scholarly journals The Burden of Pneumococcal Community-Acquired Pneumonia and Invasive Pneumococcal Disease in Hospitalized Adults: A Canadian Immunization Research Network (CIRN) Serious Outcomes Surveillance (SOS) Network Study

2016 ◽  
Vol 3 (suppl_1) ◽  
Author(s):  
Jason Leblanc ◽  
May Elsherif ◽  
Donna Mackinnon-Cameron ◽  
Lingyun Ye ◽  
Ardith Ambrose ◽  
...  
Keyword(s):  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Community Acquired Pneumonia ◽  
Research Network

scholarly journals Pneumococcal pneumonia and invasive pneumococcal disease: immunopathogenesis and diagnosis

Pneumologia ◽  
2019 ◽  
Vol 68 (1) ◽  
pp. 8-14
Author(s):  
Gina Amanda ◽  
Dianiati Kusumo Sutoyo ◽  
Erlina Burhan
Keyword(s):  
Immune System ◽  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Pneumococcal Pneumonia ◽  
Bacterial Load ◽  
Adaptive Immune System ◽  
Signs And Symptoms ◽  
Community Acquired Pneumonia ◽  
High Bacterial Load ◽  
Droplet Nuclei

Abstract Streptococcus pneumoniae is the most common aetiology of community-acquired pneumonia (CAP). It has many virulence factors, the most important being a polysaccharide capsule (Cps). There are 97 different serotypes of pneumococcal based on Cps which include both colonization and invasive serotypes. Pneumococcal pneumonia may exist as a result of either aspiration of bacteria in the nasopharynx or inhalation of droplet nuclei which contains bacteria until they reach the lower respiratory tract. This condition will activate both innate and adaptive immune system. The diagnosis of pneumococcal pneumonia is established in a patient who has the signs and symptoms of pneumonia, accompanied by the detection of S. pneumoniae in microbiology examination. Pneumococcus may also penetrate into a normally sterile site such as bloodstream, meninges, and pleural cavity, and infection of pneumococcus in those sites are defined as an invasive pneumococcal disease (IPD). High bacterial load, dysfunction of the immune system, and co-colonization of another microorganism may also lead to IPD.

scholarly journals Identification of a Candidate Streptococcus pneumoniae Core Genome and Regions of Diversity Correlated with Invasive Pneumococcal Disease

2006 ◽  
Vol 74 (8) ◽  
pp. 4766-4777 ◽  
Author(s):  
Caroline Obert ◽  
Jack Sublett ◽  
Deepak Kaushal ◽  
Ernesto Hinojosa ◽  
Theresa Barton ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Core Genome ◽  
Genomic Analysis ◽  
Community Acquired Pneumonia ◽  
Comparative Genomic ◽  
Virulence Determinants ◽  
Wild Type

ABSTRACT Streptococcus pneumoniae is a leading cause of community-acquired pneumonia and gram-positive sepsis. While multiple virulence determinants have been identified, the combination of features that determines the propensity of an isolate to cause invasive pneumococcal disease (IPD) remains unknown. In this study, we determined the genetic composition of 42 invasive and 30 noninvasive clinical isolates of serotypes 6A, 6B, and 14 by comparative genomic hybridization. Comparison of the present/absent gene matrix (i.e., comparative genomic analysis [CGA]) identified a candidate core genome consisting of 1,553 genes (73% of the TIGR4 genome), 154 genes whose presence correlated with the ability to cause IPD, and 176 genes whose presence correlated with the noninvasive phenotype. Genes identified by CGA were cross-referenced with the published signature-tagged mutagenesis studies, which served to identify core and IPD-correlated genes required for in vivo passage. Among these, two pathogenicity islands, region of diversity 8a (RD8a), which encodes a neuraminidase and V-type sodium synthase, and RD10, which encodes PsrP, a protein homologous to the platelet adhesin GspB in Streptococcus gordonii, were identified. Mice infected with a PsrP mutant were delayed in the development of bacteremia and demonstrated reduced mortality versus wild-type-infected controls. Finally, the presence of seven RDs was determined to correlate with the noninvasive phenotype, a finding that suggests some RDs may contribute to asymptomatic colonization. In conclusion, RDs are unequally distributed between invasive and noninvasive isolates, RD8a and RD10 are correlated with the propensity of an isolate to cause IPD, and PsrP is required for full virulence in mice.

scholarly journals Major Adverse Cardiovascular Events During Invasive Pneumococcal Disease Are Serotype Dependent

2020 ◽  
Author(s):  
Hector F Africano ◽  
Cristian C Serrano-Mayorga ◽  
Paula C Ramirez-Valbuena ◽  
Ingrid G Bustos ◽  
Alirio Bastidas ◽  
...  
Keyword(s):  
Invasive Pneumococcal Disease ◽  
Pneumococcal Disease ◽  
Bacterial Pathogen ◽  
Retrospective Chart Review ◽  
Clinical Information ◽  
Major Adverse Cardiovascular Event ◽  
Community Acquired Pneumonia ◽  
Major Adverse Cardiovascular Events ◽  
Adverse Cardiovascular Event ◽  
Reactive Protein

Abstract Background Up to 30% of patients admitted to hospitals with invasive pneumococcal disease (IPD) experience major adverse cardiovascular event (MACE) including new/worsening heart failure, new/worsening arrhythmia, and/or myocardial infarction. Streptococcus pneumoniae (Spn) is the most frequently isolated bacterial pathogen among community-acquired pneumonia (CAP) patients and the only etiological agent linked independently to MACE. Nevertheless, no clinical data exist identifying which serotypes of Spn are principally responsible for MACE. Methods This was an observational multicenter retrospective study conducted through the Public Health Secretary of Bogotá, Colombia. We included patients with a confirmed clinical diagnosis of IPD with record of pneumococcal serotyping and clinical information between 2012 and 2019. Spn were serotyped using the quellung method by the National Center of Microbiology. MACE were determined by a retrospective chart review. Results The prevalence of MACE was 23% (71/310) in IPD patients and 28% (53/181) in patients admitted for CAP. The most prevalent S. pneumoniae serotype identified in our study was the 19A, responsible for the 13% (42/310) of IPD in our cohort, of which 21% (9/42) presented MACE. Serotypes independently associated with MACE in IPD patients were serotype 3 (odds ratio [OR] 1, 48; 95% confidence interval [CI] [1.21–2.27]; P = .013) and serotype 9n (OR 1.29; 95% CI [1.08–2.24]; P = .020). Bacteremia occurred in 87% of patients with MACE. Moreover, serum concentrations of C-reactive protein were elevated in patients with MACE versus in non-MACE patients (mean [standard deviation], 138 [145] vs 73 [106], P = .01). Conclusions MACE are common during IPD with serotype 3 and 9n independently of frequency.

Long-term Impact of Pneumococcal Conjugate Vaccines on Invasive Disease and Pneumonia Hospitalizations in Indigenous and Non-Indigenous Australians

2019 ◽  
Vol 70 (12) ◽  
pp. 2607-2615
Author(s):  
Kelley N Meder ◽  
Sanjay Jayasinghe ◽  
Frank Beard ◽  
Aditi Dey ◽  
Martyn Kirk ◽  
...  
Keyword(s):  
Indigenous People ◽  
Conjugate Vaccine ◽  
Invasive Pneumococcal Disease ◽  
Pneumococcal Conjugate Vaccine ◽  
Pneumococcal Disease ◽  
Laboratory Data ◽  
Community Acquired Pneumonia ◽  
Indirect Impact ◽  
Long Term Impact

Abstract Background Universal pneumococcal conjugate vaccine (PCV) programs began in Indigenous Australian children in 2001 and all children in 2005, changing to 13-valent PCV (PCV13) in 2011. We used laboratory data for invasive pneumococcal disease (IPD) and coded hospitalizations for noninvasive pneumococcal community-acquired pneumonia (PnCAP) to evaluate long-term impact. Methods Annual incidence (per 100 000 population) was calculated for age-specific total IPD, PCV13 non–7-valent PCV (PCV7) serotypes, and PnCAP by Indigenous status. Incidence in the pre–universal PCV7 (2002–2004), early PCV7 (2005–2007), pre-PCV13 (2008 to mid-2011), and post-PCV13 (mid-2011 to 2016) periods was used to calculate incidence rate ratios (IRRs). Results In the total population, all-age incidence of IPD declined from 11.8 pre-PCV7 to 7.1 post-PCV13 (IRR, 0.61 [95% confidence interval {CI}, .59–.63]) but for PnCAP declined among ages <1 year (IRR, 0.34 [95% CI, .25–.45]) and 1–4 years (IRR, 0.50 [95% CI, .43–.57]) but increased significantly among age ≥5 years (IRRs, 1.08–1.14). In Indigenous people, baseline PCV13 non-PCV7 IPD incidence was 3-fold higher, amplified by a serotype 1 epidemic in 2011. By 2015–2016, although incidence of IPD and PnCAP in children aged <5 years decreased by 38%, neither decreased in people aged ≥5 years. Conclusions Fifteen years post-PCV and 5 years post-PCV13, direct and indirect impact on IPD and PnCAP differed by age and between Indigenous and non-Indigenous people, with potential implications for long-term PCV impact in comparable settings. Fifteen years after pneumococcal conjugate vaccine (PCV) introduction and 5 years post-PCV13, direct and indirect impact on invasive pneumococcal disease and pneumococcal community-acquired pneumonia differed by age and between Indigenous and non-Indigenous people, with potential implications for long-term PCV impact in comparable settings.

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