TY - JOUR
T1 - Coagulase-negative staphylococci in very-low-birth-weight infants
T2 - inability of genetic markers to distinguish invasive strains from blood culture contaminants.
AU - Bradford, R.
AU - Abdul Manan, R.
AU - Daley, A. J.
AU - Pearce, C.
AU - Ramalingam, A.
AU - D'Mello, D.
AU - Mueller, Y.
AU - Uahwatanasakul, W.
AU - Qu, Y.
AU - Grando, D.
AU - Garland, S.
AU - Deighton, M.
N1 - Funding Information:
Acknowledgement This work was partly supported by a grant from the Faculty of Life Sciences, RMIT University, Bundoora, Victoria, Australia.
PY - 2006/5
Y1 - 2006/5
N2 - Selected coagulase-negative staphylococci from the blood of very-low-birth-weight infants in the Neonatal Intensive Care Unit at the Royal Women's Hospital, Melbourne, collected over a 5-year period were examined. Isolates were classified as invasive or contaminants, speciated, typed by pulsed-field gel electrophoresis, and examined for biofilm genes (icaA, icaC, and icaD), adhesion genes (atlE, fbe), and the number of copies of IS256. Of the 24 isolates studied, there were 13 contaminants and 11 invasive isolates. The collection included 15 Staphylococcus epidermidis, eight Staphylococcus capitis, and one each of Staphylococcus warneri and Staphylococcus haemolyticus. Two small clusters of S. epidermidis that belonged to the same molecular type were identified. All S. capitis isolates belonged to the same molecular type or subtype, suggesting that a particular clone was circulating in the unit. There was no significant difference in the species found, the presence of icaA, icaC, icaD, atlE, or fbe, or the number of copies of IS256 between invasive isolates and contaminants. A series of nasal isolates from nonhospitalized adults differed from hospital isolates in the absence of IS256 and the low prevalence of icaC. There was no evidence of IS256-mediated insertion into ica genes as a mechanism of phase variation. These findings suggest that contaminants and invasive isolates derived from the same pool of hospital strains capable of causing sepsis in compromised hosts and that other mechanisms of phase variation exist, apart from IS256 insertion into ica genes.
AB - Selected coagulase-negative staphylococci from the blood of very-low-birth-weight infants in the Neonatal Intensive Care Unit at the Royal Women's Hospital, Melbourne, collected over a 5-year period were examined. Isolates were classified as invasive or contaminants, speciated, typed by pulsed-field gel electrophoresis, and examined for biofilm genes (icaA, icaC, and icaD), adhesion genes (atlE, fbe), and the number of copies of IS256. Of the 24 isolates studied, there were 13 contaminants and 11 invasive isolates. The collection included 15 Staphylococcus epidermidis, eight Staphylococcus capitis, and one each of Staphylococcus warneri and Staphylococcus haemolyticus. Two small clusters of S. epidermidis that belonged to the same molecular type were identified. All S. capitis isolates belonged to the same molecular type or subtype, suggesting that a particular clone was circulating in the unit. There was no significant difference in the species found, the presence of icaA, icaC, icaD, atlE, or fbe, or the number of copies of IS256 between invasive isolates and contaminants. A series of nasal isolates from nonhospitalized adults differed from hospital isolates in the absence of IS256 and the low prevalence of icaC. There was no evidence of IS256-mediated insertion into ica genes as a mechanism of phase variation. These findings suggest that contaminants and invasive isolates derived from the same pool of hospital strains capable of causing sepsis in compromised hosts and that other mechanisms of phase variation exist, apart from IS256 insertion into ica genes.
UR - http://www.scopus.com/inward/record.url?scp=33746766417&partnerID=8YFLogxK
U2 - 10.1007/s10096-006-0130-2
DO - 10.1007/s10096-006-0130-2
M3 - Article
C2 - 16598472
AN - SCOPUS:33746766417
SN - 0934-9723
VL - 25
SP - 283
EP - 290
JO - European Journal of Clinical Microbiology and Infectious Diseases
JF - European Journal of Clinical Microbiology and Infectious Diseases
IS - 5
ER -