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E. Coli Drug Resistance Research Paper

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Updated: Apr 28th, 2022

Introduction

In the current day, the resistance to antibiotics is very common in the bacterial isolates across the world and especially in the developing nations. According to Okeke, et al (2000), regular keeping an eye on antibiotic resistance offers data for the “antibiotic therapy and resistance control” (Okeke, et al, 2000, p.1). It is pointed out that “normal intestinal flora are a reservoir for resistance genes, the prevalence of resistance in commercial E. coli is a useful indicator of antibiotic resistance in bacterial in the community” (Okeke, et al, 2000, p.1). The researches that are conducted on E. coli are of certain significance for the reason that this species can inhabit a number of niches, animal as well as human hosts being included. Moreover, it is also pointed out that “E, coli strains efficiently exchange genetic material with pathogens such as Salmonella, Shigella, Yersinia and Vibrio species as well as pathogenic E. Coli” (Okeke, et al, 2000, p.1). The focus of this paper is to look at E. coli and its resistance to antibiotics.

E. coli: General Information

E. coli is a bacterium which is mostly found in gut of the warm-blooded animals. There exist various types of this bacterium as being part of the normal flora of the human gut and some of them serve various functions that are of benefit such as vitamin K2 production. A larger number of E. coli are not harmful to human health. However, a type of this bacterium known as serotype 0157:H7 can bring about food poisoning and can turn out to be a great threat to human health. There are other types which can cause serious infection to human beings which include; “serotypes 0104:H4, 0121, 026, 0103, 0111, 0145, and 014:H21” (medicalnestoday.com, 2011, p.1). The symptoms of infection by E. coli are, in most cases, exhibited within three to four days after exposure to these bacteria. The common signs and symptoms include; abdominal pain, diarrhea, nausea, vomiting, fever and fatigue. After being infected by E. coli 0157:H7, an adult person who is healthy is able to recover within a period of five days to one week. But on the other hand, the people with weaker immune systems including young children, the elderly people and those who are sick can experience kidney failure, a condition referred to as “haemolytic uremic syndrome” (medicalnestoday.com, 2011).

Characteristics

This bacterium is a “gram negative”, non-spore forming rod. The organism may either be mobile or immobile. E. coli is a facultative anaerobe and facilitates fermentation of the simple sugars like glucose in order to make up acids such as the acetic, formic and lactic acids. The most favourable conditions for its growth are a temperature of 98.60 F (Hi-tm.com, n.d). E. coli is regularly detected by “serological tests based on detection of somatic cell walls (o), flagellar (H) and surface (k) antigens” (Aggarwal, 2007, p.19). This bacterium has a single circular chromosome. About 90 percent of the genome “represent functional ORF while 10% of it contains regulatory sequences”(Aggarwal, 2007, p.19).

E. coli life cycle

The life cycle of this bacterium is fast in relative terms. It carries out multiplication through the binary fission process with “a generation time of about 20 minutes under best nutritional conditions” (Aggarwal, 2007, p.19). In the course of multiplication, there is elongation of cells to about two times the size of its length without alteration in the diameter by “addition of new cell wall materials to the pre-existing cell wall and then divides in to two daughter cells with the formation of septum in the center of the cell” (Aggarwal, 2007, p.19).

Multiplication commences with DNA replication. There is attachment of the DNA that has been newly formed to the “plasma membrane at adjacent sites close to the center of the cell” (Aggarwal, 2007, p.19). Each and every cellular constituent as well increase in the amount in the course of the process. At the moment the synthesis of the DNA is completed, it sends a signal “for the formation of a structure called divisome by the proteins called Fts” (Aggarwal, 2007, p.19).the main protein that is involved is referred to as Fts Z and this protein “attaches to the center of the cell cylinder in the space between the duplicated nucleotides….these polymerise to form a Z ring to which other Fts proteins bind and form a divisome” (Aggarwal, 2007, p.19). Similar protein as those that are involved in synthesizing of peptidoglycen may as well be involved in the divisome formation. This spot carries out the marking of the “cell division plane and it triggers the synthesis of new cell wall and cell membrane material in both the directions until the cell doubles in size” (Aggarwal, 2007, p.19). The elongation of the cells makes the two chromosome copies to be pulled apart. “Par A, par B, Muk B and other proteins are involved in separation of DNA” (Aggarwal, 2007, p.19). After the separation of the chromosomes, there is starting of constriction at the “site of divisome” (Aggarwal, 2007). While constriction takes place, there is depolymerising of the “FTs Z ring and wall material grows inward so as to separate the two daughter cells” (Aggarwal, 2007, p.19). This process is in turn repeated again.

E. coli Resistance

The widespread use of antibiotics for the treatment of the bacterial infections in human beings and veterinary medicine “selects for resistant micro-organisms which may in turn, transfer resistance factors to other bacteria thereby further enhancing their spread” (Levy, 1984, p.663).It is pointed out that resistant bacteria transfer has been indicated to take place between people, form people to animals, animals to people and between different animal species (Marshall, Petrowsky & Levy, 1990; Holberg, et al, 1984; Lyons et al, 1980).

According to Nijsten, London, Bogaard, & Stobberingh, (1996), looking at the case of E. Coli resistance in the case of pigs), contrary to the case of human beings as well as their pets, pigs are in most cases treated as a group and provided with mass treatment and, just like in other animals, antibiotics “may select resistant E. coli in the faecal flora which may transfer their resistance plasmids to other bacteria including pathogens such as Salmonella spp” (Smith, 1970, p.165). Furthermore, pigs are continuously in contact with faeces which they take in and are thus, as well constantly exposed to contamination by the bacteria in faeces and antibiotic resistance genes. Being in close contact with these animals as well as their products may bring about colonization with resistant bacteria found in the intestinal flora. On the other hand, endogenous flora may turn out to be resistant as a consequence of “the transfer of plasmids from bacteria of animal origin that pass through the intestinal tract” (Lyons, et al, 1980, p.547).

Moreover, E. coli commonly causes the urinary tract infections as well as bacteremia in human beings and is constantly “resistant to amin-openicillins, such as amoxicillin or ampicilin, and narrow-spectrum cephalosporins” (Allen, MacDonald, Fuite, Chan, and Stephens, 1999; Karlowsky, Kelly, Thornsberry, Jones, & Sahm, 2002). The meditation of resistance is normally carried out by acquiring of “plasmid-encoded β-lactamases such as REM-1, TEM-2, or SHV-1, which hydrolyze and inactivate these drugs” (Rupp & Fey, 2003, p.353). There are those strains that built up resistance “to third-generation cephalosprins and monobactams, through the acquisition of ESBLs commonly arising through mutation of TEM-, SHV-, or CTX-M-type enzymes” (Tenover, 2006, p.5). It is pointed out that the ESBLs, when put against the cephamycins like cefotelan and cefocitin are not active (Tenover, 2006, p.5). However, resistance to β-lactams such as cephamycins and others may come about as a consequence of the changes that occur in the porins which are found in the outer membrane. Changes like these reduce or do away with the flow of the minute hydrophilic molecules like “β-lactam drugs across the membrane” (Tenover, 2006, p.5).

Laboratory Test for resistance

One of the laboratory tests for the E. coli resistance is one given by NCBE (2009). In relation to the way this bacteria acquire antibiotic resistance through conjugation. It is pointed out that “recipient strain E. Coli J-53R bears on its chromosome a gene conferring resistance to the antibiotic rifampicin” (NCBE, 2009, p.3). The donor strain, E. Coli HT-99, facilitates harbouring of a plasmid that has a “gene conferring resistance to a second antibiotic chloramphenicol” (NCBE, 2009, p.3). There is then meting of the liquid cultures of the two strains. The meted, together with the donor and recipient cells are in turn plated on three types of media: “one containing rifampicin, one containing chloramphenicol and a one containing both antibiotics” (NCBE, 2009, p.3). After incubation taking place, the one conducting the test then interprets the results and he or she should find out that the antibiotic resistance has been moved from one strain of E. coli to the other.

Conclusion

The problem of drug resistance is currently very common and this has caused some life-threatening infections unable to treat. E. coli is one of the bacteria that are resistant that are resistant to antibiotics. There exist various types of this bacterium as being part of the normal flora of the human gut and some of them serve various functions that are beneficial. A larger number of E. coli are not harmful to human health and there is no need for much caution about the danger of being exposed to them. Even if some of the species of this bacterium are not harmful, there are other species that are quite harmful such as serotype 0157:H7 which can bring about food poisoning and can turn out to be a great threat to human health. Since this bacterium is constantly resistant to antibiotics, there is need for the researchers to study it even more closely, especially by looking closely at its life cycle among other aspects that can be helpful, in order to come up with the best possible drug that can be used to deal with it.

References

Aggarwal, S. (2007). Principles of microbial nutrition and growth. Institute of Home Economics. Web.

Allen, U. D, MacDonald N, Fuite L, Chan F, and Stephens, D.(1999). Risk factors for resistance to “first-line” antimicrobials among urinary tract isolates of Escherichia coli in children. CMAJ. 160 (1) pp.1436 –1440.

Holmberg, S. D., Osterholm, M. T., Senger, K. A. & Cohen, M. L. (1984). Drug-resistant Salmonella from animals fed antimicrobials. JVeiv England Journal of Medicine 311 (1), 617-22.

Karlowsky J. A, Kelly L. J, Thornsberry C, Jones M. E, & Sahm D. F. (2002).Trends in antimicrobial resistance among urinary tract infection isolates of Escherichia coli from female outpatients in the United States. Antimicrob Agents Chemother. 46 (1), pp.2540 –2545.

Levy, S. B.. (1984). Playing antibiotic pool: time to tally the score. New England Journal of Medicine, 311 (1), 663-5.

Lyons, R. W., Samples, C. L., DeSilva, H. N., Ross, K. A., Julian, E. M. & Checko, P. J. (1980). An epidemic of resistant Salmonella in a nursery. Journal of the American Medical Association, 243 (1), 546-7.

Marshall, B., Petrowski, D. & Levy, S. B. (1990). Inter- and intraspecies spread of Escherichia coli in a farm environment in the absence of antibiotic usage. Proceedings of the National Academy of Sciences USA, 87(1), 6609-13.

Nijsten, R. N. London, N.. Bogaard, V. & Stobberingh, T. (1996). Antibiotic resistance among Escherichia coli isolated from faecal samples of pig farmers and pigs. Journal of Antimicrobial Chemotherapy, 37 (1), 1131-1140

Okeke, I. N. et al. (2000). Antibiotic Resistance in Escherichia coli from Nigerian Students, 1986-1998. Medscape Today. Web.

Hi-tm.com, (n.d).Characteristics of E. Coli. Hi-tm.com. Web.

NCBE, (2009). Antibiotic resistance in E. Coli: A practical investigation of bacterial conjugation. National Center for Welcome Trust. Web.

Rupp, M. E. &Fey P.D. (2003).Extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae: considerations for diagnosis, prevention and drug treatment. Drugs. 63 (1), pp.:353–365.

Smith, H. W. (1970). The transfer of antibiotic resistance between strains of Enterobacteria in chicken, calves and pigs. Journal of Medical Microbiology 3(2), 165-80.

Tenover, F. C. (2006). Mechanisms of Antimicrobial Resistance in Bacteria. The American Journal of Medicine, 119 (6), pp.4 -9.

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