Single cell bottlenecks in the pathogenesis of Streptococcus pneumoniae. TLR2 signaling decreases transmission of Streptococcus pneumoniae by limiting bacterial shedding in an infant mouse Influenza A co-infection model. Influenza promotes pneumococcal growth during coinfection by providing host sialylated substrates as a nutrient source. Influenza A induces the major secreted airway mucin MUC5AC in a protease-EGFR-extracellular regulated kinase-Sp1-dependent pathway. This study demonstrates the role of influenza virus in pneumococcal transmission in an infant mouse model.īarbier, D.
Influenza A virus facilitates Streptococcus pneumoniae and disease. Influenza enhances susceptibility to natural acquisition of and disease due to Streptococcus pneumoniae in ferrets. pneumoniae to incidence of colds and serum antibody. Spread of Streptococcus pneumoniae in families.
Climate induces seasonality in pneumococcal transmission. How contagious are common respiratory tract infections? N. Decline in invasive pneumococcal disease after the introduction of protein-polysaccharide conjugate vaccine. Streptococcus pneumoniae colonisation: the key to pneumococcal disease. Prevalence and antibiotic resistance of commensal Streptococcus pneumoniae in nine European countries. The prevalence and risk factors for pneumococcal colonization of the nasopharynx among children in Kilifi District, Kenya. Here, we review the mechanistic insights provided by these studies on the multiple and varied interactions of the pneumococcus and its host.Ībdullahi, O. Furthermore, widespread vaccination and the resulting immune pressure have shed light on pneumococcal population dynamics and pathogenesis. The different stages of pneumococcal carriage and disease have been investigated in detail in animal models and, more recently, in experimental human infection. pneumoniae to evade or take advantage of the host inflammatory and immune responses. Transmission, colonization and invasion depend on the remarkable ability of S. On the other hand, they can cause severe disease when bacterial and host factors allow them to invade essentially sterile sites, such as the middle ear spaces, lungs, bloodstream and meninges. On the one hand, the pneumococci are highly adapted commensals, and their main reservoir on the mucosal surface of the upper airways of carriers enables transmission. Streptococcus pneumoniae has a complex relationship with its obligate human host.
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