Extending this analysis to allow transmission probabilities to vary with the MRSA type enabled differences between MRSA clones and wards to be quantified (table 3) and allowed hypothesis tests about whether the daily transmission probabilities differed between strains (thus allowing us to test whether the observed differences in transmissibility found using method 1 could be entirely explained by the longer length of stay of the TW patients). In ICU1 no consistent differences were seen. In ICU2 the TW clone had a higher daily transmission probability to susceptible patients in each of the four study phases under the baseline assumption of complete bacterial interference, though confidence intervals were wide and showed considerable overlap. Differences between TW and non-TW MRSA transmission probabilities reached statistical significance at the 5% level for both wards combined and for ICU1, but not for ICU2 alone, and in only one of the four phases (phase 4) using combined data from both ICUs. This phase corresponded to the introduction of the surface antiseptic bodywash protocol, which was associated with a more than halving of the transmission probability from a patient with non-TW MRSA compared to earlier phases. The fall in the transmission probability for TW MRSA in phase 4 was smaller, and likely to be confounded by the use of linezolid for TW carriers in this phase. Large differences in transmission probabilities for the two MRSA types were also seen in phase 2 (corresponding to the introduction of hand hygiene promotion), but in this case confidence intervals were wider reflecting the short duration of this phase. In other phases differences between TW and non-TW estimates were much smaller. The magnitude of the differences depended on which patients were assumed to be susceptible. Under the baseline assumption that patients colonized with one strain were not susceptible to acquiring another (complete bacterial interference) the differences were larger than in the sensitivity analysis where no bacterial interference was assumed (table 3) . This can be explained by the higher prevalence of non-TW MRSA clones; under the assumption of no bacterial interference all non-TW MRSA positive patients would be considered susceptible to infection or colonisation with TW MRSA and vice versa. Changing from complete interference to no interference therefore results in a greater increase in the number of susceptibles available for the TW clones to infect than it does for the non-TW clones. To accommodate these changes, a larger reduction in the daily transmission probability for TW clones is required. Overall, combining data from both wards, the TW clone was estimated to have a daily transmission probability that was between 63 and 100% higher than the non-TW clones in phase 4, and between 53 and 94% higher in phase 2 (the lower numbers corresponding to the no bacterial interference assumption) though the differences only reached significance at the 5% level in phase 4 and only under baseline interference assumptions. Transmission probabilities were broadly similar in the two other study phases. Estimates of the single-admission reproduction number (R a ) from the model without background transmission (and assuming TW and non-TW patients have the same length of stay distribution) are reported in the supplementary material (figure S1). Results were robust to the assumptions made about the number and timing of MRSA acquisition events (supplementary table S4), but fitting a more complex model allowing patient-to-patient transmission and transmission from background sources suggested that the relative importance of patient-to-patient and background transmission could not be reliably identified in such hyperendemic settings without additional data (supplementary table S5 ).