- Research article
- Open Access
Sccmec type II gene is common among clinical isolates of methicillin-resistant Staphylococcus aureus in Jakarta, Indonesia
BMC Research Notes volume 6, Article number: 110 (2013)
Community Acquired Methicillin Resistant Staphylococcus aureus (CA-MRSA) is a strain of MRSA that can cause infections in patients in the community, in which these patients had no previous risk factors for MRSA infection and the patient received 72 hours prior to infection when admitted to hospital. This study aims to determine and compare the characteristics of epidemiological, clinical, and molecular biology of CA-MRSA with HA-MRSA.
A total of 11 clinical strains of Methicillin-resistant Staphylococcus aureus (MRSA) and Methicillin-sensitive Stapylococcus aureus (MSSA) were collected from 2 hospitals in Jakarta, Indonesia in 2012. SCCmec typing was performed by multiplex polymerase chain reaction (PCR) and the presence of six genes (vraR, vraG, vraA, vraF,fruA, and fruB) associated with vancomycin resistance was examined by simple PCR analysis.
We found three strains of community-acquired MRSA with SCCmec type II and one strain of hospital-acquired MRSA with SCCmec type IV. The other seven strains did not contain mecA genes and SCCmec. Plasmid pUB110 was found in one strain of community-acquired MRSA and two strains of hospital-acquired MRSA. vraA genes were present in 9 of the 11 strains, vraF in 4, vraG in 5, and vraR in 4. Note worthily, three quarters of strains without pUB110 contained vraR and vraF, and 70% contained vraA, whereas 60% of strains with pUB110 contained vraG.
Based on these results, we should be concerned about the possibility of transition from MRSA strains sensitive to vancomycin in VISA strains of MRSA strains obtained in clinical trials. But first we need to look the existence of natural VISA or hVISA among these MRSA strains.
Staphylococcus aureus (S. aureus) causes a wide variety of infections with clinical symptoms ranging from mild skin infections to severe deep infections. One of the important strains frequently found among nosocomial infections is Methicillin-resistant Staphylococcus aureus (MRSA) . Data from the previous study showed higher prevalence and variations of MRSA in countries of the Asia-Pacific region than in Europe . In some countries, such as Korea, Hong Kong, and Japan, the prevalence even exceeded 70% of all S. aureus isolated from hospitalized patients [3–6].
MRSA is resistant to methicillin and other related β-lactam antibiotics, such as cefoxitin and oxacillin . Initially, MRSA infections were associated only with infection exposure in health care and hospital settings, and were therefore referred to as Hospital-acquired MRSA (HA-MRSA) . Two decades ago, Community-acquired MRSA (CA-MRSA) started to emerge among MRSA isolates from individuals with no or minimal exposure to health care facilities [8, 9]. Currently, this strain tends to be more common among S. aureus infections as it is increasingly reported, particularly among children and young adults [8–11]. CA-MRSA strains are roughly classified into two main groups. The first group consists of CA-MRSA strains that are resistant to mono beta-lactam or beta-lactams and erythromycin and usually infect healthy patients who are not predisposed to MRSA . The second group consists of MRSA strains isolated from individuals who have risk factors for infection . Clinically, the CA-MRSA strains can be isolated from severe infections such as osteomyelitis, bacteremia, endocarditis, and pneumonia [14–17].
The rapid evolvement and continuous spread of new MRSA strains may due to their capability to acquire and to use antimicrobial resistance genes encoded by mobile genetic elements such as Staphylococcal cassette chromosome mec (SCCmec)[18–21]. SCCmec is a mobile genetic element which harbors the methicillin resistance gene mecA. Based on mec and ccr gene complex variations, there are 11 SCCmec types have been described so far, and also some subtypes or sub variations have been identified [20, 23–25]. Interestingly these genotype variations also reflected their antimicrobial characteristic . SCCmec types I-III are associated with HA-MRSA isolates, while types IV and V have been found related to CA-MRSA [26, 27]. A previous study reported that up to 80% of MRSA isolates were of sequence type 22-MRSA-SCCmec type IV (ST22-MRSA-IV) .
Several reports have indicated the possibility that the incidence of CA-MRSA infection would surpass that of HA-MRSA infection [16, 29, 30]. Considering the wide spread of CA-MRSA in Asian countries in particular, there is an urgent need of epidemiological or molecular studies of this strain to guide targeting of effective therapeutic agents. In the present study, therefore, we studied the molecular variation of MRSA isolates obtained from two hospitals in Jakarta in the year 2012. We found that SCCmec type II was the predominant SCCmec type among these clinical isolates. As the main therapy for MRSA, vancomycin may contribute to the emergence of a vancomycin-intermediate S. aureus (VISA) strain. As previously reported, VISA can emerge from a vancomycin susceptible S. aureus (VSSA) strain during chronic infection – but the genetic factors tcontributing to this phenomenon still need to be further defined [31–34]. Therefore we also studied certain VISA gene variations of these strains.
A total of 11 clinical strains of S. aureus were collected in 2012 from two hospitals in Jakarta: RSAB Harapan Kita and Siloam Kebun Jeruk, Indonesia (Table 1). Only one strain per patient was included. Isolates of S.aureus colonies were identified on the basis of pigments and clotting factors. Zone barriers were determined on Mueller-Hinton agar according to the Clinical and laboratory standards institute (CLSI) guidelines. Strains were incubated at 35º for 18 hours then the diameter of inhibition zone was determined. Amoxicillin clavulanate, cefuroxime, ceftriaxone, cefotaxime, ceftazidime, cefepime, imipenem, cotrimoxazole, clindamycin, amikacin, ciprofloxacin, levofloxacin, vancomysin, linezolid, teicoplanin, tigecyclin, and fosfomycin were tested. Breakpoint for the definition of antibiotic resistance in S. aureus was based on CDC guidelines manual.
Genomic DNA isolation
Total genomic DNA was isolated using the Wizard® genomic DNA purification kit (Promega corporation, Madison, WI, USA).
Multiplex PCR for SCCmec typing
Multiplex PCR included eight loci (A through H) selected on the basis of mec element sequences described in previous reports . And the primers have been described on previous reports (Table 2) [36, 37]. PCR was performed on a volume of 50 mL using a Gene Amp PCR kit (Applied Biosystems, New Jersey, USA) and a kit containing the following: 1x PCR buffer II; 200 μM (each) deoxynucleoside triphosphate; 400 nM primer CIF2 F2, CIF2 R2, MECI P2, P3 MECI, RIF5 F10, RIF5 R13, R1 pUB110, and pT181 R1; 800 nM primer F2 DCS, DCS R2, P4 MECA, MECA P7 and P4 IS431; 200 nM primers KDP F1, KDP R1, RIF4 F3, and RIF4 R9; 1.25 U Ampli Taq, and approximately 5 ng of DNA template. The ASTEC program temperature control system PC-701 DNA thermo cycler was programmed as follows: 10 min at 95°C, 30 cycles of 30 seconds at 94°C, 30 seconds at 53°C, and 1 min at 72°C, and 10 minutes at 72°C. Samples were stored at 4°C until analysis. Ten-mL aliquot of the PCR products electrophoresed on 2% agarose gel (contained ethidium bromide) for 30 minutes at 100 V. Gel then photographed under ultraviolet light.
PCR analysis of genes related to VISA
Six genes associated with VISA strains, vraR, vraG, vraA, vraF, fruA, and fruB, were selected for PCR analysis . PCR amplification was performed using primers designed from the published NCBI sequence (Table 3). PCR reaction was performed in 13 ml reaction mixture containing 10 mM Tris (pH 8.3), 50 mM KCl, 1.5 mM MgCl2, 0.2 mM each deoksinucleotide triphosphate, 0.5 mM of each primer, and 2.5 U Taq DNA polymerase (Applied Biosystems, NewJersey, USA). The ASTEC program temperature control systemPC-701 DNA thermo cycler was programmed as follows: 10 min at 95°C, 30 cycles of 1 min at 94°C, 1 min at 58°C, and 1 min at 72°C, and 10 minutes at 72°C. Samples were stored at 4°C until analysis. Ten ml aliquot of the PCR product was electrophorese don agarose gel 1.5% for 30 min at 100 V. Gels were stained with ethidium bromide and photographed under ultraviolet light. Mu50 (ATCC; 700 699) was used as a positive control.
The project received ethical approval from the review board of the Department of National Education of the Hasanuddin University. Oral informed consent was obtained from the study participants after explanation of the procedure and the purpose of the study. Oral informed consent was applied as the collection of the specimens did not affect the intervention procedure to any extend and all clinical data was made anonymous before analysis. The collection of informed consent was witnessed by a nurse and or the medical officer in charge and was recorded on the medical file of the patient. The verbal consent procedure was approved by the ethical committee.
MRSA and MSSA strains
Of the 11 S. aureus isolates from 2012 analyzed, 5 were CA-MSSA, 2 HA-MSSA, 1 CA-MRSA and 3 HA-MRSA. The 4 MRSA isolates (CA-MRSA and HA-MRSA) were derived from different clinical samples, i.e. urine, sputum, pus, and throat swab. Sensitivity testing showed that all isolates (both MSSA and MRSA) had good sensitivity to vancomycin, teicoplanin, linezolid, tigecycline, and amikacin. Clindamycin was still sensitive for CA-MSSA, HA-MSSA and CA-MRSA.
SCCmec typing revealed that 3 of the 4 MRSA isolates contained SCCmec type II; the other 1 contained SCCmec type IV. Three of all 11 strains contained plasmid pUB110. Figure 1 shows the banding patterns of the products obtained by multiplex PCR for SCCmec typing. Four strains showed the 162-bp fragment of the mecA gene. Type II strains displayed the 284-bp fragment, 209-bpfragment, and a 342-bp fragment with or without a381-bp fragment from the plasmid pUB110; Strain type IV showed the342-bp fragment without the381-bp fragment from the plasmid pUB110.
The presence of genes associated VISA
The following six genes were studied: vraR, vraG, vraA, vraF, fruA, and fruB. Ten of the 11 S. aureus isolates contained vraA, 4 vraF, 5 vraG, and 4 vraR (Figure 2, Table 4). All 11 isolates contained fruA and 7 contained fruB. Mu50 strain was used as positive control contained all six genes. 30% of MRSA strains with pUB110 contained vraA genes, 60% vraG, 25% vraR, and 25% vraF.
In this study we found that three (27%) of our 11 S. aureus strains contained genes mecA and SCCmec type II, and 1 (9%) contained SCCmec type IV. Previous examined the study examined SCCmec types of 138 MRSA strains isolated in Japan in 1999 and found that 126 (91.3%) contained SCCmec type II, 6 (4.3%) contained SCCmec type I, and 5 (3.6%) contained SCCmec type IV . The results of this research in Japan combined with the findings in this study suggest that type II SCCmec occurs frequently in Asia pacific region. Types I and III SCCmec were not detected in this study. However, type III SCCmec has been reported in European countries, Australia, New Zealand, Thailand, Vietnam, Singapore, the Philippines, and elsewhere [40, 41].
In addition to the structural classification of four types of SCCmec, we also checked the presence of plasmid pUB110 in SCCmec. Only 3 strains (27%) contained plasmid pUB110. MRSA has been known to cause nosocomial infections. MRSA infections have been reported increased cases among the group of patients without any real connection with the hospital . CA-MRSA strains have been reported in Australia [43, 44], New Zealand , England , Canada , and the United States .
In this study we found fruA in all 11 strains and fruB in 7 of all strains (64%). Gen vraA considered as a long chain fatty acid CoA ligase, while vraF and vraG are ABC transporter genes. These genes are up-regulated in the VISA (Mu50) and may contribute to resistance to vancomycin . Furthermore, vancomycin resistance is thought to be caused by increased cell wall synthesis . The system settings are vraSR new response has been reported, and vraR, which is one of two components of the system, seems to play a role in vancomycin resistance. As a result of the introduction of genes into cells, vraR sensitive vancomycin will increase the level of resistance to vancomycin . In the present study it was found that all four MRSA isolates were sensitive to vancomycin, and that one of these contained the vraR gene. The finding of this VISA related gene in vancomycin-sensitive among MRSA strains may indicates the possible risk of transition from MRSA to VRSA but first we need to rule out the possibility of VISA or hVISA are exist among our MRSA strain. Something lacked on this study.
Note worthily, we found that three of the four MRSA strains contained plasmid pUB110, which most likely is a strain of CA-MRSA, because it only one contained genes of vraF and vraR at relatively lower frequencies than the MRSA strains containing plasmid pUB110, but contained no genes of vraR and vraF. Therefore, we need to further investigate the relationship between SCCmec typing, as a means to identify the genetic background of the bacteria, as well as the presence of genes associated VISA.
Most strains of MRSA: 75% (3/4) contains a Type II SCCmec, and only 1(25%) strain containing SCCmec type IV and the overall of S.aureus isolates containing all six genes associated VISA with different frequencies. In particular, the strain that is considered as CA-MRSA, the strain is considered to contain vraR, at 1 CA-MRSA strain was found not to contain vraR and only 33% (1/3) of vraR genes containing in HA-MRSA strains. Based on these results, we should be concerned about the possibility of transition from MRSA strains sensitive to vancomycin in VISA strains of MRSA strains obtained in clinical trials. But first we need to look the existence of natural VISA or hVISA among these MRSA strains.
In this study, we applied the multiplex PCR test to determine the type of SCCmec, and a simple PCR test to detect the presence of genes related to VISA. Both tests can be easily and rapidly performed at many hospitals and laboratories, and can therefore be considered useful tools for the investigation of clinical MRSA strains.
Shore AC, Deasy EC, Slickers P, Brennan G, O’Connell B, Monecke S, Ehricht R, Coleman DC: Detection of staphylococcal cassette chromosome mec type XI carrying highly divergent mecA, mecI, mecR1, blaZ, and ccr genes in human clinical isolates of clonal complex 130 methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother. 2011, 55 (8): 3765-3773. 10.1128/AAC.00187-11.
Reinert RR, Low DE, Rossi F, Zhang X, Wattal C, Dowzicky MJ: Antimicrobial susceptibility among organisms from the Asia/Pacific Rim, Europe and Latin and North America collected as part of TEST and the in vitro activity of tigecycline. J Antimicrob Chemother. 2007, 60 (5): 1018-1029. 10.1093/jac/dkm310.
Aires de Sousa M, Crisostomo MI, Sanches IS, Wu JS, Fuzhong J, Tomasz A, de Lencastre H: Frequent recovery of a single clonal type of multidrug-resistant Staphylococcus aureus from patients in two hospitals in Taiwan and China. J Clin Microbiol. 2003, 41 (1): 159-163. 10.1128/JCM.41.1.159-163.2003.
Boyce JM, Cookson B, Christiansen K, Hori S, Vuopio-Varkila J, Kocagoz S, Oztop AY, Vandenbroucke-Grauls CM, Harbarth S, Pittet D: Meticillin-resistant Staphylococcus aureus. Lancet Infect Dis. 2005, 5 (10): 653-663. 10.1016/S1473-3099(05)70243-7.
Lee K, Chang CL, Lee NY, Kim HS, Hong KS, Cho HC: Korean nationwide surveillance of antimicrobial resistance of bacteria in 1998. Yonsei Med J. 2000, 41 (4): 497-506.
Voss A, Doebbeling BN: The worldwide prevalence of methicillin-resistant Staphylococcus aureus. Int J Antimicrob Agents. 1995, 5 (2): 101-106. 10.1016/0924-8579(94)00036-T.
Klein E, Smith DL, Laxminarayan R: Hospitalizations and deaths caused by methicillin-resistant Staphylococcus aureus, United States, 1999–2005. Emerg Infect Dis. 2007, 13 (12): 1840-1846. 10.3201/eid1312.070629.
Fang YH, Hsueh PR, Hu JJ, Lee PI, Chen JM, Lee CY, Huang LM: Community-acquired methicillin-resistant Staphylococcus aureus in children in northern Taiwan. J Microbiol Immunol Infect. 2004, 37 (1): 29-34.
Sattler CA, Mason EO, Kaplan SL: Prospective comparison of risk factors and demographic and clinical characteristics of community-acquired, methicillin-resistant versus methicillin-susceptible Staphylococcus aureus infection in children. Pediatr Infect Dis J. 2002, 21 (10): 910-917. 10.1097/00006454-200210000-00005.
Herold BC, Immergluck LC, Maranan MC, Lauderdale DS, Gaskin RE, Boyle-Vavra S, Leitch CD, Daum RS: Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk. JAMA. 1998, 279 (8): 593-598. 10.1001/jama.279.8.593.
Kurlenda J, Grinholc M: Alternative therapies in Staphylococcus aureus diseases. Acta Biochim Pol. 2012, 59 (2): 171-184.
Naimi TS, LeDell KH, Como-Sabetti K, Borchardt SM, Boxrud DJ, Etienne J, Johnson SK, Vandenesch F, Fridkin S, O’Boyle C: Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA. 2003, 290 (22): 2976-2984. 10.1001/jama.290.22.2976.
Naimi TS, LeDell KH, Boxrud DJ, Groom AV, Steward CD, Johnson SK, Besser JM, O’Boyle C, Danila RN, Cheek JE: Epidemiology and clonality of community-acquired methicillin-resistant Staphylococcus aureus in Minnesota, 1996–1998. Clin Infect Dis. 2001, 33 (7): 990-996. 10.1086/322693.
Monaco M, Antonucci R, Palange P, Venditti M, Pantosti A: Methicillin-resistant Staphylococcus aureus necrotizing pneumonia. Emerg Infect Dis. 2005, 11 (10): 1647-1648. 10.3201/eid1110.050776.
Millar BC, Prendergast BD, Moore JE: Community-associated MRSA (CA-MRSA): an emerging pathogen in infective endocarditis. J Antimicrob Chemother. 2008, 61 (1): 1-7. 10.1093/jac/dkm441.
Seybold U, Kourbatova EV, Johnson JG, Halvosa SJ, Wang YF, King MD, Ray SM, Blumberg HM: Emergence of community-associated methicillin-resistant Staphylococcus aureus USA300 genotype as a major cause of health care-associated blood stream infections. Clin Infect Dis. 2006, 42 (5): 647-656. 10.1086/499815.
Centers for Disease C, Prevention: Severe methicillin-resistant staphylococcus aureus community-acquired pneumonia associated with influenza--Louisiana and Georgia, december 2006-january 2007. MMWR Morb Mortal Wkly Rep. 2007, 56 (14): 325-329.
Malachowa N, DeLeo FR: Mobile genetic elements of Staphylococcus aureus. Cell Mol Life Sci. 2010, 67 (18): 3057-3071. 10.1007/s00018-010-0389-4.
Hanssen AM, Ericson Sollid JU: SCCmec in staphylococci: genes on the move. FEMS Immunol Med Microbiol. 2006, 46 (1): 8-20. 10.1111/j.1574-695X.2005.00009.x.
International Working Group on the Classification of Staphylococcal Cassette Chromosome E: Classification of staphylococcal cassette chromosome mec (SCCmec): guidelines for reporting novel SCCmec elements. Antimicrob Agents Chemother. 2009, 53 (12): 4961-4967.
Otto M: Staphylococcus aureus toxin gene hitchhikes on a transferable antibiotic resistance element. Virulence. 2010, 1 (1): 49-51. 10.4161/viru.1.1.10453.
Ito T, Katayama Y, Asada K, Mori N, Tsutsumimoto K, Tiensasitorn C, Hiramatsu K: Structural comparison of three types of staphylococcal cassette chromosome mec integrated in the chromosome in methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother. 2001, 45 (5): 1323-1336. 10.1128/AAC.45.5.1323-1336.2001.
Jensen SO, Lyon BR: Genetics of antimicrobial resistance in Staphylococcus aureus. Future Microbiol. 2009, 4 (5): 565-582. 10.2217/fmb.09.30.
Lowy FD: Antimicrobial resistance: the example of Staphylococcus aureus. J Clin Invest. 2003, 111 (9): 1265-1273.
Turlej A, Hryniewicz W, Empel J: Staphylococcal cassette chromosome mec (Sccmec) classification and typing methods: an overview. Pol J Microbiol. 2011, 60 (2): 95-103.
Kuo SC, Chiang MC, Lee WS, Chen LY, Wu HS, Yu KW, Fung CP, Wang FD: Comparison of microbiological and clinical characteristics based on SCCmec typing in patients with community-onset meticillin-resistant Staphylococcus aureus (MRSA) bacteraemia. Int J Antimicrob Agents. 2012, 39 (1): 22-26. 10.1016/j.ijantimicag.2011.08.014.
Pantosti A, Sanchini A, Monaco M: Mechanisms of antibiotic resistance in Staphylococcus aureus. Future Microbiol. 2007, 2 (3): 323-334. 10.2217/174609188.8.131.523.
Rossney AS, Lawrence MJ, Morgan PM, Fitzgibbon MM, Shore A, Coleman DC, Keane CT, O’Connell B: Epidemiological typing of MRSA isolates from blood cultures taken in Irish hospitals participating in the European antimicrobial resistance surveillance system (1999–2003). Eur J Clin Microbiol Infect Dis. 2006, 25 (2): 79-89. 10.1007/s10096-006-0091-5.
Popovich KJ, Weinstein RA, Hota B: Are community-associated methicillin-resistant Staphylococcus aureus (MRSA) strains replacing traditional nosocomial MRSA strains?. Clin Infect Dis. 2008, 46 (6): 787-794. 10.1086/528716.
Davis SL, Rybak MJ, Amjad M, Kaatz GW, McKinnon PS: Characteristics of patients with healthcare-associated infection due to SCCmec type IV methicillin-resistant Staphylococcus aureus. Infect Control Hosp Epidemiol. 2006, 27 (10): 1025-1031. 10.1086/507918.
Sieradzki K, Roberts RB, Haber SW, Tomasz A: The development of vancomycin resistance in a patient with methicillin-resistant Staphylococcus aureus infection. N Engl J Med. 1999, 340 (7): 517-523. 10.1056/NEJM199902183400704.
Smith TL, Pearson ML, Wilcox KR, Cruz C, Lancaster MV, Robinson-Dunn B, Tenover FC, Zervos MJ, Band JD, White E: Emergence of vancomycin resistance in staphylococcus aureus. Glycopeptide-intermediate staphylococcus aureus working group. N Engl J Med. 1999, 340 (7): 493-501. 10.1056/NEJM199902183400701.
Moore MR, Perdreau-Remington F, Chambers HF: Vancomycin treatment failure associated with heterogeneous vancomycin-intermediate Staphylococcus aureus in a patient with endocarditis and in the rabbit model of endocarditis. Antimicrob Agents Chemother. 2003, 47 (4): 1262-1266. 10.1128/AAC.47.4.1262-1266.2003.
Howden BP, Davies JK, Johnson PD, Stinear TP, Grayson ML: Reduced vancomycin susceptibility in Staphylococcus aureus, including vancomycin-intermediate and heterogeneous vancomycin-intermediate strains: resistance mechanisms, laboratory detection, and clinical implications. Clin Microbiol Rev. 2010, 23 (1): 99-139. 10.1128/CMR.00042-09.
Ito T, Okuma K, Ma XX, Yuzawa H, Hiramatsu K: Insights on antibiotic resistance of Staphylococcus aureus from its whole genome: genomic island SCC. Drug Resist Updat. 2003, 6 (1): 41-52. 10.1016/S1368-7646(03)00003-7.
Oliveira DC, Tomasz A, de Lencastre H: The evolution of pandemic clones of methicillin-resistant Staphylococcus aureus: identification of two ancestral genetic backgrounds and the associated mec elements. Microb Drug Resist. 2001, 7 (4): 349-361. 10.1089/10766290152773365.
Oliveira DC, de Lencastre H: Multiplex PCR strategy for rapid identification of structural types and variants of the mec element in methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother. 2002, 46 (7): 2155-2161. 10.1128/AAC.46.7.2155-2161.2002.
Kuroda M, Kuroda H, Oshima T, Takeuchi F, Mori H, Hiramatsu K: Two-component system VraSR positively modulates the regulation of cell-wall biosynthesis pathway in Staphylococcus aureus. Mol Microbiol. 2003, 49 (3): 807-821.
Matsuzaki S, Yasuda M, Nishikawa H, Kuroda M, Ujihara T, Shuin T, Shen Y, Jin Z, Fujimoto S, Nasimuzzaman MD: Experimental protection of mice against lethal Staphylococcus aureus infection by novel bacteriophage phi MR11. J Infect Dis. 2003, 187 (4): 613-624. 10.1086/374001.
Katayama Y, Ito T, Hiramatsu K: A new class of genetic element, staphylococcus cassette chromosome mec, encodes methicillin resistance in Staphylococcus aureus. Antimicrob Agents Chemother. 2000, 44 (6): 1549-1555. 10.1128/AAC.44.6.1549-1555.2000.
Yamaguchi A: Bacterial resistance mechanisms for tetracyclines. Nihon Rinsho. 1997, 55 (5): 1245-1251.
Matsuhashi M, Song MD, Ishino F, Wachi M, Doi M, Inoue M, Ubukata K, Yamashita N, Konno M: Molecular cloning of the gene of a penicillin-binding protein supposed to cause high resistance to beta-lactam antibiotics in Staphylococcus aureus. J Bacteriol. 1986, 167 (3): 975-980.
Maguire GP, Arthur AD, Boustead PJ, Dwyer B, Currie BJ: Clinical experience and outcomes of community-acquired and nosocomial methicillin-resistant Staphylococcus aureus in a northern Australian hospital. J Hosp Infect. 1998, 38 (4): 273-281. 10.1016/S0195-6701(98)90076-7.
Nimmo GR, Schooneveldt J, O’Kane G, McCall B, Vickery A: Community acquisition of gentamicin-sensitive methicillin-resistant Staphylococcus aureus in southeast Queensland, Australia. J Clin Microbiol. 2000, 38 (11): 3926-3931.
Rings T, Findlay R, Lang S: Ethnicity and methicillin-resistant S. aureus in South Auckland. N Z Med J. 1998, 111 (1064): 151-
Stacey AR, Endersby KE, Chan PC, Marples RR: An outbreak of methicillin resistant Staphylococcus aureus infection in a rugby football team. Br J Sports Med. 1998, 32 (2): 153-154. 10.1136/bjsm.32.2.153.
Embil J, Ramotar K, Romance L, Alfa M, Conly J, Cronk S, Taylor G, Sutherland B, Louie T, Henderson E: Methicillin-resistant Staphylococcus aureus in tertiary care institutions on the Canadian prairies 1990–1992. Infect Control Hosp Epidemiol. 1994, 15 (10): 646-651. 10.1086/646827.
Hanaki H, Inaba Y, Sasaki K, Hiramatsu K: A novel method of detecting Staphylococcus aureus heterogeneously resistant to vancomycin (hetero-VRSA). Jpn J Antibiot. 1998, 51 (8): 521-530.
The authors declare that they have no competing interests.
LB, AR and MH carried out the molecular biology studies. LB performed data and specimens collection and also epidemiology, clinical and microbiology results analysis. RD and MS participated in the molecular biology studies. All authors read and approved the final manuscript.
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Buntaran, L., Hatta, M., Sultan, A.R. et al. Sccmec type II gene is common among clinical isolates of methicillin-resistant Staphylococcus aureus in Jakarta, Indonesia. BMC Res Notes 6, 110 (2013). https://doi.org/10.1186/1756-0500-6-110
- Multiplex Polymerase Chain Reaction
- SCCmec Type