Both analytical methods supported the hypothesis that intervention C (the surface antiseptic protocol) was associated with a sustained reduction in MRSA transmission, and both indicated a reduced effect for the TW clone. Both methods gave point estimates that indicated elevated transmission of TW MRSA compared with endemic strains in all four study phases in ICU2 but not ICU1. There were, however, some differences: the wardlevel reproduction numbers (method 1) tended to indicate greater increased transmission for the TW compared to non-TW MRSA than was seen using method 2. This reflects the fact that the two methods are quantifying different things: method 1 estimates secondary cases per case, which depends both on transmissibility and the length of ICU stay while carrying MRSA; method 2, in contrast, estimates only the daily transmission probability from one MRSA carrier to one susceptible patient. This will not be affected by length of stay. Indeed, there was some evidence that patients colonised with TW MRSA (particularly those colonised on ICU admission), had a longer length of stay than those colonised with non-TW MRSA. This may reflect the link between MRSA infection and excess length of stay in this cohort [37] , and the increased virulence of the TW strain which was over four times more likely to cause blood stream infection in colonised patients compared to non-TW MRSA strains in the same ICUs [12] . Even in the absence of an increased rate of transmission to other patients, increased length of stay would lead to a higher singleadmission reproduction number. It is possible that such differences in length of stay reflect underlying differences in the characteristics of patients most vulnerable to acquiring the different MRSA types. For example, because the TW outbreak was centred on the two ICUs, patients carrying TW on ICU admission might be more likely than patients carrying non-TW MRSA to have had recent ICU admissions. The TW clones showed a far broader range of antibiotic-resistance than endemic MRSA clones and have previously been shown to preferentially colonise vascular catheters but not carriage sites compared with endemic strains [12] . Taken together, these observations suggest that the TW MRSA could represent a phenotype particularly adapted to transmission in Table 3 . Estimates of the daily transmission probability (q) from one exposed to one susceptible patient. Estimates of the daily transmission probability (q) from one exposed to one susceptible patient. settings, such as ICUs, with high levels of antibiotic usage and patient catheterisation, perhaps at the expense of persistence outside these areas. There is some evidence that such adaptation results from both increased persistence in the ICU (perhaps by targeting long-stay patients, and causing infections that increase length of stay) and from an increased daily transmission probability (particularly in the presence of widespread antiseptic use). Caveats, of course, apply: differences in lengths of stays between TW and non-TW colonized/infected patients could be confounded by exposure history (the recent arrival of the TW clone rather than its biological properties may account for the different patient characteristics). Differences in daily transmission probabilities could also be subject to such confounding and could also have arisen by chance (in all phases -even phase 4, where the effect size was largest -confidence intervals were wide). The mechanisms underlying variations in transmissibility of different MRSA (and S. aureus) strains are poorly understood. Reasons for the differences in the two ICUs are also unclear. Chance variation cannot be ruled out, as the formal investigation of transmission potential of different MRSA types was, in part, motivated by perceived differences in transmissibility (using the same data), and the usual limitations of post hoc analyses therefore apply. Also, although the analyses accounts for demographic stochasticity, there may also be important sources of environmental stochasticity which are not accounted for. It seems unlikely that the difference in TW transmission in the two ICUs can be explained by colonized staff: a universal staff screening programme failed to detect the TW clone during the outbreak [12] . Differences in infection control practice also seem unlikely but cannot be ruled out: the two wards share the same infection control policies and staff pool, with medical and nursing staff rotating between units at 3-6 monthly intervals, though only physiotherapy, radiology and pharmacy staff worked across both units at the same time. It is possible that the built environment influences MRSA transmission. ICU2 was last refurbished in 1969, retaining a mixture of original materials including wood, and has much less open space, only eight sinks, and one side room, whereas ICU1 was refurbished in 1999 to an open plan configuration with better space utilization, 19 sinks and three side rooms. The reduced availability of sinks, side rooms and space to circulate may have adversely affected the ability to carry out infection control practice or cleaning, although it is unclear why this should only affect TW MRSA, which was not detected on environmental screening during the outbreak [12] .