Prior antimicrobials and staphylococcal bacteremia in HIV-infected patients

Styrt, Barbara; Chaisson, Richard E.; Moore, Richard D.

doi:10.1097/00002030-199710000-00007

Cited by 7 publications

(3 citation statements)

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“…We do not have information on the use of prophylaxis for Pneumocystis jirovecii and atypical mycobacterial disease or the treatment of tuberculosis. Antimicrobials with activity against P. jirovecii and mycobacteria have antibacterial activity and have been shown to reduce rates of invasive bacterial disease [33–35]. Use of such drugs would lead to an underestimation of IRs in individuals with low CD4 cell counts.…”

Section: Discussionmentioning

confidence: 99%

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*

et al. 2011

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all Danish HIV-infected individuals (n 5 4871) and population controls (n 5 92 116) matched on age and sex were enrolled in a cohort and all cases of SAB were registered. IRs and risk factors were estimated using time-updated Poisson regression analysis. ResultsWe identified 329 cases of SAB in 284 individuals, of whom 132 individuals were infected with HIV and 152 were not [crude IR ratio (IRR) 24.2; 95% confidence interval (CI) 19.5-30.0, for HIV-infected vs. non-HIV-infected individuals]. Over time, IR declined for HIV-infected individuals (IRR 0.40). Injecting drug users (IDUs) had the highest incidence and the smallest decline in IR, while men who have sex with men (MSM) had the largest decline over time. Among HIV-infected individuals, a latest CD4 count o100 cells/mL was the strongest independent predictor of SAB (IRR 10.2). Additionally, HIV transmission group was associated with risk of SAB. MSM were more likely to have hospital-acquired SAB, a low CD4 cell count and AIDS at the time of HIV acquisition compared with IDUs. ConclusionsWe found that the incidence of SAB among HIV-infected individuals declined during the study period, but remained higher than that among HIV-uninfected individuals. There was an unevenly distributed burden of SAB among HIV transmission groups (IDU4MSM). Low CD4 cell count and IDU were strong predictors of SAB among HIV-infected individuals.

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Section: Discussionmentioning

confidence: 99%

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*

et al. 2011

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“…The human CYP3A subfamily plays a dominant role in the metabolic elimination of many protease inhibitors; amprenavir (Decker et al, 1998), saquinavir (Eagling et al, 2002), nefinavir (Lillibridge et al, 1998), ritonavir (Kumar et al, 1996), and indinavir (Chiba et al, 1997), as well as reverse transcriptase inhibitors nevirapine (Erickson et al, 1999) and delavirdine (Voorman et al, 1998). Since Staphylococcus aureus is the most common microorganism causing cutaneous and systemic infections in human immunodeficiency virus-infected patients, it is possible for clindamycin to be coadministered as part of a polytherapy regimen (Styrt et al, 1997;Manfredi et al, 2002). In this light, understanding P450 enzyme interactions might allow physicians the ability to better anticipate and manage each patient's response to adding clindamycin to an established drug regimen.…”

Section: Cyp1a2mentioning

confidence: 99%

In Vitro Metabolism of Clindamycin in Human Liver and Intestinal Microsomes

Wynalda¹,

Hutzler²,

Koets³

et al. 2003

Drug Metab Dispos

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This article is available online at http://dmd.aspetjournals.org ABSTRACT:Incubations with human liver and gut microsomes revealed that the antibiotic, clindamycin, is primarily oxidized to form clindamycin sulfoxide. In this report, evidence is presented that the Soxidation of clindamycin is primarily mediated by CYP3A. This conclusion is based upon several lines of in vitro evidence, including the following. 1) Incubations with clindamycin in hepatic microsomes from a panel of human donors showed that clindamycin sulfoxide formation correlated with CYP3A-catalyzed testosterone 6␤-hydroxylase activity; 2) coincubation with ketaconazole, a CYP3A4-specific inhibitor, markedly inhibited clindamycin S-oxidase activity; and 3) when clindamycin was incubated across a battery of recombinant heterologously expressed human cytochrome P450 (P450) enzymes, CYP3A4 possessed the highest clindamycin S-oxidase activity. A potential role for flavin-containing monooxygenases (FMOs) in clindamycin S-oxidation in human liver was also evaluated. Formation of clindamycin sulfoxide in human liver microsomes was unaffected either by heat pretreatment or by chemical inhibition (e.g., methimazole). Furthermore, incubations with recombinant FMO isoforms revealed no detectable activity toward the formation of clindamycin sulfoxide. Beyond identifying the drug-metabolizing enzyme responsible for clindamycin S-oxidation, the ability of clindamycin to inhibit six human P450 enzymes was also evaluated. Of the P450 enzymes examined, only the activity of CYP3A4 was inhibited (ϳ26%) by coincubation with clindamycin (100 M). Thus, it is concluded that CYP3A4 appears to account for the largest proportion of the observed P450 catalytic clindamycin S-oxidase activity in vitro, and this activity may be extrapolated to the in vivo condition.Clindamycin (methyl 7-chloro-6,7,8-trideoxy-6-[(2S,4R)-1-methyl-4-propylpyrrolidine-2-carboxamido]-1-thio-1-threo-D-galacto-octopyranoside monohydrochloride) is an antibiotic of the "lincosamide" class (Brodasky et al., 1968). The lincosamide antibiotics seem to be most useful against the bacteria classified as Gram-positive cocci. In addition, clindamycin is helpful against protozoans such as Toxoplasma and Mycoplasma as well as many anaerobic bacteria (Luft and Remington, 1988;Dannemann et al., 1991;Mazur et al., 1999).In humans, absorption of clindamycin is rapid and virtually complete (90%) following oral administration (DeHaan et al., 1972;Metzler et al., 1973). Concentrations of clindamycin in the serum increase linearly with increased dose, and levels exceed the minimum inhibitory concentration for most indicated organisms for at least 6 h following administration of the recommended dose. Clindamycin is widely distributed throughout the body and has an average biological half-life of 2.4 h. The major bioactive metabolites excreted in urine and feces are clindamycin sulfoxide and N-desmethylclindamycin (Seaberg et al., 1984;Flaherty et al., 1988;Gatti et al., 1998).To date, there are no published reports tha...

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“…Recently documented increases in community-associated methicillinresistant S. aureus (MRSA) infection suggest that there is already a reservoir of methicillin-resistant strains [1][2][3]. The use of antimicrobials as both prophylactic and therapeutic agents for opportunistic infections in HIV-infected individuals and for cutaneous infections in injection drug users may increase the likelihood of nasal carriage of antimicrobial-resistant S. aureus [4] and suggests that these groups may be "hidden" contributors to a community-based reservoir.…”

mentioning

confidence: 99%

Incidence and Persistence of Staphylococcus aureus Nasal Colonization in a Community Sample of HIV-Infected and -Uninfected Drug Users

Miller¹,

Cespedes²,

Bhat³

et al. 2007

Clinical Infectious Diseases

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Although little is known about the correlates of Staphylococcus aureus colonization, even less is known about the predictors of incident S. aureus colonization in the community. Recently documented increases in community-associated methicillinresistant S. aureus (MRSA) infection suggest that there is already a reservoir of methicillin-resistant strains [1][2][3]. The use of antimicrobials as both prophylactic and therapeutic agents for opportunistic infections in HIV-infected individuals and for cutaneous infections in injection drug users may increase the likelihood of nasal carriage of antimicrobial-resistant S. aureus [4] and suggests that these groups may be "hidden" contributors to a community-based reservoir.We prospectively observed a subsample of participants from a large, well-characterized, community-based sample of current

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Prior antimicrobials and staphylococcal bacteremia in HIV-infected patients

Abstract: Rifabutin may be associated with diminished risk of S. aureus bacteremia incidental to use for other purposes in HIV infection. Further study is needed to assess effects on microbial resistance.

Cited by 7 publications

References 29 publications

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*

In Vitro Metabolism of Clindamycin in Human Liver and Intestinal Microsomes

Incidence and Persistence of Staphylococcus aureus Nasal Colonization in a Community Sample of HIV-Infected and -Uninfected Drug Users

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Prior antimicrobials and staphylococcal bacteremia in HIV-infected patients

Abstract: Rifabutin may be associated with diminished risk of S. aureus bacteremia incidental to use for other purposes in HIV infection. Further study is needed to assess effects on microbial resistance.

Cited by 7 publications

References 29 publications

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study*

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study*

In Vitro Metabolism of Clindamycin in Human Liver and Intestinal Microsomes

Incidence and Persistence of Staphylococcus aureus Nasal Colonization in a Community Sample of HIV-Infected and -Uninfected Drug Users

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Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*

Major but differential decline in the incidence of Staphylococcus aureus bacteraemia in HIV‐infected individuals from 1995 to 2007: a nationwide cohort study^*