|Year : 2014 | Volume
| Issue : 3 | Page : 340-343
Vancomycin-resistant Enterococcus faecium: Report of two cases
S Ahuja, A Pandey, AK Asthana, K Chauhan, Ritika, M Madan
Post Graduate Department of Microbiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh, India
|Date of Submission||01-Dec-2013|
|Date of Acceptance||28-Feb-2013|
|Date of Web Publication||10-Jul-2014|
Post Graduate Department of Microbiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Vancomycin-resistant Enterococci (VRE), especially Enterococcus faecium has emerged as an important nososcomial pathogen and represents a serious threat to patients with impaired host defense. Early detection of patients colonised or infected with VRE is an essential component of any hospital program designed to prevent nosocomial transmission of this organism. The authors report two cases of VRE isolated from blood and surgical site pus of two neonates admitted in the same neonatal unit, highlighting that early detection, prompt and appropriate infection control measures were keys to successful containment of this dreaded pathogen.
Keywords: Enterococcus faecium, infection control, Vancomycin-resistant Enterococcus
|How to cite this article:|
Ahuja S, Pandey A, Asthana A K, Chauhan K, Ritika, Madan M. Vancomycin-resistant Enterococcus faecium: Report of two cases. Indian J Med Microbiol 2014;32:340-3
|How to cite this URL:|
Ahuja S, Pandey A, Asthana A K, Chauhan K, Ritika, Madan M. Vancomycin-resistant Enterococcus faecium: Report of two cases. Indian J Med Microbiol [serial online] 2014 [cited 2020 Oct 19];32:340-3. Available from: https://www.ijmm.org/text.asp?2014/32/3/340/136597
| ~ Introduction|| |
Enterococcus species have become important nosocomial pathogens world-wide and are associated with a high mortality.  Enterococci may act as a reservoir for vancomycin resistance genes that could be transferred to more virulent bacteria, such as Staphylococcus aureus. Slowing the spread of vancomycin-resistant Enterococci (VRE) colonisation and infection, therefore, should remain a high priority for health care institutions. The treatment of these infections poses a great challenge due to the inherent resistance of Enterococci to many antibiotics and ability to acquire resistance by mutation. A combination of penicillin and gentamicin had been the mainstay of treatment till now but with the emergence of high level aminoglycoside resistance (HLAR), vancomycin is the only alternative available. The widespread use of glycopeptides in hospitals has led to the emergence of VRE which now accounts for about 30% of Enterococcal infections, with most VRE (>90%) isolates being Enterococcus faecium.  Vancomycin resistance is undoubtedly the greatest concern and is associated with severe underlying disease, compromised host defences, indwelling urinary or central venous catheters (CVC), prolonged hospitalisation and administration of multiple antibiotics especially vancomycin and cephalosporins.  We describe our clinical experience with two cases of VRE, due to E. faecium isolated from the same neonatal intensive care unit (NICU) with the aim to highlight that early detection followed by prompt and aggressive infection control measures taken by the Infection Control Team (ICT) led to successful outcome. Moreover, lack of awareness about VRE and paucity of data from this part of the country also prompted us to report this case.
| ~ Case Report|| |
A 1-day-old neonate was referred from a private nursing home to an emergency department of our hospital with clinical diagnosis of respiratory distress with sepsis. The infant was born by normal vaginal delivery at 28 weeks of gestation. His weight at birth was 1500 g. Hence it was a low birth-weight premature delivery. The mother gave history of leaking per vaginum since 15-20 days and history of Dai handling prior to the delivery. However, the delivery was conducted at a private nursing home and was uneventful. The neonate had cried immediately after birth. On admission to our hospital the child was started on inj. cefotaxime and inj. amikacin along with supportive treatment in the form of bronchodilators and digoxin. Despite therapy, there was no clinical improvement and his respiratory distress worsened with worsening saturation. Therefore, intubation was done and the neonate was placed on mechanical ventilation for respiratory failure. In view of poor response, antibiotic therapy was switched to parenteral piperacillin/tazobactam and amikacin. The baby showed mild improvement for a few days but again continued to have spikes of fever. His blood sent for culture grew E. faecium. The identification of the isolate was done by standard methods and confirmed by Vitek 2C (BioMλrieux, France). By standard Kirby-Bauer disc diffusion method, the isolate was resistant to penicillin, erythromycin, high-level gentamicin (HLG), meropenem, ciprofloxacin, vancomycin and teicoplanin but susceptible to linezolid. The isolate possessed resistance to vancomycin; the minimum inhibitory concentration (MIC) of the strain to vancomycin was ≥32 μg/ml by Vitek 2C. The report was dispatched to the NICU; the hospital infection control committee (HICC) was informed immediately which notified the staff promptly regarding appropriate infection control measures such as contact isolation of patient, barrier nursing care. The surveillance cultures were done and the source tracing was attempted. The source of VRE may be endogenous or exogenous. As Enterococcus is a part of normal vaginal flora, and there was history of leaking PV and Dai handling, the vaginal swab from the mother was taken for culture to trace the endogenous source. To trace the exogenous source surveillance cultures were taken from environmental surfaces in NICU, including warmers, bed rails, oxygen line, pulse oxymeter, bedside trolly, neonatal BP instrument (NIBP), IV stand, intercom, door handle, bed linen and gowns of health care workers. Further hand swabs of health care workers including doctors working in NICU and the care givers were also taken. However, both the endogenous and exogenous surveillance culture was negative for growth of Enterococcus species. After receiving the blood culture report the treatment was changed over to linezolid. Following treatment with linezolid at a dose of 25 mg/kg I/V x OD, the infant showed significant improvement and started taking breast feed and spoon feed 3 hourly. He gained weight (400 g) and later after a week was discharged from our hospital uneventfully.
A 1-day-old neonate born by normal vaginal delivery at home was referred to our hospital on the same day with symptoms of mass in lower back. Clinical diagnosis of meningomyelocele was made. The neonate was admitted in NICU. He was operated on the 2 rd day of admission to our hospital. Post-operatively he was shifted back to NICU and inj. cefotaxime and inj. amikacin was started and the dressing of the surgical site was done twice daily. After 2 days of surgery the patient became febrile. Due to the poor response, the treatment was changed over to inj. piperacillin/tazobactum and amikacin. Patient soon developed discharge from the surgical site which was collected and sent for culture. As the patient was not responding and was continuously febrile the treatment was changed over to inj. meropenem and inj. vancomycin. His pus culture grew E.faecium identified both by standard methods and confirmed by Vitek 2C. The isolate was resistant to penicillin, erythromycin, high level gentamicin (HLG), meropenem, ciprofloxacin, vancomycin and teicoplanin but was susceptible to linezolid by standard Kirby-Bauer disc diffusion method and MIC to vancomycin was ≥32 μg/ml. Following confirmation of the isolate the report was dispatched to the NICU and immediately HICC was informed. Source tracing was done by taking hand swabs of health care workers and environmental surfaces in NICU as discussed in the previous case. Further, with the help of the hospital management the ICT could immediately isolate both the cases by shifting them in one room and taking appropriate infection control measures more aggressively, so that there is no further transmission within the unit. Following the sensitivity report the treatment was changed over to intravenous linezolid 25 mg/kg per day. By the 3 rd day the patient became afebrile and showed significant clinical improvement. He was later (after a week) discharged from our hospital uneventfully.
| ~ Discussion|| |
VRE, especially E. faecium has emerged as an important nososcomial pathogen and represents a serious threat to patients with impaired host defences. E. faecium strains as compared to Enterococcus faecalis display a higher degree of drug resistance to multiple other antibiotics including ampicillin, gentamicin, ciprofloxacin, vancomycin and teicoplanin.  Thus emphasising the need to speciate Enterococcal isolates from clinical samples.
Emergence of VRE is of concern due to the limited therapeutic options. In the present case the first neonate had several features common with the risk of acquiring VRE as reported earlier. 
The patient was immature, had low birth weight, was administered antibiotics, notably cephalosporin. The VRE in the first case was isolated from blood and in the second case from surgical site pus. Both our isolates of VRE had a similar sensitivity pattern. The point to be noted here is that the two cases were admitted in the same neonatal unit and were reported within a period of 10 days and were being handled by the same group of staff. Therefore, we assume the source of SSI in the second case most likely might have been from the first case.
Surveillance cultures for VRE are time-consuming and expensive for the laboratory to perform. However, there is a need for surveillance cultures to trace the source which may be endogenous or exogenous. PCR may be a cost-effective alternative to surveillance cultures for VRE in some hospitals. However, in using the alternative, the laboratory may lose the ability to perform strain typing studies with the organisms in their institutions.  This case report highlights that rapid detection of VRE by the laboratory, prompt and aggressive infection control measures as per the recommendation given by CDC Hospital Infection Control Practices Advisory Committee (HICPAC),  prevented an outbreak like situation in the NICU and led to the containment of this resistant bacteria, as no further cases of VRE was isolated from NICU in that month and thereafter. Moreover, the study emphasises that these simple steps should be taken by every hospital both in government and private sectors and nursing homes where initial one or two cases are isolated and or confirmed so that an outbreak can be prevented, because if VRE are not controlled soon after introduction into a hospital, sporadic cases may evolve into a monoclonal outbreak, which may then evolve to polyclonal endemicity. VRE can spread rapidly in hospitals due to cross contamination and person to person spread. , It has also been found that being in the same ward as a VRE case carries the highest risk for acquisition of VRE. 
Resistance to vancomycin in Enterococci can be divided into six phenotypic groups of which, five are acquired (VanA, VanB, VanD, VanE and VanG) and one VanC is an intrinsic property of less commonly isolated species, such as Enterococcus gallinarum, Enterococcus casseliflavus and Enterococcus flavescens.  Out of these VanA phenotype is the most commonly encountered and confers high level resistance to vancomycin and teicoplanin. Resistance in VanB isolates results in moderate level resistance to vancomycin, except that these isolates remain susceptible to teicoplanin. Although E. faecium accounts for most VRE isolates, VanA and VanB phenotypes can be found in both E. faecalis and E. faecium. VanC confers low-level vancomycin resistance and is not associated with resistance to teicoplanin. VanD phenotype is manifested by moderate resistance to vancomycin and low level resistance or susceptibility to teicoplanin. VanE and VanG phenotypes recently described in E. faecalis, confer low- and moderate-level of resistance to vancomycin, respectively, while retaining susceptibility to teicoplanin.
Enterococci may also be tested for vancomycin resistance by using PCR assays designed to detect the genes responsible for glycopeptide resistance in these organisms. Based on its resistance to vancomycin and teicoplanin, our strains were designated as belonging to VanA phenotype. However, a limitation of this study is that we are unable to present the data of the molecular typing methods employed to identify VanA/VanB phenotype, as the number of VRE isolated was limited and we are in the process of standardising it. However, in future studies of VRE molecular typing methods will be employed to identify the VanA/VanB phenotypes. Testing VRE isolates for susceptibility to teicoplanin by using simple disk diffusion tests will differentiate between VanA (teicoplanin-resistant) and VanB (teicoplanin-susceptible) strains in most instances as reported by Mohanty et al., 2006. 
To conclude, early detection of patients colonised or infected with VRE is an essential component of any hospital program designed to prevent nosocomial transmission of VRE. The Microbiology laboratory is the first line of defence against the spread of VRE in the hospital. The ability of the laboratory to identify Enterococci and to detect vancomycin resistance promptly and accurately is essential in recognising VRE colonisation and/or infection and avoiding complex, costly containment efforts that are required when recognition of the problem is delayed. In addition, cooperation and communication between the laboratory and the ICT will facilitate control efforts substantially.
| ~ Acknowledgement|| |
We are thankful to Dr. A. K. Asthana, Principal/Dean and Chairperson HICC and Dr. D. C. Saxena, Co- chairperson HICC, Chatrapati Shivaji Subharti Hospital, Subharti Medical College, Meerut for their timely support and guidance in carrying out the infection control measures.
| ~ References|| |
|1.||Meellering RC. Emergence of Enterococcus as a significant pathogen. Clin Infect Dis 1992;14:1173-8. |
|2.||Deshpande LM, Fritsche TR, Moet GJ, Biedenbach DJ, Jones RN. Antimicrobial resistance and molecular epidemiology of vancomycin-resistant enterococci from North America and Europe: A report from the SENTRY antimicrobial surveillance program. Diagn Microbiol Infect Dis 2007;58:163-70. |
|3.||CetinyaY, Falk P, Mayhall CG. Vancomycin-resistant enterococci. Clin Microbiol Rev 2000;13:686-707. |
|4.||Murray BE. Vancomycin resistant enterococci. Am J Med 1997;102:284-93. |
|5.||Satake S, Clark N, Rimland D, Nolte FS, Tenover FC. Detection of vancomycin-resistant enterococci in fecal samples by PCR. J Clin Microbiol 1997;35:2325-30. |
|6.||Hospital Infection Control Practices Advisory Committee (HICPAC). Recommendations for preventing spread of Vancomycin resistance. Infect Control Hosp Epidemiol 1995;16:105-13. |
|7.||Ishikawa K, Hayakawa S, Katayama T, Hoshinaga K, Fukaya S, Torikai K, et al. Epidemiological study of vancomycin-resistant Enterococci isolated from a single university hospital in Japan. J Infect Chemother 2001;7:163-8. |
|8.||MacIntyre CR, Empson M, Boardman C, Sindhusake D, Lokan J, Brown GV. Risk factors for colonization with vancomycin-resistant Enterococci in a Melbourne hospital. Infect Control Hosp Epidemiol 2001;22:624-9. |
|9.||Mohanty S, Dhawan B, Gadepalli RS, Lodha R, Kapil A. Vancomycin-resistant Enterococcus faecium VanA phenotype: First documented isolation in India. Southeast Asian J Trop Med Public Health 2006;37:335-7. |
|10.||Fines M, Perichon B, Reynolds P, Sahm DF, Courvalin P. VanE, a new type of acquired glycopeptides resistance in Enterococcus faecalis BM 4405. Antimicrob Agents Chemother 1999;43:2161-4. |
|11.||McKesar SJ, Berry AM, Bell JM, Turnidge JD, Paton JC. Genetic characterizations of VanG, a novel vancomycin resistance focus of Enterococcus faecalis. Antimicrob Agents Chemother 2000;44:3224-8. |