Double coverage (generally cephalosporin + macrolide) is currently the recommended treatment for patients hospitalised with community acquired pneumonia (CAP) [1]. This seems mainly to be due to better coverage of S. pneumoniae and increases survival in pneumococcal bacteriemia [2,3]. Better coverage of atypical pathogens may play an additional role.

So the question arises: What is the pathophysiologic basis for the increased survival with double coverage for inpatient CAP?

A few hypotheses:

  1. Synergic activity against S. pneumoniae
  • In vitro data suggests that macrolides and cephalosporins actually are antagonist against S. pneumoniae [4], thus this seems unlikely to be the main cause.
  1. Immunomodulation by macrolides
  • However, in pneumococcal bacteriemia non-macrolide double coverage also improves mortality according to observational data reported by Baddour et al [5].
  1. Coverage of resistant S. pneumoniae strains

Is there are commonly accepted theory for this phenomenon ?


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