Constant readers, I am at the annual meeting of the Society for Healthcare Epidemiology of America, where there is a lot of news about MRSA in hospitals. I hope to post on that over the next few days.

In the meantime, though, I want to pass on several pieces of news about ST398, the “pig strain” that we have talked so much about.

First, the Soil Association, the British organic/sustainable farming group that has done much work elucidating the spread of ST398 and making the link between that bug and antibiotic use on farms, has released an online documentary about ST398 called Sick as a Pig. You can watch it here, and here is the Soil Association’s press release:

…40% of Dutch pigs and up to 50% of Dutch pig farmers are now carrying the new strain, which is also spreading to the wider population. Although this type of MRSA was first detected in humans in the Netherlands as recently as 2003, it now causes almost one in three cases of MRSA treated in Dutch hospitals.
It is not yet known whether any British pigs are affected by the new strain of MRSA (called ST398) since the results of testing, which was required by the EU and carried out in 2008, have not been made public.
Several countries have already published the results of their own tests revealing significant levels of MRSA in national pig herds. The European Food Safety Authority has said that, ‘It seems likely that MRSA ST398 is widespread in the food animal population, most likely in all Member States with intensive animal production’.

Second, here is a paper from last fall that somehow slipped by me: in the CDC journal Emerging Infectious Diseases, a report of two cases of ST398 infection in men in Sweden. Neither had any contact with farming or animals.

The first patient, a previously healthy 36-year-old male physiotherapist, sought medical care in March 2006 for a small abscess in his axilla. Culture of the abscess grew MRSA. Presence of mecA gene was confirmed by PCR. During the next 2 months, furunculous [sic] developed twice, caused by the same strain. His youngest child, adopted from China, had been found to be MRSA positive (throat, perineum, and a small wound) a month earlier during routine screening for adopted children. During subsequent screening of the family, the older sister, adopted from South Korea, was also found positive (throat). Both parents were negative for MRSA at that time, which suggests that the father was newly infected when his abscess developed and that he had not acquired the strain abroad. Also, spa typing indicated that the children carried different strains from that of the father and from each other (t286, t1434). Subsequent screening of family members for MRSA on several occasions found only the father to be repeatedly positive.
The second patient, a 43-year-old male clerk, also previously healthy, sought medical attention during the summer of 2007 for a MRSA-infected elbow wound. Follow-up examination determined that he carried MRSA also in the perineum and in a chronic external otitis eczema. He was later hospitalized for a larger abscess that required surgical drainage. His family members reported no symptoms and were thus not screened for MRSA.

Of note, the men’s strain (ST398, t034) carried the two genes that express the toxin PVL, which is unusual in ST398, though characteristic of CA-MRSA USA300, the dominant community strain in the US. The role that PVL plays is very controversial: Some research groups believe it is responsible for the rapid tissue destruction that can accompany USA300 infection (in penumonia and some soft-tissue infections, for instance), while others vociferously disagree.