Enterobacter cloacae

is a rod-shaped, gram-negative bacteria from the Enterobacteriaceae family. The size of

this bacteria ranges from 0.3-0.6 x 0.8-2.0 m. Enterobacter cloacae lives in the
mesophilic environment with its optimal temperature at 37 C and uses its peritrichous
flagella for movement. This organism is oxidase negative but catalase positive and is
facultative anaerobic In other words, this organism can make ATP by aerobic respiration
when oxygen is present but can switch to fermentation in the absence of oxygen.
39564Enterobacter cloacae are nosocomial pathogens that can cause a range of
infections such as bacteremia, lower respiratory tract infection, skin and soft tissue
infections, urinary tract infections, endocarditis, intra-abdominal infections, septic
arthritis, osteomyelitis, and ophthalmic infections .
Enterobacter infections can necessitate prolonged hospitalization, multiple and varied
imaging studies and laboratory tests, various surgical and nonsurgical procedures, and
powerful and expensive antimicrobial agents
Pathophysiology
Enterobacter species rarely cause disease in healthy individuals. This opportunistic
pathogen, similar to other members of the Enterobacteriaceae family, possesses an
endotoxin known to play a major role in the pathophysiology of sepsis and its
complications.
Although community-acquired Enterobacter infections are occasionally reported,
nosocomial Enterobacter infections are, by far, most common. Patients most
susceptible to Enterobacter infections are those who stay in the hospital, especially the
ICU, for prolonged periods. Other major risk factors of Enterobacter infection include
prior use of antimicrobial agents, concomitant malignancy (especially hemopoietic and
solid-organ malignancies), hepatobiliary disease, ulcers of the upper gastrointestinal
tract, use of foreign devices such as intravenous catheters, and serious underlying
conditions such as burns, mechanical ventilation, and immunosuppression.
The source of infection may be endogenous (via colonization of the skin,
gastrointestinal tract, or urinary tract) or exogenous, resulting from the ubiquitous nature
of Enterobacter species. Multiple reports have incriminated the hands of personnel,
endoscopes, blood products, devices for monitoring intra-arterial pressure, and
stethoscopes as sources of infection. Outbreaks have been traced to various common
sources: total parenteral nutrition solutions, isotonic saline solutions, albumin, digital
thermometers, and dialysis equipment.
Risk factors
nosocomial Enterobacter infections include hospitalization of greater than 2 weeks,
invasive procedures in the past 72 hours, treatment with antibiotics in the past 30 days,
and the presence of a central venous catheter. Specific risk factors for infection with

nosocomial multidrug-resistant strains ofEnterobacter species include the recent use of

broad-spectrum cephalosporins or aminoglycosides and ICU care.

Epidemiology
Frequency
United States
National surveillance programs continually demonstrate that Enterobacter species
remain a significant source of morbidity and mortality in hospitalized patients.
In the Surveillance and Control of Pathogens of Epidemiological Importance [SCOPE]
project, 24,179 nosocomial bloodstream infections from 1995-2002 were
analyzed. Enterobacter species were the second-most-common gram-negative
organism behind Pseudomonas aeruginosa; however, both bacteria were reported to
each represent 4.7% of bloodstream infections in ICU settings. Enterobacterspecies
represent 3.1% of bloodstream infections in non-ICU wards. Of nearly 75,000 gramnegative organisms collected from ICU patients in the United States between 1993 and
2004, Enterobacter species comprised 13.5% of the isolates. Multidrug resistance
increased over time, especially in infections caused by E cloacae.[3]
The National Healthcare Safety Network (NHSN) reported on healthcare-associated
infections (HAI) between 2006 and 2007. They found Enterobacter species to be the
eighth most common cause of HAI (5% of all infections) and the fourth most common
gram-negative cause of HAIs.[4]
Previous reports from the National Nosocomial Infections Surveillance System (NNIS)
demonstrated that Enterobacter species caused 11.2% of pneumonia cases in all types
of ICUs, ranking third after Staphylococcus aureus (18.1%) and P aeruginosa (17%).
The corresponding rates among patients in pediatric ICUs were 9.8% for pneumonia,
6.8% for bloodstream infections, and 9.5% for UTIs.[5, 6, 7]
Enterobacter species were also among the most frequent pathogens involved in
surgical-site infections, as reported in the NNIS report from October 1986 to April 1997.
The isolation rate was 9.5% (with enterococci, coagulase-negative staphylococci, S
aureus, and P aeruginosa rates being 15.3%, 12.6%, 11.2%, and 10.3%, respectively).
Data on antibiotic resistance are available from the Intensive Care Antimicrobial
Resistance Epidemiology (ICARE) surveillance report. The rates
of Enterobacterresistance to third-generation cephalosporins were 25.3% in ICUs,
22.3% among non-ICU inpatients, 10.1% among ambulatory patients, and as high as
36.2% in pediatric ICUs.[8]
International
Enterobacter species have a global presence in both adult and neonatal ICUs.
Surveillance data and outbreak case reports from North and South America, Europe,

and Asia indicate that these bacteria represent an important opportunistic pathogen
among neonates and debilitated patients in ICUs.
The prevalence of Enterobacter resistance to beta-lactam antibiotics, aminoglycosides,
trimethoprim-sulfamethoxazole (TMP-SMZ), and quinolones seems to be higher in
certain European countries and Israel than in the United States and Canada. Higher
rates of Enterobacter resistance to fluoroquinolones and to beta-lactam and
cephalosporin antibiotics due to the production of extended-spectrum beta-lactamases
have been reported in South America and the Asian and Pacific regions. [9, 10]
Mortality/Morbidity
Enterobacter infections cause considerable mortality and morbidity rates.

Enterobacter species can cause disease in virtually any body compartment. They are
responsible for frequent and severe nosocomial infections that require prolonged
hospitalization, multiple and varied imaging studies and laboratory tests, various
surgical and nonsurgical procedures, and powerful and expensive antimicrobial
agents. Most importantly, Enterobacter infections that do not directly causing death
cause considerable suffering in many patients, most of whom are already afflicted with
chronic diseases.
In patients with Enterobacter bacteremia, the most important factor in determining the
risk of mortality is the severity of the underlying disease. Higher 30-day mortality rates
were noted in patients presenting with septic shock and increasing Acute Physiology
and Chronic Health Evaluation II scores. Other factors implicated, independently or by
association, in the outcome of Enterobacter bacteremia include thrombocytopenia,
hemorrhage, a concurrent pulmonary focus of infection, renal insufficiency, admission
in an ICU, prolonged hospitalization, prior surgery, intravascular and/or urinary
catheters, immunosuppressive therapy, neutropenia, antibiotic resistance, and
inappropriate antimicrobial therapy.
Recent studies have demonstrated that empirical aminoglycoside use and appropriate
initial antibiotic therapy were associated with lower mortality rates, whereas
vasopressor use, ICU care, and acute renal failure were associated with higher
mortality rates. Independent risk factors for mortality included cephalosporin
resistance, trimethoprim-sulfamethoxazole resistance, mechanical ventilation, and
nosocomial infection.[11, 12]
Crude mortality rates associated with Enterobacter infections range from 15-87%, but
most reported rates range from 20-46%. Attributable mortality rates are reported to
range from 6-40%.
o E cloacae infection is associated with the highest mortality rate of
allEnterobacter infections.
o
o

Bacteremia with cephalosporin-resistant Enterobacter species is associated with a

30-day mortality rate that significantly exceeds that of infections with susceptible
strains (33.7% vs 18.6%).
Mortality rates associated with Enterobacter pneumonia are higher than those of
pneumonia due to many other gram-negative bacilli. These rates range from 14-71%.
As with bacteremia, the severity of the underlying disease is the major factor that

predicts outcome. Other factors that indicate an unfavorable outcome include the
extent of the disease as seen on chest radiographs, corticosteroid therapy, isolation
of multiple pathogens from lower respiratory tract secretions, and, possibly, treatment
with a single antibiotic.
o A review of 17 cases of Enterobacter endocarditis reported an overall mortality rate
of 44.4%.
Race

Enterobacter infections have no reported or presumed racial predilection.

Sex

The male-to-female ratio of Enterobacter bacteremia is 1.3-2.5:1. This male

predominance is also reported in the pediatric population.
Age

Enterobacter infections are most common in neonates and in elderly individuals,

reflecting the increased prevalence of severe underlying diseases at these age
extremes. In the pediatric ICU setting, an age younger than 2.5 years is a risk factor for
colonization.
Signs and symptoms
Enterobacter infections do not have a clinical presentation that is specific enough to
differentiate them from other acute bacterial infections.
Bacteremia
Signs of Enterobacter bacteremia include the following:

Physical examination findings consistent with systemic inflammatory response

syndrome (SIRS): Including heart rate that exceeds 90 bpm, a respiratory rate greater
than 20, and a temperature above 38C or below 36C
Fever: Occurring in more than 80% of children and adults with Enterobacterbacteremia
Hypotension and shock: Occur in as many as one third of cases
Septic shock: Manifested as disseminated intravascular coagulation, jaundice, acute
respiratory distress syndrome, and other complications of organ failure
Purpura fulminans and hemorrhagic bullae
Ecthyma gangrenosum
Cyanosis and mottling: Frequently reported in children with Enterobacterbacteremia
Lower respiratory tract infections
Enterobacter lower respiratory tract infections can manifest identically to those caused
by Streptococcus pneumoniae or other organisms. The physical examination findings
may include the following:

Apprehension
High fever or hypothermia
Tachycardia
Hypoxemia

Tachypnea
Cyanosis
Patients with pulmonary consolidation may present with crackling sounds, dullness to
percussion, tubular breath sounds, and egophony. Pleural effusion may manifest as
dullness to percussion and decreased breath sounds.
See Clinical Presentation for more detail.
Diagnosis
Laboratory studies
Studies for the evaluation of Enterobacter infections include the following:

Complete blood count

Creatinine level
Electrolyte evaluation
Fluid analysis, such as cells and differential, proteins, glucose, and, in some cases,
pH, lactate dehydrogenase, and amylase; required for pleural, articular, pericardial,
peritoneal, and cerebrospinal fluids
Urine analysis: Always indicated for urinary tract infections (UTIs)
Factors in the microbiologic diagnosis and assessment of Enterobacter infection include
the following:

The most important test to document Enterobacter infections is culture; when the
patient presents with signs of systemic inflammation (eg, fever, tachycardia,
tachypnea) with or without shock (eg, hypotension, decreased urinary output), blood
cultures are mandatory
Direct Gram staining of the specimen is also useful, because it allows rapid diagnosis
of an infection caused by gram-negative bacilli and helps in the selection of antibiotics
with known activity against most of these bacteria
In the laboratory, growth of Enterobacter isolates is expected to be detectable in 24
hours or less; Enterobacter species grow rapidly on selective (ie, MacConkey) and
nonselective (ie, sheep blood) agars
Imaging studies
Studies used in the investigation and management of Enterobacter infections include
the following:

Chest infections: Serial chest radiography, chest ultrasonography, and computed

tomography (CT) scanning
Intra-abdominal infections: CT scanning and ultrasonography
Endocarditis and intravascular infections: Echocardiography (preferably
transesophageal) and nuclear indium scanning
UTIs: Renal ultrasonography; occasionally, CT scanning and pyelography
Central nervous system (CNS) and ophthalmic infections: CT scanning and/or
magnetic resonance imaging (MRI)
Bone and joint infections: Plain radiography, CT scanning and/or MRI studies, nuclear
medicine studies

New technologies such as positron emission tomography (PET) scanning may be

indicated in very selective cases, particularly for differentiation of neoplasia and
infection.
ManaGEMENT
E cloacae, E aerogenes, and most otherEnterobacter species are resistant to the
narrow-spectrum penicillins that traditionally have good activity against other
Enterobacteriaceae such as E coli (eg, ampicillin, amoxicillin) and to firstgeneration and second-generation cephalosporins (eg, cefazolin, cefuroxime).
They also are usually resistant to cephamycins such as cefoxitin. Initial
resistance to third-generation cephalosporins (eg, ceftriaxone, cefotaxime,
ceftazidime) and extended-spectrum penicillins (eg, ticarcillin, azlocillin,
piperacillin) varies but can develop during treatment. The activity of the fourthgeneration cephalosporins (eg, cefepime) is fair, and the activity of the
carbapenems (eg, imipenem, meropenem, ertapenem, doripenem) is excellent.
However, resistance has been reported, even to these agents
Surgical care is indicated as for other sources of infection: drainage or debridement of
abscesses, infected collections, or osteomyelitic foci.