In the midst of an outbreak, carbapenem-resistant Acinetobacter baumannii was grown from samples of multiple environmental sites in an intensive care unit. A commercial oxidizing disinfectant (potassium peroxomonosulphate 50%, sodium alkyl benzene sulphonate 15%, and sulphamic acid 5%) was introduced throughout the intensive care unit, and its use coincided with cessation of the outbreak

Anthony M. Allworth

David L. Paterson

Graeme R. Nimmo

Hernndez

Hwee Mian Goh

Jeffrey Lipman

Kathryn O'Brien

Marion Woods

Mark A. Schembri

Michael Terry

Michelle Doidge

Narelle George

Penelope Marshall

Tenover

Crossref

Control of an Outbreak of Carbapenem-Resistant
                    Acinetobacter baumannii

Control of an Outbreak of Carbapenem-Resistant Acinetobacter baumannii in Australia after Introduction of Environmental Cleaning with a Commercial Oxidizing Disinfectant

Doidge, Michelle

Allworth, Anthony M.

Woods, Marion

Marshall, Penelope

Terry, Marshall

O'Brien, Kathryn

Goh, Hwee Mian

George, Narelle

Nimmo, Graeme R.

Schembri, Mark A.

Lipman, Jeffery

Paterson, David L.

University of Queensland eSpace

Control of an Outbreak of Carbapenem‐Resistant Acinetobacter baumannii in Australia after
Introduction of Environmental Cleaning with a Commercial Oxidizing Disinfectant • 
Author(s): Michelle Doidge; Anthony M. Allworth; Marion Woods; Penelope Marshall;
Michael Terry; Kathryn O’Brien; Hwee Mian Goh; Narelle George; Graeme R. Nimmo;
Mark A. Schembri; Jeffrey Lipman; David L. Paterson
Source: Infection Control and Hospital Epidemiology, Vol. 31, No. 4 (April 2010), pp. 418-420
Published by: Cambridge University Press on behalf of The Society for Healthcare Epidemiology of
America
Stable URL: http://www.jstor.org/stable/10.1086/651312 .
Accessed: 22/10/2015 02:25
Your use of the JSTOR archive indicates your acceptance of the Terms & Conditions of Use, available at .
http://www.jstor.org/page/info/about/policies/terms.jsp
 .
JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of
content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms
of scholarship. For more information about JSTOR, please contact support@jstor.org.
 .
Cambridge University Press and The Society for Healthcare Epidemiology of America are collaborating with
JSTOR to digitize, preserve and extend access to Infection Control and Hospital Epidemiology.
http://www.jstor.org 
This content downloaded from 23.235.32.0 on Thu, 22 Oct 2015 02:25:33 AM
All use subject to JSTOR Terms and Conditions
infection control and hospital epidemiology april 2010, vol. 31, no. 4
c o n c i s e c o m m u n i c a t i o n
Control of an Outbreak of Carbapenem-
Resistant Acinetobacter baumannii
in Australia after Introduction
of Environmental Cleaning
with a Commercial Oxidizing Disinfectant
Michelle Doidge; Anthony M. Allworth; Marion Woods;
Penelope Marshall; Michael Terry; Kathryn O’Brien;
Hwee Mian Goh; Narelle George; Graeme R. Nimmo;
Mark A. Schembri; Jeffrey Lipman; David L. Paterson
In the midst of an outbreak, carbapenem-resistant Acinetobacter bau-
mannii was grown from samples of multiple environmental sites in
an intensive care unit. A commercial oxidizing disinfectant (potas-
sium peroxomonosulphate 50%, sodium alkyl benzene sulphonate
15%, and sulphamic acid 5%) was introduced throughout the in-
tensive care unit, and its use coincided with cessation of the outbreak.
Infect Control Hosp Epidemiol 2010; 31:418-420
In 2006, an outbreak of carbapenem-resistant Acinetobacter
baumannii (CR-AB) occurred in an intensive care unit (ICU)
at a large teaching hospital in Australia. In this report, we
describe the outbreak and its successful control after attention
was placed specifically on environmental cleaning with a com-
mercially available oxidizing disinfectant (Virkon S; potas-
sium peroxomonosulphate 50%, sodium alkyl benzene sul-
phonate 15%, and sulphamic acid 5%).
methods
The outbreak occurred in a 19-bed long-stay ICU that has
an occupancy of 550–670 patient-days per month. It is within
a hospital that is a major referral center for trauma, burns,
and hematologic transplantation.
This assessment occurred during January 2004–December
2008. Patients in the ICU who were infected with CR-AB
were identified by culture of clinical specimens. Colonization
was identified by routine twice-weekly culture of endotracheal
aspirates on blood and MacConkey agar, performed for sur-
veillance purposes.1,2 On days 3–5 of ICU hospitalization and
upon discharge from the ICU, a rectal swab sample, nasal
swab sample, and wound swab sample (if a wound was pres-
ent) were also collected to determine whether carriage of CR-
AB and/or other multidrug-resistant organism were present.
As part of the investigation into this outbreak, 137 envi-
ronmental samples were collected for culture from May to
August 2006. A moistened cotton swab was swabbed over the
surface and plated onto MacConkey agar.
results
The outbreak. CR-AB isolates were recovered from 5 pa-
tients in 2004 but no patient in 2005. On January 30, 2006,
CR-AB was isolated from the respiratory tract of a patient in
the ICU. In early March 2006, CR-AB was isolated from a
second patient. Subsequently, as many as 5 new patients per
week were found to be colonized with CR-AB (Figure). In
all, 41 patients were found to be newly colonized or infected
with CR-AB during the period March 1–August 17, 2006.
In May 2006, culturing of environmental specimens com-
menced. Of 137 environmental sites sampled for culture in
the affected ICU, CR-AB was recovered from 11: a mattress,
a vital signs monitor, horizontal surfaces at the patient’s bed-
side, a computer keyboard and mouse, and a glucometer.
The CR-AB isolates of all 4 patients identified in March
2006 were found to have identical band patterns, implying
genotypic relatedness.3 We did not determine whether sub-
sequent isolates were related to these initial isolates.
Interventions. All patients identified as being colonized or
infected with CR-AB were nursed in single rooms with con-
tact isolation. In May 2006, the area within the ICU identified
as being contaminated (that is, within which environmental
specimens with positive culture results were collected) was
closed for a 3-day period. During this time, the area was
cleaned 3 times a day for 3 days with 1% neutral detergent
water solution, followed by cleaning with 70% alcohol–im-
pregnated wipes (contact time, 11 minute). Despite this in-
tense cleaning regimen, 2 of 12 cultures of environmental
samples from horizontal surfaces at the bedside yielded pos-
itive results.
A search for a new cleaning product was undertaken after
it had been clearly demonstrated that the current and in-
creased cleaning regimens were inadequate in removing CR-
AB from the environment. A commercial oxidizing disinfec-
tant (Virkon S; potassium peroxomonosulphate 50%, sodium
alkyl benzene sulphonate 15%, and sulphamic acid 5%) was
identified. This was introduced throughout the ICU on Au-
gust 17, 2006, and replaced all other cleaning solutions in
the ICU environment.
Follow-up. After the introduction of the new cleaning
product, just one new patient was found to be colonized with
CR-AB during the remainder of August 2006. In September
2006, 2 patients, and in October, 3 patients, were found to
be infected or colonized with CR-AB. There were then no
new cases until a single case on December 31, 2007. No cases
were seen in 2008, despite ongoing surveillance consisting of
twice-weekly cultures of endotracheal aspirates and rectal
swab samples. Use of the commercial surface disinfectant has
continued from August 17, 2006, to the present time.
This content downloaded from 23.235.32.0 on Thu, 22 Oct 2015 02:25:33 AM
All use subject to JSTOR Terms and Conditions
disinfectant against carbapenem-resistant a. baumannii 419
figure. Number of patients in the intensive care unit (ICU) colonized or infected with carbapenem-resistant Acinetobacter baumannii,
January 2004–December 2008. The new surface disinfectant was used in the ICU from August 17, 2006. From that point on, just 6 new
cases were detected in more than 2 years of follow-up.
Assessment of activity of the oxidizing disinfectant against
biofilm formation by A. baumannii. A strain from a patient
in the March 2006 outbreak was grown as static cultures at
37C in Luria Bertani medium. Biofilms were established by
placing a polyvinyl chloride (PVC) disk (diameter, 1 cm) in
the culture medium. After incubation for 20 hours, the PVC
disk was removed from the culture and washed extensively
in phosphatebuffered saline (PBS) to remove unbound bac-
teria. Each PVC disk was then subjected to 1 of 2 treatments:
(1) 10-minute incubation in PBS (control) or (2) 10-minute
incubation in PBS containing 0.5% this oxidizing disinfectant.
Biofilm formation was then assessed by staining with crystal
violet. Quantification of viable cells was performed by phys-
ically removing bacteria from the PVC disk, and enumeration
was performed by direct colony counting on agar plates.
The test strain formed a biofilm in this assay. Treatment
with this oxidizing disinfectant was highly efficient and re-
sulted in the killing of all viable cells within the biofilms.
discussion
In this report, we have described a discrete outbreak of in-
fection with CR-AB. The initial response to the outbreak in
our ICU was reinforcement of basic hand hygiene and contact
isolation. Despite these efforts, no reduction in the number
of cases was observed. Changes in antibiotic use appear un-
likely to have contributed to this outbreak (data not shown).
A “common source” environmental vehicle of A. baumannii
infection was sought, but diverse environmental sources were
found to be colonized. Despite intense environmental clean-
ing of affected areas within the ICU, the outbreak continued.
We found a temporal association between introduction of
a commercial oxidizing disinfectant and termination of the
outbreak. This disinfectant had not been used previously in
the institution. What are potential explanations for the ef-
fectiveness of the oxidizing disinfectant that we used and the
comparative ineffectiveness of our previous environmental
cleaning? With most disinfectants, viable A. baumannii re-
main if contact times are short or diluted agents are used.4
The bactericidal effects of agents against A. baumannii are
considerably reduced in the presence of organic material.5
These principles of decreased effectiveness if contact times
are short or organic material is present may have contribut-
ed to the lack of effect of our prior cleaning regimen. Alter-
natively, the oxidizing disinfectant that we used may have had
enhanced killing activity against A. baumannii. To our knowl-
edge, the activity of this disinfectant against A. baumannii has
not been evaluated previously. Production of biofilm by device-
related A. baumannii strains has been shown to be substantial.6
We have shown that our outbreak strain produced significant
amounts of biofilm and that when this biofilm was treated with
this oxidizing disinfectant, all of the bacterial cells were killed.
There is, therefore, a theoretical basis to our observation that
use of this product was associated with reduction in the pre-
sumed environmental acquisition of A. baumannii by our ICU
patients.
This content downloaded from 23.235.32.0 on Thu, 22 Oct 2015 02:25:33 AM
All use subject to JSTOR Terms and Conditions
420 infection control and hospital epidemiology april 2010, vol. 31, no. 4
In conclusion, we observed resolution of an outbreak of
CR-AB in an ICU. What are the limitations of our obser-
vations? Temporal associations may be misleading, because
epidemics may resolve of their own accord. We did not audit
cleaning effectiveness, hand hygiene compliance, and other
potential factors that could have influenced a reduction in
CR-AB. Finally, this oxidizing disinfectant has varied in its
sporicidal and antimicrobial activities.7 Factors that contrib-
ute to prolonged environmental contamination with CR-AB
clearly need further attention.8
acknowledgments
We thank Anthony Harris of the University of Maryland for his thoughtful
review of the manuscript.
Potential conflicts of interest. J. L. reports that he has received a re-
search grant from AstraZeneca, is a consultant to AstraZeneca and John-
son & Johnson, and has received honoraria from Wyeth. D. L. P. reports
that he has received research grants from the National Institutes of Health
(R01A1070896-01A1), the Centers for Disease Control and Prevention (U01
CI000283-02), AstraZeneca, Astellas, and Elan, and is a consultant to Acu-
reon, AstraZeneca, Merck, Advanced Life Sciences, and Johnson & Johnson.
All other authors report no conflicts of interest relevant to this article.
From the departments of Infectious Diseases (M.D., A.M.A., M.W., P.M.,
M.T., K.O., D.L.P.) and Critical Care Medicine (J.L.), Royal Brisbane and
Women’s Hospital, and the School of Molecular and Microbial Sci-
ences, University of Queensland (H.M.G., M.A.S.), the Central Microbi-
ology Laboratory, Pathology Queensland (N.G., G.R.N., D.L.P.), the Cen-
tre for Healthcare-Related Infection Surveillance and Prevention (D.L.P.),
and the University of Queensland Centre for Clinical Research (D.L.P.),
Brisbane, Australia.
Address reprint requests to David L. Paterson, 8th Fl, UQCCR Bldg, Royal
Brisbane and Women’s Hospital, Brisbane 4029, Australia (david.antibiotics@
gmail.com).
Received March 5, 2009; accepted September 29, 2009; electronically pub-
lished February 22, 2010.
 2010 by The Society for Healthcare Epidemiology of America. All rights
reserved. 0899-823X/2010/3104-0017$15.00. DOI: 10.1086/651312
references
1. Depuydt P, Benoit D, Vogelaers D, et al. Systematic surveillance cultures
as a tool to predict involvement of multidrug antibiotic-resistant bacteria
in ventilator-associated pneumonia. Intensive Care Med 2008;34:675–682.
2. Maragakis LL, Tucker MG, Miller RG, Carroll KC, Perl TM. Incidence
and prevalence of multidrug-resistant Acinetobacter using targeted active
surveillance cultures. JAMA 2008;299:2513–2514.
3. Tenover FC, Arbeit RD, Goering RV, et al. Interpreting chromosomal DNA
restriction patterns produced by pulsed-field gel electrophoresis: criteria
for bacterial strain typing. J Clin Microbiol 1995;33:2233–2239.
4. Wisplinghoff H, Schmitt R, Wohrmann A, Stefanik D, Seifert H. Resistance
to disinfectants in epidemiologically defined clinical isolates of Acineto-
bacter baumannii. J Hosp Infect 2007;66:174–181.
5. Kawamura-Sato K, Wachino J, Kondo T, Ito H, Arakawa Y. Reduction of
disinfectant bactericidal activities in clinically isolated Acinetobacter spe-
cies in the presence of organic material. J Antimicrob Chemother 2008;61:
568–576.
6. Rodriguez-Bano J, Marti S, Soto S, et al. Biofilm formation in Acinetobac-
ter baumannii: associated features and clinical implications. Clin Microbiol
Infect 2008;14:276–278.
7. Hernndez A, Martro E, Matas L, Martin M, Ausina V. Assessment of in
vitro efficacy of 1% Virkon against bacteria, fungi, viruses and spores by
means of AFNOR guidelines. J Hosp Infect 2000;46:203–209.
8. Peleg AY, Seifert H, Paterson DL. Acinetobacter baumannii: emergence of
a successful pathogen. Clin Microbiol Rev 2008;21:538–582.
This content downloaded from 23.235.32.0 on Thu, 22 Oct 2015 02:25:33 AM
All use subject to JSTOR Terms and Conditions


Control of an outbreak of carbapenem-resistant Acinetobacter baumannii in Australia after introduction of environmental cleaning with a commercial oxidizing disinfectant

http://espace.library.uq.edu.au/view/UQ:199090/UQ199090_OA.pdf

Control of an outbreak of carbapenem-resistant Acinetobacter baumannii in Australia after introduction of environmental cleaning with a commercial oxidizing disinfectant

Abstract

Similar works

Full text

Available Versions

Crossref

Crossref

University of Queensland eSpace