H E A LT H C A R E E P I D E M I O L O G Y INVITED ARTICLE

Robert A. Weinstein, Section Editor

The Epidemiology and Control of Acinetobacter baumannii

in Health Care Facilities
Pierre Edouard Fournier1,2 and Hervé Richet2

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1
Structural and Genetic Information Laboratory and 2Unité des Rickettsies, Faculté de Médecine, Marseille, France

Acinetobacter baumannii is a ubiquitous pathogen capable of causing both community and health care–associated infections
(HAIs), although HAIs are the most common form. This organism has emerged recently as a major cause of HAI because
of the extent of its antimicrobial resistance and its propensity to cause large, often multifacility, nosocomial outbreaks. The
occurrence of outbreak is facilitated by both tolerance to desiccation and multidrug resistance, contributing to the maintenance
of these organisms in the hospital environment. In addition, the epidemiology of A. baumannii infection is often complex,
with the coexistence of epidemic and endemic infections, the latter of which often is favored by the selection pressure of
antimicrobials. The only good news is that potentially severe A. baumannii infection, such as bacteremia or pneumonia in
patients in the intensive care unit who are undergoing intubation, do not seem to be associated with a higher attributable
mortality rate or an increased length of hospital stay.

Acinetobacter baumannii is a ubiquitous pathogen capable of suggest that A. baumannii is a remarkable microorganism be-
causing both community and health care–associated infections cause of the diversity of its habitat, the way it accumulates
(HAIs) that has recently emerged as a major cause of HAI, mechanisms of antimicrobial resistance, its resistance to des-
because of its propensity to accumulate mechanisms of anti- iccation, its propensity to cause outbreaks of infection, and the
microbial resistance that lead to pan-drug resistance and cause complexity of its epidemiology. Therefore, in this review, we
large HAI outbreaks that often involve multiple facilities. A. will focus on these unusual features and on unresolved issues.
baumannii mainly causes pulmonary, urinary tract, blood-
stream or surgical wound infections. Major risk factors include TAXONOMY
invasive procedures, such as the use of mechanical ventilation,
The genus Acinetobacter consists of strictly aerobic, gram-neg-
central venous or urinary catheters, and broad-spectrum
ative cocobacillary rods that grow at 20–30C on usual labo-
antimicrobials.
ratory media. Bacteria classified as members of the genus Aci-
However, knowledge about A. baumannii is much less de-
netobacter have a long history of taxonomic changes, moving
veloped than knowledge about other opportunistic pathogens,
from the family Neisseriaceae to the family Moraxellaceae.
such as Pseudomonas aeruginosa, as demonstrated by a search
Within the genus Acinetobacter, studies based on DNA/DNA
of the Medline database performed on 1 April 2005, which
hybridization have resulted in the description of 25 “genomic
revealed 30,247 citations for P. aeruginosa versus only 703 for
species” that fulfilled the criteria to be considered distinct spe-
A. baumannii. Another important limitation is the difficulty in
cies, 17 of which have officially been validated to date (http:/
correctly identifying this organism, leading to the publication
/www.bacterio.cict.fr/a/acinetobacter.html). Only 10 species
of data that are of questionable value. However, available data
have been given names, but differential biochemical and growth
tests have been published for 19 species.
Received 9 June 2005; accepted 26 October 2005; electronically published 26 January Schreckenberger and colleagues, authors of The Manual of
2006.
Reprints or correspondence: Dr. Hervé Richet, Unité des Rickettsies, Faculté de Médecine,
Clinical Microbiology [1], believe that the majority of the gen-
27, boulevard Jean Moulin, 13385 Marseille cedex 5, France (Herve.Richet@medecine ospecies cannot be reliably separated by phenotypic tests. How-
.univ-mrs.fr).
ever, because it is difficult to differentiate the isolates according
Clinical Infectious Diseases 2006; 42:692–9
 2006 by the Infectious Diseases Society of America. All rights reserved.
to their phenotypic characteristics, the term “A. calcoaceticus–
1058-4838/2006/4205-0018$15.00 A. baumannii” complex is often used.

692 • CID 2006:42 (1 March) • HEALTHCARE EPIDEMIOLOGY

HABITAT
A. baumannii is ubiquitous in nature and has been recovered
from soil, water, animals, and humans. Acinetobacter species
are normal inhabitants of human skin and are frequently iso-
lated from the throat and respiratory tract of hospitalized pa-
tients. For this reason, it has been suggested that human skin
could be the source of severe infections, such as bacteremia.
However, this hypothesis has not been confirmed in healthy
humans. Berlau et al. [2] have studied the distribution of Aci-
netobacter species on the skin of 192 healthy volunteers and
found that if 40% of volunteers carried Acinetobacter species
(Acinetobacter lwoffi in 60% of the cases), only 1 individual
carried a strain belonging to the A. baumannii–A. calcoaceticus
group. In contrast, recent studies have shown that A. baumannii
can be found in unsuspected reservoirs, such as food or ar-
thropods, and additional reservoirs remain to be discovered.
From 1 January 2002 to 31 August 2004, A. baumannii grew
from blood samples obtained from 102 patients hospitalized at
military medical facilities treating service members injured in
Afghanistan and the Iraq-Kuwait region. The sources of A.
baumannii that led to the infections are still unknown, but
during the Vietnam War, A. baumannii was the most common
gram-negative bacillus recovered from traumatic injuries to ex-
tremities. Recent reports [3–7] also have identified A. bau-
mannii infections in patients who suffered traumatic injuries,
suggesting environmental contamination of wounds as a po-
tential source, even if such a source is still unknown.
Food is known to be a source for gram-negative rods, such
as Escherichia coli, but if Acinetobacter species isolates have been
found in a variety of food items, including raw vegetables, few
data exist about the presence of A. baumannii in the food chain.
Therefore, Berlau and colleagues have sought to assess the dis-
tribution and frequency of Acinetobacter genospecies in a variety
of purchased or harvested fresh fruits and vegetables [8]. Results
showed that 17% of vegetables grew Acinetobacter in small
numbers and that A. baumannii and genospecies 11 were the
species most frequently isolated. The A. baumannii–A. cal-
coaceticus complex accounted for 56% of all strains isolated
from fruits and vegetables and were found in apple, melon,
bean, cabbage, cauliflower, carrot, potato, radish, lettuce, cu-
cumber, pepper, mushroom, and sweet corn. According to Ber-
lau et al. [8], hospital food could be a potential source for A.
baumannii acquisition. In addition, studies have shown that
digestive-tract colonization may be common in the hospital
environment, with colonization rates as high as 41% in patients
in the intensive care unit [9].
In a study seeking to isolate Bartonella quintana from body
lice collected from homeless persons in Marseille, France, La
Scola et al. [10] isolated and genotyped 40 A. baumannii strains,
of which 21 were surprisingly susceptible to ampicillin. The
genotypes of those strains were limited to 2 clones, including
1 that was susceptible to ampicillin. A. baumannii DNA was
later detected in 21% of 622 lice collected worldwide, leading
to the conclusion that there is an epidemic of A. baumanii
infection among human body lice, which may be a source of
human A. baumannii infection [10].
DESSICATION TOLERANCE
Several investigators have suspected that the survival of A. bau-
mannii in the environment could contribute to the transmission
of the organism during outbreaks. This hypothesis has been
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confirmed by several studies. By replicating hospital conditions,
Jawad et al. [11] have shown that A. baumannii organisms were
able to survive for an average of 20 days at a relative humidity
of 31%. Other investigators showed that A. baumannii strains
could be isolated from a hospital bed rail 9 days after the
discharge of an infected patient from the hospital [12]. In an-
other study, Wendt et al. [13] have shown that the ability of
A. baumannii strains to survive under dry conditions varied
greatly and was correlated with the source of the strains. Strains
isolated from dry sources had better survival rates than strains
isolated from wet sources. Of interest, Houang et al. [14] have
shown that A. baumannii underwent morphological changes
when desiccated with cells that had significantly thicker and
more electron-dense cell walls and nucleic acid than those of
control specimens. Even if such an environmental source does
not explain per se the transmission of an epidemic strain, it
suggests that hospital equipment could serve as a secondary
reservoir for A. baumannii [15]. The potential role played by
the capacity of A. baumannii to survive in the hospital envi-
ronment in the spread of epidemic strains is suggested a pos-
teriori by the success of control measures, including environ-
mental decontamination with hypochlorite solutions. However,
it is obvious that environmental decontamination is only one
measure among many and that the independent role in infec-
tion control of this approach has never been evaluated [16].
ANTIMICROBIAL RESISTANCE AND GENETICS
More than in its virulence characteristics, the main danger
associated with A. baumannii resides in its capability to acquire
antimicrobial-resistance genes extremely rapidly, leading to
multidrug resistance [17]. As a result, the management of A.
baumanii infection has become a public health problem in
many countries [18]. Of the 102 A. baumannii strains isolated
from infections in service members injured in Afghanistan and
the Iraq-Kuwait region, a high degree of antimicrobial resis-
tance was discovered, including resistance to all drugs found
in 4% of isolates [3]. In France, an outbreak of nosocomial
infections occurred from 1 April 2003 to 31 May 2004 [19]
and was caused by a multidrug-resistant A. baumannii isolate,
HEALTHCARE EPIDEMIOLOGY • CID 2006:42 (1 March) • 693
named AYE, which expressed the blaVEB-1 extended-spectrum
b-lactamase and was susceptible only to imipenem, ticarcillin-
clavulanate, and piperacillin-tazobactam.
It is estimated that the acquisition of resistance mechanisms
by A. baumannii strains is a recent phenomenon that started
in the 1970s [17]. This extremely rapid development of anti-
microbial resistance is likely to result from the ability of A.
baumannii to respond rapidly to challenges issued by antimi-
crobials, coupled with the widespread use of antimicrobials in
the hospital environment. In particular, the influence of the
wide use of extended-spectrum cephalosporins and quinolones
To date, A. baumannii has become resistant to almost all
antimicrobial agents that are currently available [42, 43]. Re-
sistance mechanisms involve antimicrobial-degradating en-
zymes, efflux pumps, target modification, and porin deficiency.
One of the main concerns about antimicrobial resistance in A.
baumannii has been the acquisition or carbapenem resistance,
mainly through the acquisition of B and D class carbapene-
mases [18, 19, 26]. The latter resistance deprives physicians of
one of the most active antimicrobials against A. baumannii.
Many reports have also described an increase in the heavy-
metal resistance mechanisms in A. baumannii [23]. For ex-

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has been demonstrated [20–21].
Mechanisms of resistance. Several mechanisms have been
shown to play a role in the acquisition of a multidrug-resistance
phenotype by A. baumannii, including the acquisition of mobile
genetic elements, such as plasmids [22], transposons [23], in-
tegrons [19–24], and natural transformation [25]. The role of
plasmids in the acquisition of antimicrobial resistance in A. bau-
mannii is mostly related to the integron structures they carry.
The presence of class I and class II integrons in A. baumannii
has been significantly associated with multiple antibiotic resis-
tance, and the nosocomial spread of isolates [19, 23, 24, 26] has
been described in both clinical and environmental strains of
Acinetobacter baumannii worldwide [27–32]. These integrons are
mostly acquired by contact with bacteria present in similar en-
vironments, such as Enterobacteriaceae [28] or Pseudomonas spe-
cies [19, 33, 34]. One of the most striking examples of integron
transfer between Pseudomonas species and A. baumannii is the
acquisition of the class I integron carrying the blaVEB-1 extended-
spectrum b-lactamase and 6 other antimicrobial resistance genes,
which were acquired from P. aeruginosa (figure 1) [19]. In ad-
dition to the acquisition of mobile genetic elements, Acinetobacter
species show a high frequency of natural transformation [35–
37]. Natural transformation in A. baumannii is made easier by
homomogy-facilitated illegitimate recombination that enables
stable integration within the chromosome of antimicrobial re-
sistance markers carried by plasmids, followed by loss of plasmid
markers [23, 25, 38–40]. The short-term accumulation and com-
bination of several of these mechanisms in A. baumannii strains
facilitate the coselective process under different antimicrobial se-
lective pressures [41].
ample, mercury-resistance operons are widely distributed
among both clinical and environmental bacteria, to which the
operons are introduced by transposons [44]. As for arsenic-
resistance operons, which have been described as encoding low
or high levels of resistance to both arsenic and antimony, they
are also widespread in environmental strains of A. baumannii
[45].
Recently, the first genome-based study has been conducted
to identify all resistance mechanisms accumulated by the AYE
strain epidemic in France [46]. The authors identified an un-
expected 86-kb resistance island, the largest in a bacterium to
date, which contained 45 clustered resistance genes. In contrast,
3 plasmids also identified in the bacterium were free of any
resistance marker.
INFECTION
Types of infection. Many A. baumannii organisms isolated
from respiratory secretion and urine specimens obtained from
hospitalized patients demonstrate colonization rather than in-
fection. Most infections involve organ systems with a high fluid
content, such as the respiratory tract, peritoneal fluid, and the
urinary tract, and are associated with indwelling devices. Path-
ological changes that are observed depend on the organ in-
volved and are not distinguishable from changes caused by
other aerobic gram-negative bacilli.
The distribution of the different types of infection varies from
one hospital to another and is probably related to the hospital
population and the type of procedures and interventions per-
formed. A prospective regional study performed in Spain of

Figure 1. Schematic representation of class I integron found in Acinetobacter baumannii strain AYE. Gene cassettes are shown as boxes, with
arrows indicating the orientation of transcription and black circles indicating the 59-base element. The intI1 gene is an integrase. Filled and empty
triangles indicate IS1999 inverted repeats. The resistance determinants carried by the integron are as follows: b-lactams, blaVEB-1 (extended spectrum
b-lactamase) and blaOXA-10 (oxacillinase); aminoglycosides, aadB and aadA1 (adenylyltransferases); rifampin, arr-2 (ADP-ribosylating transferase);
chloramphenicol, cmlA5 (major facilitator superfamily efflux pump); sulphonamides, sul1; and antiseptics, qacED1 (small multidrug resistance family
efflux pump). Adapted from [16] with permission.

694 • CID 2006:42 (1 March) • HEALTHCARE EPIDEMIOLOGY

240 A. baumannii infections showed that 190% of infections
were nosocomially acquired and that only 4% were community
acquired. In this study, respiratory tract infections were the
most common (39%), followed by exudates and abscesses (24%
each) and urinary tract infections (23%). Of interest is that
bacteremia represented only 3% of all infections [47].
A different distribution of infections was observed in a ret-
rospective study performed in a 3956-bed teaching hospital in
Marseille, France, during a 3-year period (1 January 2002–31
December 2004). In this study, 656 A. baumannii infections
were identified, and exudates and abscesses were the most com-
mon infections (32%), followed by urinary tract infections
(25%), respiratory tract infections (20%), and bacteremia
(12%). This study also showed seasonality in the occurrence
of A. baumannii infection during the 3-year period, with a
significantly greater number of infections occurring from July
through September (mean number of infections per month 
SD, 22  6) than from January through March (mean number
of infections per month  SD, 13  5; P p .005) (H. Richet,
unpublished data). The reason for this seasonality is unknown,
but it has also been observed by McDonald et al. [48], who,
by analyzing the National Nosocomial Infections Surveillance
System data for a 10-year period, showed that rates of Acine-
tobacter species infections were significantly higher during the
July–October period and that this increase was mostly attrib-
utable to bloodstream infections and pneumonia and to infec-
tions occurring in the New England region.
Outcome of A. baumannii infection. Little is known about
the genes and factors involved in virulence properties besides
that siderophore activity and adherence properties play a role
in the occurrence of colonization and infection [49]. Therefore,
the only way to assess the virulence of A. baumannii is indirectly
and consists of assessing the outcome of infections. Rates of
mortality ranging from 5% in general wards to 54% in intensive
care units have been associated with A. baumannii infections,
suggesting the existence of a certain amount of virulence in
this bacteria [50–51]. However, those are crude data, and few
studies have sought to assess the attributable mortality and to
evaluate the role of comorbidities in the outcome. Blot et al.
[52] have sought to assess outcome and attributable mortality
in critically ill patients with nosocomial A. baumannii bacter-
emia by performing a matched case-control study comparing
patients with A. baumannii bacteremia in the intensive care
unit with nonbacteriemic patients in the intensive care unit.
Matching criteria included having an equivalent APACHE II
score, having the same principal diagnosis leading to the ad-
mission to the intensive care unit, and having the same length
of stay in the intensive care unit. The crude mortality rate was
42.2% among case patients and 34.4% among control patients,
resulting in an attributable mortality of 7.8% for A. baumannii
bacteremia that was not statistically significant. In multivariate
survival analysis, older age was the only variable significantly
associated with in-hospital mortality, and A. baumannii bac-
teremia was not an independent predictor of mortality [52].
Another study seeking to assess the clinical impact of pneu-
monia caused by A. baumannii by using a matched case-control
study approach showed the same type of results. Among pa-
tients in the intensive care unit undergoing intubation, pneu-
monia due to A. baumannii was not associated with significant
differences in either attributable mortality rate or an increased
length of stay in the intensive care unit [53].
Frequency of nosocomial infections. Data exist at the na-
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tional, regional, or local level. At the national level, a prevalence
survey performed in France in June 2001 in 1533 health care
facilities containing 381,303 beds and including 305,656 pa-
tients showed a prevalence of A. baumannii infection of 0.075%.
A. baumannii was the 15th most frequently isolated microor-
ganism from nosocomial infections, representing only 1.2% of
all microorganisms [54].
In a regional prospective study performed in a network of
28 health care facilities in Spain serving a population of
11,000,000 people, the overall incidence of A. baumannii in-
fection and/or colonization was 0.39 cases per 1000 patient-
days, ranging from 0 to 1.17 cases per 1000 patient-days, de-
pending on the health care facility, and ranging from 0.14 to
4.55 cases per 1000 patient-days in intensive care units. Only
3 patients were pediatric. Among the 206 patients, 53% of cases
were infection, 43.4% of cases were colonization, and 3.6% of
cases were community acquired [47].
Therapeutic challenges. Currently, there has been renewed
interest in 2 molecules for the treatment of infections caused
by multidrug-resistant A. baumannii. Sulbactam, in combina-
tion with b-lactams, has been demonstrated to treat efficiently
infections caused by A. baumannii moderately resistant to im-
ipenem [55]. For pan-resistant strains, colistin remains the drug
of choice. This antimicrobial has been used with success to
treat severe infections, such as meningitis, bacteremia, or pneu-
monia [53, 56–61]. Deterioration of renal function was the
main adverse effect, with a prevalence ranging from 19% to
27% [59–61].
However, the results of animal studies have a tendency to
contradict the results of clinical studies regarding the role and
place of colistin for the treatment of severe infections caused
by multidrug-resistant A. baumannii [62, 63].
OUTBREAKS
One important feature of A. baumannii is its propensity to
cause outbreaks, which is probably in relation to 2 important
characteristics of the organism already described in this review:
antimicrobial resistance and resistance to desiccation. The main
results of 86 outbreaks investigations caused by A. baumannii,
which have been published in the English language literature
HEALTHCARE EPIDEMIOLOGY • CID 2006:42 (1 March) • 695
Table 1. Locations of health care outbreaks caused by Acine- shown to cause multifacility outbreaks. Such outbreaks have
tobacter baumannii. occurred in France and in the United States. In France, from
July 2003 to May 2004, 290 cases of infections and/or colo-
No. of
nizations occurred in 55 health care facilities located in 55
Location outbreaks
different administrative departments. Thirty strains were typed
Multiple health care facilities 2
by PFGE, were shown to share the same restriction profile, and
Multiple services and/or departments within
the same health care facility 2 were identical to the multidrug-resistant AYE strain described
Adult intensive care unit 26 in the Antimicrobial Resistance Section of this article. Most
Neonatal intensive care unit 3 patients were hospitalized in intensive care units. Of the 217
Burn unit 4 patients for whom clinical data were available, 73 (33%) suf-
Neurosurgery unit 3 fered from infection and 144 (67 %) were colonized. Among

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Surgery unit 2 the 73 infected patients, the deaths of 19 (26 %) were directly
Internal medicine unit 1
attributed to A. baumannii infection. It was suspected that the
Oncology unit 1
transfer of infected and/or colonized patients from one facility
to another was responsible for the spread of the epidemic strain
across France [67].
from October 1990 to October 2004, are shown below. First,
Another multifacility outbreak occurred in 15 health care
it is important to underline the fact that epidemiologic data
facilities in Brooklyn, New York, from July to September 1999,
were present in only 54% of the publications; the remaining
during which 419 isolates were collected, with 62 of them be-
articles included only microbiologic data.
longing to a single clone that was present in all 15 health care
The analysis of the locations where these outbreaks occurred
facilities. Fifty-three percent of the isolates were resistant to
shows that 2 outbreaks involved multiple health care facilities
imipenem, and 12% were resistant to all standard antimicro-
and that another 2 outbreaks involved multiple services and/or
bials [18].
departments in the same health care facility. Regarding the spe-
Control of outbreaks. When a source and/or reservoir were
cific services and/or departments involved, 26 (59%) of them
identified, the outbreak was controlled by the eradication of
were intensive care units (table 1). Many risk factors for epidemic
infections have been identified, including host factors, proce- the source/reservoir. In other circumstances, various measures
dures, treatments, or the circumstances of the hospitalization, were used, including unit closure, cohorting of patients and
and more specifically, admission to wards with a high density of staff, strict hand hygiene, contact or strict isolation, environ-
infected and/or colonized patients (table 2). Environmental con- mental disinfection, discharge of all colonized patients, con-
tamination of various hospital items has been often identified,
ranging from suctioning equipment to pillows and mattresses
Table 2. Risk factors for epidemic Acinetobacter
(table 3). The role of hands has also been investigated, showing
baumannii infections and/or colonizations.
that hand-carriage rates among staff members (nurses and phy-
sicians) ranged from 3% to 23% and that the carriage was usually High APACHE II score
transient, except in the case of damaged skin [64, 65]. It is Prematurity
important to note that strict infection-control measures, such as Procedure
contact isolation precautions, limit both staff colonization and Surgery
environmental contamination. This was clearly demonstrated by Catheterization
Paavilainen et al. [66], who performed a prospective study to Mechanical ventilation and duration
assess staff and environmental colonization following the transfer Previous antimicrobial therapy
Carbapenems
of a pediatric patient with severe burns who was colonized with
Fluoroquinolones
multidrug-resistant A. baumannii from another hospital, where
Third generation cephalosporins
this strain had caused an outbreak. Of the 1907 postexposure
Aminoglycosides
cultures performed on specimens collected from the staff and Receipt of blood products
425 environmental samples, only 0.7% and 4%, respectively, grew Contaminated parenteral solutions
this microorganism. However, it is important to emphasize that Enteral feeding
the patient was cared for in a private room, with contact isolation, Circumstances of hospitalization
by a hospital staff of 26 persons, of whom there were 7 main Length of stay
nurses who did not participate in the care of other patients in High work load
the ward [66]. Admission to wards with a high density of infected
and/or colonized patients
Multifacility outbreaks. Recently, A. baumannii has been

696 • CID 2006:42 (1 March) • HEALTHCARE EPIDEMIOLOGY

 Table 3. Acinetobacter baumannii out-
breaks and items involved in environmen-
tal contamination.
Suctioning equipment
Washbasin
Bedrail
Bedside
Table
Ventilator
Infusion pump
Sink
Hygroscopic bandage
Shower trolley
Pillow
Mattress
Resuscitation equipment
Stainless steel trolley
trolled antimicrobial use, and prompt identification of new
cases.
COMPLEXITY OF THE EPIDEMIOLOGY OF A.
BAUMANNII INFECTION
Prevention of infection requires knowledge about the epide-
miology of infection. This epidemiology can be straightforward
when sources and reservoirs have been identified and when it
is easy to differentiate between sporadic and epidemic cases of
infection. This is not the case with A. baumannii. However, the
development of molecular typing methods has provided clinical
microbiologists with powerful tools to explore the epidemiology
of infections and to reveal the molecular heterogeneity of the
isolates of A. baumannii within clinics or health care facilities.
Rodriguez-Bano et al. [47] have shown in their multicenter
study that the number of clones in an individual health care
facility ranged from 1 to 4, except in 3 health care facilities in
which 9–15 clones were identified. In addition, a predominant
clone was observed in the 14 health care facilities where the
greatest numbers of cases were observed [47]. In another study
performed in a medical intensive care unit in France, molecular
typing showed that, during an “outbreak,” epidemic cases co-
existed with sporadic cases, and the epidemiologic investigation
revealed that risk factors for epidemic cases included having
undergone a surgical procedure in the emergency operating
room, whereas the main risk factor for sporadic cases was pre-
vious receipt of fluoroquinolone. In addition, a parallelism was
shown between the incidence of A. baumannii infections and
the amount of intravenous fluoroquinolone used. In conclu-
sion, the control of these infections was made possible by the
implementation of control measures adapted to the risk factors
identified [68].
CONCLUSIONS
In conclusion, A. baumannii is a fascinating microorganism
because of the diversity of its reservoirs, its capacity to accu-
mulate genes and/or mechanisms of antimicrobial resistance,
its resistance to desiccation, and its propensity to cause out-
breaks. However, several shadow areas persist. We know very
little about the virulence of the microorganism, reservoirs re-
main to be discovered, and strategies to control the spread of
multidrug-resistant strains have to be designed and evaluated.
There is also another challenge: the treatment of infections
caused by multidrug-resistant strains.
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Acknowledgments
Potential conflicts of interest. P.E.F. and H.R.: no conflicts.
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