2010
DOI: 10.1002/ppul.21263
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Pseudomonas aeruginosain children with cystic fibrosis diagnosed through newborn screening: Assessment of clinic exposures and microbial genotypes

Abstract: Background-Chronic pulmonary infection with Pseudomonas aeruginosa (PA) is responsible for significant morbidity and mortality in cystic fibrosis (CF). Because of the limited studies evaluating early exposure and the progression of genetic variability of PA, our goal was to assess PA in young children with CF followed in two clinic types.

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Cited by 15 publications
(12 citation statements)
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“…We did not evaluate the effects of cohorting practices on risk of Pa acquisition, as this has previously been evaluated [37,38]. There is no evidence that the risk of patient-to-patient transmission is less among those with residual CFTR function, so we would not recommend that patients with residual CFTR function be managed differently from an infection control standpoint or that clinics should be segregated by CFTR function.…”
Section: Discussionmentioning
confidence: 99%
“…We did not evaluate the effects of cohorting practices on risk of Pa acquisition, as this has previously been evaluated [37,38]. There is no evidence that the risk of patient-to-patient transmission is less among those with residual CFTR function, so we would not recommend that patients with residual CFTR function be managed differently from an infection control standpoint or that clinics should be segregated by CFTR function.…”
Section: Discussionmentioning
confidence: 99%
“…New P. aeruginosa strains can appear after eradication therapies. [3] With chronicity of infection and prolonged administration of drugs, P. aeruginosa strains become resistant against antibiotics, diversifies its colony morphology, acquires mucoidity and shows multiple genotypes. [4] There are six different colony morphotypes of P. aeruginosa , type 5 (mucoid Type) was found to be the most common morphotype in chronic patients.…”
Section: Introductionmentioning
confidence: 99%
“…Regardless of the initial cause, hyperinflammation in the CF lung occurs early and continues throughout life (5). This inflammatory state is further amplified by bacterial infections, in particular, Pseudomonas aeruginosa (6,7). The presence of bacteria promotes the airway epithelium to release proinflammatory cytokines such as the potent neutrophil chemoattractant IL-8 (8).…”
mentioning
confidence: 99%