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INTRODUCTION: Late-onset disease with Group B Streptococcus (GBS LOD) remains a significant problem in neonates. Unlike early-onset disease, rates of GBS LOD have not changed with prenatal testing. Effects of GBS LOD can be severe and thus identifying risk factors for severe GBS LOD, such as hypervirulence genes, may help in managing these infants. CASE PRESENTATION: We present a case of a neonate with capsular serotype III GBS sepsis without meningitis that recurred 6 days after a 10-day-treatment period with IV ampicillin. The second episode was characterized by sepsis, neuroinvasion, meningitis and subsequent profound encephalomalacia. The short duration between the two episodes suggested recrudescence rather than reinfection. The GBS isolate was ultimately found to be positive for hypervirulence gene hvgA+, which encodes for a protein known to mediate meningeal tropism and neuroinvasion. CONCLUSION: hvgA positivity may thus potentially serve as an important biomarker for severe and neuroinvasive GBS LOD that can influence treatment decisions.
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OBJECTIVE Central-line-associated bloodstream infections (CLABSI) are an important cause of morbidity and mortality in neonates. We aimed to determine whether intra-abdominal pathologies are an independent risk factor for CLABSI. METHODS We performed a retrospective matched case-control study of infants admitted to the neonatal intensive care units (NICUs) of the Montreal Children's Hospital (Montreal) and the Royal Alexandra Hospital, Edmonton, Canada. CLABSI cases that occurred between April 2009 and March 2014 were identified through local infection control databases. For each case, up to 3 controls were matched (National Healthcare Safety Network [NHSN] birth weight category, chronological age, and central venous catheter (CVC) dwell time at the time of CLABSI onset). Data were analyzed using conditional logistic regression. RESULTS We identified 120 cases and 293 controls. According to a matched univariate analysis, the following variables were significant risk factors for CLABSI: active intra-abdominal pathology (odds ratio [OR], 3.4; 95% confidence interval [CI], 1.8-6.4), abdominal surgery in the prior 7 days (OR, 3.5; 95% CI, 1.0-10.9); male sex (OR, 1.7; 95% CI, 1.1-2.6) and ≥3 heel punctures (OR, 4.0; 95% CI, 1.9-8.3). According to a multivariate matched analysis, intra-abdominal pathology (OR, 5.9; 95% CI, 2.5-14.1), and ≥3 heel punctures (OR, 5.4; 95% CI, 2.4-12.2) remained independent risk factors for CLABSI. CONCLUSION The presence of an active intra-abdominal pathology increased the risk of CLABSI by almost 6-fold. Similar to CLABSI in oncology patients, a subgroup of CLABSI with mucosal barrier injury should be considered for infants in the NICU with active intra-abdominal pathology. Infect Control Hosp Epidemiol 2016;1446-1452.
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Infecções Relacionadas a Cateter/epidemiologia , Cateterismo Venoso Central/efeitos adversos , Cateteres Venosos Centrais/efeitos adversos , Infecção Hospitalar/epidemiologia , Infecção Hospitalar/etiologia , Gastroenteropatias/epidemiologia , Estudos de Casos e Controles , Infecções Relacionadas a Cateter/microbiologia , Cateteres Venosos Centrais/microbiologia , Bases de Dados Factuais , Feminino , Gastroenteropatias/terapia , Hospitais Pediátricos , Humanos , Lactente , Recém-Nascido , Unidades de Terapia Intensiva Neonatal , Modelos Logísticos , Masculino , Quebeque , Fatores de RiscoRESUMO
Early neonatal central cyanosis that is unrelated to cardiopulmonary causes, alerts clinicians to possibility of methaemoglobinaemia. Congenital methaemoglobinaemia due to haemoglobin M is an autosomal dominant disorder characterised by lifelong cyanosis. We report a case presentation and review of diagnostic pitfalls of a newborn who presented with central cyanosis; investigations revealed a low methaemoglobin reductase (2.2 IU/g Hb), with normal maternal levels (9.1 IU/g Hb). Therefore, haemoglobinopathy investigations were completed on the mother and her baby, which showed an α-globin variant in both. The maternal α2 globin gene sequencing showed heterozygosity for haemoglobin M Boston (α58 His â Tyr).