The first understanding of the viral/bacterial co-infection contribution to disease exacerbation came from studying the role of bacterial secondary infections during influenza pandemics. In the case of influenza virus, secondary infection has been substantially documented as ranging from 2% to 65% during a given epidemic [1]. Staphylococcus aureus, Streptococcus pneumoniae and Haemophilus influenzae are the major bacteria associated in simultaneous co-infection with influenza virus [2]. In vitro studies have shown that S. pneumoniae enhances influenza replication by producing a neuraminidase [3]. It has been suggested that it is difficult to evaluate the importance of viral/bacterial co-infection in the early years of an influenza pandemic due to low immunity. Therefore, only after immunity against influenza is built up, or after drifts have accumulated and symptoms are milder, can the effects of co-infection be better observed [2].
