Letters to the Editor / Journal of Hospital Infection 78 (2011) 335–339336

period, three patients died during hospitalization. However, theirdeaths occurred several days after the completion of treatmentand were not related to VAT. Treatment was well tolerated by allpatients and no adverse events were reported.

According to our data, monotherapy with nebulized colistin maybe effective for the treatment of patients with VAT due topolymyxin-only-susceptible Gram-negative bacteria. To our knowl-edge, this is the first study to evaluate the effect of monotherapywith inhaledcolistin inpatientswithVAT. Theeffectofnebulizedanti-biotics in the treatment of patients with nosocomial tracheobronchi-tis has been addressed previously in two studies.5,6 One studydemonstrated that treatment of VATwith inhaled antibiotics (vanco-mycin or gentamicin) was associated with reduced use of systemicantibiotics and increased weaning success.5 However, most of thepatients had VAP and simultaneously received targeted treatmentwith intravenous agents. In the other study, treatment of five patientswith nosocomial tracheobronchitis with inhaled colistin resulted ina clinical response in all patients.6 However, most patients werereceiving concomitant treatment with intravenous agents withpotential synergistic effects against Gram-negative bacteria. Inaddition, the microbiological outcomes were not assessed.

The limited evidence from this study suggests that monotherapywith inhaled colistin may be effective for the treatment of patientswith VAT due to polymyxin-only-susceptible Gram-negativebacteria. Further investigation is warranted to evaluate whethernebulized antibiotics are effective for the treatment of VAT andcan reduce the need for systemic antibiotic administration.

Conflict of interest statementNone declared.

Funding sourcesNone.

References

1. Nseir S, Di Pompeo C, Pronnier P, et al. Nosocomial tracheobronchitis in mechan-ically ventilated patients: incidence, aetiology and outcome. Eur Respir J 2002;20:1483–1489.

2. Nseir S, Di Pompeo C, Soubrier S, et al. Effect of ventilator-associated tracheo-bronchitis on outcome in patients without chronic respiratory failure: a case–control study. Crit Care 2005;9:R238–R245.

3. Craven DE, Hjalmarson KL. Ventilator-associated tracheobronchitis and pneu-monia: thinking outside the box. Clin Infect Dis 2010;51(Suppl. 1):59–66.

4. Nseir S, Favory R, Josefowicz E, et al. Antimicrobial treatment for ventilator-associated tracheobronchitis: a randomized, controlled, multicenter study. CritCare 2008;12:R62.

5. Palmer LB, Smaldone GC, Chen JJ, et al. Aerosolized antibiotics and ventilator-associated tracheobronchitis in the intensive care unit. Crit Care Med 2008;36:2008–2013.

6. Pereira GH, Muller PR, Levin AS, et al. Salvage treatment of pneumonia and initialtreatment of tracheobronchitis caused by multidrug-resistant Gram-negativebacilli with inhaled polymyxin B. Diagn Microbiol Infect Dis 2007;58:235–240.

7. Craven DE, Chroneou A, Zias N, Hjalmarson KI. Ventilator-associated tracheo-bronchitis: the impact of targeted antibiotic therapy on patient outcomes. Chest2009;135:521–528.

8. Clinical and Laboratory Standards Institute. Performance standards for antimicro-bial susceptibility testing: Seventh information supplement M100-S17. Wayne, PA,USA: CLSI; 2007.

Z.E. Athanassaa,*

P.M. Myrianthefsa

E.G. Boutzoukaa

A. Tsakrisb

G.J. BaltopoulosaaIntensive Care Unit, “KAT” University Trauma Hospital,School of Nursing, University of Athens, Athens, Greece

bDepartment of Microbiology, Medical School, University of Athens,Athens, Greece

* Corresponding author. Address: 6 Makrygianni Street,New Psychiko, 15451 Athens, Greece.

Tel.: þ30 6944620359; fax: þ30 2106857800.E-mail address: zathanassa@yahoo.gr (Z.E. Athanassa).

Accepted by J.A. Child

Available online 8 June 2011

� 2011 The Healthcare Infection Society. Published by Elsevier Ltd.All rights reserved.

doi:10.1016/j.jhin.2011.04.004

Hospital identity badges: a possible sourceof healthcare-acquired infection?

Madam,

The prevalence of healthcare-associated infections (HCAI) isincreasing.1 At any one time, it is believed that up to 9% of patientsin England will have contracted HCAI, the treatment of which coststhe UK National Health Service (NHS) up to £1 billion each year.2

The potential for healthcareworkers to act as a source of pathogenshas longbeen recognised,withprevious studies documenting contam-ination of white coats, stethoscopes and neck ties.3,4 More recently,high levels of contamination have been demonstrated on surfacesand equipment within the hospital environment. Clothing and handsof healthcare workers may become contaminated through directcontact, and thus represent possible sources of nosocomial infection.5

In September 2007, theDepartment ofHealth published guidelinesonuniform, clothing anddress to be implemented acrossNHStrusts inEngland.6 The ‘BareBelowtheElbows’policy recommends thathealth-care workers should refrain from wearing white coats, long-sleevedshirts, neck ties, wrist watches and any unnecessary badges in anattempt to reduce the spread of HCAI via direct and indirect contact.

In our unit, all clinical and non-clinical staff carry an identitybadge about their person. In addition to identification, this badgeallows secure access to restricted areas. These badges are handledfrequently and, as they have potential for patient contact, couldact as a vector for the transmission of infection.

We sampled 80 identity badges from 43 nurses, 20 doctors andseven physiotherapists from three wards (one orthopaedic traumaward and two general surgery wards), and 10 medical secretaries.The latter were recruited to act as a control group, representing a pop-ulation working within the hospital environment but without anydirect patient contact. Nursing sisters and consultants were excludedas theywere considered to have less direct patient contact than juniorcolleagues. An elective orthopaedic ward was excluded as all patientshad been screened for meticillin-resistant Staphylococcus aureus priortoadmission,andwere thereforenot representativeof surgicalpatientsin the hospital. The profession of each participant, the mode of badgecarriage and the frequency of badge cleaning were documented.

All samples were collected during the last 2 h of a working day toallow themaximumopportunity for pathogen transmission. Sampleswere obtained by passing a cotton swabmoistenedwith saline acrossthe front of each badge. All samples were handledwith sterile gloves,and the swab was passed diagonally to and fro across the badgesurface. The same author (S.H.) collected each sample, using an iden-tical sampling technique to ensure uniformity of sampling.

All identity badges sampled were of uniform design andmeasured 86 mm� 55 mm� 0.8 mm. They were constructed

Letters to the Editor / Journal of Hospital Infection 78 (2011) 335–339 337

from glossy white polyvinyl chloride, and conformed with industrystandard ISO 7811. The swab samples were plated on to blood agarplates and incubated at 37 �C in air for 24 h. The plates wereanalysed after this time, and any colonies were tested for the pres-ence of S. aureus using a latex agglutination test (PastorexTM StaphPlus, Bio-Rad Laboratories, Hemel Hempstead, UK).

The majority of staff carried their identity badge around theirneck or in a pocket of their uniform. Nursesmore commonly carriedtheir badge in a pocket, whereas doctors and physiotherapistspreferred to wear their badge around their neck. The control groupcarried their badges around their neck (N¼ 6) or in their pocket(N¼ 4). Cleaning of identity badges was uniformly poor: 58 of 80staff reported never cleaning their badge, three reported dailycleaning, 11 reported weekly cleaning and eight reported monthlycleaning. S. aureus was not detected on any of the badges.

A review of the literature revealed two previous studies thatinvestigated the contamination of identity badges.7,8 A Canadianstudy reported that significant pathogens were isolated from 13%of badges studied, irrespective of the manner in which they werecarried. However, this level of contamination was not thought tobe clinically relevant. A study from Australia investigated thecontamination of identity badges and cloth lanyards. Pathogenswere identified on 63% of badges and lanyards. However, it wasthe presence of the cloth lanyard, rather than the identity badge,that conveyed a 10-fold greater risk for the presence of bacteria.

The identity badges used within our hospital are of an industrystandard and are common to all British hospitals. Therefore, thesefindings should be applicable to other units. As bacteria havebeen shown to survive for up to 24 h on fabric and plastics, andup to 90 days on polyethylene, we recommend regular cleaningof identity badges in line with other measures taken to preventHCAI. However, we do not believe that hospital identity badgescan harbour pathogens, and consider that they pose little threatfor the spread of HCAI.

Acknowledgements

We would like to thank the Russells Hall Hospital MicrobiologyDepartment for their help in this study.

Conflict of interest statementNone declared.

Funding sourcesNone.

References

1. National Audit Office. Improving patient care by reducing the risk of hospitalacquired infection: a progress report. London: The Stationery Office; 2004.

2. National Audit Office. The management and control of hospital acquired infectionin acute NHS trusts in England. London: The Stationery Office; 2000.

3. Kennedy KJ, Dreimanis DE, Beckingham WD, Bowden FJ. Staphylococcus aureusand stethoscopes. Med J Aust 2003;178:468.

4. Ditchburn I. Should doctors wear ties? J Hosp Infect 2006;63:227–228.5. Schabrun S, Chipchase L. Healthcare equipment as a source of nosocomial

infection: a systematic review. J Hosp Infect 2006;63:239–245.6. Department of Health. Uniforms and workwear: an evidence base for developing

local policy. London: Department of Health; 2007.7. Ota K, Profiti R, Smaill F, Matlow AG, Smieja M. Identification badges: a potential

fomite? Can J Infect Control 2007;22:65–66.8. Neely AN, Maley MP. Survival of enterococci and staphylococci on hospital

fabrics and plastic. J Clin Microbiol 2000;38:724–726.

S. Hutchingsa

C. Heavera,*

A. Bhallaa

E. Reesb

E. Davisa,c

aDepartment of Trauma and Orthopaedics, Russells Hall Hospital,Dudley, UK

bDepartment of Microbiology and Pathology, Russells Hall Hospital,Dudley, UK

cThe Royal Orthopaedic Hospital NHS Foundation Trust,Northfield, Birmingham, UK

* Corresponding author. Address: Department of Orthopaedics,Russells Hall Hospital, Dudley, West Midlands DY1 2HQ, UK.

Tel.: þ44 (0) 1384 456111; fax: þ44 (0) 1384 244153.E-mail address: catriona.greenfield@doctors.net.uk (C. Heaver).

Accepted by J.A. Child

Available online 14 June 2011

� 2011 The Healthcare Infection Society. Published by Elsevier Ltd.All rights reserved.

doi:10.1016/j.jhin.2011.04.009

The challenges of implantable cardiac deviceinfection due to Helcococcus kunzii

Madam,

Implantable cardiac rhythm devices (ICRDs) are increasinglyimportant in stabilizing cardiac rhythm disorders, but their usemay be complicated by infection.1–3 Removal of these devices inthe setting of infection is often challenging, and obtaining appro-priate deep specimens is difficult. We report a delayed ICRD skininfection due to the skin commensal Helcococcus kunzii, a rarelyreported pathogen. This case highlights the importance of closecollaboration between cardiology and microbiology services.

A 75-year-old male presented to the emergency departmenteightmonths after insertion of an implantable ICRD. He had noticedswelling around the ICRD, with yellow fluid oozing from the site. Onexamination, he had a 2� 2 cm pointing abscess overlying thedevice but no evidence of cellulitis. He was commenced on fluclox-acillin 2 g four times daily i.v. and benzylpenicillin 2.4 g four timesdaily i.v. Threedays after admission, he developed progressive cellu-litis. The superficial abscess was drained, but the device was leftin situ as an ultrasound scan of the area was normal and a transtho-racic echo showed no evidence of endocarditis, suggesting that theinfection did not involve the device. The antibioticswere changed tovancomycin and clindamycin, which were received for 14 days.Following positive culture results and antibiotic susceptibilitytesting, he was discharged home on oral amoxicillin and rifampicinfor a further four weeks, with complete resolution of the infection.

Two tissue samples, a skin swab and a device swabwere received.Gram-stained smears of the two tissue samples showed pus cells andGram-positive cocci. Culture of the samples was positive at 48 hwithpure growth of an organism from all four samples. The BBL�Crystal� Identification System (Baltimore, MD, USA) and the BDPhoenix� Automated Microbiology System (Baltimore, MD, USA)identified the organism as H. kunzii. The phenotypic identificationof the isolatewas confirmed by genotypic identification by the Strep-tococcus and Diphtheria Reference Unit, Colindale, London by partialsequencing of 16S rDNA. The results from antimicrobial suscepti-bility testing, using the Clinical and Laboratory Standards Institutemethodology, were equivocal. The Antimicrobial ResistanceMonitoring Reference Laboratory at the Health Protection Agency,