172 Chapter 8 experiments suggests that may not be correct [109]. Whether hVISA in MRSAB results in increased vancomycin failure and persistent MRSAB remains debated. Some studies report worse clinical outcomes [110–116] and increased risk of persistent MRSAB [110,112–114], with others, including one systematic review and meta-analysis, showing no significant difference in mortality or persistent MRSAB [104,117–121]. Overall, the mixed data suggest that hVISA may play a role in persistent MRSAB. However, the lack of strong evidence does not necessarily justify deviating from vancomycin in routine hVISA MRSAB cases. In summary, there is unlikely to be a single pathogen component that is individually responsible for persistence in MRSAB. The inability of the host to clear the bloodstream is likely a result of complex interplay between the bacteria, the host immune system, and the circulating antibiotic (Figure 3). Understanding characteristics of S. aureus increasing the probability of persistent bacteremia opens the door to novel diagnostics, which could allow for a more aggressive antibiotic strategy up-front, potentially improving patient outcomes. Figure 3. Summary of host and pathogen factors contributing to persistent MRSAB Treatment of persistent MRSAB Limited high-quality evidence exists for the most effective treatment of MRSAB in general, and even less for the treatment of persistent MRSAB in particular [122].
RkJQdWJsaXNoZXIy MTk4NDMw