Background: Extensive drug resistance in Klebsiella pneumoniae (K. pneumoniae) causing major outbreaks in large hospitals is an emerging challenge. We describe a near fatal outbreak of colistin resistant, carbapenem resistant K. pneumoniae (CRKp) producing metallo beta-lactamases (bla_NDM) and bla_OXA-48 in the neonatal intensive care unit (NICU) at the background of a larger outbreak involving multiple parts of the hospital and the challenges in its containment. Methods: Following identification of an outbreak due to colistin resistant CRKp between April to June 2017 in the NICU, a thorough surveillance of similar cases and the hospital environment was performed to trace the source. All the isolated K. pneumoniae were tested for susceptibility to standard antibiotics by disc diffusion and microbroth dilution methods. Molecular detection of extended spectrum beta lactamases (ESBLs) and carbapenemases (classes A, B, D) genes was done. Enterobacterial repetitive intergenic consensus (ERIC) PCR and multi-locus sequence typing (MLST) was done to determine the genetic relatedness of the isolates. Characteristics of different sequence types were statistically compared (Student’s t-test). Results: A total of 45 K. pneumoniae isolates were studied from NICU (14 cases of neonatal sepsis), ICU (18 cases), other wards (7 cases) along with 6 isolates from hospital environment and human colonizers. The primary case was identified in the ICU. All the K. pneumoniae from NICU and 94.4% from the ICU were colistin resistant CRKp. Majority (59.37% and 56.25%) harbored bla_SHV/bla_CTXM and bla_OXA-48 genes, respectively. Two distinct sequence types ST5235 and ST5313 were noted with colistin resistance, distribution within the NICU and mortality as significant attributes of ST5235 (p < 0.05). The outbreak was contained with strengthening of the infection control practices and unintended short duration closure of the hospital. Conclusion: Large hospital outbreaks with considerable mortality can be caused by non-dominant clones of colistin resistant CRKp harboring bla_OXA-48 and bla_NDM carbapenemases in endemic regions. The exact global impact of these sequence types should be further studied to prevent future fatal outbreaks.

OBJECTIVES. The purpose of this work was to assess the effect of severe maternal iron-deficiency anemia and nutritional status on cord blood and breast milk iron status. METHODS. We conducted a prospective observational study over a 6-month period in a teaching hospital in central India. The study population consisted of 55 anemic (hemoglobin: <110 g/L) and 20 healthy nonanemic (hemoglobin: ≥110 g/L) pregnant women who delivered singleton live births at term gestation. We measured hemoglobin, iron, and ferritin levels in paired maternal and cord blood and iron levels in early (day 3 ± 1) and late (day 15 ± 3) transitional milk. Maternal anthropometry, including weight, height, midarm circumference, triceps skinfold thickness, and placental weight, were recorded. The main outcome measure of the study was to find out the relationship of maternal hemoglobin, iron, ferritin, and anthropometry with hemoglobin, iron, and ferritin in cord blood and iron levels in breast milk. RESULTS. Concentrations of hemoglobin, iron, and ferritin were significantly lower in the cord blood of anemic mothers and showed linear relationships with maternal hemoglobin and ferritin levels. Breast milk iron content was significantly reduced in severely anemic mothers but not in those with mild-to-moderate anemia. Breast milk iron level correlated with maternal hemoglobin and iron levels but not with ferritin levels. Maternal anthropometry had significant correlations with indices of iron nutriture in maternal and cord blood but showed no relationship with breast milk iron content. Placental weight was comparable between anemic and nonanemic mothers. CONCLUSIONS. Maternal anemia, particularly the severe type, adversely affects cord blood and breast milk iron status. Maternal nutritional status exerts a significant influence on fetal iron status but has little influence on breast milk iron content.

Respiratory distress syndrome of the neonate (neonatal RDS) is still an important problem in treatment of preterm infants. It is accompanied by inflammatory processes with free radical generation and oxidative stress. The aim of study was to determine the role of oxidative stress in the development of neonatal RDS. Markers of oxidative stress and antioxidant activity in umbilical cord blood were studied in infants with neonatal respiratory distress syndrome with reference to healthy newborns. Status of markers of oxidative stress (malondialdehyde, protein carbonyl and 8-hydroxy-2-deoxy guanosine) showed a significant increase with depleted levels of total antioxidant capacity in neonatal RDS when compared to healthy newborns. The study provides convincing evidence of oxidative damage and diminished antioxidant defenses in newborns with RDS. Neonatal RDS is characterized by damage of lipid, protein and DNA, which indicates the augmentation of oxidative stress. The identification of the potential biomarker of oxidative stress consists of a promising strategy to study the pathophysiology of neonatal RDS.