A Review of Prevalence, Antimicrobial Susceptibility Patterns and Molecular Characteristics of Methicillin-Resistant Staphylococcus aureus (MRSA) in the Caribbean ()
1. Introduction
Antimicrobial Resistance (AMR) which occurs when microorganisms (bacteria, viruses, fungi, and parasites) become able to adapt and grow in the presence of antimicrobial agents that once impacted them is a significant threat to national, regional, and global public health systems [1] [2]. An infection with AMR leads to serious illnesses and prolonged hospital admissions, increases in healthcare costs, higher costs in second-line drugs, and treatment failures [1] [3] [4]. According to the US Centers for Disease Control and Prevention (CDC), antimicrobial resistance adds 20 billion dollars in direct healthcare costs in the United States, exclusive of the 35 billion dollars in loss of productivity annually [5]. Though there were uncertainties behind the estimates, a review projected that AMR could cause 10 million deaths a year by 2050 on a global scale [6].
One of the most well-known cases of AMR, Methicillin-resistant Staphylococcus aureus (MRSA), is a major nosocomial pathogen and a cause of community-acquired infections resulting in severe morbidity and mortality worldwide [7]. Methicillin resistance is mediated by PBP-2a, a penicillin-binding protein encoded by the mecA gene that permits the organism to grow and divide in the presence of methicillin and other beta-lactam antibiotics [8] [9]. The mecA gene is located on a mobile genetic element called staphylococcal chromosome cassette (SCCmec). To date, fourteen SCCmec types have emerged world-wide; SCCmec type I (1B), type II (2A), type III (3A), type IV (2B), type V (5C2), type VI (4B), type VII (5C1), type VIII (4A), type IX (1C2), type X (7C1), type XI (8E), type XII (9C2), type XIII (9A) and type XIV (5A) [10]. The increasingly prevalent community-associated MRSA (CA-MRSA) is genetically distinct from hospital-associated MRSA (HA-MRSA), by being resistant to fewer non-β-lactam antibiotics, carrying SCCmec types IV and V, and often Panton-Valentine leukocidin (PVL) genes that encode a S. aureus exotoxin that induces lysis of monocytes and neutrophil granulocytes [11].
The epidemiology of MRSA, both circulating clones and their antibiotic resistance profiles vary throughout regions and countries [12] [13]. The Caribbean region, composed of 13 independent countries and 15 dependencies (Figure 1), is a popular international tourist destination, especially, for Americans and Europeans [14] and this would have implications for the types of multiple drug resistant organisms. Increasingly, there are reports that returning international
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Figure 1. The Caribbean map. (Source: https://www.freeworldmaps.net/caribbean/caribbean-map.jpg).
travelers with MRSA infections contracted strains specific to their country of vacation [15]. Similarly, frequent travel between Europe, Africa or North America to the Caribbean region appears to influence the local epidemiology of S. aureus infections [12]. The diversity in the socioeconomic conditions between individual countries in the Caribbean may lead us to assume that the epidemiology of MRSA might also differ between the countries. However, there was a need for a comprehensive assessment of the disparate data on the prevalence, antimicrobial susceptibility patterns and genotypes of MRSA in the Caribbean to help fill the global map of antimicrobial resistance. The present scholarly work sought to contribute to a review of the studies conducted in some English-speaking countries including Jamaica, Trinidad and Tobago, Barbados, St Kitts and Nevis, and the Dominican Republic, and a few French territories including Guadeloupe and Martinique, describing the prevalence, epidemiology, antimicrobial susceptibility patterns and molecular characteristics of MRSA in hospitalized and non-hospitalized patients.
2. Methodology
According to the framework previously described [16] [17], the methods employed in this review corresponded with the Joanna Briggs Institute Reviewer’s Manual guidelines [18]. We identified the research question, followed by relevant studies and consequently selecting them for data presentation. The search for peer-reviewed published articles conducted in PubMed and Mendeley were limited to articles in English. An exploratory search of the literature was used to develop inclusion and exclusion criteria. The strategy used in searching the keywords combined “MRSA” OR “Methicillin-resistant Staphylococcus aureus" AND “Caribbean” with some other related terms such as “Wound infection” OR “SSTI” OR “staphylococcal skin and soft tissue infections” OR “Patients” OR “Surveillance” OR “Infection control” OR “Prevalence” AND “healthcare.” Further articles were obtained using reference lists from several articles and manual searching.
This study included all types of observational studies. The relevant titles and abstracts were screened, and their full-text articles were included according to the eligibility criteria developed based on 1) region/country, 2) MRSA definitions (molecular or epidemiological), 3) study design, 4) study period and 5) settings. Articles that reported non-human isolates or did not provide a clear definition of clinical setting were excluded. Additional data extracted from each of the included studies consisted of the author, year of publication, number of patients and/or isolates of S. aureus, the type of the culture specimen and of staphylococcal infection, the percentage of MRSA to the total S. aureus isolates, molecular typing methods, the percentage of the MRSA SCCmec genotypes, the percentage of isolates positive for the Panton Valentine Leukocidin (PVL) toxin and antimicrobial resistant genes, the susceptibility of MRSA to the antibiotics tested in each study, and the status of infection control practices. The focus of this narrative review was to describe data on the percentage of MRSA to the total S. aureus isolates, assess their susceptibility to different antibiotics and document their genotypes.
3. Results
3.1. Synopsis of Staphylococcus aureus and MRSA Research Information from the Caribbean
The goal of surveillance in public health, to provide information to decrease morbidity and mortality, and to improve health, could be achieved through ongoing systematic collection, analysis, interpretation and dissemination of data regarding public health-related events. The surveillance system for MRSA in the Caribbean appears simple, most data are collected from a single or multiple, regional hospitals, primary health centers in the rural or urban communities with limited complex electronic system that receives and integrates data from the multiple sources. Out of 47 records identified during the literature screening process, an aggregate of 24 peer-reviewed publications met the search criteria, and were included in this review (Table 1), [11] [12] [19] - [38]. The publications, contributed by investigators from 10 countries (37%) of the 27 screened, ranged in dates from 1999 to 2020. The included studies were conducted in Trinidad and Tobago (n = 7), Jamaica (n = 5), Barbados (n = 2), Dominican Republic (n = 2), Martinique (n = 2), Haiti (n = 2), Cuba (n = 2), St. Kits & Nevis (n = 1), Guadeloupe (n = 1) and Guyana (n = 1).
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Table 1. Summary of included studies.
The Caribbean researchers used cohort studies, choosing equally between prospective and retrospective study designs [39] as dictated by their budgets, availability of resources and relative access to patients’ samples. For the prospective study designs, hospital and/or community clinical specimens included high vaginal swabs, urine, skin and soft tissue swabs, surgical and burn wounds, pus/abscess, respiratory tract, blood, bone, nasal cavity swabs and catheters submitted by patients or subjects being investigated for staphylococcal colonization or infections [11] [20] [29] [32] [33] [34]. For the retrospective study designs, investigators conducted cohort analysis of patients admitted to the major hospitals over a given period (years) as part of surveillance programs established to screen surgical and burn wounds, nasal, groin, and axilla for colonization with Staphylococcus aureus and prevalence of MRSA [21] [26] [37]. The main outcomes of interest in the studies were the rate of MRSA in S. aureus in hospital and/or community settings, country or regional capabilities including phenotypic characterization through antimicrobial susceptibility testing, distribution of major MRSA genotypes through various molecular genotyping methods, detection of toxin and antibiotic resistance genes, and infection control practices.
3.2. The Prevalence of MRSA in the Caribbean
An overview of the peer-reviewed articles that reported on the prevalence of MRSA in the Caribbean is shown in Table 2. The number of S. aureus or MRSA isolated from clinical samples and characterized in the included studies ranged from 16 to 1997. The results show that majority (75%) of the investigations were conducted on cultures of hospitalized patients’ samples [12] [16] [21] [23] [26] [28] [31] [32] [33] [34] [35] [37]. A few studies investigated only cultures obtained from clinical samples obtained from outpatients [24] [29], or from cultures of samples obtained from hospitalized patients and outpatients [11] [21] [27].
The results show that between 12.8% and 60% of Caribbean S. aureus isolates from samples collected from infected, hospitalized patients are MRSA [12] [16] [21] [23] [26] [28] [31] [32] [33] [34] [35] [37]. Interestingly. the prevalence of MRSA differed across the Caribbean countries and territories (Table 2). Even though the mean MRSA prevalence reported in hospitalized patients was characteristically < 21% in Barbados [11], Dominican Republic [25] and Trinidad and Tobago [27], the percentage of MRSA isolates ranged from 39% in Martinique [25], 45% in Jamaica [21] and St Kitts and Nevis [33], to 51% in Guyana [39], and 59% in Cuba [16]. Similarly, while the MRSA prevalence in the samples cultured from outpatients was 20% in the Dominican Republic [25], percentage of MRSA isolates in this patient group were, 39% and 45%, respectively, in Martinique [25], and Trinidad & Tobago [28].
Most of the MRSA isolates from hospitalized patients were associated with surgical wounds, and infections of skin and soft tissue, respiratory tract and urinary tract, age (peak range of 60 - 69 years), gender, ethnicity, duration of hospital stay, co-morbidities such as diabetes mellitus and hypertension, previous penicillin use or previous surgery [11] [12] [16] [21] [22] [25] [27] [31] [34] [35] [39]. However, prevalence of MRSA isolates in clinical samples collected from outpatients, though, associated with gender, diabetes, hypertension or asthma, some considerable proportion of the subjects tended to be healthy, students or those who participated in physical contact sports [11] [30] [33].
3.3. Antimicrobial Susceptibility Patterns of Clinical MRSA Isolates
Treatment of MRSA infections has remained problematic in the Caribbean region because of the organism’s resistance to many antimicrobial agents. Routine characterization of the clinical MRSA isolates through antimicrobial susceptibility testing and analyses, in the most instances, using the Kirby-Bauer disc diffusion method on Müller-Hinton agar [40] has been reported in approximately 50% of the studies to guide empirical treatment of mild or moderate infections [12] [21] [25] [27] [28] [30] [31] [32] [33] [35] [36]. In a study reported from Trinidad [27], involving MRSA isolates (n = 451) from clinical samples collected from hospitalized patients between 1999 and 2004, all the organisms were fully sensitive to vancomycin, while the greatest resistance was against erythromycin (86.7%) clindamycin (75.3%), tetracycline (78.7%) and ciprofloxacin (59.1%). However, the MRSA strains were less resistant to gentamicin (44.7%), chloramphenicol (17.3%) and trimethoprim-sulfamethoxazole (13%) [27].
In a study reported from Jamaica [21], all MRSA isolates (n = 80) collected from samples of hospitalized and community patients in 2002 were susceptible to vancomycin. Overall, 77.5% of the isolates were resistant to at least one antibiotic, and 10% of isolates were resistant to gentamicin, ciprofloxacin, tetracycline, chloramphenicol, and erythromycin. Sixty percent of the isolates were resistant to penicillin G, 22.5% each to trimethoprim-sulfamethoxazole and oxacillin, and 13.8% to tetracycline. More isolates from hospital sources were resistant to the antimicrobials evaluated (except for gentamicin). Notably, 82% of hospital isolates were resistant to penicillin, compared to 39% of community isolates. Further, all isolates resistant to oxacillin were from hospital sources [21]. In another study of hospitalized patients reported from Jamaica in 2010 [34], MRSA isolates (n = 33), again, showed sensitivity to vancomycin, but variable resistance to erythromycin (94%), clindamycin (52%), gentamicin (33%) and tetracycline (27%). However, resistance to trimethoprim-sulfamethoxazole and minocycline was 12% and 6%, respectively [34].
In a study reported from Barbados [11] antimicrobial susceptibility testing revealed that all hospital-associated MRSA isolates (n = 100) were resistant to ceftriaxone and ciprofloxacin, and 90% of isolates were resistant to erythromycin. All isolates were sensitive to vancomycin, rifampin, gentamicin, linezolid and trimethoprim-sulfamethoxazole; 82% were sensitive to clindamycin, with 2% inducible clindamycin resistance [11]. In the same study from Barbados, of the community-associated MRSA isolates (n = 193) evaluated, nine, or 4.7%, gave D-zones for clindamycin induction. A total of 94.3% susceptibility was recorded to trimethoprim-sulfamethoxazole. A susceptibility to vancomycin of 97.4% was observed; clindamycin susceptibility averaged 89.6%. All isolates were resistant to the β-lactam antibiotics and macrolides. However, for 4.2% of 193 MRSA isolates, four were resistant to vancomycin, whilst one isolate was resistant to cotrimoxazole, ciprofloxacin and vancomycin, and six isolates were resistant to clindamycin [11].
In a study conducted on hospitalized patients and community subjects from St Kitts & Nevis in 2019 [32], the prevalence of MRSA accounted for 46% (70/152) of the isolates. The highest rates of resistance to non-β-lactam agents were observed for daptomycin (97.1%), erythromycin (91.3%), levofloxacin (75.4%), moxifloxacin (73.9%), whereas lower proportions of resistant isolates were seen for tetracycline (10.1%), tobramycin (10.1%), gentamicin (4.3%), fusidic acid (4.3%), clindamycin (2.9), mupirocin (2.9%) and rifampicin (1.4%). All the MRSA isolates were susceptible to ceftaroline, linezolid, teicoplanin, telavancin, trimethoprim/sulfamethoxazole and vancomycin [32].
3.4. Molecular Typing of Clinical MRSA Isolates
In the last decade, six molecular typing methods have been utilized in the molecular characterization of MRSA to monitor geographic spread of one or several clones among countries in the Caribbean region [11] [12] [19] [24] [27] - [32]. These molecular techniques included pulsed field gel electrophoresis (PFGE) after SmaI digestion [37], multi-locus sequence typing (MLST) [19] [25] [28], whole genome sequencing-MLST [27], multiplex polymerase chain reaction (PCR) to detect 16SrRNA, mecA, the staphylococcal chromosomal cassette (SCC) mec types, spa types, presence of exotoxins, Panton-Valentine Leukocidin (PVL) and LukAB, and the arginine catabolic mobile element (ACME) [11] [24] [27] [29] [30] [38], microarray hybridization [12] [28], and Multiple Locus Variable-number Tandem Repeat Analysis (MLVA) [27]. Each of these genotyping methods varies regarding the equipment, cost, and expertise required, and their ability to discriminate among related isolates is not the same [10] [41]. Notwithstanding, the sequence-based techniques are specific and sensitive enough to distinguish MRSA strains based on the genes encoding the staphylococcus protein A, the SCCmec types, the PVL, and ACME [41].
Molecular typing of clinical MRSA isolates was established in approximately 60% of the studies reviewed [11] [12] [19] [24] [27] - [32]. Only 15% of the studies reported the genotypes of Methicillin sensitive S. aureus (MSSA) isolates from either hospitalized or community patients [24] [28]. More than a third of the studies did not report on the MRSA genotypes [20] [22] [25] [26] [33] [34] [36]. The clonal results of the MRSA isolates from clinical samples collected from patients in hospital and community settings in the Caribbean region (Table 2), [11] [12] [19] [24] [27] - [32] are described below.
CA-MRSA clones
There was a wide-spread occurrence of the North American epidemic or endemic ST8 MRSA SCCmec IV, PVL positive, (CA-MRSA, USA300) clone in the clinical samples of hospitalized patients studied in several countries including Barbados [11], St Kitts & Nevis [32], Trinidad & Tobago [28] [29], Jamaica [27], Cuba [30], Dominican Republic and Martinique [24]. A similar ST8 MRSA SCCmec IV, PVL positive, prevalence frequency was shown in the clinical samples of outpatients studied in Barbados [11], Trinidad & Tobago [29], Dominican Republic and Martinique [24]. However, there was occurrence of geographical differences in the prevalence of most other MRSA clones in the region. Of particular interest, was the prevalence of CC8-MRSA-IV, “Lyone” clone, CC8-MRSA-IV “UK-EMRSA” clone, and European-CA-MRSA clone in a study of clinical samples of hospitalized patients from Martinique [12]. Another CA-MRSA clone, ST72 SCCmec V was moderately prevalent [25%] in the clinical samples of outpatients reported from Dominican Republic [24], Trinidad & Tobago [29], but rarely observed in outpatients from Barbados [11] and Martinique [24]. ST72 SCCmec V was moderately prevalent [14%] in hospitalized patients studied in Cuba [30] and Haiti [31], of extremely low frequency (1.5% to 2.22%) in Trinidad & Tobago [28], and St Kitts & Nevis [32], but rare in Jamaica [27]. ST30 MRSA SCCmec IV was moderately prevalent (27%) in the samples of outpatients studied in Dominican Republic [24)] but not reported in community patients studied in Martinique [24], Trinidad & Tobago [29], and Barbados [11]. ST30 MRSA SCCmec IV was rare (1.5%) in hospitalized patients reported from St Kitts & Nevis but it was not observed in hospitalized patients’ studies from Jamaica [27], Cuba [30], Haiti [31], and Barbados [11]. Similarly, spa-CC0044-ST80 SCCmec IV was moderately prevalent (13%) in the clinical samples of outpatients studied from Martinique [24] but rare in both hospital and community settings in the other Caribbean countries with published surveillance data (Table 2).
HA-MRSA clones
According to the results shown in Table 2, ST239-MRSA-III, a common cause of hospital-acquired MRSA, was highly prevalent (60%) in the clinical samples of hospitalized patients studied in Trinidad & Tobago [28], but was of considerably low occurrence (1.45% - 3%) in the clinical samples of hospitalized patients reported from Jamaica [27] and Martinique [12]. ST5 MRSA SCCmec II (New York-Japan) clone had low prevalence (3% - 12.5%) in the clinical samples of hospitalized patients in the reports from St Kitts & Nevis [32] and Jamaica [27], and moderately prevalent (18%) in the samples of outpatients from Martinique and Dominican Republic [24]. CC5-ST5-MRSA-SCCmec 1 “Geraldine” clone was of low prevalence (3% - 13%) in the samples of hospitalized patients studied in Jamaica [27], Guadeloupe and Martinique [12].
3.5. Detection of Toxin and Antimicrobial Resistant Genes
In a population structure study on several MRSA clones (n = 45) from Trinidad and Tobago in 2014 [28], the common antimicrobial resistance markers reported were the beta-lactamase operon (blaZ/I/R; in 86.39% of isolates), erm (A) (in 9.86%, mostly ST239-MRSA-III), msr (A)/mph (C) (in 8.16% and 7.14%, respectively; mostly associated with “USA300”) and aphA3/sat (in 15.31%, largely associated with ST239-MRSA-III and “USA300”). The gentamicin/tobramycin resistance gene aacA-aphD occurred in 9.52% of isolates that all belonged to ST239-MRSA-III or “USA300”. A gene associated with mupirocin resistance, mupA, was detected in 17.78% of MRSA isolates. Other resistance markers; vanA (vancomycin resistance) and cfr (linezolid resistance) were not found [28].
Similarly, a separate study conducted on outpatients in the rural communities from the same country (Trinidad & Tobago) in 2018 showed the presence of the ermA gene in 31% (5/16) MRSA isolates tested, but none of them tested positive for the ermC and vanA genes, respectively [29]. Majority (62.5%, 10/16) of the MRSA isolates from the outpatients possessed the pvl gene, whereas 25% (4/16) possessed the alpha hemolysin (hla) gene. None of the MRSA isolates possessed the tst1 gene, 18.8% (3/16) possessed both virulence genes, pvl and hla [29]. Nearly all the MRSA (ST8, 88%) isolates from hospitalized patients and community subjects from a study reported in 2019 from St Kitts & Nevis [32] carried genes encoding resistance to streptomycin [ant (6)-Ia], amikacin and other aminoglycosides [aph (3’)-III], fosfomycin (fosD), macrolides, lincosamides and streptogramins [mph (C) and mrs (A)], and penicillin (blaZ). Additionally, genes encoding resistance to trimethoprim (dfrG) and phenicols (cat) were found in four and one isolate, respectively [32].
3.6. MRSA Infection Control Practices
MRSA infection prevention and control practices are well known, and they include effective personal hygiene, proper wound care, optimum laundry and cleaning or disinfection of high-touch or soiled surfaces [26]. However, the successful application of these practices is dependent on the knowledge, attitudes and practices of health care workers in the local or regional, major hospitals in the Caribbean. In Trinidad and Tobago, lack of effective infection control programs has been associated with poor level of knowledge, attitudes and practices among healthcare workers [42], limited resources, competing priorities, and other barriers [33]. Stringent MRSA infection control measures, on the other hand, appeared to have been set up in Barbados, which accounted for the rare prevalence of HA-associated MRSA infections in the community [11].
4. Discussion
Peer-reviewed published studies on the epidemiology of MRSA in the Caribbean remain scanty, and the true nature and extent of MRSA infections in the region are not well characterized. To our knowledge, this is the first extensive review of available peer-reviewed articles on MRSA prevalence, characteristics and clonal distributions in the Caribbean. Twenty-four studies on MRSA prevalence in different hospital and outpatient settings in 10 different Caribbean countries were analyzed. The majority (75%) of the investigations were conducted on cultures of hospitalized patients’ samples while a few studies investigated only cultures obtained from clinical samples obtained from outpatients or from cultures of samples obtained from hospitalized patients and outpatients. The MRSA isolates from hospitalized patients, clinical samples collected from outpatients, subjects who tended to be healthy, students or those who participate in physical contact sports were from major sites of MRSA colonization and infections consistent with previous reports in humans [43] [44] [45] [46].
The mean MRSA prevalence reported in hospitals and outpatients was characteristically < 21% in Barbados, Dominican Republic, Trinidad and Tobago, however, the percentage of MRSA isolates ranged from 39% in Martinique, 45% in Jamaica, St Kitts and Nevis, to 51% in Guyana, and 59% in Cuba. The heterogeneity in MRSA prevalence across the Caribbean is similar to previous reports of MRSA in Latin America which ranged from 6% in Central America to 80% in some South American countries [47], between 25% and 50% in most parts of Africa [48], or 25% - 60% in the Mediterranean European countries [49]. These different MRSA prevalence rates among different countries may be attributed to disparities in patient populations, the biological characteristics of the S. aureus strains, widespread antimicrobial use, differences in infection control practices and/or impact of regional or intercontinental travel of healthcare personnel and tourists [12] [15] [33] [50]. In a specific investigation, comparing the characteristics of MRSA clones in the French (Guadeloupe and Martinique) and non-French territories (Jamaica and Trinidad and Tobago), it has been shown that the differences in the major clones in each country most closely reflected those found in the home countries of tourists or healthcare workers and the frequency of visits to the islands [12].
This review study revealed changes in the molecular epidemiologic profile of MRSA clone in both hospital and community settings in the Caribbean. The prevalence of CA-MRSA ST8 SCC mec V, PVL+ among hospitalized patients ranged between 20% and 100% in Trinidad & Tobago, Dominican Republic, Martinique, Jamaica, St Kitts & Nevis, Barbados, and Cuba. This result is consistent with reports of continued expansion of CA-MRSA among hospitalized patients in the United States [51], Europe [52], Asia [53] [54], Africa [48] and Latin America [55], indicating the invasion of these strains into hospitals and they may replace the classical HA-MRSA strains due to their unique characteristics and faster growth patterns [11].
This study also showed that the prevalence of HA-MRSA (SCCmec type I and/or SCCmec type II) in hospitalized patients ranged between 3% to 10% in several of the Caribbean countries with the exceptions of Cuba, Trinidad & Tobago that registered HA-MRSA (ST239 SCCmec III) prevalence of 60%. The high prevalence of SCCmec type III among hospitalized patients has implications in terms of use of alternative antimicrobial treatments in the face of significant resistance to most old beta-lactam and non-beta lactam antibiotics, and the serious requirement for effective infection control to prevent spread between hospitalized patients or spread of the HA-MRSA clone to the community [56]. However, notably, there were no reports of HA-MRSA isolates in samples of outpatients from Barbados, Trinidad & Tobago and Cuba, though, reports of moderate HA-MRSA (ST5 SCCmec II) (18%) prevalence rate in the clinical samples of outpatients in the Dominican Republic and Martinique suggest that this MRSA hospital strain has spread to the community, in the two countries. The spread of HA-MRSA isolates to the community, has been demonstrated previously through the presence of SCCmec types I, II and III in CA-MRSA isolates from Taiwan (China), Korea, Hong Kong (China), Philippines, Thailand and Vietnam [56].
In addition to most β-lactams, MRSA strains are variably resistant to several antimicrobial agents, including fluoroquinolones, macrolides, lincosamides, rifampin and tetracyclines [8] [57] [58]. Resistance to trimethoprim-sulphamethoxazole, glycopeptides (vancomycin, teicoplanin), oxazolidinones (linezolid, tedizolid), daptomycin, tigecycline and the new cephalosporin, ceftaroline remains uncommon [57]. Consistent with the clonal results of the MRSA isolates from clinical samples from patients in hospital and community settings analyzed in this review study, the antimicrobial susceptibility patterns indicate wide-spread occurrence of CA-MRSA with demonstrated high resistance to β-lactam agents, macrolides and fluoroquinolones, however, with significant susceptibility to vancomycin, trimethoprim-sulphamethoxazole, clindamycin, gentamicin, rifampin and tetracycline. Similarly, the prevalence of HA-MRSA in hospitalized patients in several of the Caribbean countries with surveillance data is reflected by the antibiograms of such clones that were mostly resistant to all β-lactam antibiotics and non-β-lactam antibiotics evaluated except vancomycin and trimethoprim-sulphamethoxazole.
The major limitation of this work is that it is based on passive surveillance in the Caribbean countries that presented their findings through peer-reviewed publications. There may be additional data in grey literature or government databases from the same or other countries and territories in the region that are excluded from unfettered access and robust assessment. Second, since most of the clinical samples processed for MRSA were from hospitalized patients in the countries reporting these studies, there may have been an underestimation of the actual community prevalence of MRSA in the review study populations since there were no reports of routine sampling of patients for microbiological analyses.
5. Conclusion
In conclusion, the data from peer-reviewed articles evaluated for this report indicate the occurrence of geographical differences in the prevalence of MRSA clones within the Caribbean region. The review ascertained that a high proportion of clinical isolates from patients in the hospital and community settings of the reporting Caribbean countries were resistant to methicillin, macrolides, and fluoroquinolones, but susceptible to tetracyclines, gentamicin, clindamycin, and trimethoprim-sulphamethoxazole, due to the widespread occurrence of epidemic/endemic CA-MRSA clone ST8 SCCmec IV, PVL positive, USA300. Also, there was moderate prevalence of ST72 SCCmec V clones in both hospital and community settings in a few of the countries while ST30 SCCmec IV, PVL positive, was moderately prevalent in only one country with published research article. The moderate prevalence of HA-MRSA ST5 SCCmec II in community settings, and the high prevalence of HA-MRSA ST239 SCCmec III circulating in hospitalized patients in two countries are concerning. Future epidemiological studies which also focus on the populations outside of healthcare facilities in various countries could assist in the assessment of the burden of infections with MRSA in community settings. The implementation of stringent hospital infection control measures could substantially reduce the burden of MRSA on the healthcare systems in the Caribbean.
Acknowledgements
Access to curated literature from MEDLINE (Pubmed.gov) and 2021 Mendeley (Mendeley.com) database was appreciated. The All Saints University School of Medicine postgraduate scholarship award supported SKO to conduct this research.