these genes to other microbes worsens the situation. According to Ogura, the reason is that the bacteria are in a position to introduce their virulent and drug resistance characteristics to other microbes that were previously susceptible to antimicrobial agents (176).
The situation increases incidences of drug resistance (Martinez 50). Their population also grows in the process and can only be checked through the application of other therapies, such as macrophages. Continued application of antimicrobial elements with regards to the treatment of ST131 H30-RX and H30 subclones is, however, regarded as a futile undertaking.
Since the use of antimicrobial agents is ineffective in the control of these groups of microbes, scientists are working on ways through which the prevalence of H30 and H30-RX subclones can be reduced. Research is ongoing to develop a vaccine against pathogens. Ways to check their ability to colonise are also been devised. According to Skold, preventing their entry into the host would be easier than attempting to eradicate them (8). Stakeholders involved in the management of these organisms should take this development into consideration.
Works Cited
Giuffre, Mario, Domenico Cipolla, Celestino Bonura, Daniela Geraci, Aurora Aleo, Stefania Di Noto, Federica Nociforo, Giovanni Corsello and Caterina Mammina. “Outbreak of Colonizations by Extended-Spectrum β-Lactamase-Producing Escherichia Coli Sequence Type 131 in a Neonatal Intensive Care Unit, Italy.” Antimicrobial Resistance and Infection Control 2.1 (2013): 8. Print.
Martinez, Jose. “Natural Antibiotic Resistance and Contamination by Antibiotic Resistance Determinants: The Two Ages in the Evolution of Resistance to Antimicrobials.” Frontiers in Microbiology 3 (2012): 34-56. Print.
Ogura, Yoshitoshi. “Genomic Analyses of Mechanisms of Virulence Evolution in Enterohemorrhagic E. Coli and Enteropathogenic E. Coli.” Nippon Saikingaku Zasshi 66.2 (2011): 175-186. Print.
Skold, Ola. Antibiotics and Antibiotic Resistance, Chicester: Wiley, 2011. Print.
Vaidya, Varshak. “Horizontal Transfer of Antimicrobial Resistance by Extended-Spectrum β Lactamase-Producing Enterobacteriaceae.” Journal of Laboratory Physicians 3.1 (2011): 37. Print.