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Year : 2018  |  Volume : 20  |  Issue : 2  |  Page : 105-107

Vancomycin resistant enterococcal infections in infants and neonates

Department of Microbiology, Government Medical College, Thiruvananthapuram, Kerala, India

Date of Web Publication7-Jan-2019

Correspondence Address:
Dr. O Sasikumari
Department of Microbiology, Government Medical College, Thiruvananthapuram, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jacm.jacm_67_16

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Vancomycin-resistant Enterococci have become one of the most challenging nosocomial pathogens with limited therapeutic options. We report three cases of Vancomycin-resistant Enterococcus faecium isolated from urine, perinephric collection and blood of paediatric patients over a period of one year from June 2015–2016 in a tertiary care centre in South Kerala.

Keywords: Enterococcus faecium, nosocomial pathogens, Vancomycin-resistant Enterococci

How to cite this article:
Ligitha S G, Sasikumari O. Vancomycin resistant enterococcal infections in infants and neonates. J Acad Clin Microbiol 2018;20:105-7

How to cite this URL:
Ligitha S G, Sasikumari O. Vancomycin resistant enterococcal infections in infants and neonates. J Acad Clin Microbiol [serial online] 2018 [cited 2022 Aug 17];20:105-7. Available from: https://www.jacmjournal.org/text.asp?2018/20/2/105/249575

  Introduction Top

There are two types of Vancomycin resistance in enterococci spp. The first type is intrinsic resistance. Isolates of Enterococcus gallinarum and Enterococcus casseliflavus/Enterococcusflavescens demonstrate an inherent, low-level resistance to Vancomycin. The second type of Vancomycin resistance in enterococci spp. is acquired resistance.

Enterococci spp. can become resistant to Vancomycin by acquisition of resistance genes from another organism. Most commonly, this resistance is seen in Enterococcus faecium and Enterococcus faecalis, but also has been recognised in Enterococcus raffinosus, Enterococcus avium, Enterococcus durans and several other enterococcal species.

Several genes, including vanA,vanB, vanC, vanD and vanE, contribute to resistance to Vancomycin in enterococci spp.

E. faecium is the most frequently isolated species of Vancomycin-resistant enterococci (VRE) in hospitals and typically produces high Vancomycin (64–1000 μg/ml) and Teicoplanin (16–512 μg/ml) minimum inhibitory concentrations (MICs). These isolates typically contain vanA genes. vanB confers varied resistance to Vancomycin, ranging from moderate- to high-level resistance (MIC range, 4–1000 μg/ml) and is susceptible to Teicoplanin (MIC, 0.5–1 μg/ml).[1]

E. gallinarum and E. casseliflavus/E. flavescens isolates are intrinsically resistant to Vancomycin. These isolates contain Van C genes that typically produce Vancomycin MICs of 2–32 μg/ml.[1]

From the first isolation of Vancomycin-resistant E. faecalis and E. faecium in England in 1988, VRE have spread with unanticipated rapidity and are now encountered by hospitals in many parts of the world.[2]

We report three cases of Vancomycin-resistant E. faecium isolated from urine, perinephric collection and blood of paediatric patients over a period of one year from June 2015–2016 in a public sector, paediatric tertiary care centre in South Kerala [Table 1].
Table 1: Details of patients from whom Vancomycin-resistant enterococci were isolated

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  Case Reports Top

Case 1

An eight-month-old male baby presented with a history of fever and recurrent urinary tract infection. The patient had posterior urethral valve and micturating cysto-urethrogram showed the findings suggestive of chronic cystitis. On ultrasound examination, the patient had left hydroureteronephrosis. The perinephric collection and urine of the patient was sent for culture and sensitivity to the microbiology laboratory. From both samples, E. faecium was identified by standard methods.

Case 2

A full-term baby was delivered by vacuum extraction, due to meconium-stained amniotic fluid. The child showed poor feeding and respiratory distress. The clinical diagnosis was early-onset neonatal sepsis. The baby was admitted in neonatal intensive care unit (ICU) and started on parenteral Piperacillin–Tazobactam and Amikacin. Two blood samples collected at one-hour interval were sent to the microbiology laboratory for culture and sensitivity. Both the samples yielded E. faecium.

Case 3

A seven-month-old female baby who was severely malnourished was diagnosed to have atrioventricular cushion defect, with a history of recurrent lower respiratory tract infections. The child now presented with features of sepsis. She was started on parenteral Piperacillin-Tazobactam and Vancomycin. Since there was no clinical improvement, two blood samples collected at one-hour interval were sent to the microbiology laboratory for culture and sensitivity, and injection Meropenem was added. Both the samples yielded E. faecium in the first subculture itself by standard methods.

Antibiotic sensitivity pattern

Isolates from all the three cases had the same antibiotic sensitivity pattern. They were sensitive only to linezolid and was resistant to Penicillin, Ampicillin, Erythromycin, high-level Gentamicin and Vancomycin by Kirby–Bauer disc diffusion method. The MIC for Vancomycin was >32 μg/ml when tested with E-test strip.

In the first case, the strain was confirmed by polymerase chain reaction for Van A gene at Christian Medical College, Vellore. The positive control for vanA gene was E. faecalis (ATCC 51,299 )and negative control was E. faecalis (ATCC 29,212).[3]

In all the three cases, the identification of the organisms as Vancomycin-resistant E. faecium was confirmed by Vitek 2 (bioMerieux, France). The MICs for Vancomycin and Teicoplanin was >32 μg/ml with probably Van A phenotype as per Vitek 2 report.

  Discussion Top

VRE is a serious threat to patients with impaired host defence mechanism. The risk factors associated with colonisation and infection with VRE include prolonged hospitalisation, especially in ICU; intrahospital ward transfers; previous antimicrobial therapy, especially Vancomycin use and third-generation Cephalosporins; exposure to contaminated medical equipment such as electronic thermometers and proximity to a previously known VRE patients or staff members who had taken care of VRE patients.[4]

E. faecalis is the predominant species accounting for 80%–90% of all clinical isolates and E. faecium accounts for 5%–15%. Drug resistance is more common in E. faecium (72%) than that in E. faecalis (45%). The most common phenotype seen among VRE strains is the vanA phenotype.

Identification of VRE to species level aids in confirming whether an isolate has intrinsic (Van C) or acquired resistance (VanA or VanB). The knowledge of the type of resistance is critical for infection control purposes. vanA and vanB genes are transferable and can spread from organism to organism. In contrast, VanC genes are not transferable, have been associated less commonly with serious infections and have not been associated with outbreaks.[5] Here, the cases had occurred at different times of the year and from different locations in the hospital, and hence, the possibility of a common source was less.

In the second case, in which there was a history of difficult labour with foetal distress, high vaginal swab of the mother also grew E. faecium with same antibiotic sensitivity pattern. However, in other two cases, the source could not be identified. Contact isolation was done to prevent the spread of infection. All the three cases responded well to treatment with Linezolid.

  Conclusion Top

This case series signifies the emergence of VRE in this geographical area. The emergence and spread of this pathogen show the need for appropriate infection control policies and strict enforcement of antibiotic policies. Well-planned screening programs with barrier nursing and isolation of patient may help prevent the spread of such pathogens.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

O'Driscoll T, Crank CW. Vancomycin-resistant enterococcal infections: Epidemiology, clinical manifestations, and optimal management. Infect Drug Resist 2015;8:217-30.  Back to cited text no. 1
Cetinkaya Y, Falk P, Mayhall CG. Vancomycin-resistant enterococci. Clin Microbiol Rev 2000;13:686-707.  Back to cited text no. 2
Praharaj I, Sujatha S, Parija SC. Phenotypic and amp; genotypic characterization of vancomycin resistant Enterococcus isolates from clinical specimens. Indian J Med Res 2013;138:549-56.  Back to cited text no. 3
[PUBMED]  [Full text]  
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:DD03-4.  Back to cited text no. 4
Tschudin Sutter S, Frei R, Dangel M, Gratwohl A, Bonten M, Widmer AF, et al. Not all patients with vancomycin-resistant enterococci need to be isolated. Clin Infect Dis 2010;51:678-83.  Back to cited text no. 5


  [Table 1]


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