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Journal of Medical Microbiology (2005), 54, 901–903
Case Report
DOI 10.1099/jmm.0.46169-0
Community-acquired vancomycin-resistant
Enterococcus faecium: a case report from Malaysia
N. S. Raja,1 R. Karunakaran,1 Y. F. Ngeow1 and R. Awang2
Correspondence
1
Department of Medical Microbiology, University of Malaya Medical Center, Kuala Lumpur 59100,
Malaysia
2
Department of Oral & Maxillofacial Surgery, Faculty of Dentistry, University of Malaya, 59100 Kuala
Lumpur, Malaysia
N. S. Raja
[email protected]
Received 24 May 2005
Accepted 20 June 2005
Vancomycin-resistant enterococci (VRE) are formidable organisms renowned for their ability to
cause infections with limited treatment options and their potential for transferring resistance genes
to other Gram-positive bacteria. Usually associated with nosocomial infections, VRE are rarely
reported as a cause of community-acquired infection. Presented here is a case of communityacquired infection due to vancomycin-resistant Enterococcus faecium. The patient had been
applying herbal leaves topically to his cheek to treat a buccal space abscess, resulting in a burn of the
overlying skin. From pus aspirated via the skin a pure culture of E. faecium was grown that was
resistant to vancomycin with a MIC of .256 ìg ml 1 by the E test and resistant to teicoplanin by disc
diffusion, consistent with the VanA phenotype. The organism was suspected of contaminating the
leaf and infecting the patient via the burnt skin. This case highlights the need for further studies on the
community prevalence of VRE among humans and animals to define unrecognized silent reservoirs
for VRE, which may pose a threat to public health.
Introduction
The emergence of antimicrobial-resistant organisms, including vancomycin-resistant enterococci (VRE), poses a challenge to clinicians due to the lack of effective antimicrobial
agents available against them and associated infectioncontrol implications. VRE were first reported in Europe in
1988, and have since emerged as a global threat to public
health. Increasingly recognized as nosocomial pathogens,
they tend to colonize or infect severely debilitated hospitalized patients on prolonged courses of antibiotics (Kapil,
2005; D’Agata et al., 2001). Community-acquired infections
with VRE, however, have rarely been described (Coque et al.,
1996). There are five phenotypes of VRE, i.e. VanA, VanB,
VanC, VanD and VanE, recognized by their susceptibility
pattern to vancomycin and teicoplanin (Cetinkaya et al.,
2000). We report here a case of community-acquired buccal
space abscess caused by vancomycin-resistant Enterococcus
faecium from the University of Malaya Medical Center, Kuala
Lumpur, Malaysia.
Case report
A 38-year-old man presented to the Accident and Emergency
Unit of the University of Malaya Medical Center, Kuala
Lumpur, with a 3 day history of pain and swelling of the right
Abbreviation: VRE, vancomycin-resistant enterococci.
cheek associated with pain in the right upper and lower teeth.
There was no significant past medical history. A firm believer
in traditional medicine, he had initially sought the advice of a
‘bomoh’ (the local term for a traditional medicine man) and
had been given some herbal leaves to apply over his right
cheek, following which he had developed further pain,
redness and a burnt area over the affected cheek skin.
On examination, the man was febrile, with a temperature of
38.4 8C. There was a swelling over the right cheek area
extending from the right zygomatic arch to the right lower
border of the mandible. The overlying skin was inflamed,
with a burnt, black and dry central area, but no apparent
sinus was visible. The patient was unable to fully open his
mouth, and palpation revealed the swelling to be tender and
fluctuant. A clinical diagnosis of right buccal abscess of the
cheek secondary to infected molar roots with cellulitis of the
cheek was made, and an orthopanthomogram revealed
radiolucency over the right mandibular molar alveolar
regions suggestive of retained roots. His haemoglobin level
was 14.9 g dl 1 and white blood cell count was 12.33109 l 1
(82 % neutrophils, 11 % lymphocytes). The renal function
was normal.
The patient was admitted to the Ear, Nose and Throat ward
and intravenous cefuroxime (750 mg) and metronidazole
(500 mg) were administered every 8 h. Aspiration of the
swelling under local anaesthetic was also carried out in the
ward. About 5 ml of pus was aspirated externally via the right
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N. S. Raja and others
cheek and another 5 ml was aspirated intraorally via the right
buccal mucosa, and the specimens were sent for culture and
antimicrobial susceptibility testing.
The patient’s condition improved dramatically and by the
next day, the fever had subsided, the size of the swelling had
decreased and the patient was able to open his mouth. He was
discharged with instructions to complete a weeks’ course of
oral cefuroxime and metronidazole.
Microbiological investigations
The two pus specimens received at the Microbiology
Laboratory of the University of Malaya Medical Centre were
processed using standard laboratory procedures, and susceptibility testing was in accordance with the NCCLS disc
diffusion method (NCCLS, 2004).
The intraorally aspirated pus grew Streptococcus milleri that
was sensitive to penicillin, erythromycin, clindamycin, imipenem and vancomycin. The pus aspirated externally via the
right cheek grew E. faecium, which was identified using
standard biochemical tests (Cetinkaya et al., 2000) and the
API Strept kit (Biomérieux). This was resistant to ampicillin,
erythromycin, clindamycin, teicoplanin and vancomycin,
and susceptible to amoxycillin clavulanate, imipenem and
linezolid. High-level resistance to gentamicin was tested for,
using the 120 ìg gentamicin disc; however, resistance was
not detected. MIC testing using the E test (AB biodisk)
performed according to the manufacturer’s guidelines on
Mueller–Hinton agar revealed a vancomycin MIC of
.256 ìg ml 1 . PCR amplification revealed the presence of
the vanA gene.
By the time the laboratory had confirmed isolation of VRE,
the patient had already been discharged from hospital. He
remains well to today.
Discussion
The UK, France, Turkey and Malaysia are among the many
countries that have reported infection or colonization with
VRE, and the spectrum of documented infections includes
endocarditis, thrombophlebitis and bacteraemia (Riley et al.,
1996; Babcock et al., 2001; Basustaoglu et al., 2001). Community-acquired VRE infections are scarce though, and the
only published reports to date have been of urinary-tract
infections (Aznar et al., 2004; Taneja et al., 2004). To our
knowledge, this is the first community-acquired soft-tissue
infection caused by VRE in the literature.
Scientists and researchers have considered the mechanism
for the development of vancomycin resistance in E. faecium.
Possible contributing factors include the frequent parenteral
use of vancomycin to treat methicillin-resistant Staphylococcus aureus and penicillin-resistant enterococcal infections, as
well as the oral use of vancomycin for the treatment of
Clostridium difficile enterocolitis. Coque et al. (1996) have
established that large numbers of VRE may be isolated from
hospitalized patients after glycopeptide administration and
902
that this may result in an increased risk of nosocomial
transmission as well as spread of vancomycin resistance to
other species of bacteria in the gut. The use of avoparcin in
animal husbandry in Europe has also been linked to the
emergence of VRE, which can reach humans via the food
chain (WHO, 1997). Other glycopeptides like teicoplanin
and ristocetin, and non-glycopeptide agents such as bacitracin, polymixin B and robenidine (used in the treatment of
coccidial infections in poultry) can also induce vancomycin
resistance (Lai & Kirsch, 1996). Other farm animals or pets,
including horses, dogs, chickens and pigs, may also be
potential sources of VRE (Cetinkaya et al., 2000).
The source of the VRE in our patient was not identified, but
this patient had no direct exposure to livestock or pet faeces.
However, we suspect that the source of the VRE might have
been the medicinal leaf that the ‘bomoh’ applied to his outer
cheek, which possibly was contaminated with VRE from a
community source and infected the cheek through skin
burns caused by the leaf. Traditional medicine from a
‘bomoh’ is a form of alternative medicine available in
Malaysia that is especially popular among the rural community. In this case, the leaf itself caused a burn on the
patient’s skin, which probably led to the entry of the VRE.
Also evident is the need for further studies on the community
prevalence of VRE among both the animal and human
population in Malaysia to define the extent of VRE in the
community.
Typically resistant to multiple antimicrobial agents, VRE
infections present a therapeutic challenge due to the limited
treatment options available. Penicillin or ampicillin with or
without a synergistic option (aminoglycosides) is a favourable choice in cases of penicillin-susceptible VRE. Published
reports have also described successful treatment of VRE
infections with teicoplanin and linezolid (Cetinkaya et al.,
2000; Babcock et al., 2001). Our patient responded to
drainage of the pus and treatment with cefuroxime and
metronidazole. As these antimicrobials are not effective
against enterococci, it is likely that the VRE infection of the
cheek resolved with surgical drainage without the need for
specific anti-VRE antimicrobial therapy.
It is worrying that we have detected VRE with the vanA gene,
which, along with the van B gene, is plasmid-borne and hence
readily transferable from organism to organism (CDC,
1999). This would be especially menacing if spread were to
occur to methicillin-resistant Staphylococcus aureus, as it
would result in highly limited treatment options. Conjugative transfer of the vanA gene from enterococci to S. aureus
has been demonstrated in a laboratory setting (Noble et al.,
1992), and since 2002, three cases of vancomycin-resistant
S. aureus possessing the vanA gene have been reported from
clinical settings (Chang et al., 2003; Tenover et al., 2004;
CDC, 2004). In the first case, the vanA gene from the
vancomycin-resistant S. aureus was postulated to have
originated from VRE that were also isolated from the patient
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Journal of Medical Microbiology 54
Community-acquired vancomycin-resistant E. faecium
(Chang et al., 2003). The implications of this finding have
been the cause for much concern among scientists and
clinicians.
Infection-control measures are always a priority when VRE is
isolated from a hospitalized patient, but in this case, by the
time we had confirmed VRE in the pus sample, the patient
had already been discharged. It is worrying that the patient
had been in the open ward for 2 days, providing a silent
reservoir for the dissemination of VRE. No screening of
patients was done, and there is a possibility that transmission
to asymptomatic carriers may have occurred.
Chang, S., Sievert, D. M., Hageman, J. C. & 10 other authors (2003).
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D’Agata, E. M., Jirjis, J., Gouldin, C. & Tang, Y. W. (2001). Community
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Kapil, A. (2005). The challenge of antibiotic resistance: need to
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Acknowledgements
resistance encoded by the vanA gene cluster in Enterococcus faecium.
Antimicrob Agents Chemother 40, 1645–1648.
We would like to thank Miss Tiang Yee Peng for her technical help
rendered in carrying out the VRE PCR.
NCCLS (2004). Performance Standards for Antimicrobial Susceptibility
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