Double coverage (generally cephalosporin + macrolide) is currently the recommended treatment for patients hospitalised with community acquired pneumonia (CAP) . 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:
- Synergic activity against S. pneumoniae
- In vitro data suggests that macrolides and cephalosporins actually are antagonist against S. pneumoniae , thus this seems unlikely to be the main cause.
- Immunomodulation by macrolides
- However, in pneumococcal bacteriemia non-macrolide double coverage also improves mortality according to observational data reported by Baddour et al .
- Coverage of resistant S. pneumoniae strains
Is there are commonly accepted theory for this phenomenon ?