References

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Jevons MP. “Celbemom”–resistant staphylococci. Br Med J. 1961; 14:113-114
Lubelchek RJ, Weinstein R. Antibiotic resistance and nosocomial infections. In: Mayer KH, Pizer HF London: Academic Press; 2008
Oliveira DC, Tomasz A, de Lencastre H. Secrets of success of a human pathogen: molecular evolution of pandemic clones of meticillin-resistant Staphylococcus aureus. Lancet Infect Dis. 2:180-189
Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus: Minnesota and North Dakota, 1997–1999. MMWR Morb Mortal Wkly Rep. 1999; 48:707-710
Nathwani D, Morgan M, Masterton RG Guidelines for UK practice for the diagnosis and management of methicillin-resistant Staphylococcus aureus (MRSA) infections presenting in the community. J Antimicrob Chemother. 2008; 61:976-994
Que Y, Moreillon P. Staphylococcus aureus (including Staphylococcal toxic shock), 7th edn. In: Mandell GL, Bennett JE, Dolin R Philadelphia: Churchill Livingstone; 2010
Jackson MS, Bagg J, Gupta MN, Sturrock RD. Oral carriage of staphylococci in patients with rheumatoid arthritis. Rheumatology. 1999; 38:572-575
Dahlen G, Linde A, Moller AJR, Ohman A. A retrospective study of microbiologic samples from oral mucosal lesions. Oral Surg Oral Med Oral Pathol. 1982; 53:250-255
Tawara Y, Honma K, Naito Y. Methicillin-resistant Staphylococcus aureus and Candida albicans on denture surfaces. Bull Tokyo Dent Coll. 1996; 37:119-128
Owen MK. Prevalence of oral methicillin-resistant Staphylococcus aureus in an institutionalized veterans population. Spec Care Dentist. 1994; 14:75-79
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Coming to a practice near you? community-acquired meticillin resistant staphylococcus aureus (ca-mrsa)

From Volume 38, Issue 4, May 2011 | Pages 254-260

Authors

Emer O’Leary

BDS, MFDS RCS(Glas)

Senior House Officer, University of Glasgow, Glasgow

Articles by Emer O’Leary

Deborah EA Lockhart

BSc(DentSci), BDS(Hons), MFDS RCSEd

Specialist Registrar and Honorary Clinical Teacher Microbiology, University of Glasgow, Glasgow

Articles by Deborah EA Lockhart

Andrew Smith

BDS, FDS RCS(Edin), FRCPath, PhD

Glasgow Dental Hospital and School

Articles by Andrew Smith

Abstract

Hospital-acquired meticillin resistant Staphylococcus aureus (HA-MRSA) arose in the 1960s, but the last decade saw the emergence of a new entity: community-acquired MRSA (CA-MRSA). Unlike HA-MRSA, patients affected by CA-MRSA have no obvious risk factors and may present with recurrent skin and soft tissue infections (SSTI) or, rarely, severe necrotizing pneumonia. This article provides an overview of CA-MRSA and reinforces the standard infection control procedures required to prevent further spread.

Clinical Relevance: The dental team require an awareness of emerging infections, their relevance to dentistry and the infection control procedures necessary to prevent transmission.

Article

Introduction

Meticillin resistant Staphylococcus aureus (MRSA) is classically associated with healthcare interventions. Consequently, hospital admission represents a prominent risk factor for the acquisition of certain epidemic strains of MRSA, leading to the term ‘hospital-acquired infection’ (HAI). This was modified to ‘healthcare associated infection’ acknowledging patient movement between healthcare and community settings, despite the MRSA strains remaining identical.

New strains termed community-associated MRSA (CA-MRSA), with distinct phenotypic and genotypic characteristics, emerged in the last ten years and are now widespread in the USA. As cases have been reported in the UK and the incidence is likely to increase,1 the dental team should have an understanding of this emerging pathogen and their role in preventing further spread. This article provides a background on the origins of this bacterium, discusses its occurrence in the oral cavity and highlights current treatment and prevention strategies. Dental healthcare workers should have sufficient knowledge to manage patients colonized or infected with any strain of MRSA competently.

Background

Staphylococcus aureus is a Gram-positive coccus that colonizes the nose, skin and oral cavity of approximately 20–30% of healthy individuals. Although S. aureus may exist as a commensal, it is responsible for a variety of infections, ranging from superficial skin infections to invasive life-threatening conditions, including septicaemia, endocarditis, osteomyelitis, pneumonia and toxic shock syndrome. There is political pressure to reduce the incidence of this important nosocomial pathogen2 and Figure 1 demonstrates an overall reduction in the number of S. aureus bacteraemias reported in Scotland between 2005 and 2009 as part of a mandatory surveillance scheme.3

Figure 1. Quarterly numbers of S. aureus bacteraemias (including MRSA) in Scotland from April 2005 to March 2009.3

Emerging resistance

Prior to the 1940s, virtually all S. aureus isolates were susceptible to penicillin. Following the introduction of this therapeutic agent in the mid 1940s, widespread resistance appeared as a result of the enzyme penicillinase hydrolysing the beta-lactam ring, rendering the drug inactive. Meticillin, a semi-synthetic penicillinase stable derivative, became available in the late 1950s and the first MRSA was described around the same time.4 Meticillin is no longer used clinically with flucloxacillin, the preferred agent for a meticillin sensitive S. aureus (MSSA). This pattern of emerging resistance has been repeated following the introduction of other antibiotics (Figure 2).5

Figure 2. Time-line of emergence of resistance in S. aureus.

MRSA refers to a strain of S. aureus that has acquired the mecA gene coding for an altered penicillin-binding protein (PBP2A) that renders the organism resistant to all current beta-lactam antibiotics, including penicillin, amoxicillin, flucloxacillin and the cephalosporins. Many HA-MRSA isolates demonstrate resistance to other antibiotic classes, such as the macrolides (eg erythromycin), lincosamides (eg clindamycin) and fluoroquinolones (eg ciprofloxacin). Serious infections with MRSA are treated with intravenous glycopeptides, such as vancomycin or teicoplanin. Newer oral agents, such as linezolid, have a role in special circumstances, although there are concerns regarding bone marrow toxicity.

Types of MRSA

Understanding the evolution of MRSA has improved with a range of phenotypic and genotypic (fingerprinting) techniques that can trace the spread of successful clones. There are thought to be five major lineages that spread throughout the world following the introduction of meticillin.6 The main HA-MRSA strains in the UK are epidemic (E) MRSA15 and EMRSA16.

Advances in the sequencing of bacterial housekeeping genes has led to the use of a technique called multi-locus sequence typing (MLST) that assigns a unique ‘sequence type’ to identify a particular S. aureus strain accurately. Common MLST types are ST22 (EMRSA15) and ST36 (EMRSA16), for hospital-acquired strains, and ST8 (USA 300) and ST1 (USA 400), for those originating in the community.

Hospital and community-acquired MRSA – what is the difference?

In 1999, one of the first cases of CA-MRSA was reported in the USA, causing the death of four previously healthy children.7 Cases of CA-MRSA have continued to increase in the USA, particularly amongst young people; often running a rapid and devastating course. Worldwide prevalence, however, remains low.8 There are important phenotypic and genotypic differences between HA- and CA-MRSA, which are used to distinguish them (Table 1). Skin and soft tissue infections are among the most common manifestations of CA-MRSA and patients may report recurrent abscesses. Less common, but more severe, infections include necrotizing pneumonia and severe sepsis.


Parameter HA-MRSA CA-MRSA
Patient group Chronically or critically ill and/or immunocompromised patients in healthcare settings or with recent healthcare exposure. Nursing home residents. Generally young healthy individuals with no healthcare exposure. Often occurs in settings where people are crowded, frequent skin to skin contact, lack adequate hygiene, share personal items and may have open cuts/abrasions on their skin.
Infection site Variable including bacteraemia, surgical site, IV lines, bone/joint, pneumonia and catheter urines. Predilection for recurrent skin and soft tissue infections (abscess, cellulitis). Rarely necrotizing pneumonia.
Transmission Within healthcare settings. Often prior colonization. Community-acquired. Spreads in sports teams and household contacts.
Panton-Valentine Leucocidin (PVL) Usually absent. Often present.
Antibiotic susceptibility Often multi-resistant to several classes of antibiotics, eg macrolides, licosamides, fluoroquinolones, Treatment options may be limited. Often resistant only to beta-lactam antibiotics. More treatment options.
Lineage ST 22 (EMRSA 15).ST 36 (EMRSA 16). ST 8 (USA 300).ST 1 (USA 400).

An array of pathogenic determinants may facilitate host colonization and disease in S. aureus, including:

  • Surface proteins (eg fibronectin binding protein A/B);
  • Antiphagocytic polysaccharide capsules;
  • Cytotoxins;
  • Superantigens; and
  • Enzymes facilitating spread (eg proteases and hyaluronidase).
  • Panton-Valentine Leucocidin (PVL) toxin production is an important virulence factor in CA-MRSA, causing destruction of white blood cells and leading to massive tissue necrosis. The precise role of PVL in disease remains unresolved, although epidemiologically associated with SSTI and believed to have a role in the pathogenesis of severe necrotizing. While almost all CA-MRSA strains carry the PVL toxin, it is also found in MSSA.9

    Staphylococcus aureus in the oral cavity

    Colonization

    There is sufficient evidence that S. aureus is an oral commensal, although its role in oral mucosal disease in immunocompetent hosts is unclear. The carriage rate in healthy adults ranges from 24–36%.10 Prosthetic materials, such as acrylic dentures, increase the incidence of S. aureus, with one study reporting colonization in 23–48% of denture wearers, with 10% MRSA positive. Owing to the formation of biofilms, MRSA is difficult to eradicate using conventional denture cleansers, with some requiring heat sterilization or even re-making.11,12 Another study suggested that 19% of institutionalized veterans were MRSA positive in the oral cavity.13

    Children may have a higher incidence of S. aureus carriage compared to older dentate patients, with one study reporting 64% of children having S. aureus in the oral cavity.14 Studies examining MRSA carriage in the oral flora of children revealed much lower incidence rates of up to 1.6%.15

    Infection

    Staphylococcus aureus is implicated in a spectrum of oral diseases, including angular cheilitis (Figure 3), parotitis, osteomyelitis and mucositis (especially in the immunocompromised).

    Figure 3. Clinical photograph of patient with angular cheilitis.

    A 3-year study of laboratory data from Glasgow found a 5% incidence rate of MRSA from the 5,005 specimens analysed. Patients with MRSA were more commonly seen in primary care settings, such as nursing homes, hospices and general dental practice, rather than the dental hospital where the majority of MSSAs were isolated.16

    Diagnosis

    Diagnosis of suspected oral infections should be confirmed by appropriate specimens submitted to a diagnostic microbiology laboratory for culture, identification and susceptibility testing. This is particularly important for recurrent and/or difficult to treat infections that have not responded to first-line therapy. For example, intra- and peri-oral mucosal lesions should be swabbed, alongside other potential reservoirs of infection, such as the anterior nares and dentures. An oral rinse is also useful for angular cheilitis as S. aureus has been implicated in 63% of cases.17

    General dental practitioners are advised to contact their local microbiology laboratory that will provide advice and supply specimen collection materials. The poor uptake of diagnostic microbiology facilities in general dental practice probably underestimates the role of S. aureus in oral disease.

    Treatment

    The successful treatment of any suspected infection, including MRSA, depends on an accurate diagnosis and removing the source of infection. Severe infections with systemic involvement require admission to tertiary referral centres and will not be discussed further here, aside from commenting that intravenous antibiotics are usually required guided by appropriate susceptibility results.

    For more minor infections, including angular cheilitis, the use of topical miconazole (primarily an anti-fungal agent but with some anti-staphylococcal properties) or topical naseptin (a combination of neomycin and chlorhexidine) may suffice. Prolonged courses of topical fusidic acid monotherapy must be avoided as this leads to the emergence of resistance, thereby reducing the availability of a useful oral anti-MRSA agent in more severe infections.

    Other infections, including mucositis and parotitis, often require systemic antibiotics, and these must be guided by susceptibility testing, as the resistance pattern of oral anti-MRSA agents is difficult to predict. Specific advice should be sought from a microbiologist, however, treatment usually involves combination therapy, eg doxycycline and fusidic acid to minimize resistance. Flucloxacillin is advocated for MSSA infections. Treatment of MRSA colonization is generally not advocated.

    Antibiotic prescribing and MRSA

    An important role in the control of MRSA by dentists is responsible prescribing of antibiotics. Frequent antibiotic use has been linked to increased MRSA acquisition.18 One study showed that, among professional football players, the risk of contracting MRSA was almost eight times higher if players had taken antibiotics in the previous year versus those who had not.19 A study of general dental practitioners in England found that, of the 2,951 prescriptions issued over a time period, only 29% were considered justifiable using published guidelines.20 Another study,21 examining prescribing practices of general dental practitioners in England, found 69% of dentists prescribed antibiotics prior to drainage and 45% when it was established, despite research demonstrating that drainage of an infection is the only treatment necessary for the majority of infected swellings without systemic symptoms. As S. aureus may colonize various body sites, systemic antibiotics prescribed inappropriately for other conditions will affect the endogenous flora and potentially drive resistance.

    Prevention of MRSA transmission

    The dental team has a responsibility for the prevention of spread of MRSA. Therefore, it is essential that high standards of infection control are adhered to for every patient in the practice, as most patients are unaware of their MRSA status. Furthermore, it is not feasible to screen for MRSA carriage in dental practice. Table 2 outlines the standard infection control procedures (SICPs) that must be followed. No additional precautions are required to manage a patient known to have MRSA in the dental setting.


  • Hand hygiene
  • Personal protective equipment
  • Cleanliness of care equipment
  • Cleanliness of environment
  • Prevention of occupational exposure
  • Management of blood and body fluid spillage
  • Safe handling of uniforms
  • Safe disposal of waste
  • Patient placement (applicable in secondary care facilities)
  • There have been documented cases of MRSA oral infection transmitted by a dentist.22 A study in Japan23 of nosocomial transmission of MRSA, via the surfaces of the dental surgery, found that 6% (8/140) of patients treated in an oral and maxillofacial surgery were found to be colonized after treatment, after identical strains were isolated on the dental chair and air syringe. A further study of S. aureus environmental contamination in an 89 chair dental clinic in a dental hospital in Brazil identified MRSA colonized surfaces in the emergency dental clinic and that clinical procedures increased the dispersal of S. aureus into the environment.24 Both these studies highlight the need for strict adherence to SICPs in dental settings.

    Conclusions

    CA-MRSA is a significant problem in the USA and is of growing concern in the UK. These new strains appear to have a predilection for damaged skin and airways, and may be PVL toxin positive. CA-MRSA strains are transmissible, especially amongst family members, staff/children in nurseries and in sports teams. Therefore, it is essential that the dental team follow SICPs, practise prudent antimicrobial prescribing and do not discriminate against MRSA positive patients.

    The incidence of documented oral S. aureus infections is low, but this may be masked by an equally low number of diagnostic samples taken by dentists. We strongly encourage all dentists to consider using diagnostic microbiology laboratories to facilitate in the diagnosis of oral infections.