Infection withBurkholderia cepaciaComplex Genomovars in Patients with Cystic Fibrosis: Virulent Transmissible Strains of Genomovar III Can ReplaceBurkholderia multivorans

Abstract

Infection with Burkholderia cepacia complex in patients with cystic fibrosis (CF) results in highly variable clinical outcomes. The purpose of this study was to determine if there are genomovar-specific disparities in transmission and disease severity. B. cepacia complex was recovered from 62 patients with CF on > or =1 occasions (genomovar III, 46 patients; genomovar II [B. multivorans], 19 patients; genomovar IV [B. stabilis], 1 patient; genomovar V [B. vietnamiensis], 1 patient; and an unclassified B. cepacia complex strain, 1 patient). Patient-to-patient spread was observed with B. cepacia genomovar III, but not with B. multivorans. Genomovar III strains replaced B. multivorans in 6 patients. Genomovar III strains were also associated with a poor clinical course and high mortality. Infection control practices should be designed with knowledge about B. cepacia complex genomovar status; patients infected with transmissible genomovar III strains should not be cohorted with patients infected with B. multivorans and other B. cepacia genomovars.

Widespread clone of Burkholderia cenocepacia in cystic fibrosis patients in the Czech Republic

“…In this study, we performed random amplified polymorphic DNA (RAPD) analysis (Mahenthiralingam et al, 1996) and macrorestriction typing followed by PFGE (Mahenthiralingam et al, 2001) to investigate genetic relatedness between Czech clinical isolates and to compare them with major epidemic strains from other CF centres. In addition, the isolates were also screened for the presence of genetic markers of strain transmissibility, i.e.…”

Transmissible Burkholderia cepacia genomovar IIIa strains bind and convert monomeric iron(III) protoporphyrin IX into the μ-oxo oligomeric form

“…These findings are important since they show that genomovar IIIa strains would be able to generate the m-oxo oligomer from any free iron(III) protoporphyrin IX monomers both in the healthy lung (at neutral pH) and under the slightly lower pH conditions which may prevail during chronic lung inflammation. These observations may explain why epidemic genomovar IIIa strains are frequently found able to superinfect lungs already colonized by other species, including Pseudomonas aeruginosa and other B. cepacia genomovars (Hart & Winstanley, 2002;Mahenthiralingam et al, 2001) where, in the presence of chronic inflammation, the pH is likely to be lower than neutral (Bodem et al, 1983).…”

“…A survey of a previously well-characterized panel of strains belonging to the Burkholderia cepacia complex (Mahenthiralingam et al, 2000(Mahenthiralingam et al, , 2001 has revealed the possession of a putative 97 kDa haem-binding protein (HBP) by epidemic strains of genomovar IIIa (Smalley et al, 2001). Such isolates have been described as highly transmissible among cystic fibrosis (CF) patients (Mahenthiralingam et al, 2001) and can cause the socalled 'cepacia syndrome', a necrotizing pneumonia leading to a fatal clinical deterioration.…”

“…Such isolates have been described as highly transmissible among cystic fibrosis (CF) patients (Mahenthiralingam et al, 2001) and can cause the socalled 'cepacia syndrome', a necrotizing pneumonia leading to a fatal clinical deterioration. The exact role of the 97 kDa HBP in pathogenesis during lung infection with epidemic genomovar IIIa strains is not yet clear.…”

Burkholderia cenocepacia J2315-mediated destruction of Staphylococcus aureus NRS77 biofilms.

“…The ET12 epidemic lineage encodes a cable pilus that can assist in binding to both mucins [84] and host tissue [85], and isolates have been shown to dominate and replace infections originally caused by B. multivorans [86].…”