Development of neonatal sepsis is not dependent on the presence of magA, k2A, rmpA and kfu genes in Klebsiella pneumoniae
Abstract number: P1981
Huik K., Parm Ü., Denks K., Pauskar M., Avi R., Metsvaht T., Ilmoja M., Lutsar I.
Background:K. pneumoniae is one of the leading causes of infections in neonatal intensive care units (NICU). In adults its pathogenicity has been associated with virulence genes like magA, k2A, rmpA and kfu. Their role in neonatal infections is less well known.
Objectives: To determine the population dynamics of K. pneumoniae in two NICUs in Estonia and evaluate the presence of the above mentioned virulence genes among invasive and colonising strains.
Methods: From Aug 2006 to Dec 2007 rectal and nasopharyngeal (NP) surveillance cultures were collected from all neonates admitted with suspected or confirmed early onset sepsis. Blood cultures were obtained as clinically indicated. Isolates were typed using amplified fragment length polymorphism (AFLP) PCR analysis. In parallel, 5 mucosal and 5 invasive isolates in 5 pts with invasive disease were typed using pulse field gel electrophoresis (PFGE). Hypermucoviscosity test was defined as positive string test. The magA (specific to K1 capsule serotype), k2A (specific to K2 capsule serotype), rmpA (regulator of mucoid phenotype) and kfu (an iron uptake system) were detected by PCR using specific primers.
Results: A total of 47/278 pts had mucosal carriage of K. pneumoniae and 6 had BSI including 38 colonised pts in unit A (5 with BSI) and 9 in unit B (1 with BSI). Altogether, 88 rectal, 55 NP, and 5 BSI isolates were analysed. The ALFP analysis identified 6 different clonal groups 2 of which predominated in unit A (type A in 26 pts over 7mo and, type K in 6 pts over 2mo), while in unit B all colonising K. pneumoniae strains were different. 5/6 BSI were caused by type A; the invasive and colonising strains had similar genotype in PFGE analysis. Hypermucoviscosity strains were detected only among mucosal isolates; in 16/30 isolates in pts with and in 0/118 without BSI (P < 0.001). No magA and rmpA genes were detected. The k2A and kfu genes were rare and present in 7/143 and 4/143 mucosal isolates, respectively but only in pts without BSI. A concordance between AFLP type and presence of k2A and kfu genes was identified type B was related to k2A and type P to kfu.
Conclusions: AFLP method is an alternative in evaluating the spread of K. pneumoniae in NICU and allows to identify potential cross-colonisation clusters. Although none of the tested virulence genes was associated with BSI, the testing of colonising strains for hypermucoviscosity appeared to be a simple method identifying patients at risk for BSI.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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