Host-microbe interplay in persistent Staphylococcus aureus nasal carriage in HIV patients.
It has been shown that persistent Staphylococcus aureus nasal carriage results in increased bacterial dispersal and a higher risk of infection compared to non-or-intermittent S. aureus carriage. Although many studies investigated S. aureus nasal carriage in HIV patients, none compared persistent carriage to non-persistent carriage nor were studies performed in the HAART era. We investigated the host-microbe interplay of persistent S. aureus nasal carriage in HIV-infected patients by studying host determinants of persistent carriage as well as the genetic structure of S. aureus strains isolated. We compared this genetic structure with the previously determined population structure of S. aureus isolates obtained from healthy individuals. Between February 2004 and June 2005 all HIV patients visiting the outpatient department of Erasmus MC (Rotterdam, The Netherlands) were asked to participate in this study. Participants were interviewed and screened for persistent S. aureus carriage using two semi-quantitative nasal swab cultures. For 443 patients two cultures were available, 131 (29.6%) were persistent carriers, which is significantly higher as compared to healthy individuals from the same geographic region (17.6%; P<0.0001). Male sex (odds ratio [OR], 2.22; 95% confidence interval [CI], 1.32-3.73), current smoking (OR, 0.58; 95% CI, 0.38-0.90), Pneumocystis jiroveci pneumonia (PCP) prophylaxis (OR, 0.39; 95% CI, 0.16-0.97) and antiretroviral therapy (OR, 0.61; 95% CI, 0.38-0.98) were independent determinants of persistent carriage. Only two strains were mecA positive (1.2%) and no PVL positive strains were detected. The population structure of S. aureus strains isolated from HIV patients appeared to be strongly overlapping with that of S. aureus isolates from healthy individuals.
Melles
Damian C
DC
Department of Medical Microbiology and Infectious Diseases, room L-313, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands. d.melles@erasmusmc.nl
Pauw
Erna
E
van den Boogaard
Linda
L
Boelens
Hélène A M
HA
Peters
Jenny
J
Peeters
Justine K
JK
Witsenboer
Hanneke
H
van Leeuwen
Willem B
WB
Verbrugh
Henri A
HA
van Belkum
Alex
A
Nouwen
Jan L
JL
D000328:Adult; D000368:Aged; D000553:Ambulatory Care; D054458:Amplified Fragment Length Polymorphism Analysis; D019380:Anti-HIV Agents / Q000627:therapeutic use; D001426:Bacterial Proteins / Q000235:genetics; D001427:Bacterial Toxins / Q000235:genetics; D002353:Carrier State / Q000453:epidemiology / Q000382:microbiology*; D018890:Chemoprevention; D016000:Cluster Analysis; D004269:DNA, Bacterial / Q000235:genetics; D005098:Exotoxins / Q000235:genetics; D005260:Female; D015658:HIV Infections / Q000150:complications*; D006801:Humans; D007956:Leukocidins / Q000235:genetics; D008297:Male; D008875:Middle Aged; D009426:Netherlands; D009666:Nose / Q000382:microbiology*; D046915:Penicillin-Binding Proteins; D011020:Pneumonia, Pneumocystis / Q000517:prevention & control; D012307:Risk Factors; D012737:Sex Factors; D012907:Smoking; D013203:Staphylococcal Infections / Q000453:epidemiology / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000145:classification / Q000235:genetics / Q000302:isolation & purification*
D019380:Anti-HIV Agents; D001426:Bacterial Proteins; D001427:Bacterial Toxins; D004269:DNA, Bacterial; D005098:Exotoxins; D007956:Leukocidins; C078284:Panton-Valentine leukocidin; D046915:Penicillin-Binding Proteins; C487789:mecA protein, Staphylococcus aureus