|
| ORIGINAL ARTICLE |
|
| Year : 2017 | Volume
: 63
| Issue : 3 | Page : 162-168 |
Changing trend in bacterial etiology and antibiotic resistance in sepsis of intramural neonates at a tertiary care hospital
MP Roy1, M Bhatt1, V Maurya2, S Arya1, R Gaind2, HK Chellani1
1 Department of Pediatrics, VMMC and Safdarjung Hospital, New Delhi, India
2 Department of Microbiology, VMMC and Safdarjung Hospital, New Delhi, India
Correspondence Address:
R Gaind
Department of Microbiology, VMMC and Safdarjung Hospital, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0022-3859.201425
Background: Septicemia is an important cause of neonatal morbidity and mortality. However, organized data on causative organisms and their resistant pattern are scanty from developing countries. The changing trend in causative organisms and their antibiotic resistance is yet to be documented in India. The present study examines the trends in bacterial profile and antibiotic resistance of the organisms causing sepsis in hospitalized neonates. Materials and Methods: A retrospective laboratory-based analysis of blood cultures obtained from Neonatal Intensive Care Unit of a tertiary care hospital in New Delhi was done for the period of 1999–2014, divided into five phases. Results: A total of 4700 isolates were considered. Over time, Gram-negative organisms have replaced Gram-positives as frequent isolates. Initially, there was predominance of Klebsiella pneumoniae, then of Staphylococcus aureus which recently has been changed with coagulase negative-Staphylococcus and Acinetobacter. Growing resistance against the first and second line of drugs has been noted, including methicillin-resistant S. aureus and vancomycin-resistant Enterococcus. Conclusion: The etiological profile of neonatal sepsis has changed tremendously in the past 15 years. High resistance against common drugs necessitates continued surveillance and review of empirical antibiotic policy for neonatal sepsis. These steps are important to effectively curtail the surge of further antibiotic resistance.
[FULL TEXT] [PDF]*
|
