MICROBIOLOGY


appearance when cultured on mannitol salt agar, characterised by round golden/ yellow pigmented colonies (Fig 1b).3 This distinctive feature differentiates S. aureus from another staphylococcal commensal, Staphylococcus epidermidis, which produces white colonies.4


exhibits rapid growth in rich medium and yields yellow colonies on the plate, attributed to the production of the carotenoid pigment staphyloxanthin.4 S. aureus is a natural constituent of the skin flora, notably inhabiting areas such as the nasal passages and perineum in humans and animals.1


Approximately


a quarter of individuals in good health carry one or more strains of S. aureus asymptomatically at any given time. Infections often arise from the patient’s own colonising strain. Owing to its niche as a commensal, S. aureus is readily exposed to all antibiotic treatments, which has led to the selection of drug- resistant strains such as methicillin- resistant S. aureus (MRSA).4 Standard treatment protocols for staphylococcal infections typically involve antibiotic therapy and surgical drainage. However, the proliferation of resistance to penicillin, methicillin and other β-lactam antibiotics has severely constrained treatment options. It is a prevalent causative agent of infections within hospital and community environments.7


S. aureus resistance mechanisms S. aureus strains can develop resistance to antibiotics either naturally or during treatment. The widespread use of penicillin in the 1940s and 1950s initially proved successful in treating S. aureus infections.8


However, over time, the


overuse of this antibiotic led to the development of resistance among various bacterial pathogens. Resistance to penicillin in S. aureus is primarily attributed to the activity of penicillinase, a type of β-lactamase encoded by the blaZ gene. This enzyme, found on a plasmid within a transposon in S. aureus, renders penicillin and ampicillin ineffective by hydrolysing the β-lactam ring.8 This phenomenon was initially observed by Spink and Ferris in 1947 when they identified penicillin-resistant S. aureus strains in hospital settings. This resistance soon transcended the confines of healthcare facilities. Particularly the virulent and transmissible phage type 80/81 strains, later identified as clonal complex 30 (CC30) through molecular typing methods, disseminated into the community, causing infections.8 The emergence of MRSA followed the development of semi-synthetic anti-staphylococcal penicillins in the


46


HEALTHCARE-ACQUIRED MRSA Typical patients


Infection site Transmission


S. aureus Clinical setting of diagnosis Medical history


Elderly, debilitated and/or critically or chronically ill. Often bacteraemia with no obvious infection focus.


Within healthcare settings; little spread among household contacts.


In an inpatient setting, but increasingly HA-MRSA infections in soft tissue and urine are occurring in primary care.


History of MRSA colonisation, infection, recent surgery; admission to a hospital or nursing home, antibiotic use; dialysis, permanent indwelling catheter.


Virulence of infecting strain Community spread is limited, PVL genes usually absent. Antibiotic susceptibility


COMMUNITY-ACQUIRED MRSA Typical patients


Infection site Transmission Often multi resistant with result that choice of agents often very limited.


Young, healthy people; students, professional athletes and military service personnel.


Predilection for skin and soft tissue, producing cellulitis and abscesses. May cause necrotising community acquired pneumonia, septic shock or bone and joint infections.


Community-acquired. It may spread in families and sports teams.


Clinical setting of diagnosis In an outpatient or community setting. Medical history


Antibiotic susceptibility No significant medical history or healthcare contact.


Virulence of infecting strain Community spread occurs easily. PVL genes often present, predisposing to necrotising soft tissue or lung infection.


Generally susceptible to more antibiotics than HA-MRSA.


Table 1. Differences between HA-MRSA and CA-MRSA. Information adapted from ‘Guidelines for UK practice for the diagnosis and management of methicillin-resistant Staphylococcus aureus (MRSA) infections presenting in the community’.15


1960s. Evidence suggests that methicillin resistance may have even preceded the clinical use of these antibiotics. Methicillin resistance is mediated by the mecA gene, acquired through horizontal transfer of the staphylococcal cassette chromosome mec (SCCmec). The mecA gene encodes penicillin-binding protein 2a (PBP2a), which exhibits low affinity for β-lactam antibiotics. This reduced affinity leads to resistance against the class of β-lactam antibiotics.9


Molecular epidemiology MRSA infections have evolved, with initial cases mainly associated with healthcare settings. However, in the 1990s a shift occurred. MRSA infections began appearing in individuals without prior hospitalisation, leading to the distinction between healthcare-associated (HA-MRSA) and community-associated (CA-MRSA) strains.10


Table 1 elaborately


illustrates the differences between HA- MRSA and CA-MRSA. CA-MRSA strains are characterised by lower clindamycin resistance rates, increased likelihood of Panton-Valentine leukocidin (PVL) expression, and predominance of SCCmec type IV or V strains, particularly in the United States.11


that produces PVL is associated with numerous outbreaks and is the primary cause of skin and soft tissue (SSTI) infections in the US.12


HA-MRSA strains typically harbour


more prominent SCCmec elements, categorised as type I, II, or III. Conversely, CA-MRSA isolates carry smaller SCCmec elements, typically type IV or V, which also contain the mecA gene. Research has suggested that these smaller elements confer resistance to select non-β-lactam antimicrobials and often harbour PVL genes.10


The clonal complexes of CA-MRSA,


prevalent in Australia, Europe and North America, are characterised by the Type IV SCCmec element and the presence of the PVL locus.13


The shorter SCCmec


elements are also believed to play a role in these strains’ survival and faster replication. The SCCmecIV USA300 clone stands out as a predominant and highly virulent strain14


in the United


States. International travel significantly influences the spread of hypervirulent strains, such as the USA300 clone. Consequently, timely diagnosis and effective antimicrobial therapy are paramount in managing CA-MRSA infections.


MRSA is primarily transmitted through The USA300 clone


direct skin-to-skin contact with individuals directly exposed to the bacteria. This exposure can occur through contact with wounds, dressings, or objects that have been in contact with MRSA-infected patients or with individuals who are colonised with the organism.


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