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Annals of Medicine and Medical Sciences
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  2. Vol. 05, No. 08, (2026)
  3. Prevalence and Characterisation of Methicillin Resistant Staphylococcu…
Original Article Open Access

Prevalence and Characterisation of Methicillin Resistant Staphylococcus Aureus Isolated in a Tertiary Laboratory, Pretoria, South Africa

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Annals of Medicine and Medical SciencesVol. 05, No. 08, (2026) August 1, 2026pp. 1062 - 1069
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Abstract

Objectives: Methicillin resistant Staphylococcus aureus (MRSA) remains the pathogen of major public health significance globally. This study aimed to characterize MRSA isolates at Dr George Mukhari tertiary microbiology laboratory in Pretoria, South Africa. Methods: Clinical MRSA isolates were collected over a 12 months period. Antibiotic susceptibility profile of the isolates was determined using disc diffusion and E test methods. Antibiotic resistance genes, SCCmec types and virulence genes were detected using multiplex PCR assays. Results: From the 1,135 S. aureus isolates cultured, 303 (27%) were confirmed as MRSA. Resistance to erythromycin, clindamycin and high-level mupirocin was 59%, 52% and 22% respectively. No resistance to vancomycin was found; however, 11% of the isolates tested had vancomycin MICs at 2 µg/µl. The ermA was the most common antibiotic resistance gene detected. The SCCmec type III was the most prevalent (40%) followed by SCCmec type V (25.5%). The sea, psm-mec and lukS/F-PV were the predominant virulence genes detected. Conclusion: This study reported a 27% prevalence of MRSA and noticed an increase in vancomycin MICs. Resistance and virulence genes across different SCCmec types were diverse. There is a need for reinforcement of infection, prevention, and control strategies to mitigate MRSA spread.

Keywords

Antibiotic resistance genes SCCmec types virulence genes South Africa.

Introduction

Staphylococcus aureus (S. aureus) is a Gram-positive bacterium considered as part of normal flora of humans’ skin, nasal passages as well as the mucosal surfaces of the upper respiratory and the urogenital tract of some healthy individuals [1]. Staphylococcus aureus is well known for its pathogenic ability of causing a wide range of suppurative and toxin mediated infections ranging from superficial infections such as skin lesions (boils and furunculosis) to serious infections such as pneumonia, osteomyelitis, endocarditis and toxic shock syndrome [2]. The main mode of transmission of S. aureus is through contact with human skins and hands [2].

Staphylococcus aureus has evolved into drug resistance over the years after the initial development of resistance to methicillin [3]. Methicillin-resistant S. aureus (MRSA) refers to any strain of S. aureus that has gained resistance to the first-line agent, cloxacillin and other β-lactam antibiotics such as cephalosporins [3]. The MRSA strains emerged in early 1960s and were mainly acquired in medical settings, causing outbreaks and were considered to be hospital-associated MRSA (HA-MRSA) [4]. However, in the 1990s a change was observed, MRSA strains were detected in community settings among individuals without previous health care contact and were referred to as community-associated (CA-MRSA) [5]. Since then, cases of CA-MRSA have been reported globally [2].

Methicillin resistance is commonly caused by the mecA gene, which encodes for a penicillin-binding protein (PBP2a) that has decreased β-lactam antibiotic binding affinity [5]. It is part of a mobile genetic element (MGE) known as the Staphylococcal cassette chromosome (SCCmec), which has two vital genetic parts: the mec gene and the cassette chromosome recombinase (ccr) genes. SCCmec is integrated into the S. aureus chromosome at a unique site which contributes to the characterization of S. aureus into different SCCmec types [6]. The ccr gene complex and the two other putative genes (cch and ccu) are for further subtyping of the SCCmec types [7]. Initially, five SCCmec types (I–V) were described, however, to date 15 SCCmec types (I–XV) with several subtypes and variants, with different characteristics have been identified [8]. In most cases, HA-MRSA were known to typically carry SCCmec types I, II, and III, while CA-MRSA carries SCCmec IV and V [9].

MRSA has numerous virulence factors that enable it to trigger pathogenesis and spread infection in the body. These include a variety of enzymes, proteins, and toxins encoded by different genes, some on MGE such as plasmids [10]. Examples of these are Panton-Valentine Leukocidin encoded by the lukS/F-PV gene; exfoliative toxins encoded by the eta and etb genes; the staphylococcal enterotoxin encoded by the sea gene, the toxic shock syndrome toxin encoded by the tsst-1 gene and phenol-soluble modulins encoded by the psm-mec gene [11].

Material and Methods

Study design, demographic data collection and Bacterial isolation

This was a cross-sectional descriptive study in which Staphylococcus aureus isolates cultured at the DGM laboratory between June 2019 and June 2020 were documented. Those identified as MRSA by the VITEK®-2 automated system (bioMérieux, Etoile, France) were collected and stored at -70°C for further processing. Patients’ information was documented from the Laboratory Information System –Trackcare (LIS).

Antibiotic susceptibility testing of the isolates

Antibiotic susceptibility testing was done using the disc diffusion and the gradient diffusion, Epsilometer (E) test methods according to the Clinical Laboratory Standard Institute (CLSI) guidelines [18]. The following antibiotic discs were tested: clindamycin (2µg/ml), erythromycin (15µg/ml), low-level mupirocin (5µg/ml), and high-level mupirocin (20µg/ml). The cefoxitin (10µg/ml) disc was tested to confirm the phenotypic identity of MRSA isolates. Double disc diffusion method was done to determine the inducible resistance (macrolide-linconsamide-streptogramin B [MLSB] cross resistance). The E test method was done to determine the minimum inhibitory concentration (MIC) of vancomycin on the first 100 selected MRSA isolates.

Multiplex PCR assays for antibiotic resistance genes of MRSA isolates

DNA extraction of isolates was performed using the boiling method. Conventional multiplex PCR assays were carried out for mecA gene confirmation in the isolates and for the detection of antibiotic resistance genes using sets of primers and conditions previously reported (Supplementary materials [S1]). All primers used in this study were synthesised by Inqaba Biotechnical Industries (Pty) Ltd, Pretoria, South Africa. The PCR was performed in a 25 µl reaction consisting of 11 µl of MyTaq™ HS Red mix (Bioline, UK), 1 µl of each primer solution (forward and reverse), 10 µl of nuclease-free water, and 2 µl of DNA templates. The PCR products were separated on 1% agarose gel and images visualised and captured using a Gel DocTM EZ system (Bio-Rad, USA).

Detection of SCCmec types and cassette chromosome recombinase and putative genes

Multiplex PCR assay was performed for the screening of MRSA SCCmec types I, II, III, V and type IV sub-types IVa, IVb, IVc, IVd based on the methods and conditions previously described (S1). The cassette chromosome recombinases genes (ccrA and ccrB) and putative genes (cch, and ccu) were also screened for using a multiplex PCR assay using sets of primers and conditions listed in S1.

Detection of MRSA virulence genes

Multiplex PCR assay was performed for the detection of MRSA virulence genes including eta, etb, lukS/F-PVL, psm-mec, sea and the tsst-1 following procedures and conditions previously described (S1).A total volume of 25 μl consisted of 8 μl of EmeraldAmp MAX PCR Master Mix (Takara, Japan), 0.5 μl primer mix (forward and reverse), 5μl DNA template and PCR grade water.

Control strains and data analysis

The control strains used in this study included MRSA ATCC BAA1026, methicillin-susceptible S. aureus (MSSA) ATCC 29213 and strains previously sequenced in-house. All data obtained was recorded and exported into a Microsoft Excel sheet and analysed using STATA 18.

Results

Baseline characteristics of clinical MRSA isolates

A total of 1135 S. aureus were isolated at the DGM laboratory during the study period. The prevalence of MRSA identified using the VITEK®-2 automated system was 27% (303/1135) and the first 200 MRSA isolates were selected for the analysis. Of these, 142 were samples from DGM Hospital, 35 from Jubilee, 10 from Odi, 6 from Brits, 3 from Mmametlhake, and 2 from KwaMhlanga Hospitals. The frequency of MRSA isolates was higher in the male (56%) as compared to female (43.5%) patients with a p-value of 0.365. The 20-29 years age group had the highest number of MRSA isolates followed by the 5-14 years age group. The isolates were from diverse clinical specimens, the majority of which were pus/pus swabs followed by blood culture as shown in Table 1.

Table 1 Types of clinical specimens collected.
Specimen types Frequency %
Pus/ Pus swabs 143 71.5
Blood culture 43 21.5
Sputum 12 6.0
CSF 1 0.5
Urine 1 0.5
Total 200 100

Antibiotic Susceptibility profile of MRSA isolates.

Of the MRSA isolates tested, 66% (132/200) were resistant to cefoxitin while 34% (68/200) were cefoxitin sensitive. Resistance to erythromycin, clindamycin, low-level mupirocin (LLRM) as well as high-level mupirocin (HLRM) was observed in 59%, 52%, 44%, and 22% of the isolates respectively. The double disc diffusion method showed D zones in 58 isolates (resistant to erythromycin but susceptible to clindamycin), indicating the inducible MLSB phenotype (Table 2A).

Table 2 Susceptibility profile of MRSA isolates (n=200).
Antibiotic Susceptible Intermediate Resistant
Erythromycin 81 (40.5%) 1 (0.5%) 118 (59%)
Clindamycin 93 (46.5%) 4 (2%) 103 (52%) *
Mupirocin low-level (5µg) 112 (56%) - 88 (44%)
Mupirocin high-level (200µg) 156 (78%) - 44 (22%)

*This included 45 + 58 D-zone positive isolates

The MICs of vancomycin on the first 100 selected MRSA isolates showed that all the isolates were in the susceptible range. However, increased vancomycin MIC of 1 to 2 and above 2 µg/ml were observed in 26 and 11 isolates respectively as shown in Table 2B.

Table 3 Vancomycin MIC results of MRSA isolates (n=100).
Vancomycin MIC ranges (µg/ml)
0.38 0.5 0.75 1 1-2 >2
Number of isolates 3 8 11 41 26 11

Molecular detection of antibiotic resistance genes of MRSA isolates.

The PCR assay detected methicillin resistance mecA gene in 66% of isolates while 34% of isolates did not show the presence of mecA gene. Among the 119 isolates which were resistant to either erythromycin and/or clindamycin, the ermA gene was present in 20% followed by ermC in 12% as shown in Table 3. Five of the 44 isolates with high-level mupirocin resistance had the mupA gene. A combination of two resistance genes was observed in five isolates. None of the 11 isolates with vancomycin MIC >2 had positive vancomycin resistance genes.

Table 4 Antibiotic resistance genes present in MRSA isolates.
Gene Present (%)
ermA 24/119 (20%)
ermB 4/119 (3%)
ermC 14/119 (12%)
msrA 10/119 (8%)
mefA 4/119 (3%)
ermC + msrA mefA + mupA 4/119 (3%) 1/119 (0.8%)
mupA 5/44 (11%)
vanA, B & C 0 (0%)

Determination of SCCmec types, cassette chromosome recombinase and putative genes.

Multiplex PCR assay showed that 40% of the isolates were SCCmec type III, 25% were SCCmec type V and 5.5% of the isolates were non-typable. Three isolates had two SCCmec types simultaneously. A complete distribution of SCCmec types identified in this study is shown in Table 4.

Table 5 SCCmec type distribution among MRSA isolates (n=200).
SCCmec type Number of positive isolates (n=200) Source of samples (n)
SCCmec types I 0 (0) -
SCCmec types II 19 (9.5%) Pus (8), blood culture (11)
SCCmec type III 80 (40%) Pus (69), blood culture (11)
SCCmec type IVa 10 (5%) Pus (10)
SCCmec type IVb 14 (7%) Pus (14)
SCCmec type IVc 8 (4%) Pus (7), blood culture (1)
SCCmec type IVd 5 (2.5%) Pus (4), urine (1)
SCCmec type V 50 (25%) Pus (39), sputum (9), blood culture (2), urine (1)
SCCmec types II + IVb* 1 (0.5%) Pus (1)
SCCmec types IVc + V* 2 (1%) Pus (2)
Non-typable 11 (5.5%) -
Total 200

*Three isolates had two SCCmec types simultaneously.

Two cassette chromosome recombinase genes (ccrA and ccrB) and two putative genes (cch, and ccu) were detected among the isolates, with ccrA, ccrB, cch, and ccu detected in 55% (110), 26% (52), 13.5% (27) and 5.5% (11) respectively.

Detection of virulence genes among MRSA isolates.

All six genes screened for were detected among the isolates. Overall, sea gene was the most prevalent virulence gene detected in a total of 94 (47%) isolates followed by psm-mec in 90 (45%) of isolates. A total of 61 (30.5%) isolates had more than 1 virulence genes (Table 5). Two isolates did not carry any of the virulence genes screened for.

Table 6
Virulence genes detected Positive isolates (n=200) %
Single virulence gene detected (134) (67)
sea 47 23.5
psm-mec 39 19.5
lukS/F-PV 30 15
eta 6 3
tsst-1 6 3
etb 2 1
None of genes 4 1
Combination of two virulent genes (31) (15.5)
sea + psm-mec 11 5.5
psm-mec + eta 9 4.5
sea + lukS/F-PV 7 3.5
psm-mec+ tsst-1 2 1
psm-mec + lukS/F-PV 2 1
Combination of three virulent genes (29) (14.5)
sea +psm-mec + eta 16 8
sea + psm-mec + tsst-1 10 5
sea + psm-mec + lukS/F-PV 2 1
sea + eta +tsst-1 1 0.5
Combination of four virulent genes psm-mec + tsst-1 + eta + lukS/F-PV (1) 1 (0.5) 0.5
Total 200 100

The SCCmec types were associated with virulence genes. The distribution of SCCmec types associated with different virulence

genes of MRSA isolates a in Pretoria is shown in Table 6.

Table 7 The association between SCCmec types and virulence genes.
Virulence genes detected Number of Positive isolate Associated SCCmec type detected N p-value
psm-mec 135 (67.5%) SCCmec type III 73 p < 0.0001
SCCmec type II 14
SCCmec type IVb 14
SCCmec type IVa 8
SCCmec type V 8
SCCmec type IVc 3
SCCmec type IVd 1
SCCmec type II + IVb * 1
Non-typable 11
Sea 116 (58%) SCCmec type III 56 p = 0.003
SCCmec type IVb 12
SCCmec type V 12
SCCmec type II 11
SCCmec type IVc 4
SCCmec type IVd 1
SCCmec type II + IVb * 1
Non-typable 11
Luks/F-PV 56 (28%) SCCmec type V 44 p ˂ 0.0001
SCCmec type IVc 5
SCCmec type IVc + V * 2
SCCmec type II 1
SCCmec type III 1
SCCmec type IVa 1
SCCmec type IVb 1
Non-typable 1
Eta 41 (20.5%) SCCmec type III 19 p = 0.002
SCCmec type IVb 6
SCCmec type IVa 5
SCCmec type V 3
SCCmec type II 2
Non-typable 6
tsst-1 20 (10%) SCCmec type II 14 p ˂ 0.0001
SCCmec type V 5
SCCmec type II + IVb * 1
Etb 2 (1%) SCCmec type IVd 2 p = 0.0001

*Isolates with more than one SCCmec type.

Discussion

This study was undertaken to characterize clinical MRSA isolates from the DGM laboratory in Pretoria, South Africa. The study reported an MRSA prevalence of 27%. This rate is in agreement with other reports which indicated that the prevalence of MRSA in Sub-Saharan Africa is between 25% and 50% [1619]. However, the present finding is lower than the 46% previously reported by Perovic et al. in South Africa [17]. Higher rates of 82% and 72% have been reported in Rwanda and Eritrea respectively [2021]. In Colombia, a 90% MRSA prevalence was reported [22]. This confirms the variations in MRSA prevalence geographically which might be due to socio-economic, environmental and demographic factors [23]. In this study, males had a higher number of MRSA isolates as compared to females and mostly this was in patients aged from 20 to 29 years. This is consistent with another study in Ethiopia [24]. Similar to what has previously been reported in Ethiopia and Eritrea, MRSA isolation was highest in pus/pus swab samples (72%) followed by blood culture samples (22%) [2124].

The cefoxitin disk diffusion test was used to screen for MRSA phenotypically. Of the 200 MRSA isolates analysed, 66% were resistant and 34% were susceptible to cefoxitin. Comparative to our finding, Perovic et al. reported 43% of MRSA isolates resistant to cefoxitin [17]. The PCR detection of mecA gene has been proposed as a reliable indicator of resistance to methicillin. In this study, 66% of isolates were mecA positive and 34% of isolates did not show the presence of the mecA gene using PCR although identified as MRSA by the VITEK®-2 automated system. This suggests that resistance in these isolates was not mediated by the mecA gene which is consistent with the cefoxitin screening, but could be by other non-mecA genes such as mecC or other resistance mechanisms [25]. There is no evidence that the non-mecA-mediated resistance is of less clinical relevance [25]. These reports suggest that the VITEK-2 system is still a reliable method for the identification of MRSA isolates because it identifies MRSA regardless of the underlying mechanism of resistance.

This study reported a 59% and 52% resistance to erythromycin and clindamycin, respectively. Fifty eight of the 103 clindamycin resistant isolates showed the inducible clindamycin resistance phenotype (iMLSB) detected by a D-zone. A similar situation has been reported in Pakistan [26]. Of the antibiotic resistance determinants screened for, the ermA gene was the most prevalent, accounting for 20% followed by ermC (15%). This confirms what has previously been reported that the ermA gene encoding for MLS cross-resistance has the highest frequency rate among MRSA isolates [27]. However, this rate is much lower than the 86% reported in Iran [27]. In contrast to our finding, another study in India reported ermC gene being the most prevalent (23.4%) [28]. The frequency of ermB gene, previously reported to have originated from animal strains was low (3%) [29]. In this study, low prevalences of msrA (8%) and mefA (3%) genes were recorded. Similar, to our finding, a Turkish study reported the msrA gene in 7% of the isolates [30]. The msrA and mefA genes are acquired genes for mechanisms of inducible resistance to erythromycin by encoding an ATP-dependent efflux pump to mediate resistance [31]. This trend of more than 50% resistance rates of MRSA to MLSB antibiotics renders the empiric use of these antibiotics unreliable; hence alternative antibiotics such as linezolid must be considered.

In this study, 100% of the isolates were susceptible to vancomycin. However, an increase of vancomycin MICs to heterogeneous vancomycin reduced susceptibility, hVISA ranges were observed in 78% of the isolates (Table 2B). This demonstrates MIC creep, a drift in the clinical isolates of MRSA towards reduced vancomycin susceptibility [32]. The implication of this is of concern as vancomycin is the standard therapy for MRSA infections, it might suggest the need for combination therapy or adoption of alternative regimens for the treatment of invasive MRSA infections [32], which will be a challenge for resource constrained countries. None of the isolates had glycopetide resistance genes. Vancomycin-resistant MRSA strains have been reported in other countries such as the US and India [33].

Mupirocin is the cornerstone of decolonisation regimens, a successful strategy to prevent MRSA spread in healthcare facilities [34]. Increased usage has resulted in emergence of mupirocin resistance [35]. The mupA gene is a plasmid gene encoding for an additional isoleucyl-tRNA synthetase for which mupirocin has no affinity [35]. Our findings showed 44 (22%) of the isolates with high-level mupirocin resistance (HLMR) and mupA gene was detected in five of these isolates. This prevalence rate is double the 11% reported in Iran, which also showed that previous exposure to mupirocin can be related to the HLMR in MRSA [35]. Our finding is higher than that reported in GermAny which recorded mupirocin-resistant MRSA with mupA gene prevalence of 7.3% [36]. An association between HLMR and MDR MRSA has been demonstrated and the emergence of HLMR in isolates indicates an expanding reservoir of plasmids encoding mupirocin resistance, which can be transferred to other strains [37]. Low-level mupirocin resistance (LLMR) was shown in 44% of the isolates in this study. The increasing prevalence of reduced susceptibility to mupirocin might have major implications for Infection Prevention Control (IPC) guidelines in hospitals [37].

The staphylococcal cassette chromosome mec (SCCmec) is a large movable staphylococcal chromosomal element that contains mecA and ccr genes [6]. These have been used to characterise MRSA into several types and subtypes with different characteristics [6]. This study showed a predominance of SCCmec type III (39%), which is known to be associated with HA-MRSA, followed by SCCmec type V (25%) and SCCmec type II (9.5%). The rate of SCCmec type III found in this study is similar to those reported in two other South African studies [17,38] and in a Saudi Arabian study [9]. SCCmec V, which is traditionally linked to CA-MRSA, was the second most common type. This finding may indicate that CA-MRSA strains are circulating in clinical settings. A similar situation has previously been reported in Detroit, USA [39]. In this study, 9.5% of MRSA isolates were found to carry SCCmec type II. This SCCmec type has been reported to occur mostly in patients with severe conditions and lengthy hospital stays [40]. The majority, 11 of the 20 SCCmec type II isolates were from blood cultures, suggesting that the patients could have been more sick. Other types found in this present study were subtypes of SCCmec IV which were types IVa (5%), IVb (7%), IVc (4%), and IVd (2.5%). This again overlaps with CA-MRSA. This finding of CA-MRSA SCCmec types from hospital patients could probably be because of samples taken from patients at the time of their admission, implying that they had community-acquired infections. A similar situation has been reported in India [41]. Three isolates had two SCCmec types each and they are subject to further investigation.

The ccr gene is one of the fundamental components of SCCmec that encode DNA recombinase enzymes that catalyse the mobility of the SCCmec cassette [42]. In this study, 55% and 26% of MRSA isolates possessed ccrA and ccrB genes respectively. These genes play an important role in the excision and insertion into several integration sites and possibly facilitate the spread of resistance genes to susceptible strains [42]. Our results showed that ccrA and ccrB genes were also carried in isolates of SCCmec types II, III, and V. These findings agree with the phylogenetic relationship of ccr genes and SCCmec elements previously reported in Japan [43].

In this study, all the six virulence genes screened for, were detected in the isolates. Overall, the sea was the most prevalent virulence gene detected as a single gene in 23.5% of isolates and in a total of 116 (58%) isolates, followed by psm-mec and luks-pvl. The sea gene is known to cause food poisoning and can also lead to toxic shock syndrome [44]. It was found to be significantly associated with SCCmec III (p = 0.003). The psm-mec gene was the second most detected single gene (19.5%), overall in 67.5% of the isolates and was mostly associated with SCCmec III (p ˂ 0.0001). This gene is known to influence cytolytic capacity, stimulate inflammatory responses and contribute to biofilm development [45]. The lukS/F-PV was the third most detected as a single gene at 15%; overall, in 28% of isolates, and was mostly found in SCCmec V (p ˂ 0.0001). A study in Lyon (France) found lukS/F-PV genes in 93% of S. aureus strains recovered from furunculosis [46]. This gene known to be responsible for skin and soft tissue infections by killing white blood cells, interfere with phagocytosis, and is found mostly in CA-MRSA strains [46]. This study detected the exfoliative toxins eta and etb genes at the rates of 3% and 1% isolates respectively. Overall in combinations, eta was found in 20.5% of the isolates and mostly in SCCmec III (p = 0.2). Exfoliative toxins cause the breakdown of cohesiveness between neighbouring keratinocytes in the superficial epidermis in scalded skin syndrome. A study done in Durban, South Africa, didn’t detect any of these genes [47]. In this study, the tsst-1 gene was detected in 3% of the isolates as a single gene and overall in 10%. Fourteen of 20 (10%) of isolates with tsst-1 gene were SCCmec type II. The toxic shock syndrome was originally diagnosed in women and was initially associated with an unidentified factor, correlated with tampon use [48].

Of concern, several virulence gene combinations were detected among the MRSA isolates as shown in Table 5. Overall, the combination of two, three and four virulence genes were simultaneous detected in 31 (15.5%), 29 (14.5%) and 1 (0.5%) isolates respectively. These results may suggest that hyper-virulent MRSA strains are circulating in our area. Furthermore, this study reported an association of virulence genes with SCCmec types as previously reported [45]. In Iran, the association of psm-mec with SCCmec type III was found in 95.4% of the isolates [45]. In Switzerland, lukS/F-PV was associated with SCCmec type V (83%) [49]; while in Korea, 62.8% (86/137) isolates harbouring the tsst-1 gene were found associated with SCCmec type II [50]. This supports previous reports showing that different SCCmec types are associated with certain virulence genes and diseases [45,49,50].

Conclusion

This study reported MRSA prevalence of 27% and the predominating SCCmec type was III (40%) followed by V (25%). Resistance to erythromycin and clindamycin was more than 50%. There was a noticeable increase in vancomycin MICs which may suggest the need for combination therapy or adoption of an alternative agent like linezolid for the treatment of invasive MRSA infections. There was 22% high-level resistance to mupirocin which has implication for infection, prevention and control (IPC) guidelines. This study reported diverse virulence determinants, 31% of isolates having combinations of more than one gene with the predominance of sea followed by psm-mec and lukS/F-PV genes across the SCCmec types. There is a need for reinforcement of IPC strategies to mitigate MRSA spread. Further testing will also confirm the presence of known hypervirulent strains.

Competing interests

The authors declare that they have no conflicts or competing interests.

Funding sources

None declared.

Acknowledgements

The authors thank all the staff of the Department of Microbiological Pathology, School of Medicine, Sefako Makgatho Health Sciences University, as well as the National Health Laboratory Services Microbiology, Dr George Mukhari Tertiary Laboratory, South Africa for the technical support.

Author contributions

All authors provided critical input and contributed to the manuscript writing and approved its final version. MN and MLR conceived and designed the study. GBS and CCN collected samples and performed laboratory experiments. OK, MLR and MN supervised and analysed the data. JYB and drafted the original manuscript and MH finalised. All authors approved the final version to be published.

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