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) [1]. Data from the previous study showed higher prevalence and variations of MRSA in countries of the Asia-Pacific region than in Europe [2]. 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 [1]. 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) [7]. 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 [12]. The second group consists of MRSA strains isolated from individuals who have risk factors for infection [13]. 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[22]. 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 [26]. 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) [28].

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.

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 [39]. 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 [42]. CA-MRSA strains have been reported in Australia [43, 44], New Zealand [45], England [46], Canada [47], and the United States [41].

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 [48]. Furthermore, vancomycin resistance is thought to be caused by increased cell wall synthesis [38]. 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 [38]. 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.