Enterobacteriaceae
Microbiologists carry out studies to determine the antibiotic resistances of the major types of microorganisms that they can give relevant epidemiological information to the personnel in charge, which assists them in making appropriate recommendations on the suitable antibiotics to be used. Drastic increase in resistance among the Enterobacteriaceae, which are known to lead to nosocomial infections to the amoxicillin, has raised great concern. Enterobacteriaceae family is resistant to amoxicillin, ampicilin and amoxicillin-clavulanate (Bouza & Cercenado, 2002, par.1).
The major cause of amoxicillin resistant in the family of Enterobacteriaceae is the β-lactamases, which is plasmid-mediated. This mechanism involves high or hyper-generation of the β-lactamase belonging to chromosomal class C, hyper-production of oxacillinases, production of TEM enzymes that is plasmid-mediated and hyper-production of TEM enzymes where its β-lactamase cannot be inhibited by amoxicillin as antibiotics. For instance, resistance of E.coli to amoxicillin is mainly because of β-lactamase TEM, which is plasmid-encoded and is very sensitive to inhibitors of β-lactamase like clavulanic acid. Hence, it is clear that they are several mechanisms in which the pathogen becomes resistant to the inhibitor like amoxicillin of the combination of β-lactam-β-lactamase. Beta lactamases, which is plasmid-mediated or “ESBLs” (Plasmid-mediated Extended Spectrum Beta Lactamases) were established first in the year 1983 in Germany in Klebsiella pneumonia. From that time, diseases that result from ESBL-generating members of the Enterobacteriaceae family have increased drastically (Okesola & Makanjuola, 2009, pp. 5-8).
In the year 1988 in Spain in a certain regional hospital, a study of the strains that generated the beta-lactamase enzymes was carried out. The investigation involved 1,207 strains whereby each strain was per individual/client. Vulnerability to ampicillin was conducted through the disc-diffusion method. Among the 528 resistant strains that were represented by 52 percent, the MICs of cefotaxime, amoxicillin, clavulanic acid and carbenicillin were measured in Mueller-Hilton agar by using 50,000 CFU inoculums as per the NCCLS recommendations. Therefore, by use of an uncomplicated acidimetric test, a beta-lactamase activity substrate summary was measured which permitted strains to be differentiated. Determination or measurement of beta-lactamase and recognition of enzymes that is plasmid-mediated was conducted by use of analytical isoelectric to compare the satellite and main bands with the normal/standard enzymes. Hence, the double-disc investigation for synergy among amoxicillin, clavulanic acid, aztreonam, cefotaxime and ceftriaxone was carried out to screen for generators of ESLBs. The results showed compatible information for beta-lactam and beta-lactamases venerability patterns. In addition, strains believed to be hypergenerators of chromosal beta-lactamase that were based on the vulnerability of the information and features of the beta-lactamases were conducted through qualitative method, which assessed the acceleration/speed of nitrocefin hydrolysis and its inhibition when amoxicillin and aztreonam are used (Fuster, Roy, Reig, Raya & Coira, 2005, p.67).
S. pneumoniae
Since the period of antibiotic began in the year 1970s, streptococcus pnemoniae has been vulnerable to all categories of antibiotics, which have been known to be perfect in fighting against the pathogens apart from tetracycline. Some of the risk factors that have been associated with the resistant of S. pnemoniae strains to antibiotics are as follows. These are, the use of antibiotic in the past, children spending much time in the health care and previous respiratory tract infections. Streptococcus pneumoniae (S. pneumoniae) is a major microorganism that causes respiratory tract diseases like pneumonia. The medical management of these diseases has been multi-faceted due to the widespread and emergence of the resistance of the pathogen to the commonly utilized antibiotics like especially macrolides and beta-lactams (amoxicillin). This resistance in S. Pneumoniae is arbitrated by two main mechanisms. These mechanisms are methylation of the target site of the ribosomal macrolide that is encoded/predetermine by the erm gene or B gene and the drug efflux, encoded/predetermined by the mef gene or A gene. The ribosomal target methylation (erm/B) gene leads to resistance to 16-, 15- and 14-membered streptogramin B, macrolides and lincosamides. On the other hand, drug efflux (meff/A) gene leads to resistance to ring macrolides15- and 14-membered only. Therefore, the prevalence of ribosomal target site and drug efflux mechanisms among S.Pneumoniae of the macrolide resistant are different in varies geographical areas (Wierzbowski, Nichol, Laing, Nikulin &Karlowsky, 2007, pp.1-2).
Moreover, S. Pneumoniae isolates/separates positive for both mef(A) and erm(B) are so common recently and have been recognized in several nations like South Korea, Japan, USA, Hungary and Mexico. These both mef (A) and erm (B) isolates of S.Pneumoniae have been verified to be in one main clonal multifaceted and exhibit great resistant rate to several classes of antibiotics including amoxicillin. Similarly, their probable widespread is of great interest and may ned up having medical impact for failure of treatment. In addition, S. pneumoniae resistant to amoxicillin might be due to ribosomal mutation or imitation (genes encoding riboproteins L22 and L4 and encoding 23S rRNA) though such reports are rare (Wierzbowski et al 2007, pp. 4-7).
For instance, a study was conducted by Beijing children suffering from respiratory tract illnesses to investigate S. pneumoniae resistant to macrolide like amoxicillin. S pneumoniae for nasopharyngeal were tested with 15 antibiotics for their sensitivity and later evaluated for phenotypes of the strains of macrolide resistant and for the genes of macrolide resistant like tet(M), erm(B), mef(A) and int(T)n, PCR was used. Among the 185 S. pneumonia strains, pneumoniae exhibited large cross-resistance to several macrolides like amoxicillin, clindamycin, azithromycin, acetylspiramycin among others. Genes like mef (A) and erm (B) were also observed. Therefore, the increased widespread and emergence of S. pnemoniae to macrolides like amoxicillin has led to medical or clinical implications like increased prospective for failure in treatment with several antibiotics that are currently being recommended to treat the respiratory tract illnesses. Thus, the persistence surveillance or monitoring of the resistance of S. pnemoniae is crucial to make sure that appropriate recognition of MDR clones is performed (Wierzbowski etal 2007, pp. 9-12).
Shigella
Dysentery is one of the main endemic infections that has resulted to several mortality cases in most parts of the world and shigellae is one of the contributing proportion to the disease in most of the subtropical and tropical regions of the globe. Therefore, the drastic increase of the antimicrobial resistance of this pathogen to several antibiotics like amoxicillin makes it crucial to understand the widespread antibiogram to lower the morbidity and mortality rates related to shigellosis. Studies have indicated that the species of shigella generate low-level of beta lactamases that are chromosomally mediated that does not significantly influence the amount of resistant to beta-lactams. In addition, the high level of resistant of Shigella to amoxicillin and ampicillin is because of the production or generation of beta-lactamases, which is equivalent to OXA-1 Or TEM-1that are produced in Shigella flexneri in the resistant of ampicillin (American Society for Microbiology, 2001, p. 2179).
In addition, shigellosis is an outbreak all over the world through effective antibiotic medication can be utilized to lower the rate of disease occurrence. However, the range of antibiotic medication against this pathogen is becoming inadequate because of the rising resistance of the pathogen to the available antibiotics like amoxicillin (Dagan, Orr, Yavzori, Yuhas, Meron, Ashkenazi & Cohen, 2002, pp. 887-889). For instance, one of the species of Shigella, S. sonnei can be described in this case which was recognized by the antiserum agglutination and by Bio-merieux in the year 1998 from samples of stool of a young boy who had been admitted in a hospital. This boy was suffering from a diarrhoeal disease, which occurred two months after staying in Turkey. This strain of shigella was resistant to antibiotics like amoxicillin and ticarcillin whether they were administered as a single dose or in combination (American Society for Microbiology, 2001, p. 2179).
Moderate resistant of S. flexneri isolates to amoxicillin has been recorded due to its production of relatively OXA type enzyme (2, 8) of inhibitor-resistant. In addition, the high-level resistant of S. sonnei to amoxicillin-clavulanate (2,048 µg/ml) related to vulnerability to cephalothin implied the availability of a previously unrecorded TEM-33 variation in the species. The progression variety seen for the TEM-33/IRT-3 genes gives weight to the concept that there are various genes of TEM in nature (American Society for Microbiology, 2001, p. 2180).
Studies to determine the molecular foundation of the amoxicillin-clavulanate resistant in the isolates of S. sonnei was carried out. In this case, TEM-I-hyper-generating strain of S. sonnei and OXA-I-generating strain of S. flexneri were investigated as MIC determinations comparators. The MICs of amoxicillin-clavulanate, amoxicillin and cephalothin were measured through dilution in the Mueller-Hinton agar where a certain amount of inoculum was utilized per spot. Therefore, the S. sonnei pattern of resistant was characterized by great MICs of more than 2,048 microgram/milliliter ticarcillin and amoxicillin while that of OXA-I-generating S. flexneri were much lesser (American Society for Microbiology, 2001, p. 2179).
Salmonella
Beta-Lactam antibiotics are mostly utilized in the medication of salmonellosis. Currently, reports have been mentioned concerning the rapid increase of the resistant of the microorganism to the antibiotics including Typhimurium, Typi, Enteritidis and Panama in many nations. Clinical or medical strains of the species of Salmonella generating large amount of beta-lactamases and are resistant to several antibiotics like amoxicillin have been separated or isolated from the big epidemics or outbreaks and the sporadic cases (Llanes, Kirchgesner & Plesiat, 1999, par.1).
A study carried out by the University of Hospital of Besancon located in France between the year 1987 and 1994, indicated a drastic rise from zero to 42 percent in the amoxicillin resistant prevalence rate among the species of Salmonella. In the 96 isolates of Salmonella gathered at that time, 54 of them generated TEM-1 beta-lactamase, 40 were found to generate PSE-1, one generated PSE-1 and PSE-2
and one generated OXA-1 through DNA hybridization and isoelectric focusing investigations or experiments. In addition, plasmids coding for the above-mentioned beta-lactamases were later featured by replicon typing, profile analysis, hybridization with an “spvCD-orfE virulence probe” and restriction combination pattern evaluation or analysis. Moreover, S. typhimurium isolates were compared genotypically through electrophoresis of pulsed gel of the chromosomal DNA of Xbal-macrorestricted. In addition, DT104 isolates that are resistant to amoxicillin is through the generation of PSE-1 beta-lactamase and they have contributed to several outbreaks. On the contrary, other DT104 isolates identified in hospital in British, French and Danish consisted of blaPSE-1 gene that was integrated or combined in the chromosome of the bacteria. Therefore, in the second strains, aadA2 and blaPSE-1 genes were available on two different integrons, while the hereditary determinants accountable for tetracycline and chloramphenicol resistance were believed to dwell on transposons. Hence, it is thought that the plasmid genes, which measure the Salmonella resistances are ferried by transposons and integrons that are in a position to fly from the chromosome to dwell in plasmid or the other way round. Thus, is clear that integrons are accountable for the acquirement and distribution of the resistance genes of the species of Salmonella through plasmid transfer (Llanes et al, 1999, par. 3-4).
DNA-based typing techniques have offered very valuable data/information on the distribution of resistant Salmonella to studies of epidemiology. In some situations, the R plasmid relatedness hidden by strains of different origin would be exhibited through “restriction fragmentation pattern analysis” permitting a better comprehending of the way R factors or resistant strains might propagate. From the year 1987 to 1994, there was dramatic rise in the occurrence of resistant to amoxicillin by the species of Salmonella that had been isolated at the university mentioned above. To determine whether the tremendous increase was because of the propagation of few resistant clones within the society or it was due to acquirement of resistant determinants that had been obtained by Salmonella from multiple bacteria sources, several typing techniques were utilized. This was for comparison of the R plasmid hidden by the resistant separates or isolates and isolates or separates (Llanes et al, 1999, par. 6).
Reference list
American Society for Microbiology (2001). Inhibitor-Resistant TEM-33 b-Lactamase in a Shigella sonnei Isolate. Antimicrobial Agents And Chemotherapy, 45, (7): 2179-2180. Web.
Bouza E, Cercenado E., (2002). Klebsiella and enterobacter: antibiotic resistance and treatment implications. U.S. National Library of Medicine National Institutes of Health, 17 (3): 215-230. Web.
Dagan, D., Orr, N., Yavzori, M., Yuhas, Y., Meron, D., Ashkenazi, S., & Cohen, D., (2002). Retrospective Analysis of the First Clonal Outbreak of Nalidixic Acid-Resistant Shigella sonnei Shigellosis in Israel. Eur J Clin Microbiol Infect Dis, 21:887–889. Web.
Fuster, C., Roy, C., Reig, R., Raya, C., & Coira, A., (2005). Frequency of plasmid-mediated beta-lactamases in Enterobacteriaceae isolated in Spain. European Journal of Clinical Microbiology & Infectious diseases, 12, (1). Web.
Llanes, C., Kirchgesner, V., & Plesiat, P., (1999).Propagation of TEM- and PSE-Type β-Lactamases among Amoxicillin-Resistant Salmonella spp. Isolated in France. American Society for Microbiology. Web.
Okesola, A., & Makanjuola, O., (2009). Resistance to Third-Generation Cephalosporins and Other Antibiotics by Enterobacteriaceae in Western Nigeria. American Journal of Infectious Diseases, 5 (1): 17-20. Web.
Wierzbowski, K., K. Nichol1, K., Laing, N., Hisanaga, T., Nikulin, A., Karlowsky, A., Hoban, D., & Zhanel, G., (2007). Macrolide resistance mechanisms among Streptococcus pneumoniae isolated over 6 years of Canadian Respiratory Organism Susceptibility Study. Journal of Antimicrobial Chemotherapy, 60, 733–740