Expulsion of group a hemolytic streptococci in droplets and droplet nuclei by sneezing, coughing and talking

Hamburger, Morton; Robertson, O. H.

doi:10.1016/s0002-9343(48)90392-1

Cited by 54 publications

(54 citation statements)

References 13 publications

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“…One possible explanation for this observation is that covS mutant strains are attenuated in the ability to disseminate throughout the population. As the main portal of GAS transmission is the upper respiratory tract (17,26) and as dissemination commonly occurs through dispersal of aerosolized saliva (17,18), covS mutant strains may be attenuated in the ability to colonize, proliferate, and/or persist in the upper respiratory tract. Using growth and persistence in human saliva as a surrogate for growth and persistence in the upper respi-FIG.…”

Section: Comparison Of Gene Expression Of Wild-type and Covr And Covsmentioning

confidence: 99%

CovS Simultaneously Activates and Inhibits the CovR-Mediated Repression of Distinct Subsets of Group A Streptococcus Virulence Factor-Encoding Genes

et al. 2009

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To colonize and cause disease at distinct anatomical sites, bacterial pathogens must tailor gene expression in a microenvironment-specific manner. The molecular mechanisms that control the ability of the human bacterial pathogen group A Streptococcus (GAS) to transition between infection sites have yet to be fully elucidated. A key regulator of GAS virulence gene expression is the CovR-CovS two-component regulatory system (also known as CsrR-CsrS). covR and covS mutant strains arise spontaneously during invasive infections and, in in vivo models of infection, rapidly become dominant. Here, we compared wild-type GAS with covR, covS, and covRS isogenic mutant strains to investigate the heterogeneity in the types of natural mutations that occur in covR and covS and the phenotypic consequences of covR or covS mutation. We found that the response regulator CovR retains some regulatory function in the absence of CovS and that CovS modulates CovR to significantly enhance repression of one group of genes (e.g., the speA, hasA, and ska genes) while it reduces repression of a second group of genes (e.g., the speB, grab, and spd3 genes). We also found that different in vivo-induced covR mutations can lead to strikingly different transcriptomes. While covS mutant strains show increased virulence in several invasive models of infection, we determined that these mutants are significantly outcompeted by wild-type GAS during growth in human saliva, an ex vivo model of upper respiratory tract infection. We propose that CovS-mediated regulation of CovR activity plays an important role in the ability of GAS to cycle between pharyngeal and invasive infections.

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Section: Comparison Of Gene Expression Of Wild-type and Covr And Covsmentioning

confidence: 99%

CovS Simultaneously Activates and Inhibits the CovR-Mediated Repression of Distinct Subsets of Group A Streptococcus Virulence Factor-Encoding Genes

et al. 2009

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“…The main portal of GAS transmission is the upper respiratory tract (Hamburger & Robertson, 1948;Shelburne et al, 2005a), and dissemination commonly occurs through dispersal of aerosolized saliva (Hamburger & Robertson, 1948;Katzenell et al, 2001). To investigate the contribution of the 4.5S RNA to the ability of GAS to cause upper respiratory tract infections we used growth and persistence in human saliva as a surrogate for growth and persistence in the upper respiratory tract, as previously described (Shelburne et al, 2005b;Trevino et al, 2009).…”

Section: Contribution Of the 45s Rna To Gas Growth And Persistence Imentioning

confidence: 99%

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

2010

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The signal recognition particle (SRP) is a ribonucleoprotein complex that targets proteins for secretion in a co-translational manner. While originally thought to be essential in all bacteria, recent data show that the SRP is dispensable in at least some streptococcal species. The SRP from the human pathogen group A Streptococcus (GAS, Streptococcus pyogenes) is predicted to be composed of protein Ffh and 4.5S RNA. Deletion of ffh alters the secretion of several GAS proteins, and leads to a severe reduction in virulence. Here, we report that mutation of the gene encoding 4.5S RNA results in phenotypes both similar to and distinct from that observed following ffh mutation. Similarities include a reduction in secretion of the haemolysin streptolysin O, and attenuation of virulence as assessed by a murine soft tissue infection model. Differences include a reduction in transcript levels for the genes encoding streptolysin O and NADglycohydrolase, and the reduced secretion of the SpeB protease. Several differences in transcript abundance between the parental and mutant strain were shown to be dependent on the sensorkinase-encoding gene covS. Using growth in human saliva as an ex vivo model of upper respiratory tract infection we identified that 4.5S RNA mutation leads to a 10-fold reduction in colony-forming units over time, consistent with the 4.5S RNA contributing to GAS growth and persistence during upper respiratory tract infections. Finally, we determined that the 4.5S RNA was essential for GAS to cause lethal infections in a murine bacteraemia model of infection. The data presented extend our knowledge of the contribution of the SRP to the virulence of an important Gram-positive pathogen.

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“…Saliva is ubiquitous in the human oropharynx and is an essential part of both the acquired and innate immune defense systems (25,39). Landmark experiments conducted more than 60 years ago demonstrated the important role played by saliva in the establishment of GAS infection and the subsequent transmission of infectious organisms (18)(19)(20). These studies revealed that large numbers of live GAS were present in the saliva of individuals with GAS pharyngitis (19).…”

mentioning

confidence: 99%

“…These studies revealed that large numbers of live GAS were present in the saliva of individuals with GAS pharyngitis (19). Moreover, it was established that a major route for dissemination of GAS from infected individuals into the environment was via dispersal of aerosolized saliva (20). Other investigators have reported that pharyngitis patients with detectable levels of GAS in their saliva were more likely to transmit the organism than were individuals whose saliva did not contain GAS (26,58).…”

mentioning

confidence: 99%

Growth Characteristics of and Virulence Factor Production by Group A Streptococcus during Cultivation in Human Saliva

et al. 2005

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Group A Streptococcus (GAS) commonly infects the human oropharynx, but the initial molecular events governing this process are poorly understood. Saliva is a major component of the innate and acquired immune defense in this anatomic site. Although landmark studies were done more than 60 years ago, investigation of GAS-saliva interaction has not been addressed extensively in recent years. Serotype M1 GAS strain MGAS5005 cultured in human saliva grew to ϳ10 7 CFU/ml and, remarkably, maintained this density for up to 28 days. Strains of several other M-protein serotypes had similar initial growth patterns but did not maintain as high a CFU count during prolonged culture. As revealed by analysis of the growth of isogenic mutant strains, the ability of GAS to maintain high numbers of CFU/ml during the prolonged stationary phase in saliva was dependent on production of streptococcal inhibitor of complement (Sic) and streptococcal pyrogenic exotoxin B (SpeB). During cultivation in human saliva, GAS had growth-phase-dependent production of multiple proven and putative extracellular virulence factors, including Sic, SpeB, streptococcal pyrogenic exotoxin A, Mac protein, and streptococcal phospholipase A 2 . Our results clearly show that GAS responds in a complex fashion to growth in human saliva, suggesting that the molecular processes that enhance colonization and survival in the upper respiratory tract of humans are well under way before the organism reaches the epithelial cell surface.One hallmark of a successful microorganism is the ability to adapt to new host environments. Group A Streptococcus (GAS) causes a wide variety of diseases in humans, ranging from impetiginous skin lesions to invasive diseases, such as necrotizing fasciitis and meningitis. GAS is particularly suited to inhabit the human oropharynx, colonizing as many as onehalf of school-age children in nonepidemic periods and causing an estimated 15 million cases of pharyngitis in the United States each year (3,43). Moreover, the presence of GAS in the oropharynx generally is required for the subsequent development of rheumatic fever, the leading cause of preventable heart disease in children (10, 28).The oropharynx is the major site of entry for GAS into the human body and its main portal of transmission (19,43,46). Saliva is ubiquitous in the human oropharynx and is an essential part of both the acquired and innate immune defense systems (25,39). Landmark experiments conducted more than 60 years ago demonstrated the important role played by saliva in the establishment of GAS infection and the subsequent transmission of infectious organisms (18)(19)(20). These studies revealed that large numbers of live GAS were present in the saliva of individuals with GAS pharyngitis (19). Moreover, it was established that a major route for dissemination of GAS from infected individuals into the environment was via dispersal of aerosolized saliva (20). Other investigators have reported that pharyngitis patients with detectable levels of GAS in their saliva were more l...

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Expulsion of group a hemolytic streptococci in droplets and droplet nuclei by sneezing, coughing and talking

Cited by 54 publications

References 13 publications

CovS Simultaneously Activates and Inhibits the CovR-Mediated Repression of Distinct Subsets of Group A Streptococcus Virulence Factor-Encoding Genes

CovS Simultaneously Activates and Inhibits the CovR-Mediated Repression of Distinct Subsets of Group A Streptococcus Virulence Factor-Encoding Genes

The 4.5S RNA component of the signal recognition particle is required for group A Streptococcus virulence

Growth Characteristics of and Virulence Factor Production by Group A Streptococcus during Cultivation in Human Saliva

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