Robert G. Deiss

We evaluated differences in pretravel care, exposures, and illnesses among pediatric and adult travelers, using a prospective, observational cohort. Eighty-one pediatric travelers were matched 1:1 with adult military dependents by travel region, destination’s malaria risk, and travel duration. Pediatric travelers were more likely to have coverage for hepatitis A and B (90% versus 67% of adults; 85% versus 44%), visit friends and relatives (36% versus 16%), report mosquito bites (69% versus 44%), and have close contact with wild or domesticated animals (40% versus 20%) than adults (P < 0.05). Subjects < 10 years of age were less likely to be prescribed antibiotics (28% versus 95%; RR = 0.63; 95% CI: 0.46–0.85) and antidiarrheals (9% versus 100%; RR = 0.10; 95% CI: 0.03–0.29) for travelers’ diarrhea (TD) self-treatment than adults. Travel medicine providers should emphasize strategies for vector avoidance, prevention of animal bites and scratches, and TD self-treatment in pediatric pretravel consultations.

Varicella-zoster virus (VZV) reactivation is common but difficult to predict in HIV-infected persons. Since qualitative VZV antibodies can determine past VZV disease or vaccination, we evaluated whether quantitative VZV antibody levels over time can predict future zoster. US Military HIV Natural History (NHS) participants with a zoster diagnosis at least 5 years after HIV diagnosis (n = 100) were included. Zoster-negative controls (n = 200) were matched by age, race, gender, and CD4 count at HIV diagnosis. Repository plasma specimens collected at baseline and prior to zoster diagnosis were evaluated using a quantitative anti-VZV ELISA assay. Differences in quantitative VZV levels were analyzed by Wilcoxon Mann–Whitney and Fisher’s exact tests. Median CD4 count at HIV diagnosis was similar for cases and controls (535 [IQR 384–666] vs. 523 [IQR 377–690] cells/μL; p = 0.940), but lower for cases at zoster diagnosis (436 [IQR 277–631] vs. 527 [IQR 367–744] cells/μL; p = 0.007). Antiretroviral therapy (ART) use prior to zoster diagnosis was lower for cases (52.0%) compared to controls (64.5%; p = 0.025). Cases had similar mean VZV antibody levels prior to zoster diagnosis compared to controls [2.25 ± 0.85 vs. 2.44 ± 0.96 index value/optical density (OD) ratio; p = 0.151] with no difference in the change in antibody levels over time (0.08 ± 0.71 vs. 0.01 ± 0.94 index value/OD per year; p = 0.276). Quantitative VZV antibody levels are stable in HIV-infected persons and do not predict zoster reactivation. Low CD4 count and lack of ART use appear to be better predictors of future zoster diagnosis.

Background The effects of at‐risk drinking on HIV infection remain controversial. We investigated the impact of self‐reported alcohol consumption on surrogate markers of HIV progression among individuals initiated on highly active antiretroviral therapy (HAART). Methods We analyzed individuals who were surveyed on alcohol use within a year of HAART initiation between 2006 and 2014. At‐risk drinking was defined as consumption of at least 3 or 4 drinks/d, or 7 and 14 drinks/wk among women and men, respectively. We performed time‐updated generalized estimating equation logistic regression to determine the effect of at‐risk drinking on virologic failure (VF) and mixed‐effects linear regression on CD4 count reconstitution, controlling for potential confounders. Results Of 801 individuals initiated on HAART, 752 individuals with alcohol survey data were included in the analysis. Of these, 45% (n = 336) met criteria for at‐risk drinking at HAART initiation on at least 1 survey. The rates of VF were 4.30 per 100 person‐years (95% CI [2.86, 6.21]) for at‐risk drinkers and 2.45 per 100 person‐years (95% CI [1.57, 3.65]) for individuals without at‐risk drinking. At‐risk drinking was not significantly associated with VF (OR 1.73, 95% CI [0.92, 3.25]) (p = 0.087) or CD4 reconstitution (CD4 increase 11.4; 95% CI [−19.8, 42.7]) in univariate analyses; however, in our multivariate model, a statistically significant relationship between VF and at‐risk drinking was observed (OR 2.28, 95% CI [ 1.01, 5.15]). Conclusions We found a high proportion of at‐risk drinking in our military cohort, which was predictive of VF in multivariate analysis. Given alcohol's effect on myriad HIV and non‐HIV outcomes, interventions to decrease the prevalence of at‐risk drinking among HIV‐infected individuals are warranted.