# 50 - 167 Acinetobacter Infections

### 167 Acinetobacter Infections

EDWARDSIELLA INFECTIONS
E. tarda is the only member of the genus Edwardsiella that is associated 
with human disease. This organism is found predominantly in freshwa­
ter and marine environments and in the associated aquatic animal spe­
cies. Human acquisition occurs primarily from interaction with these 
reservoirs or ingestion of raw or inadequately cooked aquatic animals. 
E. tarda infection is rare in the United States, where acquisition occurs 
mainly along the Gulf of Mexico; recently reported cases are mostly 
from Asia. This pathogen shares clinical features with Salmonella spe­
cies (as an intestinal pathogen; Chap. 171), Vibrio vulnificus (as an 
extraintestinal pathogen; Chap. 173), and Aeromonas hydrophila (as 
both an intestinal and an extraintestinal pathogen; Chap. 173).

■
■INFECTIOUS SYNDROMES
Gastroenteritis is the predominant Edwardsiella-associated infectious 
syndrome (50–80% of reported cases). Self-limiting watery diarrhea 
is most common, but severe colitis also occurs. The most common 
extraintestinal infection is wound infection due to direct inoculation, 
which is often associated with brackish or freshwater injuries, snake­
bites, or fish-related trauma. A case of pneumonia occurred after a 
near-drowning incident. Cholecystitis, cholangitis, and hepatic abscess 
may be due to ascending infection via the biliary tree. Other infec­
tious syndromes result from invasion of the gastrointestinal tract and 
subsequent bacteremia. A primary bacteremic syndrome, sometimes 
complicated by meningitis, has a 40% case–fatality rate; hematogenous 
seeding may result in hepatic and intra- and extraperitoneal abscesses, 
endocarditis, mycotic aneurysm, septic arthritis, osteomyelitis, nec­
rotizing fasciitis, and empyema. Most hosts who develop systemic 
Edwardsiella infection have significant comorbidities (e.g., hepatobili­
ary disease, iron overload, cancer, or diabetes mellitus).
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Infectious Diseases
■
■DIAGNOSIS
Although E. tarda can readily be isolated and identified, most laborato­
ries do not routinely screen for or identify it in stool samples. Produc­
tion of hydrogen sulfide is a characteristic biochemical property.
TREATMENT
Edwardsiella Infections
E. tarda is susceptible to most antimicrobial agents appropriate for 
use against GNB. Gastroenteritis is generally self-limiting, but treat­
ment with a fluoroquinolone may hasten resolution. In the setting 
of severe sepsis, fluoroquinolones, third- and fourth-generation 
cephalosporins, carbapenems, and amikacin—either alone or in 
combination—are the safest choices pending susceptibility data.
INFECTIONS CAUSED BY MISCELLANEOUS 
GENERA
Other gram-negative organisms such as Hafnia, Kluyvera, Cedecea, 
Pantoea, Ewingella, Leclercia, Raoultella, and Photorhabdus spp. are 
occasionally isolated from diverse clinical specimens, including blood, 
sputum, urine, cerebrospinal fluid, joint fluid, bile, and wounds. Such 
organisms cause infection predominantly in compromised hosts or 
in association with an invasive procedure or foreign body. Cephalo­
sporinases from Kluyvera have been implicated as the progenitors of 
CTX-M ESBLs. Kluyvera and Raoultella may produce carbapenemases.
■
■FURTHER READING
Antimicrobial Resistance Collaborators: Global burden of bac­
terial antimicrobial resistance in 2019: A systematic analysis. Lancet 
399:629, 2022. [Erratum in Lancet 400:1102, 2022.]
Bonten M et al: Epidemiology of Escherichia coli bacteremia: A sys­
tematic literature review. Clin Infect Dis 72:1211, 2021.
Cheng MP et al: Beta-lactam/beta-lactamase inhibitor therapy for 
potential AmpC-producing organisms: A systematic review and 
meta-analysis. Open Forum Infect Dis 6:ofz248, 2019.
David S et al: Epidemic of carbapenem-resistant Klebsiella pneumoniae 
in Europe is driven by nosocomial spread. Nat Microbiol 4:1919, 2019.

Harris PNA et al: Effect of piperacillin-tazobactam vs meropenem 
on 30-day mortality for patients with E coli or Klebsiella pneumoniae 
bloodstream infection and ceftriaxone resistance: A randomized 
clinical trial [published correction appears in JAMA 321:2370, 2019]. 
JAMA 320:984, 2018.
Holy O, Forsythe S: Cronobacter spp. as emerging causes of health­
care-associated infection. J Hosp Infect 86:169, 2014.
Kamiyama S et al: Edwardsiella tarda bacteremia, Okayama, Japan, 
2005–2016. Emerg Infect Dis 25:1817, 2019.
Russo TA, Marr CM: Hypervirulent Klebsiella pneumoniae. Clin 
Microbiol Rev 32:e00001, 2019.
Tamma PD et al: Infectious Diseases Society of America 2022 Guid­
ance on the Treatment of Extended-Spectrum β-lactamase Producing 
Enterobacterales (ESBL-E), Carbapenem-Resistant Enterobacterales 
(CRE), and Pseudomonas aeruginosa with Difficult-to-Treat Resis­
tance (DTR-P. aeruginosa). Clin Infect Dis 75:187, 2022.
van Duin D et al: Molecular and clinical epidemiology of carbapenemresistant Enterobacterales in the USA (CRACKLE-2): A prospective 
cohort study Lancet Infect Dis 20:731, 2020. [Erratum in Lancet 
Infect Dis 19:30755, 2020.]
Weiner-Lastinger LM et al: Antimicrobial-resistant pathogens asso­
ciated with adult healthcare-associated infections: Summary of data 
reported to the National Healthcare Safety Network, 2015–2017. 
Infect Control Hosp Epidemiol 41:1, 2020.
Rossana Rosa, Christine A. Vu

Acinetobacter Infections
■
■DEFINITION
Acinetobacter species were first described in 1911 and named Micro­
coccus calcoaceticus. Thereafter, the genus was renamed multiple 
times; since 1950, it has been known as Acinetobacter. Acinetobacter 
species are gram-negative, oxidase-negative, nonmotile, nonferment­
ing coccobacilli that are easily recovered on standard culture media. 
Differentiation among Acinetobacter species on the basis of phenotypic 
characteristics alone is very difficult. Molecular-based methods such as 
matrix-assisted laser desorption–ionization–time-of-flight mass spec­
trometry (MALDI-TOF-MS) and quantitative real-time polymerase 
chain reaction (PCR) are usually necessary to identify Acinetobacter 
baumannii, the most clinically relevant species of the genus.
■
■ETIOLOGY AND EPIDEMIOLOGY
Acinetobacter species are naturally encountered in water and soil 
and have also been recovered from fruits and vegetables. In humans, 
Acinetobacter can be found on the skin and in the respiratory and 
gastrointestinal tracts. A. baumannii is capable of surviving environ­
mental desiccation for weeks; this characteristic is important from an 
infection-control perspective as it allows this organism to persist in the 
hospital environment and on equipment.
Acinetobacter was historically considered a pathogen of hot and 
humid climates. In recent years, however, hospital outbreaks caused 
by A. baumannii have been reported worldwide, even in temperate 
climates. In the United States, the Centers for Disease Control and 
Prevention (CDC) estimates that 12,000 Acinetobacter infections occur 
every year, 7300 of which are caused by multidrug-resistant strains, 
with 500 attributable deaths. The increase in the number of infections 
with A. baumannii is suspected to be due to the rapid spread of certain 
genetically distinct lineages; of the three international clonal lineages 
(ICLs), ICL I and ICL II are multidrug resistant. The predominance 
of these lineages remains unexplained, although it has been proposed 
that this population structure is the result of two waves of expansion.

The first wave followed a bottleneck (possibly linked to a restricted 
ecologic niche) that occurred in the distant past. The second wave is 
ongoing and is being driven by the rapid expansion of a limited num­
ber of multidrug-resistant clones. The COVID-19 pandemic resulted 
in a setback to the efforts to control the spread of multidrug-resistant 
organisms, with significant increases in the rates of infections with 
carbapenem-resistant Acinetobacter reported worldwide.
Analysis of the A. baumannii pangenome (the sum of the core and 
dispensable genomes) has shown that its organization is charac­
terized by a small core genome and a large accessory or disposable 
genome. This organization reflects A. baumannii’s high plasticity, 
which enables it to acquire exogenous genetic material. With few 
exceptions, gene functions associated with virulence are found in the 
core genome; this observation suggests a limited role for the acquisi­
tion of new virulence traits in the recent nosocomial expansion of A. 
baumannii clones. Genes associated with resistance to antimicrobial 
agents are found in both the species core genome and the accessory 
genome. In the accessory genome, these genes have been found in alien 
islands, often flanked by integrases, transposases, or insertion 
sequences. This pattern suggests possible acquisition by horizontal 
gene transfer from other Acinetobacter strains or even from different 
bacterial species present in the immediate environment. Acquisition of 
these antimicrobial resistance genes is hypothesized to have led to the 
recent rapid expansion of highly homogeneous clonal lineages, whose 
main difference from nonclonal A. baumannii appears to be their anti­
microbial resistance.
Health Care–Associated Infections 
Infections caused by A. 
baumannii occur frequently among patients admitted to intensive 
care units (ICUs). Risk factors for colonization and infection with this 
pathogen include nursing home residence, prolonged ICU stay, central 
venous catheterization, tracheostomy, mechanical ventilation, enteral 
feedings, and treatment with third-generation cephalosporins, fluoro­
quinolones, and carbapenems. Acquisition of carbapenem-resistant A. 
baumannii is most common among patients exposed to carbapenems. 
Spread of A. baumannii across different regions is facilitated by the 
movement of patients between health care systems and throughout the 
continuum of health care. Within the hospital, environmental spread of 
A. baumannii occurs as a result of inappropriate hand hygiene among 
workers providing health care for infected or colonized patients and 
the contamination of hospital equipment, such as respiratory therapy 
and ventilation equipment. The air surrounding the patient may also 
play a role in environmental colonization with A. baumannii, especially 
in inpatient areas without physical barriers between patients and with 
an inadequate number of air exchanges.
A. baumannii strains identified during hospital outbreaks are typi­
cally resistant to more antibiotic classes than strains from the commu­
nity. The prevalence of colonization with A. baumannii at the time of 
admission or during a stay in a long-term acute-care hospital (LTACH) 
or nursing home is variable and depends on regional flora. Outbreaks 
of A. baumannii in acute-care hospitals and LTACHs that “share” 
patients have been described in Ohio, Michigan, Illinois, and Indiana.
Community-Acquired Infections 
Community-acquired infec­
tions caused by Acinetobacter have been described in Australia and 
Asia. Few cases have been reported in regions with a temperate climate, 
and even those few cases have taken place during warm and humid 
months. Risk factors for community-acquired pneumonia due to this 
organism include a history of alcohol abuse, diabetes mellitus, smok­
ing, and chronic lung disease.
War Zone–Associated Infections 
Infections caused by Acineto­
bacter in war zones include skin and soft tissue infections associated 
with traumatic injuries and bloodstream infections. Outbreak investi­
gations of A. baumannii infections among military personnel returning 
from Iraq and Afghanistan suggested the acquisition of A. baumannii 
in field hospitals rather than colonization of the skin before an injury. 
This view is supported by the recovery of A. baumannii isolates with 
similar genetic characteristics from inanimate surfaces in field hospi­
tals and from patients.

Disaster Medicine 
A. baumannii is linked to infections among 
victims of trauma during tsunamis, earthquakes, and terrorist attacks. 
The types of infections most frequently observed in these settings are 
soft tissue injuries, but bloodstream infections and pneumonia have 
also been reported. In addition, outbreaks of A. baumannii infection in 
ICUs caring for disaster victims have been described.

■
■PATHOGENESIS
Mechanisms of pathogenesis and virulence in Acinetobacter spe­
cies have not been fully elucidated. However, A. baumannii seems 
to have greater virulence potential than other Acinetobacter species, 
as evidenced by its ability to grow at 37°C and to resist uptake by 
macrophages.
Initial A. baumannii colonization of the host and the environment 
is facilitated by the organism’s ability to adhere to surfaces and human 
cells and to create biofilms. The ability to form a biofilm is phenotypi­
cally associated with exopolysaccharide production and pilus forma­
tion. A quorum-sensing molecule encoded by the abaI autoinducer 
synthase gene has been implicated in A. baumannii biofilm formation 
on abiotic surfaces. Outer-membrane porins appear to mediate cell 
apoptosis. A. baumannii can survive in harsh environments within 
the host and on inanimate surfaces by modifying the structure of its 
lipid A, with a consequent decrease in susceptibility to antibiotics and 
antimicrobial peptides and an increase in survival upon desiccation.
Acinetobacter species produce an extracellular capsule that protects 
the bacteria from external threats, including complement-mediated 
killing. Studies of mouse models showed that Acinetobacter species can 
increase capsule production in the presence of subinhibitory levels of 
antibiotic—an ability that leads to increased resistance to complementmediated killing and a hypervirulent phenotype.
CHAPTER 167
Phospholipase C and phospholipase D have been identified as viru­
lence factors in A. baumannii. These enzymes exert cytotoxic effects on 
epithelial cells and facilitate their invasion.
Iron-acquisition systems are also important virulence mechanisms 
in A. baumannii. Through secretion of siderophores (low-molecularmass ferric-binding compounds), A. baumannii is able to grow despite 
iron deficiencies in the surrounding environment (e.g., in the human 
host).
Acinetobacter Infections
Several protein-secretion systems have been identified in A. bau­
mannii. The most recently described is a type II secretion system. 
The substrate for this system, the LipA lipase, is required for growth 
on medium containing lipids as a sole carbon source. Mutants lack­
ing the genes for the type II secretion system or its substrate exhibit 
defective in vivo growth in a neutropenic murine model of bacteremia. 

A. baumannii also has a type VI secretion system whose primary 
function seems to be to secrete antibacterial toxins that kill competing 
bacteria, including other strains in the same species.
The type V autotransporter system has been characterized in 

A. baumannii. In a murine systemic model of Acinetobacter infection, 
the Acinetobacter trimeric autotransporter mediates biofilm formation 
and maintenance; adherence to extracellular matrix components such 
as collagen I, II, and IV; and virulence.
Outer-membrane vesicles (OMVs) play a special role in protein 
secretion. Many A. baumannii strains secrete OMVs containing vari­
ous virulence factors, including outer-membrane protein A (OmpA), 
proteases, and phospholipases. The membrane proteins in OMVs are 
responsible for eliciting a potent innate immune response. Several 
studies have shown that A. baumannii OMVs could be used as an acel­
lular vaccine to effectively control A. baumannii infections.
Nosocomial strains of Acinetobacter can deploy multiple mecha­
nisms of resistance, including alterations in porins and efflux pumps 
and expression of β-lactamases. More specifically, Acinetobacter spe­
cies can reduce the expression of porins, thus hindering the passage 
of β-lactam antibiotics into the periplasmic space. These species can 
overexpress bacterial efflux pumps and decrease the concentration of 
β-lactam antibiotics in the periplasmic space. Efflux pumps can also 
actively remove quinolones, tetracyclines, chloramphenicol, disinfec­
tants, and tigecycline. Acinetobacter species possess chromosomally 
encoded cephalosporinases and are capable of acquiring β-lactamases,

including serine and metallo-β-lactamases. AmpC β-lactamases are 
class C β-lactamases intrinsic to all A. baumannii strains. Although 
these enzymes are expressed at low levels and are not inducible, the 
addition of the insertion sequence ISAba1 next to the AmpC gene 
increases β-lactamase production, with resulting resistance to most 
cephalosporins.

Carbapenem resistance in Acinetobacter species is mostly tied to 
the emergence of Ambler class D oxacillinases of group 2d, some of 
which are intrinsic and chromosomal (e.g., OXA-51-like) while others 
are acquired and are found in plasmids or are chromosomally encoded 
(e.g., OXA-23-like, 24 [33-like, 40-like], 58-like, 143-like, and 235-like).
■
■CLINICAL MANIFESTATIONS
Pneumonia 
A. baumannii is a notorious cause of nosocomial pneu­
monia, most frequently among patients requiring prolonged mechani­
cal ventilation. The onset of disease tends to be later than that caused 
by other gram-negative bacilli; however, clinical symptoms of hospitalacquired or ventilator-associated pneumonia due to A. baumannii are 
similar to those of nosocomial or ventilator-associated pneumonia 
due to other nosocomial pathogens. Thus, the most common indica­
tors of infection include fever and increased sputum production. The 
positivity of respiratory cultures in most cases may present a challenge 
for the clinician since airway colonization with A. baumannii may not 
always indicate a diagnosis of pneumonia, but it is a known risk factor 
for infection itself. In addition, radiologic findings are nonspecific and 
can include lobar consolidations and pleural effusions, with cavitations 
being rarely seen. The crude mortality rates associated with nosoco­
mial pneumonia due to A. baumannii are reported as high as 65%. 
However, since these infections occur in debilitated patients, their 
attributable mortality has been difficult to establish.
PART 5
Infectious Diseases
Community-acquired pneumonia due to A. baumannii is relatively 
rare. Its clinical presentation is characterized by fever, severe respira­
tory symptoms, and multiple-organ dysfunction. Patients frequently 
have a cough productive of purulent sputum, shortness of breath, and 
chest pain. Imaging studies usually show lobar consolidation. Mortality 
rates associated with this process are >50%.
Bloodstream Infections 
Bloodstream infections due to A. bau­
mannii are most frequent among ICU patients and usually occur in the 
presence of a central venous catheter or as a secondary complication of 
hospital-acquired or ventilator-associated pneumonia. Polymicrobial 
growth has been reported in 20–36% of bacteremia episodes. Fever 
is the most common sign of infection (developing in >95% of cases), 
and presentation with septic shock and disseminated intravascular 
coagulopathy has been described in as many as 25 to 30% of patients, 
respectively. A. baumannii bloodstream infections often result in 
higher hospitalization costs and longer ICU stays. Crude mortality 
rates from this infection are as high as 40%; however, rates can be as 
high as 70% from infections caused by carbapenem-resistant isolates. 
In patients with infections caused by extremely drug-resistant strains, 
poor outcomes are thought to be driven by delays in the initiation of 
adequate antimicrobial therapy.
Skin and Soft Tissue Infections 
Acinetobacter species have been 
described as part of the skin flora, yet the majority of the organisms 
from this genus that colonize the skin are not those associated with 
nosocomial infections. Discerning infection from wound coloniza­
tion is challenging. Gunshot wounds and the presence of orthopedic 
external-fixation devices are common among patients with combat 
trauma–associated A. baumannii skin and soft tissue infections. The 
report on a case series of eight U.S. military patients described the 
clinical presentation of their infections as evolving from an edematous 
peau d’orange appearance to a sandpaper appearance with overlying 
vesicles and then to a necrotizing process with hemorrhagic bullae. 
Other case series have also included necrotizing fasciitis. A. baumannii 
is an important pathogen in burn units worldwide. Large burns pro­
vide ideal conditions for A. baumannii and facilitate patient-to-patient 
transmission. The presence of A. baumannii in wounds contributes to 
healing delays and graft loss. In addition, wound colonization is a risk 

factor for bloodstream infections among patients with extensive burn 
injuries.
A. baumannii infections resulting from trauma to soft tissues in the 
setting of natural disasters, such as tsunamis and earthquakes, have 
been reported. The implication is that A. baumannii should be con­
sidered in the differential diagnosis of soft tissue infections following 
exposure to tropical and subtropical environments.
Urinary Tract Infections 
A. baumannii is an infrequent cause of 
urinary tract infections. The majority of cases reported are catheterassociated infections, reflecting the ability of A. baumannii to form 
biofilms on these devices. A few reports have described communityacquired infections occurring in the setting of nephrolithiasis and after 
renal transplantation.
Meningitis 
Central nervous system infections with A. baumannii 
have been reported in the context of outbreaks, traumatic injuries, 
neurosurgical procedures, and external ventricular drains. One case 
series described a petechial rash in up to 30% of patients. Acinetobacter 
species may look similar to Neisseria meningitidis on a Gram stain of 
cerebrospinal fluid; both appear as gram-negative paired cocci. Eradi­
cation of A. baumannii from the cerebrospinal fluid can be challenging 
and requires careful selection of antibiotics that adequately penetrate 
the site of infection.
Other Miscellaneous Infections 
A few cases of A. baumannii ker­
atitis associated with the use of contact lenses have been reported. Cases 
of native- and prosthetic-valve endocarditis have also been described.
TREATMENT
Acinetobacter Infections
Treatment of Acinetobacter infections is challenging due to difficul­
ties in differentiating colonization versus infection and because 
Acinetobacter can develop resistance to most available antibiotics. 
Therefore, the choice of empirical therapy should be based on local 
epidemiology and, if available, the patient’s colonization status 
with a carbapenem-resistant isolate. Definitive therapy should be 
determined by antimicrobial susceptibility testing. Antimicrobial 
options for the management of infections caused by A. baumannii 
are displayed in Table 167-1.
Acinetobacter species possess intrinsic β-lactamases that inacti­
vate first- and second-generation cephalosporins. Through acquisi­
tion of extended-spectrum β-lactamases, these organisms can also 
become resistant to third- and fourth-generation cephalosporins, 
along with carbapenems. Nevertheless, when the isolate is suscep­
tible, β-lactam agents should be used. Ampicillin-sulbactam (due to 
its sulbactam component) is the treatment of choice, with cefepime, 
meropenem, and imipenem as alternative options based on in vitro 
susceptibility testing.
Currently, there is no antibiotic regimen that has been proven 
superior for the treatment of carbapenem-resistant A. baumannii. 
The 2024 Infectious Diseases Society of America (IDSA) “Guidance 
on the Treatment of Antimicrobial Resistant Gram-Negative Infec­
tions” recommends sulbactam-durlobactam in combination with a 
carbapenem as their preferred regimen, and high-dose ampicillinsulbactam in combination with either polymyxin B, minocycline, 
tigecycline, or cefiderocol is an alternative. Pairing of sulbactam 
with durlobactam makes a novel diazabicyclooctane non-β-lactam 
β-lactamase inhibitor with activity against the Acinetobacterderived cephalosporinases and class D β-lactamases including car­
bapenemases of the OXA family. High-dose ampicillin-sulbactam 
is recommended in combination with either polymixn B, mino­
cycline, tigecycline, or cefiderocol. The use of high-dose over 
standard dose ampicillin-sulbactam increases binding of sulbactam 
to its penicillin-binding proteins (PBP) targets (PBP2 and PBP3) 
in order to optimize inhibition of cell wall synthesis. This recom­
mendation is based on two meta-analyses of small clinical trials 
and observational data. In a randomized clinical trial including 125 
patients with carbapenem-resistant A. baumannii, patients treated

TABLE 167-1  Therapeutic Options for the Management of MultidrugResistant Acinetobacter baumannii Infections
ANTIBIOTIC
DOSINGa
COMMENTS
Sulbactam
6–9 g/d
Unavailable as single drug 
in many countries (including 
the United States). Different 
dosing strategies proposed 
if administered with 
ampicillin.
Ampicillinsulbactam
3 g q4h
9 g q8h
27 g q24h
Infuse over 30 min
Infuse over 4 h
Infuse as continuous 
infusion
Sulbactamdurlobactam
1 g/1 g q6h
Infuse over 3 h
Meropenem
2 g q8h
Carbapenem-susceptible 
isolates only; infuse over 3 h
Imipenemcilastatin
500 mg q6h
Carbapenem-susceptible 
isolates only; infuse over 3 h
Cefiderocol
2g q8h
Use in combination therapy; 
infuse over 3 h
Colistin
Dosing per the international 
consensus guidelines on 
polymixins (Tsuji BT et al, 
Pharmacotherapy 39:10, 2019)
Colistin is preferred for 
urinary tract infections.
Polymyxin B
Dosing per the international 
consensus guidelines on 
polymixins (Tsuji BT et al, 
Pharmacotherapy 39:10, 2019)
Polymyxin B is preferred 
over colistin for 
bloodstream infections.
Tigecycline
200-mg loading dose followed by 
100 mg q12h
Use in combination therapy
Minocycline
200 mg q12h
IV/PO. Use in combination 
therapy
aAll drugs are given by the IV route unless otherwise stated.
with sulbactam-durlobactam had a 28-day all-cause mortality of 19% 
compared to 32% in patients treated with colistin, and with lower 
rates of nephrotoxicity in the sulbactam-durlobactam arm.
Cefiderocol is a siderophore cephalosporine with in vitro stabil­
ity against the Acinetobacter-derived cephalosporinase and other 
-Hand hygiene
-Contact precautions
Health care worker’s
hands 
A. baumannii–
positive patient
Shared equipment 
Health care
environment
-Physical separation from
 A. baumannii–negative
 patients
-Rectal surveillance
-Cohorting nursing
 personnel
-Chlorhexidine baths
-Antibiotic stewardship
-Daily and terminal
 disinfection
-Limits on shared equipment
-Disinfection of equipment
 between patients
FIGURE 167-1  Strategies for the prevention of dissemination of Acinetobacter baumannii in health care facilities.

extended-spectrum β-lactamases. However, A. baumannii isolates 
with reduced cefiderocol susceptibility have been described, and 
in a randomized clinical trial that included 54 critically ill patients 
with carbapenem-resistant A. baumannii, the end-of-study mortal­
ity was 50% in the cefiderocol arm, compared to 18% in the best 
available therapy arm (mostly consisting of colistin).

Polymyxins are cationic detergents that have become less popu­
lar as a result of nephrotoxicity and neurotoxicity. Additionally, 
polymyxins are difficult to dose, have a narrow therapeutic win­
dow, and do not reach optimal tissue concentration in the lungs, 
which is a common site of infection for A. baumannii. Despite its 
disadvantages, polymyxin B and polymyxin E (colistin) have been 
reintroduced in clinical practice as they retain in vitro activity 
against carbapenem-resistant A. baumannii. In a randomized study 
of patients with pneumonia due to carbapenem-resistant Acineto­
bacter, patients receiving colistin in combination with high-dose 
ampicillin-sulbactam had a higher rate of clinical improvement 
by day 5 compared to those receiving colistin monotherapy. The 
combination of colistin plus meropenem was long favored due to 
in vitro synergy; however, two randomized controlled trials showed 
this strategy had comparable outcomes to colistin monotherapy.
Several tetracycline derivatives have in vitro activity against A. 
baumannii. Of them, tigecycline and minocycline could be con­
sidered as part of a combination regimen, used at high doses when 
minimum inhibitory concentrations are low. Although doxycycline 
is a widely available agent with established breakpoints against A. 
baumannii, it is usually less active than minocycline. Eravacycline is 
a newer tetracycline with promising activity against A. baumannii; 
however its use has been limited; it is currently being marketed to 
treat more resistant strains.
CHAPTER 167
Bacteriophage therapy against multidrug-resistant A. baumannii 
has been reported with varied success rates. Furthermore, dosing 
and duration of therapy vary by syndrome and resistance can also 
arise during treatment.
Acinetobacter Infections
■
■COMPLICATIONS AND PROGNOSIS
Infections caused by A. baumannii can be associated with high mor­
tality rates. Factors contributing to higher mortality are thought to 
include severity of the patient’s underlying illness and drug resistance 
in the infecting strain.
A. baumannii–
negative patient
-Physical separation from
 A. baumannii–positive
 patients
-Cohorting nursing
 personnel
-Chlorhexidine baths
-Antibiotic stewardship