The bacterial coinfection rate of 28% amongst our H1N1 hospitalized patients was higher compared to other studies [8, 9]. A large laboratory-based study in the United States demonstrated comparable bacterial coinfection rates to our study with similarly very low frequency of viral copathogen detection . Whilst our finding concurred with several studies [1, 8, 9, 11, 12] that showed H1N1 infections having a predilection for younger patients, patients > 50 years had higher risk of bacterial coinfection in our study.
Although concurrent bacterial infection was shown to have a major influence on mortality in previous influenza pandemics , its' role in the current H1N1 pandemic is still evolving. Recent postmortem studies amongst fatal H1N1 cases established a link between bacterial lung infections and increased deaths . Whilst an earlier study showed bacterial coinfection not to be a major contributor to severe disease , a more recent study demonstrated otherwise . In our study, patients with bacterial coinfection were found to have higher risk of developing complications. The presence of underlying comorbidity, liver impairment and supplemental oxygen requirement were significantly higher in bacterial coinfected patients in univariate analysis, although these factors were not predictive in multivariate analysis.
Unlike S.pneumoniae, S.aureus and S.pyogenes which are repeatedly reported as coinfecting agents [4, 8, 10, 13], the high rates of M.pneumoniae coinfection was unique to our study. Although hematological parameters have been mentioned in few other studies [8, 9, 12], to our best knowledge this is the first study that specifically explored the impact of bacterial coinfection on these parameters. CDC recognizes the importance of early empirical antibiotics in H1N1 infected patients who might have concurrent bacterial pneumonia . Our study showed that leukocytosis and neutrophilia were notably higher in bacterial coinfected patients. This finding could alert physicians about the possibility of bacterial coinfection, as clinical diagnosis may be insufficient and bacterial cultures take time. Eighty-two percent of our patients received empiric or definitive antibiotics at some point during admission which was comparable to high rates in a China study .
The limitation of our study includes its' retrospective design and a small sample size which was unavoidable, as we were limited by the actual number of cases during the study period and because it was a single centre study. As such, our study was inadequately powered to examine the influence of certain characteristics. Nasopharyngeal aspirates may have questionable pathogenic role, however the 3 patients with positive NPA were treated with appropriate antibiotics as they were felt to be clinically relevant. Mycoplasma serology was not performed in all patients and the request was based upon physicians' discretion, this may have underestimated the actual number of cases. The preadmission antibiotic therapy could underestimate the bacterial coinfection rates. Despite these limitations, we identified bacteria coinfection in 28% of our patients.
In conclusion, our study suggests that bacterial coinfection is not uncommon in H1N1 infected patients and laboratory investigations should go beyond establishing a viral cause alone. Bacterial coinfection was more frequently seen in the older age group and was associated with higher rates of complications. As adjunct to clinical findings, clinicians need to have a high index of suspicion if neutrophilia was identified on admission as it may denote bacterial coinfection. A larger scale study will be useful to further confirm our findings.