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      Drugs & Diseases > Infectious Diseases

      Enterobacter Infections Clinical Presentation

      Updated: Jun 02, 2022
      • Author: Susan L Fraser, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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      Presentation

      History

      Enterobacter infections do not produce a unique enough clinical presentation to differentiate them clinically from other acute bacterial infections. Consequently, details on the patient history and physical examination findings for each infected body compartment are not provided in this article, with the exception of lower respiratory tract infections and bacteremia. Details regarding similar disease presentations are available throughout Medscape Reference via the links provided in the Differentials section.

      Bacteremia

      Most cases of Enterobacter bacteremia are nosocomial, frequently acquired in the ICU.

      E cloacae, followed by E hormaechei, are the species implicated most frequently in Enterobacter bacteremia cases.

      Mixed bacteremia is common (14-53%).

      The portal of entry into the bloodstream is frequently unknown, but any infected organ, central line, or arterial catheters may be the primary source of bacteremia.

      Symptoms of Enterobacter bacteremia are similar to those of bacteremia due to other gram-negative bacilli.

      Lower respiratory tract infections

      The clinical presentations caused by Enterobacter lower respiratory tract infections include asymptomatic colonization, tracheobronchitis, pneumonia, lung abscess, and empyema.

      As with other respiratory pathogens, chronic obstructive pulmonary disease, diabetes mellitus, alcohol abuse, malignancy, and neurologic diseases are risk factors for the acquisition of lower respiratory tract infections.

      Prior antimicrobial therapy may predispose to Enterobacter pneumonia.

      Enterobacter species are a significant cause of ventilator-associated pneumonia.

      Enterobacter species are major pathogens in early post–lung transplant pneumonia. In most cases, the bacteria are transmitted from the donor.

      Symptoms of Enterobacter pneumonia are not specific to these bacteria. Fever, cough, production of purulent sputum, tachypnea, and tachycardia are usually present.

      As with infections caused by organisms such as Streptococcus pneumoniae, many Enterobacter infections in elderly debilitated patients do not cause a systemic inflammatory reaction. However, this clinical presentation is by no means benign, and the associated mortality rate is particularly high in this population.

      Skin and soft tissue infections

      In most cases, Enterobacter skin and soft tissue infections are hospital-acquired and include cellulitis, fasciitis, myositis, abscesses, and wound infections.

      Enterobacter species can infect surgical wounds in any body site, and these infections are clinically indistinguishable from infections caused by other bacteria.

      In 1985, Palmer et al reviewed an outbreak of postsurgical Enterobactermediastinitis. [22] Cases varied in severity from fulminant bacteremic infections to less-severe wound infections. The source was unknown, and a case-control analysis suggested that surgical complications and prophylaxis with cephalosporins were associated with the infection. The level of skin and wound colonization was high among patients who underwent cardiac surgery during this outbreak. The outbreak was controlled with barrier isolation, restriction of contacts, and a reduction in the duration of cephalosporin prophylaxis.

      Other Enterobacter wound infections have been reported in the literature. Infected body sites have included a posterior spinal wound, burn wounds (many reports), and different types of injuries involving trauma to multiple sites. Some of the infections were polymicrobial. Some authors have noted a trend of traditional wound bacteria (eg, S aureus) being replaced by Enterobacter species and other nosocomial pathogens. Some trauma-related wound infections are acquired before hospital admission. This was the case with agricultural mutilating wounds caused by corn-harvesting machines. Gram-negative rods were predominant (81%), the most common being Enterobacter species and Stenotrophomonas maltophilia.

      Enterobacter species occasionally cause community-acquired soft-tissue infections in healthy individuals, including those who sustain war-related or trauma-related injuries.

      Endocarditis

      A case report described a patient with E cloacae endocarditis on a porcine mitral heterograft. An accompanying literature review disclosed 17 additional cases. Two thirds of the patients had underlying cardiac disease; most had mitral valve infection, and 4 patients had concomitant aortic valve involvement. [23]

      A few more case reports subsequent to this case series have been published in both English and non-English literature, including one case of E asburiae causing both cotton fever and native valve endocarditis in an intravenous drug user.  [24, 25]

      Urinary tract infections

      Enterobacter UTI is indistinguishable from a UTI caused by other gram-negative bacilli.

      Pyelonephritis with or without bacteremia, prostatitis, cystitis, and asymptomatic bacteriuria can be caused by Enterobacter species, as with Escherichia coli and other gram-negative bacilli.

      Most Enterobacter UTIs are nosocomial and are associated with indwelling urinary catheters and/or prior antibiotic therapy.

      Intra-abdominal infections

      Enterobacter species may be isolated together with colonic flora in intra-abdominal abscesses or peritonitis following intestinal perforation or surgery.

      A frequent cause of Enterobacter involvement is prior digestive-tract colonization by Enterobacter species during hospitalization.

      Case reports have described Enterobacter hepatobiliary sepsis, including emphysematous cholecystitis, suppurative cholangitis, and hepatic gas gangrene in a child after liver transplantation. Hemorrhagic necrotizing pancreatitis developed in a 72-year-old woman with obstructive jaundice.

      Central nervous system infections

      Neonatal meningitis resulting from C sakazakii infection is described in Age.

      In 1993, Durand et al published a review of 493 episodes of acute bacterial meningitis. [26] This study involved patients aged 16 years or older admitted to Massachusetts General Hospital from January 1962 through December 1988. Gram-negative bacilli were the etiologic agents in 4% and 38% of community-acquired and nosocomial meningitis, respectively. In community-acquired infections, Enterobacter was isolated in one of the 9 cases of meningitis caused by gram-negative bacilli (E coli 4 times, Klebsiella species 3 times, and Proteus once) and in 5 of the 57 episodes of nosocomial meningitis (E coli 17 times, Klebsiella species 13 times, Pseudomonas species 6 times, and Acinetobacter species 6 times).

      Other series were reported from various countries (United States, Iceland, United Kingdom, Senegal, Brazil). Gram-negative bacilli were not among the 5 most common causes of meningitis in any of these countries.

      Ophthalmic infections

      Enterobacter species account for a small fraction of postsurgical endophthalmitis and posttraumatic cases. [27]

      Most ophthalmic infections are caused by gram-positive organisms, but Enterobacter species and Pseudomonas species are among the most aggressive pathogens.

      Bone and joint infections

      Enterobacter species are occasionally implicated in septic arthritis, on both native and prosthetic joints, and can result in osteomyelitis and discitis in adults and children.

      Enterobacter bone and joint infections are usually more difficult to cure than those caused by S aureus. They often occur in patients with complex surgical and medical histories.  [28] The authors have observed relapses that required additional treatment following the initial 6 weeks of intravenous therapy. 

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      Physical

      Bacteremia

      Physical examination findings consistent with systemic inflammatory response syndrome (SIRS) include heart rate that exceeds 90 bpm, a respiratory rate of greater than 20, and temperature of greater than 38°C or less than 36°C.

      More than 80% of children and adults with Enterobacter bacteremia develop fever.

      Hypotension and shock occur in as many as one third of cases.

      Disseminated intravascular coagulation, jaundice, acute respiratory distress syndrome, and other organ failures reflect the severity of septic shock.

      Purpura fulminans and hemorrhagic bullae usually observed with meningococci or viruses causing hemorrhagic fever may be part of the clinical presentation of Enterobacter bacteremia.

      Ecthyma gangrenosum, usually associated with Pseudomonas or Aeromonas bacteremia, may also be observed.

      Cyanosis and mottling is frequently reported in children with Enterobacter bacteremia.

      Lower respiratory tract infections

      The physical manifestations caused by Enterobacter are not specific for infection with these bacteria. Enterobacter lower respiratory tract infections can manifest identically to those caused by S pneumoniae or other organisms.

      The physical examination findings may include apprehension, high fever or hypothermia, tachycardia, hypoxemia, tachypnea, and 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.

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      Causes

      Species of the Enterobactercloacae complex are gram-negative bacilli that belong to the Enterobacteriaceae family. Other members of this family include Klebsiella, Escherichia, Citrobacter,Cronobacter, Serratia, Salmonella, and Shigella species, among many others. Enterobacteriaceae are the most common bacterial isolates recovered from clinical specimens. These bacteria have an outer membrane that contains, among other things, lipopolysaccharides from which lipid-A plays a major role in sepsis. Lipid-A, also known as endotoxin, is the major stimulus for the release of cytokines, which are the mediators of systemic inflammation and its complications.

      In the microbiology laboratory, colonies of Enterobacteriaceae appear large, dull-gray, and dry or mucoid on sheep blood agar. All Enterobacteriaceae ferment glucose and, consequently, are able to grow in aerobic and anaerobic atmospheres.

      MacConkey agar is a lactose-containing medium that is selective for nonfastidious gram-negative bacilli such as Enterobacteriaceae. Using the enzymes beta-galactosidase and beta-galactoside permeases, the most frequently encountered species of Enterobacter strains activate the pH indicator (neutral red) included in MacConkey agar, giving a pink or red stain to the growing colonies. Klebsiella and Enterobacter species may appear similar as mucoid colonies but can be differentiated with a few specific tests. In contrast to Klebsiella species, Enterobacter organisms are motile, usually ornithine decarboxylase-positive, and urease-negative. E sakazakii (reclassified into the Cronobacter genus in 2007) produces a characteristic yellow pigment.

      Six different species comprise the E cloacae complex. Some have never been associated with human infections. The most commonly isolated species include E cloacae and E hormaechei, followed by the rarely encountered Enterobacter asburiae, Enterobacter gergoviae, Enterobacter taylorae, and Enterobacter cancerogenus. Enterobacter aerogenes was renamed K aerogenes in 2017. [6]

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