We were interested to read the recent publication in CMI concerning the role of superantigenic strains in the prognosis of infections caused by community-acquired methicillin-susceptible Staphylococcus aureus (CA-MSSA) [1]. The authors reported that 73% of CA-MSSA isolates, recovered from 37 immunocompetent patients with CA-MSSA, produced at least one superantigen, but that carriage of superantigens by S. aureus did not affect mortality. We wish to report similar findings concerning the relationship between virulence genes carried by methicillin-resistant S. aureus (MRSA) and the potential for invasive infection.

We determined the occurrence of 18 virulence determinants (including adhesins and toxins) among 26 invasive and 20 colonising isolates of MRSA, using six separate multiplex PCRs [2–6]. Invasive isolates were recovered over a 3-year period from patients with device-related bacteraemia as part of a previous study [7]. Colonising isolates were from nasal swabs, collected from patients who were MRSA-positive on their first admission to the hospital, but who had no apparent infection.

The distribution of toxin genes was reported to be similar in MSSA survivors and non-survivors [1]; similarly, we found no significant correlation between the carriage of almost all the virulence genes and the invasiveness of MRSA isolates (Table 1). The only exception was a significantly greater frequency of the seg gene in colonising isolates compared with invasive isolates (100% and 73%, respectively; p 0.028 by Fisher’s exact test). The seh gene was harboured by 5% of colonising isolates and 19.2% of invasive isolates, but this difference was not statistically significant (p 0.212). Nashev et al. [8] also reported an increased frequency of seg among colonising isolates compared with invasive isolates of MSSA (73% and 52% [8]) and an increased frequency of seh in invasive isolates (6.7% vs. 21.4%), but Desachy et al. [1] reported no difference in the distribution of these genes. Our study suggested some variability of the egc cluster, as isolates positive for sei were not always positive for seg. Therefore, the presence of one or two egc genes may not indicate the presence of the entire egc cluster, as suggested by Desachy et al. [1]. The absence of an association between these genes and invasive isolates in our study parallels the absence of a significant role for superantigens in the prognosis of patients with sepsis caused by S. aureus [1].

Table 1.   Prevalence of 18 virulence determinants among colonising and invasive isolates of methicillin-resistant Staphylococcus aureus
GenePrevalence of virulence gene (%)
Colonising isolates (= 20)Invasive isolates (= 26)

Characterisation of potential virulence features of MRSA that are of relevance for pathogenicity in hospital settings has been the subject of several recent studies [1,8–10]. As highlighted by previous studies [1,8–10] and the present findings, the inability to find a definitive correlation between invasive S. aureus strains and the carriage of virulence genes suggests that either the expression of virulence determinants in vivo mediates pathogenicity, or that host immune factors may play a significant role in outcome. The mechanism by which compromised immunity facilitates S. aureus infection is probably complex, and is likely to involve several different aspects of innate immunity, e.g., compromised neutrophil function, variations in cytokine or antimicrobial peptide expression, and the possible involvement of some components of acquired immunity. The elucidation of these mechanisms in patients who are colonised or infected with MRSA will contribute to our understanding of the complexities of S. aureus pathogenesis.


  1. Top of page
  2. Acknowledgements
  3. References

Reference strains were kindly supplied by C. Smyth (Trinity College Dublin, Ireland) (strains NY19, FRI472, FRI569, FRI913, DXD10, DX41) and A. Rossney (MRSA Reference Laboratory, St James Hospital, Dublin, Ireland) (MO50076). The colonising isolates were provided by O. Sherlock, E. Creamer and the Microbiology Laboratory at Beaumont Hospital (Dublin, Ireland). This work was funded, in part, by a Summer Research Grant to SOD from the Royal College of Surgeons in Ireland. The authors declare that they have no conflicting interests in relation to this work.


  1. Top of page
  2. Acknowledgements
  3. References
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