JAC Advance Access originally published online on May 30, 2006
Journal of Antimicrobial Chemotherapy 2006 58(2):480-481; doi:10.1093/jac/dkl230
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Correspondence |
The ‘Oxford Staphylococcus’: a note of caution
Staphylococcus Reference Unit, Centre for Infections, Health Protection Agency 61 Colindale Avenue, London NW9 5EQ, UK
*Corresponding author. Tel: +44-208-3277227; Fax: +44-208-2007449; E-mail: angela.kearns{at}hpa.org.uk
Keywords: Panton-Valentine leucocidin , Staphylococcus aureus , antibiotic control strain
Sir,
The discovery of penicillin prompted a period of intense activity among the scientific community. In the early 1940s, workers sought to characterize penicillin and assess its suitability for therapeutic use.1 Heatley subsequently described a standardized method for the biological assay of penicillin and recommended the use of a particular test strain of Staphylococcus aureus.2 The organism was deposited in the National Collection of Type Cultures (NCTC) in 1943 and assigned reference number NCTC 6571. In recognition of the fact that much of the early work on penicillin was carried out by workers in Oxford, S. aureus NCTC 6571 (cross-referenced in the American Type Culture Collection as ATCC 9144) has become known as the ‘Oxford Staphylococcus’.
The Oxford Staphylococcus is used widely in clinical diagnostic microbiology laboratories throughout the UK. It serves as a reference strain for antimicrobial susceptibility testing, being susceptible to antistaphylococcal antibiotics tested in such laboratories. It is also commonly used as a control organism for the phenotypic characterization of S. aureus including coagulase testing (regarded as a weak positive control) and determination of DNase activity.
The reference strain has been regarded as rather innocuous and safe to handle. However, through the ongoing programme of work to characterize reference strains and clinical isolates of S. aureus referred to the Staphylococcus Reference Unit (SRU, Centre for Infections, London), we have found that the Oxford Staphylococcus harbours the Panton-Valentine leucocidin (PVL) genes. This toxin has also been detected in a control strain of S. aureus used in the USA, isolated in Seattle in 1945 (ATCC 25923, NCTC 12981).3 PVL is regarded as a marker of virulence in S. aureus. It is strongly associated with skin and soft tissue infections (SSTIs)4 and published data suggest that where PVL genes are present they are expressed.5 The toxin induces pore formation in leucocytes, triggering the release of interleukins and other inflammatory mediators, leading to tissue necrosis and abscess formation.4 PVL-positive S. aureus have been circulating in the UK and causing disease for over 50 years. For example, phage type 80/81 strains prevalent in the 1950s and 1960s that caused a pandemic of community-acquired SSTIs, pneumonias and septicaemias in children and young adults were PVL-positive.6
Review of the SRU database has shown that among over 13 000 S. aureus isolates referred for typing and characterization from November 2003 to January 2006 15 have been identified as being closely related to the Oxford Staphylococcus by phage typing and/or PFGE. The majority (12 of 15; 80%) were referred as MRSAs or coagulase-negative staphylococci, suggesting that the reference strain had been submitted, probably as a result of transposition errors occurring in the referring laboratory. The remaining three, however, were referred as MSSA recovered from patients with abscesses or community-acquired pneumonia, both of which are clinical presentations associated with PVL.4 In these instances, it is likely that the organism referred was the aetiological agent. All three were unrelated temporally and occurred in geographically distinct areas of England. PCR- and DNA-sequence based analyses4,6 showed the clinical isolates were indistinguishable from each other and the Oxford Staphylococcus: they encoded PVL, enterotoxins G and I; were multi-locus sequence type 30 (ST30); were protein A (spa) type t318; and belonged to accessory gene regulator (agr) allele group 3. All four cultures were susceptible to antistaphylococcal antibiotics (one clinical isolate was resistant to penicillin only) and PFGE profiles obtained by macro-restriction of chromosomal DNA with SmaI4 confirmed that they were closely related (Figure 1).
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These data, together with previously published reports,4 show that representatives of this MSSA lineage continue to circulate in the UK with potential to cause community-acquired disease 60 years following the primary isolation of the Oxford Staphylococcus. From an evolutionary perspective, it is noteworthy that members of this clonal lineage have subsequently acquired methicillin resistance [specifically following acquisition of the staphylococcal chromosome cassette mec (SCCmec) type IV element] and emerged as a community-associated MRSA strain (ST30-MRSA-SCCmecIV) which has been found in the Southwest Pacific and some other regions, including the UK.4,6
The Oxford Staphylococcus has been used as a control organism for some 60 years and we are not aware of any infections resulting from acquisition of this organism by laboratory personnel. Although the provenance of the control strain is unclear, it is tempting to speculate that it was originally isolated from a pyogenic infection associated with the presence of the PVL genes. It may be argued that the organism may have become attenuated following repeated subculture over the years following its initial isolation. Nevertheless, these observations serve as an alert to microbiologists: good laboratory practice should be adhered to where this organism is handled, particularly following the report of infection due to PVL-positive MRSA occurring in a microbiologist working with such organisms.7 Attention should be paid to the covering of cuts and wounds and/or wearing of gloves to minimize any risk of infection among laboratory workers. Crucially, healthcare personnel should remain vigilant to the possible occurrence of SSTIs in individuals handling the Oxford Staphylococcus and, where S. aureus is identified as the aetiological agent, the isolate should be fully characterized to determine its PVL status and relatedness to the control strain.
Transparency declarations
None to declare.
Acknowledgements
We thank Dr Robert Hill (Antibiotic Resistance Evaluation Unit, Centre for Infections, London) for provision of antimicrobial susceptibility data.
References
1 Abraham EP, Chain E, Fletcher CM, et al. (1941) Further observations on penicillin. Lancet ii:177–89.
2 Heatley NG. (1944) A method for the assay of penicillin. Biochem J 38:61–5.[Medline]
3
Dunne WM. (2006) Panton-Valentine leukocidin genes in a laboratory quality control strain of Staphylococcus aureus. J Clin Microbiol 44:287.
4
Holmes A, Ganner M, McGuane S, et al. (2005) Staphylococcus aureus isolates carrying Panton-Valentine leucocidin genes in England and Wales: frequency, characterization and association with clinical disease. J Clin Microbiol 43:2384–90.
5
Prevost G, Couppie P, Prevost P, et al. (1995) Epidemiological data on Staphylococcus aureus strains producing synergohymenotropic toxins. J Med Microbiol 42:237–45.
6 Robinson DA, Kearns AM, Holmes A, et al. (2005) Re-emergence of early pandemic Staphylococcus aureus as a community-acquired methicillin-resistant clone. Lancet 365:1256–8.[CrossRef][Web of Science][Medline]
7
Nordmann P and Naas T. (2005) Transmission of methicillin-resistant Staphylococcus aureus to a microbiologist. New Engl J Med 352:1489–90.
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