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CASE REPORT  
Year : 2016  |  Volume : 59  |  Issue : 4  |  Page : 548-550
Vancomycin-resistant enterococci in neonatal stool as a cause of septicemia: Challenges for infection control practices


1 Department of Microbiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India
2 Department of Pediatrics, Institute of Medical Sciences, Banaras Hindu University, Varanasi, Uttar Pradesh, India

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Date of Web Publication10-Oct-2016
 

   Abstract 

The increasing reports of vancomycin-resistant enterococci (VRE) as a cause of neonatal septicemia are of recent interest. However, in majority of the cases, the source of VRE could not be located. As a consequence, the real importance of VRE and its control measures is undermined. Herein, we report a case of neonatal septicemia due to VRE (Enterococcus faecalis) of vanA genotype with VRE carriage in stool of the neonates as a possible source of sepsis. The report put forwards some lacunae in the infection control practices that are presently followed in the country.

Keywords: Infection control, neonatal Intensive Care Unit, septicemia, vancomycin-resistant enterococci

How to cite this article:
Kaushal S, Banerjee T, Anupurba S, Kumar A. Vancomycin-resistant enterococci in neonatal stool as a cause of septicemia: Challenges for infection control practices. Indian J Pathol Microbiol 2016;59:548-50

How to cite this URL:
Kaushal S, Banerjee T, Anupurba S, Kumar A. Vancomycin-resistant enterococci in neonatal stool as a cause of septicemia: Challenges for infection control practices. Indian J Pathol Microbiol [serial online] 2016 [cited 2019 Feb 23];59:548-50. Available from: http://www.ijpmonline.org/text.asp?2016/59/4/548/191802



   Introduction Top


The emergence of multidrug-resistant enterococci, especially vancomycin-resistant enterococci (VRE), and its spread has facilitated the occurrence of several hospital outbreaks worldwide. The prevalence in Asian countries is not so high, probably due to recent emergence of this resistance in this continent and only a handful of studies to document. [1] In India, the prevalence of VRE has been reported as' 8%, 5.5% and 23% in New Delhi, Chandigarh, and Mumbai, respectively, all of vanB phenotype. [2] We report a case of neonatal septicemia caused by VRE of vanA genotype, the likely source of infection being the neonate's colonized gut.


   Case Report Top


A less than 1-day-old male, preterm, very low birth weight neonate was admitted to the Neonatal Intensive Care Unit (NICU) with body weight of 1065 g, an Apgar score of 2/10, and features of sepsis. The neonate was delivered from a multigravida mother by lower segment cesarean section with bad obstetric history and history of per vaginal leakage with cord prolapse and oligohydramnios. She had received treatment with ceftriaxone (500 mg intravenous (IV) twice daily) for 5 days. The neonate had received bag and tube ventilation for 2 min following birth using 100% oxygen and had been on bubble continuous positive airway pressure since the 1 st day of life. He has also received phototherapy. His blood was sent for culture but failed to grow any organism initially. He was put on empirical therapy with amikacin (15 mg IV once daily) and piperacillin-tazobactam (50 mg IV twice daily) followed by vancomycin (10 mg IV twice daily) but without any improvement. His initial blood cultures did not show the presence of any organism. On the 10 th day, his blood culture grew Enterococcus faecalis identified by extensive biochemical tests. [3] The isolate was sensitive to linezolid and resistant to ampicillin, high-strength gentamicin, and grew on vancomycin screen agar, with vancomycin minimum inhibitory concentration >256 μg/ml detected both by broth microdilution and E-test method [Figure 1]. The isolate harbored vanA gene as detected by polymerase chain reaction (PCR) [Figure 2]. [4] A preliminary report was immediately dispatched, and surveillance cultures were done to trace the source of VRE. Samples were collected from different surfaces of the neonate such as heel pad, umbilical cord/stump, wrist, oral and nasal mucosa, webs of the fingers, intravenous and urinary catheter, oxygen mask tube, feeding tube, and also from the close environment such as bed and beddings, common door handle of the NICU, wash basin and hand wash, personal belongings such as stethoscope and mobile phones of attending doctors and nurses, and hands of all associated health-care workers. Stool samples both of the neonate and mother were collected and processed. Interestingly, VRE was isolated from unenriched stool of the neonate with comparable susceptibility pattern and genotype profile as that of the blood isolate. Typing the isolates by enterobacterial repetitive intergenic consensus PCR [5] showed that both the isolates from blood and stool were clonally related. The neonate was treated with linezolid (12 mg IV twice daily) and showed improvement and weight gain with an Apgar score of 8/10 on discharge after 19 days of hospital stay.
Figure 1: Vancomycin-resistant Enterococcus faecalis isolated from blood of the neonate

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Figure 2: Polymerase chain reaction amplification of vanA gene in Enterococcus faecalis isolated from blood and stool of the neonate

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   Discussion Top


The case report is important in this perspective that we were able to trace the likely source of infection in the septicemic neonate. Most of the recent case reports from India have not been able to trace the source of VRE or detect the genotype. [6],[7] Consequently, the importance of VRE surveillance in stool, especially in ICU and NICU, as an integral part of infection control monitoring has been undermined.

The predominance of vanA gene in East Asian region has already been documented in studies from Japan, Korea, and China. [8] The high rate of transmission of vanA gene to other isolates itself is a potential threat in the hospital environment. We have also reported high vanA genotype VRE carriage rate in stool in association with antibiotic usage in the adult ICU of our tertiary care hospital. [9] However, isolation of VRE in neonate stool with septicemia deserves a special mention due to additional challenges put forward in the management and care of this vulnerable group of patients.

Due to excessive usage of antibiotics other than glycopeptides in nosocomial settings, hospital staff and patients who have survived with prolonged hospital stay like in our case serve as potent VRE reservoirs. Unlike ours, in developed countries, where surveillance culturing systems are taken seriously, patients who are colonized with VRE are routinely identified and the choice of which empiric antibiotic to administer for a presumed nosocomial infection is usually decided by the colonization status of the patients. [10] In patients known to be colonized with VRE, broad-spectrum agents that lack a significant activity against anaerobes would be preferred, on the assumption that potent anaerobic activity would not be required for treating the infection. If the patient is not colonized with VRE, administration of a potent antienterococcal broad-spectrum agent such as piperacillin-tazobactam may be preferred. In this manner, both the establishment of new colonization and the level of colonization of those already colonized could be minimized. [10] Due to lack of any such guideline for the management of VRE-colonized patients in India, we were not able to intervene with the colonization status of the neonate.

Most infections and colonizations with VRE are due to patient's endogenous flora that can spread directly from the patient or indirectly through contaminated surfaces, shared equipment, or hands of health-care workers. [11] In this case, due to strict infection control measures, VRE was not found in the environment of NICU. Therefore, we concluded that translocation of gut flora colonized with VRE might have been responsible for VRE sepsis in the neonate.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Cattoir V, Leclercq R. Twenty-five years of shared life with vancomycin-resistant enterococci: Is it time to divorce? J Antimicrob Chemother 2013;68:731-42.  Back to cited text no. 1
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2.
Sood S, Malhotra M, Das BK, Kapil A. Enterococcal infections & antimicrobial resistance. Indian J Med Res 2008;128:111-21.  Back to cited text no. 2
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3.
Facklam RR, Collins MD. Identification of Enterococcus species isolated from human infections by a conventional test scheme. J Clin Microbiol 1989;27:731-4.  Back to cited text no. 3
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4.
Arbour N, Weirich A, Cornejo-Palma D, Prevost S, Ramotar K, Harder CJ. Real-time PCR detection of VRE. AN0019, Version 1.1. Canada: Spartan Bioscience Inc.; 2008.  Back to cited text no. 4
    
5.
Wang A, Yang Y, Lu Q, Wang Y, Chen Y, Deng L, et al. Presence of qnr gene in Escherichia coli and Klebsiella pneumoniae resistant to ciprofloxacin isolated from pediatric patients in China. BMC Infect Dis 2008;8:68.  Back to cited text no. 5
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6.
Ahuja S, Pandey A, Asthana AK, Chauhan K, Ritika, Madan M. Vancomycin-resistant Enterococcus faecium: Report of two cases. Indian J Med Microbiol 2014;32:340-3.  Back to cited text no. 6
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7.
Shantala GB, Nagarathnamma T, Pooja DR, Harsha TR, Karthik R. Neonatal septicaemia caused by vancomycin resistant Enterococcus faecium - A case report. J Clin Diagn Res 2014;8:DD03-04.  Back to cited text no. 7
    
8.
Zheng B, Tomita H, Xiao YH, Wang S, Li Y, Ike Y. Molecular characterization of vancomycin-resistant Enterococcus faecium isolates from mainland China. J Clin Microbiol 2007;45:2813-8.  Back to cited text no. 8
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9.
Banerjee T, Anupurba S, Filgona J, Singh DK. Vancomycin-resistance enterococcal colonization in hospitalized patients in relation to antibiotic usage in a tertiary care hospital of North India. J Lab Physicians 2015;7:108-11.  Back to cited text no. 9
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10.
Rice LB. Emergence of vancomycin-resistant enterococci. Emerg Infect Dis 2001;7:183-7.  Back to cited text no. 10
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11.
Huycke MM, Sahm DF, Gilmore MS. Multiple-drug resistant enterococci: The nature of the problem and an agenda for the future. Emerg Infect Dis 1998;4:239-49.  Back to cited text no. 11
    

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Correspondence Address:
Shampa Anupurba
Department of Microbiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.191802

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