Search

BACKGROUND AND OBJECTIVES Asthma is considered a precaution for use of quadrivalent live attenuated influenza vaccine (LAIV4) in persons aged ≥5 years because of concerns for wheezing events. We evaluated the safety of LAIV4 in children with asthma, comparing the proportion of children with asthma exacerbations after LAIV4 or quadrivalent inactivated influenza vaccine (IIV4). METHODS We enrolled 151 children with asthma, aged 5 to 17 years, during 2 influenza seasons. Participants were randomly assigned 1:1 to receive IIV4 or LAIV4 and monitored for asthma symptoms, exacerbations, changes in peak expiratory flow rate (PEFR), and changes in the asthma control test for 42 days after vaccination. RESULTS We included 142 participants in the per-protocol analysis. Within 42 days postvaccination, 18 of 142 (13%) experienced an asthma exacerbation: 8 of 74 (11%) in the LAIV4 group versus 10 of 68 (15%) in the IIV4 group (LAIV4-IIV4 = −0.0390 [90% confidence interval −0.1453 to 0.0674]), meeting the bounds for noninferiority. When adjusted for asthma severity, LAIV4 remained noninferior to IIV4. There were no significant differences in the frequency of asthma symptoms, change in PEFR, or childhood asthma control test/asthma control test scores in the 14 days postvaccination between LAIV4 and IIV4 recipients. Vaccine reactogenicity was similar between groups, although sore throat (P = .051) and myalgia (P CONCLUSIONS LAIV4 was not associated with increased frequency of asthma exacerbations, an increase in asthma-related symptoms, or a decrease in PEFR compared with IIV4 among children aged 5 to 17 years with asthma.

BACKGROUND: Hospital-associated venous thromboembolism (HA-VTE) is an increasing cause of morbidity in pediatric populations, yet identification of high-risk patients remains challenging. General pediatric models have been derived from case-control studies, but few have been validated. We developed and validated a predictive model for pediatric HA-VTE using a large, retrospective cohort. METHODS: The derivation cohort included 111 352 admissions to Monroe Carell Jr. Children’s Hospital at Vanderbilt. Potential variables were identified a priori, and corresponding data were extracted. Logistic regression was used to estimate the association of potential risk factors with development of HA-VTE. Variable inclusion in the model was based on univariate analysis, availability in routine medical records, and clinician expertise. The model was validated by using a separate cohort with 44 138 admissions. RESULTS: A total of 815 encounters were identified with HA-VTE in the derivation cohort. Variables strongly associated with HA-VTE include history of thrombosis (odds ratio [OR] 8.7; 95% confidence interval [CI] 6.6–11.3; P < .01), presence of a central line (OR 4.9; 95% CI 4.0–5.8; P < .01), and patients with cardiology conditions (OR 4.0; 95% CI 3.3–4.8; P < .01). Eleven variables were included, which yielded excellent discriminatory ability in both the derivation cohort (concordance statistic = 0.908) and the validation cohort (concordance statistic = 0.904). CONCLUSIONS: We created and validated a risk-prediction model that identifies pediatric patients at risk for HA-VTE development. We anticipate early identification of high-risk patients will increase prophylactic interventions and decrease the incidence of pediatric HA-VTE.

BACKGROUND AND OBJECTIVES: Staphylococcus aureus (SA) is the second leading cause of late-onset sepsis among infants in the NICU. Because colonization of nasal mucosa and/or skin frequently precedes invasive infection, decolonization strategies, such as mupirocin application, have been attempted to prevent clinical infection, but data supporting this approach in infants are limited. We conducted a phase 2 multicenter, open-label, randomized trial to assess the safety and efficacy of intranasal plus topical mupirocin in eradicating SA colonization in critically ill infants. METHODS: Between April 2014 and May 2016, infants RESULTS: A total of 155 infants were randomly assigned. Mupirocin was generally well tolerated, but rashes (usually mild and perianal) occurred significantly more often in treated versus untreated infants. Primary decolonization occurred in 62 of 66 (93.9%) treated infants and 3 of 64 (4.7%) control infants (P < .001). Twenty-one of 46 (45.7%) treated infants were persistently decolonized compared with 1 of 48 (2.1%) controls (P < .001). CONCLUSIONS: Application of mupirocin to multiple body sites was safe and efficacious in eradicating SA carriage among infants in the NICU; however, after 2 to 3 weeks, many infants who remained hospitalized became recolonized.

[Figure: see text] BACKGROUND AND OBJECTIVES: Staphylococcus aureus (SA) is the second leading cause of late-onset sepsis among infants in the NICU. Because colonization of nasal mucosa and/or skin frequently precedes invasive infection, decolonization strategies, such as mupirocin application, have been attempted to prevent clinical infection, but data supporting this approach in infants are limited. We conducted a phase 2 multicenter, open-label, randomized trial to assess the safety and efficacy of intranasal plus topical mupirocin in eradicating SA colonization in critically ill infants. METHODS: Between April 2014 and May 2016, infants

OBJECTIVE: To compare the effectiveness of clindamycin, trimethoprim-sulfamethoxazole, and β-lactams for the treatment of pediatric skin and soft-tissue infections (SSTIs). METHODS: A retrospective cohort of children 0 to 17 years of age who were enrolled in Tennessee Medicaid, experienced an incident SSTI between 2004 and 2007, and received treatment with clindamycin (reference), trimethoprim-sulfamethoxazole, or a β-lactam was created. Outcomes included treatment failure and recurrence, defined as an SSTI within 14 days and between 15 and 365 days after the incident SSTI, respectively. Adjusted models stratified according to drainage status were used to estimate the risk of treatment failure and time to recurrence. RESULTS: Among the 6407 children who underwent drainage, there were 568 treatment failures (8.9%) and 994 recurrences (22.8%). The adjusted odds ratios for treatment failure were 1.92 (95% confidence interval [CI]: 1.49–2.47) for trimethoprim-sulfamethoxazole and 2.23 (95% CI: 1.71–2.90) for β-lactams. The adjusted hazard ratios for recurrence were 1.26 (95% CI: 1.06–1.49) for trimethoprim-sulfamethoxazole and 1.42 (95% CI: 1.19–1.69) for β-lactams. Among the 41 094 children without a drainage procedure, there were 2435 treatment failures (5.9%) and 5436 recurrences (18.2%). The adjusted odds ratios for treatment failure were 1.67 (95% CI: 1.44–1.95) for trimethoprim-sulfamethoxazole and 1.22 (95% CI: 1.06–1.41) for β-lactams; the adjusted hazard ratios for recurrence were 1.30 (95% CI: 1.18–1.44) for trimethoprim-sulfamethoxazole and 1.08 (95% CI: 0.99–1.18) for β-lactams. CONCLUSIONS: Compared with clindamycin, use of trimethoprim-sulfamethoxazole or β-lactams was associated with increased risks of treatment failure and recurrence. Associations were stronger for those with a drainage procedure.

OBJECTIVE: The study aimed to assess whether maternal colonization with Staphylococcus aureus during pregnancy or at delivery was associated with infant staphylococcal colonization. METHODS: For this prospective cohort study, women were enrolled at 34 to 37 weeks of gestation between 2007 and 2009. Nasal and vaginal swabs for culture were obtained at enrollment; nasal swabs were obtained from women and their infants at delivery and 2- and 4-month postbirth visits. Logistic regression was used to determine whether maternal colonization affected infant colonization. RESULTS: Overall, 476 and 471 mother-infant dyads had complete data for analysis at enrollment and delivery, respectively. Maternal methicillin-resistant S aureus (MRSA) colonization occurred in 10% to 17% of mothers, with the highest prevalence at enrollment. Infant MRSA colonization peaked at 2 months of age, with 20.9% of infants colonized. Maternal staphylococcal colonization at enrollment increased the odds of infant staphylococcal colonization at birth (odds ratio; 95% confidence interval: 4.8; 2.4–9.5), hospital discharge (2.6; 1.3–5.0), at 2 months of life (2.7; 1.6–4.3), and at 4 months of life (2.0; 1.1–3.5). Similar results were observed for maternal staphylococcal colonization at delivery. Fifty maternal-infant dyads had concurrent MRSA colonization: 76% shared isolates of the same pulsed-field type, and 30% shared USA300 isolates. Only 2 infants developed staphylococcal disease. CONCLUSIONS: S aureus colonization (including MRSA) was extremely common in this cohort of maternal-infant pairs. Infants born to mothers with staphylococcal colonization were more likely to be colonized, and early postnatal acquisition appeared to be the primary mechanism. * Abbreviations: CA-MRSA — : community-associated methicillin-resistant Staphylococcus aureus GBS — : group B Streptococcus GEE — : generalized estimating equation MRSA — : methicillin-resistant Staphylococcus aureus MSSA — : methicillin-susceptible Staphylococcus aureus PCR — : polymerase chain reaction PVL — : Panton-Valentine leukocidin SSTIs — : skin and soft-tissue infections VUMC — : Vanderbilt University Medical Center