Abstract:
Community-acquired pneumonia (CAP) remains an important cause of morbidity and
mortality throughout the world with much recent and ongoing research focused
on the occurrence of cardiovascular events (CVEs) during the infection, which are
associated with adverse short-term and long-term survival. Much of the research
directed at unraveling the pathogenesis of these events has been undertaken in
the settings of experimental and clinical CAP caused by the dangerous, bacterial
respiratory pathogen, Streptococcus pneumoniae (pneumococcus), which remains the
most common bacterial cause of CAP. Studies of this type have revealed that although
platelets play an important role in host defense against infection, there is also increasing
recognition that hyperactivation of these cells contributes to a pro-inflammatory,
prothrombotic systemic milieu that contributes to the etiology of CVEs. In the case of
the pneumococcus, platelet-driven myocardial damage and dysfunction is exacerbated
by the direct cardiotoxic actions of pneumolysin, a major pore-forming toxin of this
pathogen, which also acts as potent activator of platelets. This review is focused on
the role of platelets in host defense against infection, including pneumococcal infection
in particular, and reviews the current literature describing the potential mechanisms
by which platelet activation contributes to cardiovascular complications in CAP. This
is preceded by an evaluation of the burden of pneumococcal infection in CAP, the
clinical features and putative pathogenic mechanisms of the CVE, and concludes with
an evaluation of the potential utility of the anti-platelet activity of macrolides and various
adjunctive therapies.
