Recurrent multidrug-resistant Salmonella enterica serovar Typhimurium bacteremia in a returned traveller.

This case report describes a 68-year-old male with recurrent multidrug-resistant Salmonella enterica serovar Typhimurium bacteremia acquired during travel abroad. He experienced a recurrence of bacteremia without a clear source and was successfully treated with 10 weeks of intravenous ertapenem. Post hoc genome sequencing revealed an isolate bearing class A, C, and D extended-spectrum ß-lactamases (ESBLs). A review of English- and French-language literature since 2000 revealed eight publications that discussed recurrent S. enterica serovar Typhimurium bacteremia. Patients with multidrug-resistant S. enterica serovar Typhimurium should be monitored frequently for recrudescence, even in the absence of risk factors.

Le présent rapport décrit le cas d'un homme de 68 ans atteint d'une bactériémie à Salmonella enterica sérovar Typhimurium multirésistante contractée lors d'un voyage à l'étranger. Un traitement à l'ertapénem par voie intraveineuse pendant dix semaines a guéri cette récidive de la bactériémie, dont la source n'a pu être décelée. Le séquençage génétique de l'isolat clinique effectué a posteriori a révélé des bêta-lactamases à spectre élargi de classe A, C et D. Grâce à une analyse bibliographique des publications en anglais et en français après 2000, huit publications sur la bactériémie récurrente à S. enterica sérovar Typhimurium ont été recensées. Les patients atteints d'une bactériémie à S. enterica sérovar Typhimurium multirésistante devraient faire l'objet d'une surveillance fréquente pour écarter les recrudescences, même en l'absence de facteurs de risque.

Protease inhibitor use and the incidence of diabetes mellitus in a large cohort of HIV-infected women.

OBJECTIVE: To assess the association between protease inhibitor (PI) use and the incidence of diabetes mellitus (DM) among participants in the Women's Interagency HIV Study. DESIGN: Prospective multicenter cohort study. The diagnosis of DM was based on self-report at semiannual interviews conducted from 1994 to 1998. SETTING: Six inner-city clinical sites in the United States (Brooklyn, NY; Bronx, NY; Washington, DC; Chicago, IL; San Francisco, CA; and Los Angeles, CA). PARTICIPANTS: A total of 1785 nonpregnant women who had no history of prior DM. The women made up four groups: 1) PI users (n = 609, person-years [PY] at risk = 707); 2) reverse transcriptase inhibitor (RTI)-only users (n = 932, PY = 1486); 3) HIV-infected women reporting no antiretroviral therapy (ART) ever (n = 816, PY = 1480); and 4) HIV-uninfected women (n = 350, PY = 905). MAIN OUTCOMES: Incidence of DM and median body mass index (BMI) from 1995 to 1998 were compared among the four groups. RESULTS: Sixty-nine incident cases of DM occurred among 1785 women (1.5 cases per 100 PY; 95% CI: 1.2-1.9). The incidence of DM among PI users was 2.8 cases per 100 PY (2.8%) versus 1.2% among both RTI users and women on no ART (95% CI: 1.6-4.1 [PI]; 0.7-1.8 [RTI and no ART]; P = 0.01 for comparison of the PI group with the RTI group) and 1.4% among HIV-uninfected women (95% CI: 0.7-2.2, P = 0.06 for comparison with PI group). Weight gain was not associated with either PI or RTI use. Multivariate models identified PI use (hazard ratio [HR] = 2.90 [95% CI: 1.50-5.60]; P = 0.002), age (HR = 1.75 per 10 years [95% CI: 1.31-2.34]; P = 0.0002) and BMI as independent risk factors for DM. CONCLUSIONS: PI use was associated with a threefold increase in the risk of reporting incident DM. Routine screening for diabetes, particularly among older and heavier patients using PI therapy, is advisable.

Serum immunoglobulin G response to human papillomavirus type 16 virus-like particles in human immunodeficiency virus (HIV)-positive and risk-matched HIV-negative women.

Baseline serum samples from 2815 human immunodeficiency virus (HIV)-positive and 963 HIV-negative women enrolled in 2 cohort studies were tested for immunoglobulin G antibodies to human papillomavirus type 16 (HPV-16) capsids. HPV-16 seropositivity was associated with lifetime number of sex partners (P<.001) among both HIV-positive and HIV-negative women. Approximately 50%-60% of HPV-16 DNA-positive women were HPV-16 positive. HPV-16 seropositivity was associated with HIV infection; however, after adjustment for baseline cervical HPV infection and disease, the association disappeared. Thus, the high seroprevalence of HPV-16 among HIV-positive women may be explained by a high prevalence of HPV of all types. Approximately 50% of HIV-positive women had serological evidence of prior HPV-16 infection, but only approximately 5% had an HPV-16 cervical infection at baseline. Despite the higher prevalence of HPV infection in this group, most HIV-positive women are able to control HPV-16 replication at the cervix, and reactivation, if it occurs, is not very common.

Prevalence and predictors of Toxoplasma seropositivity in women with and at risk for human immunodeficiency virus infection.

We assessed the prevalence and predictors of latent Toxoplasma infection in a large group of human immunodeficiency virus (HIV)-infected and HIV-uninfected at-risk US women. The prevalence of latent Toxoplasma infection was 15% (380 of 2525 persons) and did not differ by HIV infection status. HIV-infected women aged > or =50 years and those born outside of the United States were more likely to have latent Toxoplasma infection, with prevalences of 32% and 41%, respectively.

The impact of HIV infection and immunodeficiency on human papillomavirus type 6 or 11 infection and on genital warts.

BACKGROUND: HIV infection and associated immunodeficiency are known to alter the course of human papillomavirus (HPV) infections and of associated diseases. GOAL: This study investigated the association between HIV and HPV and genital warts. STUDY DESIGN: HPV testing and physical examinations were performed in two large prospective studies: the Women's Interagency HIV Study (WIHS) and the HIV Epidemiology Research Study (HERS). Statistical methods incorporating dependencies of longitudinal data were used to examine the relationship between HIV and HPV and genital warts. RESULTS: A total of 1008 HIV-seronegative and 2930 HIV-seropositive women were enrolled in the two studies. The prevalence of HPV 6 or 11 was 5.6 times higher in HIV-seropositive women in the WIHS and 3.6 times higher in the HERS. Genital wart prevalence increased by a factor of 3.2 in the WIHS and 2.7 in the HERS in HIV-seropositive women. In the WIHS, infection with HPV type 6 or 11, in comparison with no HPV infection, was associated with odds of genital wart prevalence of 5.1 (95% CI: 2.9-8.8), 8.8 (95% CI: 6.1-12.8), and 12.8 (95% CI: 8.8-18.8) in HIV-seronegative women, HIV-seropositive women with > or =201 CD4 cells/microl, and HIV-seropositive women with < or =200 CD4 cells/microl, respectively. In the HERS, infection with HPV type 6 or 11 was associated with odds of 2.7 (95% CI: 1.6-4.6), 4.9 (95% CI: 3.2-7.7), and 5.3 (95% CI: 3.3-8.5) in these same groups. Other HPV types showed a similar dose-response relation, but of substantially lower magnitude and statistical significance. CONCLUSIONS: HIV infection and immunodeficiency synergistically modified the relation between HPV 6 or 11 infection and genital wart prevalence.