Article

Influenza-associated pediatric mortality in the United States: Increase of Staphylococcus aureus coinfection

Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.
PEDIATRICS (Impact Factor: 5.3). 11/2008; 122(4):805-11. DOI: 10.1542/peds.2008-1336
Source: PubMed

ABSTRACT Pediatric influenza-associated death became a nationally notifiable condition in the United States during 2004. We describe influenza-associated pediatric mortality from 2004 to 2007, including an increase of Staphylococcus aureus coinfections.
Influenza-associated pediatric death is defined as a death of a child who is younger than 18 years and has laboratory-confirmed influenza. State and local health departments report to the Centers for Disease Control and Prevention demographic, clinical, and laboratory data on influenza-associated pediatric deaths.
During the 2004-2007 influenza seasons, 166 influenza-associated pediatric deaths were reported (n = 47, 46, and 73, respectively). Median age of the children was 5 years. Children often progressed rapidly to death; 45% died within 72 hours of onset, including 43% who died at home or in an emergency department. Of 90 children who were recommended for influenza vaccination, only 5 (6%) were fully vaccinated. Reports of bacterial coinfection increased substantially from 2004-2005 to 2006-2007 (6%, 15%, and 34%, respectively). S aureus was isolated from a sterile site or endotracheal tube culture in 1 case in 2004-2005, 3 cases in 2005-2006, and 22 cases in 2006-2007; 64% were methicillin-resistant S aureus. Children with S aureus coinfection were significantly older and more likely to have pneumonia and acute respiratory distress syndrome than those who were not coinfected.
Influenza-associated pediatric mortality is rare, but the proportion of S aureus coinfection identified increased fivefold over the past 3 seasons. Research is needed to identify risk factors for influenza coinfection with invasive bacteria and to determine the impact of influenza vaccination and antiviral agents in preventing pediatric mortality.

1 Follower
 · 
112 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Ninety staphylococci carrying the mecA gene, including 17 strains of methicillin-resistant Staphylococcus aureus (MRSA), were isolated from environmental settings within New York State. Waterborne staphylococci harboring mecA were isolated from multiple sources: the Hudson River near a combined sewage overflow; urban streams; freshwater and marine beaches; a swimming pool; swimming pool decks; combined sewage; as well as wastewater treatment plant (WWTP) primary sewage influent, mixed liquor, aeration water, and final (unchlorinated) effluent. Environmental MRSA strains were isolated from beach water (n=3); swimming pool deck water (n=1); Hudson River water (n=2); combined sewage (n=3); as well as wastewater treatment plant mixed liquor (n=4), aeration water (n=2) and final effluent (n=2). MRSA strains were isolated from 3/75 (4%) of surface water samples collected from beaches near bathers. Characterization of MRSA isolates by pheno- and genotypic methods included antibiotic resistance testing, polymerase chain reaction amplification of portions of two genes encoding Panton-Valentine leukocidin, partial amplification and sequencing of variable regions within genes encoding staphylococcal protein A (spa) and hypothetical gene SACOL0058, and Pulsed-Field Gel Electrophoresis. The majority of environmental MRSA isolates resembled hospital-acquired MRSA strains in terms of genetic profiles. One MRSA isolate from swimming pool deck water, and another from WWTP aeration water, were indistinguishable from epidemic CA-MRSA (spa type t008; pulsotype USA300). Four Staphylococcus fleurettii isolates from surface water samples carried novel mecA variants, although mecI sequences were identical to that of pre-MRSA strain N315 (GenBank: BA000018.30). This is the first report of MRSA in swimming pool deck water, in river water at a combined sewer overflow discharge point, in surface water at freshwater beaches, and in WWTP final effluent, as well as the first extensive characterization of antibiotic resistance profiles among waterborne mecA-positive staphylococci. Study findings demonstrated that human exposure to MRSA may occur in more non-clinical settings than were previously known. This is also the first description of novel mecA variants in S. fleurettii, and the first report of cultivable S. fleurettii in surface water, indicating that the reported livestock colonizer is a potential reservoir of novel antibiotic resistance genomes that may be shared with S. aureus.
    03/2010, Degree: PhD, Supervisor: Ellen Braun-Howland
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Influenza is a common respiratory virus and Staphylococcus aureus frequently causes secondary pneumonia during influenza infection, leading to increased morbidity and mortality. Influenza has been found to attenuate subsequent Type 17 immunity, enhancing susceptibility to secondary bacterial infections. IL-27 is known to inhibit Type 17 immunity, suggesting a potential critical role for IL-27 in viral and bacterial co-infection.MethodsA murine model of influenza and Staphylococcus aureus infection was used to mimic human viral, bacterial co-infection. C57BL/6 wild-type, IL-27 receptor ¿ knock-out, and IL-10 knock-out mice were infected with Influenza H1N1 (A/PR/8/34) or vehicle for 6 days followed by challenge with Staphylococcus aureus or vehicle for 24 hours. Lung inflammation, bacterial burden, gene expression, and cytokine production were determined.ResultsIL-27 receptor ¿ knock-out mice challenged with influenza A had increased morbidity compared to controls, but no change in viral burden. IL-27 receptor ¿ knock-out mice infected with influenza displayed significantly decreased IL-10 production compared to wild-type. IL-27 receptor ¿ knock-out mice co-infected with influenza and S. aureus had improved bacterial clearance compared to wild-type controls. Importantly, there were significantly increased Type 17 responses and decreased IL-10 production in IL-27 receptor ¿ knock-out mice. Dual infected IL-10¿/¿ mice had significantly less bacterial burden compared to dual infected WT mice.Conclusions These data reveal that IL-27 regulates enhanced susceptibility to S. aureus pneumonia following influenza infection, potentially through the induction of IL-10 and suppression of IL-17.
    Respiratory Research 02/2015; 16(1):10. DOI:10.1186/s12931-015-0168-8 · 3.13 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Post influenza pneumonia is a leading cause of mortality and morbidity, with mortality rates approaching 60% when bacterial infections are secondary to multi-drug resistant (MDR) pathogens. Staphylococcus aureus, in particular community acquired MRSA (cMRSA), has emerged as a leading cause of post influenza pneumonia. Linezolid (LZD) prevents acute lung injury in murine model of post influenza bacterial pneumonia. Mice were infected with HINI strain of influenza and then challenged with cMRSA at day 7, treated with antibiotics (LZD or Vanco) or vehicle 6 hours post bacterial challenge and lungs and bronchoalveolar lavage fluid (BAL) harvested at 24 hours for bacterial clearance, inflammatory cell influx, cytokine/chemokine analysis and assessment of lung injury. Mice treated with LZD or Vanco had lower bacterial burden in the lung and no systemic dissemination, as compared to the control (no antibiotic) group at 24 hours post bacterial challenge. As compared to animals receiving Vanco, LZD group had significantly lower numbers of neutrophils in the BAL (9×103 vs. 2.3×104, p < 0.01), which was associated with reduced levels of chemotactic chemokines and inflammatory cytokines KC, MIP-2, IFN-γ, TNF-α and IL-1β in the BAL. Interestingly, LZD treatment also protected mice from lung injury, as assessed by albumin concentration in the BAL post treatment with H1N1 and cMRSA when compared to vanco treatment. Moreover, treatment with LZD was associated with significantly lower levels of PVL toxin in lungs. Linezolid has unique immunomodulatory effects on host inflammatory response and lung injury in a murine model of post-viral cMRSA pneumonia.
    PLoS ONE 10(1):e0114574. DOI:10.1371/journal.pone.0114574 · 3.53 Impact Factor

Full-text

Download
6 Downloads
Available from
Oct 13, 2014