Is Enterobacter cloacae infection Dangerous in the Elderley?

2 ANSWERS

1. jane
   

   Hello,
   
   
   Enterobacter species, particularly Enterobacter cloacae and Enterobacter aerogenes, are important nosocomial pathogens responsible for various infections, including bacteremia, lower respiratory tract infections, skin and soft-tissue infections, urinary tract infections (UTIs), endocarditis, intra-abdominal infections, septic arthritis, osteomyelitis, and ophthalmic infections. Enterobacter species can also cause various community-acquired infections, including UTIs, skin and soft-tissue infections, and wound infections, among others.
   
   Risk factors for 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 of Enterobacter species include the recent use of broad-spectrum cephalosporins or aminoglycosides and ICU care.
   
   These "ICU bugs" cause significant morbidity and mortality, and infection management is complicated by resistance to multiple antibiotics. Enterobacter species possess inducible beta-lactamases, which are undetectable in vitro but are responsible for resistance during treatment. Physicians treating patients with Enterobacter infections are advised to avoid certain antibiotics, particularly third-generation cephalosporins, because resistant mutants can quickly appear. The crucial first step is appropriate identification of the bacteria. Antibiograms must be interpreted with respect to the different resistance mechanisms and their respective frequency, as is reported for Enterobacter species, even if routine in vitro antibiotic susceptibility testing has not identified resistance.
   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.
   
   Enterobacter species contain a subpopulation of organisms that produce a beta-lactamase at low-levels. Once exposed to broad-spectrum cephalosporins, the subpopulation of beta-lactamase–producing organisms predominate. Thus, an Enterobacter infection that appears sensitive to cephalosporins at diagnosis may quickly develop into a resistant infection during therapy. Carbapenems and cefepime have a more stable beta-lactam ring against the lactamase produced by resistant strains of Enterobacter.
   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. Enterobacter species represent 3.1% of bloodstream infections in non-ICU wards. In a more recent report, of nearly 75,000 gram-negative 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.1
   
   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.2,3,4
   
   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 Enterobacter resistance 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.5
   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.6,7
   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.8,9
       * 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 all Enterobacter infections.
             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%).
             o 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.
   
   s*x
   
       * 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.
       * Enterobacter sakazakii has been reported as a cause of sepsis and meningitis, complicated by ventriculitis, brain abscess, cerebral infarction, and cyst formation.10 This clinical pattern appears to be specific to E sakazakii in neonates and infants infected with this bacterium. E sakazakii has also been associated with many outbreaks due to contaminated powdered formula for infants.11
   
   Clinical
   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 the eMedicine journal via the links provided in Differentials.
   
       * Bacteremia
             o Most cases of Enterobacter bacteremia are nosocomial, frequently acquired in the ICU.
             o E cloacae, followed by E aerogenes, are by far the species implicated most frequently in Enterobacter bacteremia cases.
             o Mixed bacteremia is common (14-53%).
             o The portal of entry into the bloodstream is frequently unknown, but any infected organ may be the primary source of bacteremia.
             o Symptoms of Enterobacter bacteremia are similar to those of bacteremia due to other gram-negative bacilli.
       * Lower respiratory tract infections
             o The clinical presentations caused by Enterobacter lower respiratory tract infections include asymptomatic colonization, tracheobronchitis, pneumonia, lung abscess, and empyema.
             o 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.
             o Prior antimicrobial therapy may predispose to Enterobacter pneumonia.
             o Enterobacter species are a significant cause of ventilator-associated pneumonia.
             o Enterobacter species are major pathogens in early post–lung transplant pneumonia. In most cases, the bacteria are transmitted from the donor.
             o Symptoms of Enterobacter pneumonia are not specific to these bacteria. Fever, cough, production of purulent sputum, tachypnea, and tachycardia are usually present.
             o 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
             o In most cases, Enterobacter skin and soft-tissue infections are hospital-acquired and include cellulitis, fasciitis, myositis, abscesses, and wound infections.
             o Enterobacter species can infect surgical wounds in any body site, and these infections are clinically indistinguishable from infections caused by other bacteria.
             o In 1985, Palmer et al reviewed an outbreak of postsurgical Enterobacter mediastinitis.12 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.
             o 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.
             o Enterobacter species occasionally cause community-acquired soft-tissue infections in healthy individuals, including those who sustain war-related injuries.
       * Endocarditis
             o 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.13
             o A few more case reports subsequent to this case series have been published in both English and non-English literature.
       * Urinary tract infections
             o Enterobacter UTI is indistinguishable from a UTI caused by other gram-negative bacilli.
             o 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.
             o Most Enterobacter UTIs are nosocomial and are associated with indwelling urinary catheters and/or prior antibiotic therapy.
       * Intra-abdominal infections
             o Enterobacter species may be isolated together with colonic flora in intra-abdominal abscesses or peritonitis following intestinal perforation or surgery.
             o A frequent cause of Enterobacter involvement is prior digestive-tract colonization by Enterobacter species during hospitalization.
             o 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
             o Neonatal meningitis resulting from E sakazakii infection is described in Age.
             o In 1993, Durand et al published a review of 493 episodes of acute bacterial meningitis.14 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).
             o 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
             o Enterobacter species account for a small fraction of postsurgical endophthalmitis cases.
             o 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
             o 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.
             o Enterobacter bone and joint infections are usually more difficult to cure than those caused by S aureus. The authors have observed relapses that required additional treatment following the initial 6 weeks of intravenous therapy.
   
   Physical
   
       * Bacteremia
             o 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.
             o More than 80% of children and adults with Enterobacter bacteremia develop fever.
             o Hypotension and shock occur in as many as one third of cases.
             o Disseminated intravascular coagulation, jaundice, acute respiratory distress syndrome, and other organ failures reflect the severity of septic shock.
             o Purpura fulminans and hemorrhagic bullae usually observed with meningococci or viruses causing hemorrhagic fever may be part of the clinical presentation of Enterobacter bacteremia.
             o Ecthyma gangrenosum, usually associated with Pseudomonas or Aeromonas bacteremia, may also be observed.
             o Cyanosis and mottling is frequently reported in children with Enterobacter bacteremia.
       * Lower respiratory tract infections
             o 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.
             o 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.
   
   Causes
   
       * Enterobacter is a gram-negative bacillus that belongs to the Enterobacteriaceae family. Other members of this family include Klebsiella, Escherichia, Citrobacter, 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 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.
   
   Hope it helps

   Report (1) (0)  |   12 years, 8 month(s) ago  

2. amomipais82
   

   Hi,
   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.
   
   Enterobacter species contain a subpopulation of organisms that produce a beta-lactamase at low-levels. Once exposed to broad-spectrum cephalosporins, the subpopulation of beta-lactamase–producing organisms predominate. Thus, an Enterobacter infection that appears sensitive to cephalosporins at diagnosis may quickly develop into a resistant infection during therapy. Carbapenems and cefepime have a more stable beta-lactam ring against the lactamase produced by resistant strains of Enterobacter.
   
   thanks

   Report (1) (0)  |   12 years, 8 month(s) ago