The trimethoprim and sulfamethoxazole combination, co-trimoxazole, plays a vital role in the treatment of infections. Previous studies demonstrated that the BpeEF-OprC efflux pump confers widespread trimethoprim resistance in clinical and environmental isolates, but this is not accompanied by significant resistance to co-trimoxazole. Using the excluded select-agent strain Bp82, we now show that acquired trimethoprim versus co-trimoxazole resistance is mainly mediated by constitutive BpeEF-OprC expression due to mutations or by BpeEF-OprC overexpression due to mutations.
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