This study was conducted to determine the prevalence of MRSA among school children and to detect the mecA gene. In this study, 44.7% (n = 85) of healthy children attending school were the nasal carrier of S. aureus. This finding is higher than that reported by Adhikari et al. [16] and Rijal et al. [17] in school children. Hence, regular surveillance of MRSA carriers among the school children seems to be required to identify, treat, and prevent a possible spread of such isolates among other school children and the community. The high isolation of S. aureus in this study might be because this study was conducted in Kathmandu valley, which is highly crowded and polluted. Furthermore, school itself is a crowded place and crowded place often leads to spread of disease in local population [26]. Similarly, pollution can lead to increased adhesion, colonization and invasion of S, aureus [27]. Other studies have reported 5.10% [2], 52.5% [28], 18.35% [29], and 47.3% [30] S. aureus colonization from Tibet, India, Ethiopia, and China respectively. The variations in prevalence rate may be due to characteristics of the study population, sampling, or culture techniques. A high isolation rate of S. aureus and MRSA was observed in children attending private school, which might reflect the family's socioeconomic status, the easy approach of the children to the hospital, and the risk factor associated with colonization.
In this study, the prevalence of MRSA was found to be 53% (n = 45), which is similar to the prevalence rate reported in previous studies [17, 31]. A lower prevalence of MRSA in school children was reported in India (15.4%) by Vinodhkumaradithyaa et al. [32] and in Nepal (17.1%) by Adhikari et al. [16]. Studies carried out in hospital settings in different parts of Nepal from 2004 to 2019 report MRSA prevalence ranging from 14.6–72.4% [13]. Among them, Jaiswal et al. [33] and Sapkota et al. [34] reported a much higher prevalence of MRSA than ours i.e 70.6% and 72.4% respectively. On the other hand, Bhatt et al. [35] and Rai et al. [36], 19.0% each, Khanal et al. [37] (2.1%) and Shrestha et al. [38] (16.7%) reported a much lower prevalence than ours. The difference in the isolation rate of MRSA could be due to differences in isolation techniques such as the use of oxacillin disk only, the test conditions, study population, sample type, study site, or the variations in the specific risk factors.
To better control the spread of MRSA colonization in the community, it is essential to know about risk factors for colonization. We found that the odds of MRSA coloinzation decreases as the age of the children increases. This is evident as the older aged children are more aware about the hygiene practices. Although, the crude OR showed higher nearly 2.4 times higher odds of MRSA colonization in students having frequent handshaking practices than in the ones not having the practice, upod adjustedm the associateion seemed insignificant. Hands remain ones of the major causes of infection in children and handshaking often leads to bacterial transmission between individuals [39, 40]. Furthermore, if there is frequent contact with the nose without washing hands after shaking hands with others, MRSA can easily enter the nose and be colonized, leading to outbreaks [41, 42]. However, other risk factors such as sex, family history of diabetes, frequent wound infection, regular hospital visits, socialization, frequent nose touching practices, and topical medication were not significantly associated with nasal MRSA colonization. In a similar study, age, sex, hygienic practices, living in urban areas, daycare attendance, and seasonality were reported as the significant risk factors [43].
The meta-analysis by Khanal et al. [13] reported penicillin as the least sensitive antibiotic (pooled susceptibility 0%), followed by ampicillin. Reduced susceptibility in most of the studies was reported for erythromycin and gentamycin. Similar susceptibility for penicillin was obtained in our study as all the MRSA isolates and 97.55% of the MSSA isolates showed resistance to penicillin. This finding is consistent with a study conducted in Jimma [30], Ethiopia [44], and Nigeria [45] where the resistance was 100% towards penicillin. Unlike other studies mentioned in the meta-analysis, where vancomycin followed by chloramphenicol (pooled susceptibility 98.0% and 91.0% resp) was found to be the most sensitive drug against MRSA, gentamycin was found to be the most sensitive drug in our study (91.9%) followed by linezolid (84.4%) and vancomycin (75.5%). High sensitivity towards vancomycin in other studies and ours might be because it is not a commonly prescribed drug owing to its higher price and unavailability in many parts of the country. Mishra et al. [46] and Raut et al. [47] also reported high sensitivity (100%) of linezolid. Around half of our isolates were resistant to erythromycin, compared to previous studies in Nepal reporting resistance rates of 63.6% [46], 7.1% [48], 11.0% [49], and 32.7% [50]. We observed 24.4% resistance to cotrimoxazole in MRSA isolates. Other studies report variable resistance rates for cotrimoxazole; 72.7% [46], 64.0% [49], 81.7% [50], 42.96% [51], and 12.5% [52] in Nepal. Except for penicillin, all other tested antibiotics showed less than 40% resistance against all MSSA strains in our study. Differences in susceptibility patterns may be due to the geographical differentiation, the time when the MRSA isolates first occurred in the area, and the selectivity of antibiotics.
The presence of the mecA gene is the most crucial evidence for the detection of MRSA isolates [53–55]. In this research, among 45 MRSA isolates mecA gene was present in 41 (91.1%) isolates in this study. A slightly lower prevalence of the mecA gene in MRSA isolates has been reported by Kandel et al. [15] (72.2%) and Adhikari et al. [16] (82.0%). Our result is consistent with that of the study performed by Nikfar et al. [56] in Iran, where out of 11 MRSA isolates, only seven were positive for the mecA gene. The absence of the mecA gene in some phenotypic MRSA isolates might be due to the differing levels of mecA gene expression of methicillin resistance [25] or borderline resistant S. aureus; S. aureus resistant to methicillin but lacking mecA gene. The latter could be due to hyperproduction of β-lactamase, specific alternations in different amino acids present in penicillin-binding proteins cascade (PBPs 1, 2, and 3) [57], or the presence of toxin genes such as lukS and lukF that encode for PVL or femA and blaZ genes [58, 59]. Similarly, among 40 MSSA isolates, the mecA gene was present in 38 (95%) isolates. It has been found that a small percentage of highly heteroresistant isolates that are phenotypically sensitive to methicillin carry the mecA gene. It is believed that, besides the presence of the mecA gene, a reduced expression or mutations in femA and femB genes leads to the absence of phenotypic resistance in those isolates that contained the mecA gene [59]. This type of strain may lead to the failure of therapy using β-lactam antibiotics as they can become highly resistant if exposed to anti-staphylococcal penicillin [60].
The presence of the mecA gene itself is not a criterion for induced resistance [61], and questions can be raised in considering mecA as the sole genetic marker for methicillin resistance, although more research is needed [16]. Other mechanisms or genes other than the mecA gene could also be responsible for developing resistance.
Identification of the MRSA carriers and treatment is much required to prevent the spread of community-acquired MRSA. Our findings will be valuable to access the prevalence of MRSA carriers among school-going children in the Kathmandu valley. Furthermore, the AST pattern reported in our study will be beneficial in optimizing the treatment therapies for infections caused by such isolates. The findings may also open the door to search for other intrinsic factors that may produce resistance competing with the mecA gene.