Intermittent and sustained low-level HIV viral rebound in patients receiving potent antiretroviral therapy.
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Biomedical subjects
Publications and source records attributed to Patrick Francioli.
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OBJECTIVE: HIV-1 post-exposure prophylaxis (PEP) is frequently prescribed after exposure to source persons with an undetermined HIV serostatus. To reduce unnecessary use of PEP, we implemented a policy including active contacting of source persons and the availability of free, anonymous HIV testing ('PEP policy'). METHODS: All consultations for potential non-occupational HIV exposures i.e. outside the medical environment) were prospectively recorded. The impact of the PEP policy on PEP prescription and costs was analysed and modelled. RESULTS: Among 146 putative exposures, 47 involved a source person already known to be HIV positive and 23 had no indication for PEP. The remaining 76 exposures involved a source person of unknown HIV serostatus. Of 33 (43.4%) exposures for which the source person could be contacted and tested, PEP was avoided in 24 (72.7%), initiated and discontinued in seven (21.2%), and prescribed and completed in two (6.1%). In contrast, of 43 (56.6%) exposures for which the source person could not be tested, PEP was prescribed in 35 (81.4%), P < 0.001. Upon modelling, the PEP policy allowed a 31% reduction of cost for management of exposures to source persons of unknown HIV serostatus. The policy was cost-saving for HIV prevalence of up to 70% in the source population. The availability of all the source persons for testing would have reduced cost by 64%. CONCLUSION: In the management of non-occupational HIV exposures, active contacting and free, anonymous testing of source persons proved feasible. This policy resulted in a decrease in prescription of PEP, proved to be cost-saving, and presumably helped to avoid unnecessary toxicity and psychological stress.
OBJECTIVE: To assess the epidemiology of methicillin-resistant Staphylococcus aureus (MRSA) in Switzerland. MATERIAL AND METHODS: One-year national survey of all MRSA cases detected in a large sample of Swiss healthcare institutions (HCI). Analysis of epidemiological and molecular typing data (PFGE) of MRSA strains. RESULTS: During 1997, 385 cases of MRSA were recorded in the 5 university hospitals, in 33 acute care community hospitals, and 14 rehabilitation or long-term care institutions. Half of the cases were found at the University of Geneva Hospitals where MRSA was already known to be endemic (41.1 cases/10,000 admissions). The remaining cases (200) were distributed throughout Switzerland. The highest rates (>100 cases/10,000 admissions) were reported from non-acute care institutions. Rates ranged from 3.3 to 41.1 cases/10,000 admissions for university hospitals (mean 15.5); 0.67 to 90.4 for community hospitals (mean 4.8), and 28.2 to 315 for non-acute care institutions reporting MRSA (mean 85.7). Forty percent of MRSA patients were infected, while 60% were only colonised. The leading infection sites were skin and soft tissue (21%), surgical site (15%), and the urinary tract (26%). Whereas in Eastern Swiss HCI most MRSA cases occurred in acute care hospitals (n = 47, 98%), rehabilitation and long-term care institutions accounted for an important number of the identified cases (n = 107, 38%) in Western Switzerland. CONCLUSION: Low rates of MRSA were still observed in Swiss HCI, despite one outlying acute care centre with endemic MRSA and some nonacute care institutions with epidemic MRSA. Rehabilitation and long-term care institutions contributed to a substantial proportion of cases in Western Switzerland and may constitute a significant reservoir. Overall, a national approach to surveillance and control of MRSA is mandatory in order to preserve a still favourable situation, and to decrease the risk of epidemic MRSA dissemination.
BACKGROUND: Although studies have reported large reductions in the risks of AIDS and death since the introduction of potent anti-retroviral therapies, few have evaluated whether this has been similar for all AIDS-defining diseases. We wished to evaluate changes over time in the risk of specific AIDS-defining diseases, as first events, using data from individuals with known dates of HIV seroconversion. METHODS: Using a competing risks proportional hazards model on pooled data from 20 cohorts (CASCADE), we evaluated time from HIV seroconversion to each first AIDS-defining disease (16 groups) and to death without AIDS for four calendar periods, adjusting for exposure category, age, sex, acute infection, and stratifying by cohort. We compared results to those obtained from a cause-specific hazards model. RESULTS: Of 6,941, 2,021 (29%) developed AIDS and 437 (6%) died without AIDS. The risk of AIDS or death remained constant to 1996 then reduced; relative hazard = 0.89 (95% CI: 0.77-1.03); 0.90 (95% CI: 0.81-1.01); and 0.32 (95% CI: 0.28-0.37) for 1979-1990, 1991-1993, and 1997-2001, respectively, compared to 1994-1996. Significant risk reductions in 1997-2001 were observed in all but two AIDS-defining groups and death without AIDS in a competing risks model (with similar results from a cause-specific model). There was significant heterogeneity in the risk reduction across events; from 96% for cryptosporidiosis, to 17% for death without AIDS (P < 0.0001). CONCLUSION: These findings suggest that studies reporting a stable trend for particular AIDS diseases over the period 1979-2001 may not have accounted for the competing risks among other events or lack the power to detect smaller trends.
Broncho-alveolar lavage specimens from patients with Pneumocystis carinii pneumonia were investigated by PCR-single strand conformation polymorphism (SSCP) analysis of four genomic regions for P. carinii f. sp. hominis. In all, 32% of specimens produced two bands (one allele) for each of the four genomic regions, suggesting an infection with a single P.c. hominis type. The other specimens displayed more than two bands for at least one of the four genomic regions, suggesting several theoretical possibilities: co-infections, heterozygosity of diploid or polyploid organisms, or multicopy genes. Quantification of the different alleles and analysis of mixtures of specimens showed that different alleles of a genomic region were most often present in different proportions in a given specimen. In contrast, experiments with plasmid insertion of two alleles resulted in the detection of identical proportions of the two alleles. This suggests that neither heterozygosity of diploid organisms nor multicopy genes are responsible for the presence of two alleles. Unequal proportions are most likely explained by the occurrence of co-infections. The putative co-infecting types could be identified in the majority of specimens.
OBJECTIVE: To assess the molecular epidemiology and risk factors for Pseudomonas aeruginosa colonization and infection in hospitalized patients. METHODS: In a 1000-bed university hospital, newly admitted patients were assessed prospectively for colonization and infection with P. aeruginosa. Anal swabs were obtained upon admission and at discharge. Ribotyping was used for the typing of isolates. Epidemiologic and clinical data were recorded prospectively. Independent risk factors were assessed using multivariate analysis. RESULTS: The recovery rate of patients with P. aeruginosa from anal specimens on admission was 6.7% (42/628). Infection due to P. aeruginosa was observed in 20 of 628 (3.2%) patients, of whom 10 (1.6%) were already infected on admission. Independent risk factors for colonization/infection on admission were age, indwelling urinary catheter, the presence of wound and seropositivity for HIV. Independent risk factors for nosocomial infection were anal colonization on admission, alcoholism, indwelling urinary catheter and antibiotic treatment during hospitalization. Ribotyping revealed that 27 patients were colonized or infected with a unique ribotype, whereas 24 shared one or more ribotypes with other patients. Analysis of epidemiologic and molecular typing data revealed that transmission from patients to patients or from patients to environment was documented on only three occasions. CONCLUSIONS: A great many P. aeruginosa strains were isolated from patients and the environment, and most environmental strains were different from those recovered in patients, suggesting a low rate of hospital acquisition of P. aeruginosa from the environment. The main risk factors for hospital-acquired infection were detectable colonization on admission, antibiotic treatment and urinary catheter.
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