title: Do HIV-seropositive patients become colonised with drug-resistant microorganisms?
abstract: The aim of the present study was to investigate whether HIV-infected patients, a group that is supposedly at risk for infection with antibiotic-resistant microbes, really does so, and to assess possible risk factors for acquiring these organisms. During the period from January 1998 to July 1999, samples of normal flora were obtained from 107 HIV-infected patients attending an outpatient clinic in Oslo, Norway. The samples were cultured for Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, coagulase-negative staphylococci and Candida spp., and the resulting isolates were tested for antimicrobial susceptibility. The patients studied represented all stages of HIV infection, from recently infected to severely immunocompromised. Samples were taken at one, two or three time-points to determine whether antimicrobial resistance in colonising microorganisms increases over time. Antimicrobial resistance was linked primarily to antimicrobial prophylaxis, but it did not increase during the observation period. The level of a patient's immunodeficiency and the consequently intensified medical care was also of some importance. Even though about 50% of the patients were receiving antimicrobial agents at the time of sampling, the level of resistance found in these patients was very similar to that found in other patient groups in Norway; except for Candida albicans isolates, which were less susceptible to fluconazole. Overall, antimicrobial resistance was uncommon in the HIV-seropositive patients studied, a finding that is probably related to the overall low prevalence of antimicrobial resistance in the general population in Norway.
authors.affiliation: Division of Infectious Disease Control, Norwegian Institute of Public Health, PO Box 4404 Nydalen, 0403 Oslo, Norway. truls.leegaard@labmed.uio.no
authors.forename: T M
authors.initials: TM
authors.lastname: Leegaard
authors.forename: D A
authors.initials: DA
authors.lastname: Caugant
authors.forename: L O
authors.initials: LO
authors.lastname: Frøholm
authors.forename: E A
authors.initials: EA
authors.lastname: Høiby
authors.forename: E J
authors.initials: EJ
authors.lastname: Rønning
authors.forename: P
authors.initials: P
authors.lastname: Sandven
authors.forename: J N
authors.initials: JN
authors.lastname: Bruun
mesh_terms: D000328:Adult; D000900:Anti-Bacterial Agents; D000890:Anti-Infective Agents / Q000494:pharmacology; D000935:Antifungal Agents / Q000494:pharmacology; D002175:Candida / Q000187:drug effects / Q000302:isolation & purification; D024881:Drug Resistance, Bacterial; D025141:Drug Resistance, Fungal; D004926:Escherichia coli / Q000187:drug effects / Q000302:isolation & purification; D005260:Female; D006678:HIV; D015658:HIV Infections / Q000150:complications* / Q000382:microbiology*; D006193:Haemophilus influenzae / Q000187:drug effects / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008826:Microbial Sensitivity Tests; D012307:Risk Factors; D013210:Staphylococcus / Q000187:drug effects / Q000302:isolation & purification; D013296:Streptococcus pneumoniae / Q000187:drug effects / Q000302:isolation & purification; D013997:Time Factors
chemical_list: D000900:Anti-Bacterial Agents; D000890:Anti-Infective Agents; D000935:Antifungal Agents