what happens if mrsa becomes resistant to all antibiotics

• Journal List
• J Glob Infect Dis
• v.7(ii); Apr-Jun 2015
• PMC4448330

J Glob Infect Dis. 2015 Apr-Jun; 7(2): 78–84.

Study of Antibiotic Resistance Pattern in Methicillin Resistant Staphylococcus Aureus with Special Reference to Newer Antibiotic

Dardi Charan Kaur

Department of Microbiology, Maharashtra Establish of Medical Education and Enquiry Medical College, Talegaon, Dabhade, Pune, Maharashtra, India

Sadhana Sanjay Chate

Department of Microbiology, Maharashtra Institute of Medical Instruction and Enquiry Medical College, Talegaon, Dabhade, Pune, Maharashtra, India

Abstruse

The worldwide epidemic of antibiotic resistance is in danger of ending the golden age of antibiotic therapy. Resistance impacts on all areas of medicine, and is making successful empirical therapy much more hard to achieve. Staphylococcus aureus demonstrates a unique ability to quickly respond to each new antibody with the development of a resistance mechanism, starting with penicillin, until the most recent, linezolid and daptomycin. Methicillin resistant South. aureus (MRSA) has become owned today in hospitals worldwide. Resistance to the newer antimicrobial-agents — linezolid, vancomycin, teicoplanin, and daptomycin are been reported and also the fear of pandrug-resistance. This report was carried out to know the antimicrobial resistant blueprint of MRSA to newer antibiotic, to know any isolates are extensively-drug resistant (XDR)/pandrug resistant (PDR), inducible macrolide-lincosamide streptogramin B (iMLSB), and mupirocin resistance. Xxx-vi MRSA isolates resistant to the routinely tested antibiotic were further tested for list of antibiotic by a grouping of international experts. Isolates were tested for iMLSB and mupirocin resistance past the disk diffusion method. Of 385 MRSA, 36 (nine.35%) isolates of MRSA were resistant to the routinely tested antibiotic. Amidst these 36 MRSA isolates, none of our isolates were XDR/PDR or showed resistant to anti-MRSA cephalosporins (ceftaroline), phosphonic acids, glycopeptides, glycylcyclines, and fucidanes. Lower resistance was seen in oxazolidinones (2.78%), streptogramins (v.56%), lipopeptide (5.56%). Thirty-four (94.44%) isolates showed constitutive MLSB (cMLSB) resistance and two (5.56%) iMLSB phenotypes. Loftier- and low-level mupirocin resistance were seen in 13 (36.eleven%) and half-dozen (16.67%), respectively. In our report, none of our isolates were XDR or PDR. No resistance was observed to ceftaroline, telavancin, teicoplanin, and vancomycin; but the presence of linezolid resistance (1, two.28%) and daptomycin resistance (two, 5.56%) in our rural set-up is a cause of business organization.

Keywords: Ceftaroline, Daptomycin, inducible clindamycin resistance, Linezolid, Mupirocin resistance, Newer antibiotic, PDR, Telavancin, XDR

MICROBIOLOGY Study

T he emergence of resistance to antibiotics in Gram-positive pathogens has become a major international problem equally there are fewer, or even sometimes no, effective antimicrobial agents bachelor for infections caused by these bacteria.[ane] The problem of increasing antimicrobial resistance is even more threatening when because the very limited number of new antimicrobial agents that are in development. As rapidly as new antibiotics are introduced, Staphylococci have adult efficient mechanisms to neutralize them; inevitably this has left fewer effective bactericidal antibiotics to treat these often life-threatening infections.

Multidrug-resistant (MDR) Staphylococci pose a growing problem for human health. The ascent of drug-resistant virulent strains of Staphylococcus aureus, peculiarly methicillin-resistant S. aureus (MRSA) is a serious trouble in the treatment and control of Staphylococcal infections.[2,three] Methicillin-resistant Staphylococci (MRS) crusade difficult-to-treat infections. The most hitting state of affairs is that MRSA strains have emerged with concomitant resistance to many usually used antibiotics of groups, aminoglycosides, macrolides, fluoroquinolones, chloramphenicol, and tetracycline.[iv]

A special rule has been practical in defining antimicrobial resistance in Southward. aureus. Once a Southward. aureus isolate is characterized as an MRSA, it is instantly classified as an MDR, because resistance to oxacillin or cefoxitin infers nonsusceptibility to all categories of β-lactam antimicrobials listed in this certificate (i.e., all categories of penicillins, cephalosporins, β-lactamase inhibitors, and carbapenems).[5] Thus, MDR-MRSA is the new or rather a continually evolving paradigmatic pathogen.[six]

MDR-MRSA strains, the silently violent incarnations of Due south. aureus widespread in community and hospital environments take posed serious clinical imbroglio.[four] MRSA strains are labeled every bit a "superbug" in the heath domain.[half dozen]

First reported in 1960, the growing problem in the Indian scenario is that MRSA prevalence has increased from 12% in 1992 to lxxx.89% in 1999.[7] MRSA has go endemic today in hospitals covertly worldwide, and 30% of South. aureus isolates are MDR, 2 decades ago, as conjectured from surveillance in the U.s.a..[8]

At all the fourth dimension, the full range of antibiotics is available but, an utterly sad fact today is that more than 95% MRSA worldwide practice non respond to the commencement-line antibiotics, due to artifices in bacterial genomes confirming the constabulary that unproblematic genomes evolve faster than complex genomes.[9] The following antibacterial agents have been canonical during the last five years: Quinupristin/dalfopristin, linezolid, daptomycin, and tigecycline. Novel lipoglycopeptide agents liketelavancin, novel cephalosporins (ceftaroline) with enhanced activeness against MRSA are in the pipeline.

Several studies have reported the resistance to the newer antimicrobial agents like linezolid, vancomycin, teicoplanin, and daptomycin.[x,xi,12] The fear of pandrug-resistance (resistance to all antibiotics and drugs in present use), equally cautioned in Gram-negative pathogens,[13] cannot exist ruled out in S. aureus and our return to a post-antibioticera. The truthful extent of antimicrobial resistance in MRSA in our area is unknown. Thus, this study was carried out to with the aim:

• To know the antimicrobial resistant pattern of MRSA to newer antibiotic.

• To know the number of isolates showing extensively-drug resistant (XDR)/pandrug resistant (PDR).

• To notice out the percentage of MRSA having constitutive (constitutive macrolide-lincosamide-streptogramin B (cMLS_B) phenotype) and inducible (iMLS_B) using D-test.

• To find out the percent of MRSA isolates having loftier- and depression-level mupirocin resistance in MRSA by disk improvidence.

A prospective study was carried out in the Section of Microbiology during the period January 2012-August 2014. Approval was obtained from the Institutional Ethics Committee IEC/204, local review board for carrying out the study. A full of 335 nonduplicate MRSA isolated from diverse clinical specimens similar pus, claret, urine, central venous catheters tips, tracheal aspirates, and sputum were randomly selected. MRSA isolates were identified by standard microbiological techniques. This isolates was tested for routine antibiotic by Kirby–Bauer disk improvidence method on Mueller–Hinton agar as per Clinical and Laboratory Standards Institute (CLSI). The antibiotics tested were ciprofloxacin, cefotaxime, gentamycin, oflaxacin, amoxicillin+clavulanic acid, amikacin, ampicillin, tobramycin, cefuroxime, and erythromycin.[4]

Sample size — Xxx-half dozen MRS Aisolates resistant to the routinely tested antibiotic were further tested for list of antibody past a group of international experts: A articulation initiative by the European Centre for Disease Prevention and Command (ECDC) and the Centers for Disease Control and Prevention (CDC) [Table 1].[five]

Table 1

Listing of antibiotic by a grouping of international experts: Antimicrobial categories and agents[v]

A bacterial isolate was considered resistant, intermediate, or nonsusceptible to an antimicrobial agent by using interpretive criteria provided by European Committee on Antimicrobial Susceptibility Testing (EUCAST), the CLSI, and/or the Food and Drug Administration (FDA).[v]

The isolates were tested for inducible clindamycin resistance (iMLS_B) and mupirocin resistance by the disk diffusion method.[iv] Statistical analysis was done past using standard normal test (z-test). Antibiotic disk were obtained from HiMedia Laboratories Pvt Ltd, Mumbai, India; Oxoid Limited, Britain; and Mast grouping, U.k..

Out of 385 MRSA isolated from diverse clinical specimen, 36 (9.35%) isolates of MRSA were resistant to the routinely tested antibiotic. [Tabular array 2]. The distribution of the MRSA (resistant to routinely tested antimicrobial agents) was college among female (19, 52.78%) than males (17, 147.22%). Gender-wise no statistical significance was noted. Ward-wise college distribution of MRSA (resistant to routinely tested antimicrobial agents) was observed in Obstetrics and Gynecology (Obgy; 12, 33.33%) and Surgery (11, 30.56%) followed by Medicine (7, 19.44%), Intensive Care Unit (ICU;4, 11.eleven%), and ane each from Pediatrics (Ped;ii.78%) and Skin (two.78%) [Figure ane].

Table ii

Distribution of MRSA among the specimen

Ward-wise distribution of 36 MRSA. The to a higher place nautical chart depicts higher distribution of MRSA isolates (resistant to routinely tested antimicrobial agents) in Obgy (33.33%) and Surgery (thirty.56%). MRSA: Methicillin resistant Staphylococcus aureus, ICU: intensive care unit, Obgy: Obstetrics and Gynecology, Ped: Pediatrics

Among these 36 MRSA isolates, none of our isolates were XDR or PDR. Also none of the 36 isolates were resistant to antimicrobial category like anti-MRSA cephalosporins (ceftaroline), phosphonic acids, glycopeptides, glycylcyclines, and fucidanes. But 100% resistance was noted to fluoroquinolones, aminoglycosides, macrolides, and lincosamides showed 97.22% resistance. Lower resistance was seen in oxazolidinones (2.78%), streptogramins (5.56%), and lipopeptides (v.56%) [Tabular array 3].

Tabular array 3

Antibody resistant pattern of 36 isolates of MRSA (resistant to the routinely tested antibody)

In our study, erythromycin resistance was noted to the tune of 100%. These isolates were subjected to D-test. Nosotros observed 34(94.44%) isolates who showed constitutive MLS_B resistance and two (5.56%) iMLS_B phenotypes. Of 36 MRSA isolates, low-level resistance in half dozen (16.67%) and high-level mupirocin resistance was observed in 13 (36.11%).

Antibiotic resistance amongst pathogenic bacteria is a well-documented phenomenon that has astringent consequences for the treatment of infections in the hospital setting and increasingly in the community. The Infectious Diseases Guild of America recently published a striking list of bacterial pathogens whose antibody resistance severely impacts the ability to treat infections in the U.s.a. infirmary setting.[14]

In our study, out of 385 MRSA isolated from various clinical specimens, 36 (9.35%) isolates of MRSA were resistant to the routinely tested antibody. In our report, we analyzed the antimicrobial resistance pattern as per the classification of an international expert proposal for interim standard definitions for caused resistance by Magiorakos et al., and found none of our isolates were XDR or PDR.[five]

Out of 36 MRSA isolates (resistant to routinely tested antimicrobial agents) none of the isolates were resistant to antimicrobial category similar anti-MRSA cephalosporins (ceftaroline), phosphonic acids, glycopeptides, glycylcyclines, and fucidanes. Whereas, 100% resistance was noted to fluoroquinolones, aminoglycosides, macrolides, and lincosamides showed 97.22% resistance. Lower resistance was seen in oxazolidinones (two.78%), streptogramins (5.56%), and lipopeptides (5.56%).

S. aureus demonstrates a unique power to quickly respond to each new antibody with the development of a resistance mechanism, starting with penicillin and methicillin, until the well-nigh recent, linezolid and daptomycin.[15]

Deoxyribonucleic acid restriction enzyme polymorphism of t-half dozen ribosomal RNA gene is reported to exist distributed throughout S. aureuschromosome, which has the methicillin resistant determinant (mec) equally an episome (or fifty-fifty as a plasmid); the mecsequences could enter into the bacterial sequences at 3 points in the genome of Southward. aureus.[xvi] Unfortunately, the plasmid/episome confers rapid resistance to a lot of antibiotics of dissimilar classes/generations. Gene transfers through conjugation involving the transposon, "Tn-1546" with the gene mecA, encoding a modified penicillin binding poly peptide confers resistance to the methicillin and other penicillin derivatives was reported. The mecA gene encodes the penicillin-bounden protein PBP2a, which cannot be bound by β-lactam antibiotics and in turn prevents the disruption of cell wall germination by these antibiotics. This mec-gene is located on mobile genetic element called the, "staphylococcal cassette chromosome-mec" (SCC-mec).[17]

In fact, when an antibody binds to the protein that prevents the synthesis of peptidoglycan in the bacterial cell wall, the resistance is conferred. Some bacteria can produce a "modified penicillin binding protein" that ceases to demark to the antibiotic, which eventually prevents the targeted furnishings of the antibody.[18] Indeed, resistance of S. aureus to β-lactam antibiotics is attributed to the presence of the mecA gene.

Ceftaroline fosamil, the prodrug of the active metabolite, ceftaroline, is a new, broad-spectrum cephalosporin recently approved in the USA for the treatment of astute bacterial pare and pare structure infections (ABSSSIs) and community-acquired bacterial pneumonia (CABP). Ceftaroline has potent in vitro activeness confronting Gram-positive organisms, including MRSA and Streptococcus pneumoniae, too as common Gram-negative organisms.[19] In our written report, we observed none of our isolates showed resistance to ceftaroline. Clark et al., in their report concluded, prolonged choice in the presence of ceftaroline demonstrated no evidence of resistance development for the bulk of isolates and lack of cross-resistance with other antibody classes among tested species important in complicated skin and soft-structure infections (cSSSI) and customs-acquired pneumonia (CAP).[20] While Laudano in his in vivo comparison of ceftaroline fosamil with daptomycin showed the greatest reduction in bacterial titers in vegetations after iv days of handling. But ceftaroline demonstrated 100% sterilization of vegetations in all strains. Resistance to ceftaroline is expected to be express, every bit demonstrated in multistep resistance option studies.[19,21]

Vancomycin, teicoplanin, and daptomycin resistance pattern was as well studied. We found none of our isolates were resistant to vancomycin and teicoplanin, but 2 isolates were institute resistant to daptomycin. Susceptibility breakpoint for daptomycin was considered equally <1 μg/ml for Staphylococci as recommended by the CLSI.[four]

Dubey in their study reported, out of 390 MRSA strains isolated from outpatient department (OPD), 80 (20.51%) were vancomycin resistant (vancomycin resistant South. aureus (VRSA)) and 173 (44.35%) strains were vancomycin intermediate Southward. aureus (VISA) and the rest 137 (35.12%) strains were sensitive to vancomycin. Similarly from nosocomial sources, out of 461 MRSA isolates, 110 (23.86%) strains were VRSA and 208 (45.11%) were VISA strains; while 143 (31.01%) strains were totally sensitive to vancomycin; whereas, out of 363 MRSA isolates obtained from ICU and NICU, 61 (sixteen.8%) VRSA strains and 164 (45.17%) VISA strains were institute; whereas, the remainder 138 (38.01%) isolates were vancomycin sensitive.[6]

Biedenbach et al., in their study reported a 3.2% rate of tolerance to vancomycin and a 31.6% rate of tolerance to teicoplanin for 76 MRSA isolates from a collection of SENTRY Antimicrobial Surveillance Plan strains collected from eight medical centers in the Asia-Pacific region.[22]

Reduced susceptibility to vancomycin has been reported to exist associated with reduced susceptibility to daptomycin. Diederen et al., reported seven of the 17 VISA isolates to take daptomycin minimum inhibitory concentration (MIC) of ii μg/ml and one isolate to have MIC four μg/ml. Nonetheless, such clan was not seen in our report.[12]

Maria et al., observed daptomycin were more potent in vitro than either vancomycin or teicoplanin against MRSA according to its MIC for 90% of isolates (MIC90) and was more bactericidal according to its minimum bactericidal concentration for 90% isolates (MBC90) and MBC/MIC ratios. A total of 6.1% (29/479) and 18.8% (90/479) of the strains tested exhibited tolerance to vancomycin and teicoplanin, while tolerance to daptomycin was non observed for whatever of the 479 isolates. Twenty-four (5%) of all strains were tolerant to both vancomycin and teicoplanin.[ten]

Celikbilek et al., on the base of operations of MIC90 values, in their study observed daptomycin was four to 16 times more effective than vancomycin, teicoplanin, and linezolid.[23]

In our written report, we observed that one (2.78%) of our MRSA isolates was resistant to linezolid. Gu et al., systematically reviewed the published literature and observed <1% of S. aureus and 2% of coagulase-negative Staphylococcus (CoNS) are linezolid resistant. Nonetheless, multifocal outbreaks of linezolid-resistant Staphylococcus (LRS) have been reported and both vertical and horizontal manual. The most common mechanisms for linezolid resistance were mutation (G2576T) to the 23S rRNA or past acquisition of a plasmid-borne ribosomal methyltransferase gene, cfr.[24] Linezolid resistance in Staphylococcus is defined by both the CLSI and the EUCAST equally a linezolid MIC of ≥8 mg/L. The majority of LRS were isolated from patients in Northward America and Europe. Overall, 46.2% (30/65) of LRSA were reported in Due north America, 30.8% (twenty/65) in Europe, xx.0% (13/65) in Asia, and 3.ane% (2/65) in South America. Linezolid susceptibility among clinically significant isolates is monitored through ii surveillance programs, the global Zyvox Annual Appraisal of Potency and Spectrum (ZAAPS), and the USA Linezolid Experience and Accurate Conclusion of Resistance (LEADER).[24]

In a study by Kevin et al., stelavancin was consistently more active than vancomycin and teicoplanin confronting all organisms tested and showed authorisation equal to or greater than daptomycin and linezolid against all strain types except VanA-type vancomycin-resistant Enterococci (VRE).[xi]

In our study, erythromycin resistance was noted to the tune of 100%. This isolates were subjected to D-test, where nosotros establish 34 (94.44%) isolates equally cMLS_B resistance and two (v.56%) iMLS_B phenotypes. The resistance to macrolide tin exist mediated by msrAgene or via erm gene encoding for enzymes that confer inducible or constitutive resistance to macrolide, lincosamide, and type B streptogramin. Nagarajan et al., observed all MRSA ST239 isolates showed high level mupirocin resistance and inducible clindamycin resistance.[25]

Fokas et al., found iii.five% S. aureus isolates had inducible, 60% had constitutive MLS resistance.[26] Interestingly, in a study by Angel et al., at that place has been no constitutive MLS_B resistance.[27]

Mupirocin (pseudomonic acrid A) derived from Pseudomonas fluorescens is a topical antibiotic widely used for treatment of MRSA-associated skin and soft-tissue infections. Prolonged, widespread, or uncontrolled and multiple courses of mupirocin are all associated with the development of mupirocin resistance.

Of 36 MRSA isolates, low-level mupirocin resistance was noted in six (16.67%) and high-level mupirocin resistance in thirteen(36.eleven%). Nicholson et al., observed the higher prevalence of low- and loftier-level resistance to mupirocin to the tune of 30 and 24%, respectively.[28]

Low-level mupirocin resistance is usually associated with point mutations in the chromosomally encoded ileSgene; whereas, high-level resistance is mostly due to a plasmid-mediated gene, mupA. The mupAgene is typically located on mobile genetic elements, these plasmids typically comport resistance determinants to other antimicrobial agents, including macrolides, gentamicin, tetracycline, and trimethoprim.[29] Suggesting that mupirocin use could select for increased drug resistance in Southward. aureus.

The emergence and spread of antibiotic resistance remains a global public wellness concern. A cadre role of all clinical laboratories is to decide the antibiotic susceptibility pattern of bacterial isolates. This would guide the clinicians in treating the patient infected with MRSA and also in conception of a definite antibiotic policy; and in effective hospital infection command policy.

Conclusion

In our study, none of the isolates showed resistance to ceftaroline, telavancin, teicoplanin, and vancomycin; simply the presence of linezolid (one,2.28%) and daptomycin resistance (2, 5.56%) in our rural set-up is cause of concern.

Higher resistance was noted to gentamicin, ciprofloxacin, moxifloxacin, clindamycin, and chloramphenicol. This could exist selective antibody pressure. But to the relief, none of our isolates were XDR or PDR. To prevent the emergence of pandrug resistance isolates, we recommend:

1. MRSA strains may spread readily in hospitals from colonized or infected persons. Colonized employees are generally asymptomatic, although they are a potential reservoir of infections acquired by patients. Colonized or infected hospital personnel (healthcare workers) may serve equally reservoir and disseminator of MRSA in hospitals. So screening for MRSA among healthcare workers and patients.

2. The choice of antimicrobial agent should be based on in vitro susceptibility and the hospital-based antibiotic policies must be strictly followed and abiding surveillance of drug resistance for all bacterial pathogens is needed.

3. Curtail the large corporeality of unnecessary antibiotic use in many areas of life.

4. National surveillance of antibody resistance and antibiotic use. Setting upwardly and/or strengthening infection control committees in hospitals.

5. Antimicrobial stewardship programs can exist implemented to reduce inappropriate use of antimicrobials, thereby decision-making the development of resistance.

6. Biomedical waste management: Genetic recombination mechanisms-conjugation and transformation occur more likely than expected in untreated hospital sewage system, because all sorts of bacteria with grading levels of antibiotic resistance are physically together, thereby inducing jail cell-to-cell contact or DNA intake from some lysed pathogenic strain.[xxx]

ACKNOWLEDGEMENTS

I am grateful to the Management of MIMER Medical College, Talegaon Dabhade, Pune for their support and encouragement. Thanks to Mrs. Hemwati Kaple for technical back up.

Footnotes

Source of Support: Nil.

Disharmonize of Interest: None alleged.

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