Methicillin-resistant Staphylococcus aureus (MRSA) was first discovered on 2nd October 1960 by Prof Margaret Patricia Jevons at the Public Health Laboratory in Collindale, London, UK.

Photo of Prof Jevons, obtained via a screenshot of a Lancet publication on October 2011.

Methicillin (or celbenin as it was also known as then) became available for prescription in 1959, and the conventional narrative has always been that MRSA arose as a consequence of rapid resistance development to the widespread use of the antibiotic. I have myself told the story this way to students and other healthcare professionals during lectures on MRSA.

There are a couple of inconvenient truths that one had to close a blind eye to when explaining the initial appearance of MRSA this way:

Now, the question of MRSA’s origin has been tackled in another way, using next generation sequencing and sophisticated (to me anyway) bioinformatics techniques on a collection of the original MRSA preserved by the Public Health England Staphylococcal Reference Laboratory, as well as MRSA (and MSSA) from the Statens Serum Institute in Denmark – the latter used as a representative of early European MRSA. This work is published on the preprint server BiorXiv (more on preprints at a later date – definitely a topic worthy of discussion especially with respect to the contentious issue of availability of scientific research findings), led by my former supervisor at the Wellcome Trust Sanger Institute Dr Matthew Holden – now a full professor at the University of St Andrews in Scotland.

Screenshot from the preprint server BiorXiv.

Their findings suggest strongly that MRSA actually arose in the 1940s, likely as a consequence of widespread penicillin use (and to a lesser extent, other antibotics such as tetracycline or streptomycin). Because evolutionarily it is a less efficient mechanism of penicillin resistance compared to penicillinase production, MRSA likely comprised a very small fraction of the overall S. aureus population until they underwent positive selection pressure from widespread methicillin (and oxacillin) use, and no doubt subsequently also from fluoroquinolone use subsequently.

Screenshot from one of the figures in the “MRSA origins BiorXiv” article

What does this work mean, besides being a piece of “revisionist history”? It also adds to the evidence that antibiotic resistance is a web of unintended consequences, rather than a simplistic cause-effect model that we often find (too much) comfort in.

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