Tools
Enterobacter Infections
Introduction
Enterobacter are gram-negative, facultatively anaerobic bacilli within Enterobacteriaceae that inhabit soil and water and comprise part of the normal human gastrointestinal microbiota.[1] Although they are frequently commensal, these organisms can act as opportunistic pathogens in hospitalized or immunocompromised hosts. Clinically important species include the Enterobacter cloacae complex and Klebsiella aerogenes (formerly Enterobacter aerogenes).[2] These organisms are significant causes of healthcare-associated infections, including bloodstream infections, ventilator-associated pneumonia, urinary tract infections, surgical-site infections, and device-associated infections. Less commonly, they can cause meningitis and intra-abdominal infection.[3]
Indwelling devices, recent invasive procedures, prior exposure to broad-spectrum antibiotics, and admission to intensive care or neonatal intensive care units increase risk.[4] Transmission typically occurs through contaminated equipment or the hands of healthcare personnel when infection prevention practices are not followed.[5] Outbreaks in high-acuity units, particularly among premature infants and critically ill adults, are associated with substantial morbidity and mortality.[4]
A major challenge in managing Enterobacter infections is the development of multidrug resistance. Enterobacter species possess inducible chromosomal AmpC β-lactamases and frequently acquire extended-spectrum β-lactamases or carbapenemases, narrowing therapeutic options.[6][7]][8] Current guidance emphasizes that organisms at moderate risk for clinically significant AmpC β-lactamase production (eg, Enterobacter cloacae complex and K aerogenes) often fail third-generation cephalosporins and piperacillin–tazobactam in invasive disease, and treatment strategies increasingly depend on carbapenems or newer β-lactam/β-lactamase inhibitor combinations when indicated.[7][6]
As of 2024, carbapenem-resistant Enterobacterales remain designated by global and national health authorities as critical-priority and urgent threats, reflecting high mortality, rapid spread, and limited treatment options.[7][9][10] Surveillance indicates an increasing global prevalence of carbapenem-resistant Enterobacterales, with the E cloacae complex prevalent in North America and Europe and frequent carriage of transferable carbapenemases, eg, KPC (Klebsiella pneumoniae carbapenamase), NDM (New Delhi metallo-β-lactamase), and OXA-48 (Oxacillinase-48). Recent reports from the United States and Europe highlight shifts, including the rising detection of NDM and the continued transmission of high-risk clones.[9][11]
Etiology
Register For Free And Read The Full Article
Search engine and full access to all medical articles- 10 free questions in your specialty
- Free CME/CE Activities
- Free daily question in your email
- Save favorite articles to your dashboard
- Emails offering discounts
Learn more about a Subscription to StatPearls Point-of-Care
Etiology
Enterobacter species are motile, nonspore-forming, lactose-fermenting, often urease-positive gram-negative rods within the Enterobacteriaceae family. These pathogens are ubiquitous in water, soil, and vegetation and constitute part of the normal human gut microbiota. In healthcare settings, they behave as opportunistic pathogens, particularly in hosts with significant comorbidities or immunosuppression. Clinically, the most relevant species are the Enterobacter cloacae complex and Klebsiella aerogenes.[2]
Infections predominantly arise in hospitalized individuals, especially those with malignancy, corticosteroid exposure, recent invasive procedures, or indwelling devices (eg, central venous and urinary catheters, endotracheal tubes). Although largely nosocomial, some species, eg, Pantoea agglomerans (formerly Enterobacter agglomerans), have been implicated in community-acquired neonatal infections. Rare, recently described species (eg, Enterobacter chinensis and Enterobacter rongchengensis) have also been isolated from human diseases and may harbor multiple putative virulence determinants.[12]
Virulence mechanisms include adhesins that mediate attachment to host tissues and device surfaces, capsular polysaccharide, which impairs opsonophagocytosis, lipopolysaccharide (LPS), which triggers proinflammatory cascades, and robust biofilm formation, all of which support persistent colonization and antimicrobial tolerance.[13][14] In E cloacae, virulence, and interbacterial competition are further promoted by type VI secretion systems regulated by the nucleoid-associated HU protein.[15][16] Tissue tropism may modulate clinical phenotype, as E cloacae demonstrates variable adhesion and invasion across host cell types. Beyond species-specific traits, conserved fitness factors across Enterobacterales enhance survival and dissemination during bacteremia. Clinically resistant isolates can persist within macrophages without replicating or inducing cytotoxicity, which may contribute to developing chronic or relapsing infections.[17] E hormaechei can exploit mucus metabolism to enhance colonization and persistence in hospitalized hosts, particularly among carbapenem-resistant strains.[18]
A major clinical concern is the development of intrinsic and acquired multidrug resistance. The principal intrinsic mechanism is chromosomal AmpC β-lactamase, which may be inducible or derepressed and confers resistance to many β-lactams, including third-generation cephalosporins. Additionally acquired determinants, notably plasmid-mediated extended-spectrum β-lactamases and carbapenemases such as KPC and NDM, further restrict therapeutic options.[19][20][21] Horizontal gene transfer facilitates rapidly disseminating these resistance genes within healthcare environments.[20] Enterobacter infections are opportunistic and nosocomial, typically emerging in immunosuppression, antibiotic exposure, invasive devices, and chronic illnesses. Environmental ubiquity, biofilm formation, intracellular persistence, and formidable multidrug resistance collectively drive clinical persistence and adverse outcomes.
Epidemiology
Historical Background
Late 20th-century United States surveillance consistently identified Enterobacter as a leading pathogen in intensive care units and a frequent cause of hospital-acquired bacteremia, underscoring its longstanding impact on nosocomial infections.[3]
Contemporary Molecular Epidemiology
Recent genomic studies have demonstrated substantial clonal and resistance diversity, with region-specific patterns. In parts of Europe, bloodstream infections due to Enterobacter cloacae complex have involved high-risk international clones, eg, ST66, ST171, and ST78, often carrying carbapenemase and colistin-resistance determinants.[22][23] Across Asia, outbreaks of E hormaechei coharboring carbapenemases and additional resistance mechanisms illustrate the convergence of resistance to carbapenems, tigecycline, and colistin (eg, blaNDM-1 with tmexCD2-toprJ2 and mcr-9).[23]
Reports from Taiwan highlight ST78 E hormaechei as a driver of plasmid-mediated β-lactamase gene spread across lineages via transferable OXA-48 plasmids.[24] Longitudinal surveillance in France (including overseas territories) documents persistence and local endemicity of IMI-type carbapenemase–producing Enterobacter cloacae complex.[25] In the United States, genomic surveillance has identified clusters of KPC-producing Enterobacter cloacae complex alongside broad species diversity and multiple resistance determinants.[26][21] One health syntheses from Africa further confirm Enterobacter as an ESKAPE pathogen across human, animal, and environmental niches, emphasizing reservoirs beyond acute-care hospitals.
ESKAPE pathogens
- Enterococcus faecium
- Staphylococcus aureus
- Klebsiella pneumoniae
- Acinetobacter baumannii
- Pseudomonas aeruginosa
- Enterobacter species
Disease Burden and Outcomes
Incidence of Enterobacter cloacae complex and related Enterobacter bloodstream infections has risen over recent decades, with the highest rates observed in older adults and patients with advanced comorbidity or critical illness. Population-based studies report an estimated 28-day mortality of 21% and a 1-year mortality of approximately 38% after Enterobacter bacteremia. Prognosis worsens with severe sepsis or shock and with delays in active therapy. Resistant phenotypes also portend poorer outcomes, including derepressed AmpC-mediated cephalosporin resistance and the emergence of extended-spectrum β-lactamase and carbapenemase-producing strains.[27]
History and Physical
Enterobacter species cause a broad spectrum of clinical syndromes, most often in healthcare-associated settings and in patients with significant comorbidity or immunosuppression. Risk increases with recent or prolonged exposure to broad-spectrum antimicrobials (especially third-generation cephalosporins or fluoroquinolones), systemic corticosteroids, and proton pump inhibitors, the presence of indwelling devices, and states of impaired host defense (eg, malignancy or neutropenia).
Clinical Features
Common clinical presentations of Enterobacter infections include bloodstream infections (bacteremia),[28][29] lower respiratory tract infections (particularly ventilator-associated pneumonia) [30], urinary tract infections [31], surgical site infections [32], and intravascular catheter–associated infections.[33][34] These manifestations represent the most frequently encountered presentations in hospitalized or immunocompromised patients.
Less common or organ-specific presentations
Less common or organ-specific infections often relate to host factors or medical devices and are typically reported as case series or individual case reports. Central nervous system involvement may include nosocomial meningitis, neonatal meningitis caused by the Enterobacter cloacae complex, and rare cases of encephalitis or brain abscess attributed to Klebsiella aerogenes.[35] Endocarditis caused by E cloacae is uncommon but serious, often healthcare-associated, and linked to poorer outcomes.[36] Musculoskeletal infections encompass vertebral osteomyelitis, discitis, postoperative ankle fracture infections, prosthetic joint infections requiring individualized surgical and antimicrobial strategies, and sporadic native joint infections, even in immunocompetent hosts.[32]
Pediatric bone and joint infections, including osteomyelitis and septic arthritis, have been documented in regional series.[37] Ophthalmic infections, though rare, include dacryocystitis and preseptal cellulitis caused by multidrug-resistant E cloacae.[38] Trauma-associated cases include bacteremia due to Enterobacter cancerogenus following pelvic trauma and multidrug-resistant Enterobacter infections in battlefield trauma patients with invasive devices and complex wounds.[39][40] Diabetic foot infections involve multidrug-resistant Enterobacter species, with risk heightened by prior antibiotic exposure, suboptimal glycemic control, and chronic ulceration.[41][42]
Evaluation
Microbiologic Diagnostic Studies
Microbiologic identification of Enterobacter infections relies on culture from the involved site and is considered the gold standard for diagnosis. For suspected bacteremia, clinicians should obtain at least 2 sets of aerobic and anaerobic blood cultures before initiating antibiotic therapy.[43][44]
Conventional Laboratory Studies
Conventional laboratory methods include Gram staining for early detection of gram-negative bacilli and MacConkey agar to assess lactose fermentation, as Enterobacter species typically ferment lactose.[45][46] Biochemical differentiation helps distinguish indole-negative Enterobacter and Klebsiella from indole-positive E coli, and motile Enterobacter species from nonmotile Klebsiella species.[47]
Rapid Identification Laboratory Studies
Rapid identification techniques, where available, include matrix-assisted laser desorption/ionization time-of-flight mass spectrometry.[48][49] Targeted molecular assays, eg, multiplex polymerase chain reaction, allow differentiation within the Enterobacter cloacae complex, including E cloacae, E hormaechei, E roggenkampii, and E kobei.[50][51] Carbapenemase detection in suspected resistant strains may involve phenotypic tests, eg, the modified carbapenem inactivation method with ethylenediaminetetraacetic acid for metallo-β-lactamases, molecular assays targeting KPC, NDM, or OXA-48–like genes, and lateral-flow immunochromatographic assays.[52][53] Rapid results should be integrated with antimicrobial stewardship to expedite initiation of an active agent.[54]
Antimicrobial Susceptibility Testing
Antimicrobial susceptibility testing should follow standardized CLSI or EUCAST methods using broth microdilution or validated automated systems.[55][56] Detection strategies for AmpC, extended-spectrum β-lactamase, and carbapenemase mechanisms, including β-lactam/β-lactamase/inhibitor disks (ESBL), ESBL screens, and carbapenemase testing, guide mechanism-directed therapy.[57]
Adjunctive Evaluation
The clinical presentation should guide adjunctive evaluation. Laboratory assessments include complete blood count, comprehensive metabolic panel, and urinalysis with culture when a urinary source is suspected.[58] Imaging may include chest radiography for pneumonia, computed tomography or magnetic resonance imaging for deep-seated, device-related, or musculoskeletal infections, echocardiography for suspected endocarditis, and ultrasound to evaluate drainable collections. Source assessment involves evaluating and, when feasible, removing or exchanging implicated devices, eg, central venous or urinary catheters, and obtaining appropriate intraoperative or percutaneous specimens for culture in suspected deep or prosthetic infections.
Treatment / Management
Management should be individualized and guided by resistance mechanisms, the source of infection, illness severity, and host comorbidities. Core elements include timely initiation of an active agent, prompt source control (eg, drainage, device removal/exchange), and strong antimicrobial stewardship. Engage infectious diseases consultation early for multidrug-resistant or complicated infections; deprescribe proton-pump inhibitors when not indicated; minimize corticosteroid exposure when clinically feasible; and deescalate to the narrowest active agent once susceptibilities are known.[7][59][60]
General Principles
General principles for managing Enterobacter infections emphasize timely, targeted interventions. Empiric therapy should be guided by patient risk factors, the suspected source of infection, and the local antibiogram, with prompt narrowing of therapy once susceptibility results become available.[7] Early and definitive source control, including removal or exchange of infected hardware, remains essential for effective management.
Complex or resistant infections require active involvement of antimicrobial stewardship and infectious diseases teams to optimize therapy and patient outcomes. Clinicians should review inpatient proton-pump inhibitor (PPI) use and discontinue therapy when not clinically indicated. PPIs reduce gastric acidity, alter gut microbiota, and promote bacterial overgrowth, including Enterobacter species.[59][60] Corticosteroid exposure should be minimized in dose and duration whenever feasible to reduce risk factors contributing to infection severity.
AmpC β-Lactamase-Producing Enterobacter Infections
AmpC β-lactamase–producing Enterobacter, including the Enterobacter cloacae complex and Klebsiella aerogenes, presents unique therapeutic challenges due to inducible resistance mechanisms. For these infections, the following management is recommended:
- Serious nonurinary tract infection: For these conditions, clinicians should use high-dose cefepime with pharmacokinetic/pharmacodynamic (PK/PD) optimization, eg, extended infusion, or a carbapenem when the infection is severe or source control is limited. Third-generation cephalosporins should be avoided because they risk selecting derepressed AmpC and clinical failure. Fourth-generation cephalosporins demonstrate greater stability against AmpC when ESBLs are absent. Evidence supports cefepime as a carbapenem-sparing option for AmpC producers when minimum inhibitory concentrations fall within the susceptible range and dosing is optimized.[7][61][62]
- Urinary tract infection: For uncomplicated cystitis, urinary tract infections (UTI) can be treated with nitrofurantoin or trimethoprim–sulfamethoxazole (TMP-SMX) when susceptibility is confirmed. Fluoroquinolones or a single intravenous aminoglycoside may serve as alternatives in select patients. Complicated UTIs or pyelonephritis may warrant an aminoglycoside if renal function allows, with therapy tailored to susceptibility results. After clinical stabilization, oral step-down therapy with TMP-SMX or a fluoroquinolone is appropriate because AmpC β-lactamase does not hydrolyze these agents.[7] (A1)
Extended-Spectrum β-Lactamases-producing Enterobacter
ESBL–producing Enterobacter requires careful therapeutic selection to ensure effective treatment and minimize the development of resistance. Carbapenems, eg, meropenem or imipenem-cilastatin, remain the preferred agents for infections outside the urinary tract and severe diseases. Ertapenem provides a reasonable option for stable, noncritical patients without a risk of Pseudomonas infection. Due to poor clinical reliability, cefepime and aztreonam should not be used as monotherapy in invasive ESBL-producing Enterobacter. TMP-SMX or fluoroquinolones may be used for urinary tract infections when susceptibility is documented, reserving carbapenems for cases in which these alternatives are inactive or contraindicated.[7][63]
Carbapenem-Resistant Enterobacter
Carbapenem-resistant Enterobacter (CRE) requires mechanism-directed and site-specific therapy. For Klebsiella pneumoniae carbapenemase producers, active options include ceftazidime–avibactam, meropenem–vaborbactam, or imipenem–cilastatin–relebactam.[7][64] If susceptibility is confirmed, OXA-48–like producers can often be treated with ceftazidime–avibactam. Metallo-β-lactamase producers, eg, NDM or VIM, may respond to cefiderocol or the combination of ceftazidime–avibactam with aztreonam, administered simultaneously by prolonged infusion, when active.[65](A1)
In situations with limited options or uncertain susceptibility, combination regimens may be considered for septic shock or rapidly progressive infections, though new β-lactam/β-lactamase inhibitor agents remain the preferred approach when active. Polymyxins and tigecycline are generally deprioritized due to toxicity concerns and inferior clinical outcomes. Aminoglycosides or fosfomycin may be considered for noncritical individuals with CRE UTI if the organism is susceptible. Fosfomycin is not recommended for treating pyelonephritis due to its poor oral bioavailability. Tigecycline and colistin are not recommended for UTI because of minimal urinary excretion.[7]
Dosing and Administration
PK/PD-optimized dosing is recommended for time-dependent β-lactams (eg, extended or continuous infusions where appropriate). For aminoglycosides, use once-daily dosing with therapeutic drug monitoring and careful renal surveillance. After clinical stabilization and confirmation of susceptibility, transition to active oral agents (eg, TMP-SMX or a fluoroquinolone) for step-down in selected infections (excluding endocarditis or undrained foci), consistent with evidence supporting shorter courses and oral completion for uncomplicated Enterobacterales bacteremia after source control.[7][66]
Stewardship and Prevention
Stewardship and prevention strategies are central in managing Enterobacter infections and limiting the spread of resistance. Prospective audit and feedback, preauthorization for last-line antimicrobial agents, and early deescalation once susceptibilities become available should be embedded into routine practice. Infection-prevention bundles strengthen these efforts by emphasizing hand hygiene, minimizing device use with prompt removal when feasible, rigorous environmental disinfection, and active surveillance in high-risk units. Sustained success depends on interprofessional coordination among infectious disease specialists, pharmacists, microbiologists, and nursing teams to ensure consistent, durable outcomes.[7]
Investigational and Adjunctive Approaches
Investigational and adjunctive approaches remain under evaluation for multidrug-resistant Enterobacter. Bacteriophage therapy and other emerging modalities are promising, particularly for biofilm-associated infections; however, current evidence supports their use only in research settings. These approaches remain investigational and have not been established as standard of care.[67][68][69](B2)
Differential Diagnosis
Enterobacter infections mimic many gram-negative and gram-positive syndromes. Prompt species identification and delineation of resistance mechanisms (inducible AmpC, ESBLs, carbapenemases) are critical for guiding therapy and preventing on-treatment resistance.[7]
Symptom-Based Differential Diagnoses
Differential diagnoses associated with various conditions that should be considered based on the presentation include:
- Sepsis/bloodstream infections: E coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, and assess device-related sources
- Lower respiratory tract/ventlator-associated pneumonia: Aspiration pneumonitis, viral (influenza, RSV, SARS-CoV-2), bacterial (S pneumoniae, H influenzae), acute respiratory distress syndrome (ARDS), complications (parapneumonic effusion, empyema, lung abscess) [70][71]
- Urinary tract: Other Enterobacterales, Proteus spp, Pseudomonas spp, fungal UTI in select hosts
- Skin, soft tissue, bone, and joint infections: Staphylococcus aureus (including MRSA), β-hemolytic streptococci, postoperative and catheter-related infections, osteomyelitis/septic arthritis
- Prostatitis: Typically E coli or Klebsiella [72]
- Intra-abdominal: Polymicrobial Enterobacterales with anaerobes
- Central nervous system (uncommon): Nosocomial meningitis/ventriculitis, neonatal gram-negative Bacilli, including E cloacae complex
Organism-Specific Differential Diagnoses
Differentiation between etiologic organisms is essential, given distinct intrinsic or acquired resistance profiles. Pathogens that can present with clinical features similar to Enterobacter infections include Klebsiella pneumoniae/oxytoca, E coli, Citrobacter freundii, Serratia marcescens, Proteus spp, Morganella morganii, Providencia spp, Hafnia alvei, and Yersinia enterocolitica.[6] Nonfermenting organisms to consider in healthcare-associated infections include P aeruginosa, Acinetobacter baumannii, Stenotrophomonas maltophilia, and Burkholderia cepacia complex.[73][74] In patients who are immunocompromised or being treated in the intensive care unit, the most likely alternative diagnoses include Klebsiella pneumoniae (including hypervirulent forms), E coli, P aeruginosa, Serratia, Citrobacter, and Proteus mirabilis (notably with catheter-associated UTI).[75][76]
Laboratory Studies to Differentiate Diagnoses
Key laboratory methods for diagnosing Enterobacter infections and differentiating between similar conditions rely on a combination of conventional, rapid, and susceptibility approaches. Traditional methods include Gram staining, growth on MacConkey agar to evaluate lactose fermentation, and biochemical testing (eg, indole, citrate, urease, ornithine decarboxylase, and motility assays).[46] Rapid species identification and resistance characterization can be achieved using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and targeted PCR for complex resolution and detection of ESBL or carbapenemase genes.[77][78] Antimicrobial susceptibility testing should follow CLSI or EUCAST standards, prioritizing mechanism testing when AmpC, ESBL, or carbapenemase production is suspected.[7][79]
Taxonomy and Resistance Considerations
Taxonomy and resistance patterns hold particular importance. Enterobacter species—especially the E cloacae complex and Klebsiella aerogenes—and Serratia, Morganella, Providencia, and Citrobacter harbor inducible chromosomal AmpC β-lactamases. Third-generation cephalosporins should be avoided in serious infections caused by these organisms.[80]
Diagnostic Prompts
Diagnostic evaluation should account for recent hospitalization, invasive devices or procedures, and host immunosuppression, including neutropenia, malignancy, diabetes, or corticosteroid therapy. Site-specific symptoms and signs of sepsis warrant the timely collection of cultures before antibiotics whenever feasible. Clinicians should request susceptibility and molecular resistance testing as indicated. Imaging studies, eg, chest radiography, CT, MRI, or ultrasound, help localize infection, identify complications, and guide decisions on device removal or source control.[44][81]
Prognosis
Outcomes in Enterobacter infections remain heterogeneous, shaped by host factors, infection site, severity of illness, timeliness of active therapy, adequacy of source control, and underlying resistance mechanisms. Prognosis often depends on how quickly effective treatment is initiated and whether resistant pathogens complicate management.
Mortality
Mortality in bloodstream infections (BSIs) within 30 days ranges from 8% to 40%, with one study's results reporting an overall mortality rate of 24.6%. A mortality rate of 34.7% was reported in cases involving cephalosporin resistance.[28][82] Population-based BSI cohorts demonstrate 28-day mortality rates of approximately 21% and 1-year mortality rates of around 38%. Infections caused by metallo-β-lactamase (MBL)–producing Enterobacterales demonstrate approximately 30% 30-day mortality in some series.[65][83][84] Resistance plays a significant role in outcomes. Broad-spectrum cephalosporin resistance, often resulting from AmpC derepression or carbapenemase production, increases the risk of death, while CRE markedly worsens survival.[28][85] Among immunocompromised patients, mortality can approach 60%.[86][87][88]
Care-Process Failure Predictors
Care-process failures strongly influence prognosis. Delayed initiation of active therapy, inadequate source control, and persistent bacteremia consistently predict worse outcomes.[82]
High-Risk and Special Populations
High-risk groups include patients with hematologic malignancies, solid tumors, or transplants, where BSI mortality ranges from 14% to more than 30%, rising further with polymicrobial infection, septic shock, or resistance to extended-spectrum cephalosporins.[86][87][89][90] Nosocomial acquisition, device-related infections, advanced age, and major comorbidities, eg, organ failure, further heighten risk.[28] Special populations demonstrate distinct patterns. In pediatrics, microbiologic failure often occurs when drainage is delayed or infection extends beyond urinary or bloodstream sites. By contrast, uncomplicated lower UTIs in otherwise healthy individuals generally resolve with excellent outcomes when managed promptly with targeted therapy.
Species Notes
Species-specific outcomes show similarity, with Klebsiella aerogenes and Enterobacter cloacae carrying comparable mortality risk, though the clinical course may differ and influence management decisions.[28][91] Ultimately, the rapid delivery of effective therapy, combined with timely source control, drives survival, while resistance mechanisms—especially derepressed AmpC and carbapenemases—represent the most significant adverse modifiers of prognosis.[28][82][28][83][84]
Complications
Clinical complications of Enterobacter infection depend on the disease site, host factors, resistance mechanisms, and the adequacy of therapy and source control. These outcomes highlight the need for rapid diagnosis, effective therapy, and aggressive source control to minimize both acute mortality and long-term morbidity.
Severe Complications
Major clinical manifestations include sepsis and septic shock, which can cause rapid decline and carry particularly high mortality in critically ill or immunosuppressed patients.[7][28][86] Multiorgan dysfunction frequently develops, presenting as respiratory failure, acute kidney injury, hepatic injury, or disseminated intravascular coagulation, especially when active therapy is delayed. Pulmonary complications include lung abscesses, parapneumonic effusions or empyema, and acute respiratory distress syndrome, most often in ventilated patients.
Central nervous system involvement ranges from nosocomial meningitis and ventriculitis to neonatal meningitis, brain abscess, or ventriculitis, with Cronobacter reclassification recognized in infant disease. Neonatal gastrointestinal complications include necrotizing enterocolitis, particularly in premature infants. Catheter-related bloodstream infection often produces persistent or recurrent bacteremia when device removal is delayed.[92] Persistence or recurrence may also result from inadequate empiric coverage, incomplete source control, or on-therapy resistance.[28][92] Metastatic foci can develop as endocarditis, osteomyelitis, septic arthritis, or deep abscesses.[93][94] Polymicrobial disease occurs frequently in malignancy or profound immunosuppression and is associated with worse outcomes.[95][96]
Resistance-Related Complications
Resistance further complicates clinical progression. AmpC derepression during exposure to third-generation cephalosporins can drive multidrug resistance, while carbapenem-resistant Enterobacter leaves few treatment options and requires complex management strategies.[7][86]
Complications in High-Risk Groups
High-risk groups include neonates and premature infants, patients with malignancy or neutropenia, individuals with indwelling devices or prostheses, and critically ill or immunosuppressed adults.[28][86]
Long-Term Sequelae
Long-term sequelae can be substantial. Adults may experience functional decline, prolonged rehabilitation, and increased susceptibility to future healthcare-associated infections.[97] Pediatric survivors face risks of neurodevelopmental impairment, chronic lung disease, and recurrent hospitalizations.[4]
Deterrence and Patient Education
Deterrence and patient education focus on preventing infections, limiting their spread, and reducing relapse, particularly in individuals with catheters or weakened immune systems. Enterobacter commonly inhabit the gastrointestinal tract and the environment, with some strains resistant to multiple antibiotics. Prevention relies on coordinated teamwork. Healthcare professionals should minimize or remove devices as early as possible, initiate empiric antibiotics promptly, tailor therapy based on culture results, enforce strict hand hygiene and isolation precautions, and pursue timely drainage of abscesses or removal of infected lines.
Patients play a crucial role by asking whether proton-pump inhibitors remain necessary, using corticosteroids only as prescribed, and taking antibiotics exactly as directed. Consistent hand hygiene, careful catheter, wound, or line care, adherence to follow-up appointments, and reporting of drug allergies strengthen outcomes. Immediate medical attention should be sought for fever, chills, worsening symptoms during antibiotic therapy, redness, swelling, pain, or drainage at catheter or surgical sites, as well as for rash, hives, breathing difficulty, severe diarrhea, or confusion. Patients should contact their care team or seek urgent evaluation without delay when uncertain.
Pearls and Other Issues
The following factors should be kept in mind when managing Enterobacter infections:
- A mechanism-first approach remains essential: Clinicians should assume inducible AmpC production in Enterobacter cloacae complex and Klebsiella aerogenes. Third-generation cephalosporins should be avoided in severe disease because of the risk of derepressed mutants. AmpC-stable agents should be selected according to susceptibilities, with extended-infusion dosing considered when appropriate.
- Early confirmation of resistance is equally important; rapid identification combined with phenotypic or molecular testing for ESBLs and carbapenemases informs both therapeutic selection and infection-control measures.
- Successful outcomes depend heavily on timely source control, which involves removal or exchange of infected lines, drainage of abscesses, and relief of obstructive uropathy.
- Once patients demonstrate clinical improvement, hemodynamic stability, and availability of an active oral option, transition from intravenous to oral therapy reduces hospital stay and catheter-associated risks.
- Management must also emphasize the treatment of clinical syndromes rather than colonization, particularly in device-bearing hosts, where respiratory or urinary isolates may not represent an infection.
- Accurate recording of β-lactam allergies, distinguishing between intolerance and true anaphylaxis, preserves access to first-line agents.
Common Pitfalls
Several pitfalls commonly undermine care. The use of third-generation cephalosporins for likely AmpC producers in serious infections contributes to therapeutic failure. Delays in ordering or performing ESBL or carbapenemase testing lead to ineffective empiric coverage and potential transmission. Treating colonization, eg, isolates from ventilated airways or catheterized urine without clinical evidence of infection, results in unnecessary antibiotic exposure.
Neglecting device removal or source control can prolong infection, while relying on drugs with poor tissue penetration—eg, fosfomycin for pyelonephritis or tigecycline and colistin for urinary tract infections—limits their effectiveness. Inadequate dose adjustment for renal or hepatic impairment and overlooked drug–drug interactions increase the risk of adverse outcomes. Prolonged use of proton-pump inhibitors or corticosteroids without indication further increases the risk of infection.
Enhancing Healthcare Team Outcomes
Optimal management of Enterobacter infections depends on rapid diagnostics, mechanism-aware therapy, early source control, and antimicrobial stewardship. These infections frequently involve invasive devices and high-acuity settings, making timely action and interprofessional collaboration critical. Outcomes hinge on recognizing resistance patterns, eg, AmpC derepression, ESBL production, and carbapenemase activity, while aligning therapy with susceptibility data.[7][98] Coordinated, patient-centered care reduces mortality, shortens hospital stay, and limits relapse or recurrence.
Effective care requires clearly defined skills, strategies, and responsibilities across the healthcare team. Infectious disease specialists guide empiric and definitive therapy, interpret resistance mechanisms, and advise on duration and device removal. Clinical microbiologists deliver rapid organism identification and resistance testing, enabling early tailoring of therapy. Pharmacists optimize pharmacokinetics and pharmacodynamics, manage interactions, and coordinate the transition from intravenous to oral administration, while nurses reinforce prevention practices, monitor for adverse effects, and support device care. Surgeons and interventional radiologists provide timely drainage and hardware removal, while case managers and social workers arrange follow-up, outpatient therapy, and adherence support.[44] Strong interprofessional communication, reliable handoffs, and stewardship-aligned workflows ensure early active therapy, daily reassessment, safe transitions, and documentation of care plans. This coordinated approach improves outcomes, enhances patient safety, and elevates team performance.
References
Moreira de Gouveia MI, Bernalier-Donadille A, Jubelin G. Enterobacteriaceae in the Human Gut: Dynamics and Ecological Roles in Health and Disease. Biology. 2024 Feb 23:13(3):. doi: 10.3390/biology13030142. Epub 2024 Feb 23 [PubMed PMID: 38534413]
Level 2 (mid-level) evidenceWesevich A, Sutton G, Ruffin F, Park LP, Fouts DE, Fowler VG Jr, Thaden JT. Newly Named Klebsiella aerogenes (formerly Enterobacter aerogenes) Is Associated with Poor Clinical Outcomes Relative to Other Enterobacter Species in Patients with Bloodstream Infection. Journal of clinical microbiology. 2020 Aug 24:58(9):. doi: 10.1128/JCM.00582-20. Epub 2020 Aug 24 [PubMed PMID: 32493786]
Level 2 (mid-level) evidenceTobin EH, Zahra F. Nosocomial Infections. StatPearls. 2025 Jan:(): [PubMed PMID: 32644738]
Rahal A, Andreo A, Le Gallou F, Bourigault C, Bouchand C, Ferriot C, Corvec S, Guillouzouic A, Gras-Leguen C, Launay E, Flamant C, Lepelletier D. Enterobacter cloacae complex outbreak in a neonatal intensive care unit: multifaceted investigations and preventive measures are needed. The Journal of hospital infection. 2021 Oct:116():87-90. doi: 10.1016/j.jhin.2021.07.012. Epub 2021 Aug 19 [PubMed PMID: 34419520]
Boyce JM. Hand and environmental hygiene: respective roles for MRSA, multi-resistant gram negatives, Clostridioides difficile, and Candida spp. Antimicrobial resistance and infection control. 2024 Sep 27:13(1):110. doi: 10.1186/s13756-024-01461-x. Epub 2024 Sep 27 [PubMed PMID: 39334403]
Tebano G, Zaghi I, Cricca M, Cristini F. Antibiotic Treatment of Infections Caused by AmpC-Producing Enterobacterales. Pharmacy (Basel, Switzerland). 2024 Sep 21:12(5):. doi: 10.3390/pharmacy12050142. Epub 2024 Sep 21 [PubMed PMID: 39311133]
Tamma PD, Heil EL, Justo JA, Mathers AJ, Satlin MJ, Bonomo RA. Infectious Diseases Society of America 2024 Guidance on the Treatment of Antimicrobial-Resistant Gram-Negative Infections. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024 Aug 7:():. pii: ciae403. doi: 10.1093/cid/ciae403. Epub 2024 Aug 7 [PubMed PMID: 39108079]
Castanheira M, Deshpande LM, Mendes RE, Doyle TB, Sader HS. Prevalence of carbapenemase genes among carbapenem-nonsusceptible Enterobacterales collected in US hospitals in a five-year period and activity of ceftazidime/avibactam and comparator agents. JAC-antimicrobial resistance. 2022 Oct:4(5):dlac098. doi: 10.1093/jacamr/dlac098. Epub 2022 Sep 30 [PubMed PMID: 36196444]
Sati H, Carrara E, Savoldi A, Hansen P, Garlasco J, Campagnaro E, Boccia S, Castillo-Polo JA, Magrini E, Garcia-Vello P, Wool E, Gigante V, Duffy E, Cassini A, Huttner B, Pardo PR, Naghavi M, Mirzayev F, Zignol M, Cameron A, Tacconelli E, WHO Bacterial Priority Pathogens List Advisory Group. The WHO Bacterial Priority Pathogens List 2024: a prioritisation study to guide research, development, and public health strategies against antimicrobial resistance. The Lancet. Infectious diseases. 2025 Sep:25(9):1033-1043. doi: 10.1016/S1473-3099(25)00118-5. Epub 2025 Apr 14 [PubMed PMID: 40245910]
Smith HZ, Hollingshead CM, Kendall B. Carbapenem-Resistant Enterobacterales. StatPearls. 2025 Jan:(): [PubMed PMID: 31869168]
Devinney K, Burton N, Alroy KA, Crawley A, Da Costa-Carter CA, Kratz MM, Lin Y, Montfort-Gardeazabal J, Portier T, Santiago C, Siemetzki-Kapoor U, Sullivan M, Wiegartner RJ, McPherson TD, Greendyke WG. Notes from the Field: Increase in New Delhi Metallo-β-Lactamase-Producing Carbapenem-Resistant Enterobacterales - New York City, 2019-2024. MMWR. Morbidity and mortality weekly report. 2025 Jun 26:74(23):401-403. doi: 10.15585/mmwr.mm7423a2. Epub 2025 Jun 26 [PubMed PMID: 40568976]
Mustapha SS, Ibrahim M, Aliyu S, Abdulkadir I. Enterobacter agglomerans, an uncommon cause of community-acquired bacterial infection in neonates. Journal of tropical pediatrics. 2022 Oct 6:68(6):. pii: fmac085. doi: 10.1093/tropej/fmac085. Epub [PubMed PMID: 36228308]
Misra T, Tare M, Jha PN. Insights Into the Dynamics and Composition of Biofilm Formed by Environmental Isolate of Enterobacter cloacae. Frontiers in microbiology. 2022:13():877060. doi: 10.3389/fmicb.2022.877060. Epub 2022 Jul 5 [PubMed PMID: 35865928]
Liu HY, Prentice EL, Webber MA. Mechanisms of antimicrobial resistance in biofilms. npj antimicrobials and resistance. 2024:2(1):27. doi: 10.1038/s44259-024-00046-3. Epub 2024 Oct 1 [PubMed PMID: 39364333]
Hernández-Martínez G, Ares MA, Rosales-Reyes R, Soria-Bustos J, Yañez-Santos JA, Cedillo ML, Girón JA, Martínez-Laguna Y, Leng F, Ibarra JA, De la Cruz MA. The nucleoid protein HU positively regulates the expression of type VI secretion systems in Enterobacter cloacae. mSphere. 2024 May 29:9(5):e0006024. doi: 10.1128/msphere.00060-24. Epub 2024 Apr 22 [PubMed PMID: 38647313]
Soria-Bustos J, Ares MA, Gómez-Aldapa CA, González-Y-Merchand JA, Girón JA, De la Cruz MA. Two Type VI Secretion Systems of Enterobacter cloacae Are Required for Bacterial Competition, Cell Adherence, and Intestinal Colonization. Frontiers in microbiology. 2020:11():560488. doi: 10.3389/fmicb.2020.560488. Epub 2020 Sep 24 [PubMed PMID: 33072020]
Parau G, Parks HJ, Anderson AJG, Bisaro F, García-Romero I, Gilmore MC, Korankye SO, Marshall H, Valvano MA. Clinical Isolates of Antimicrobial-Resistant Enterobacter Species Can Persist in Human Macrophages Without Replication and Overt Cellular Cytotoxicity. The Journal of infectious diseases. 2025 Jul 30:232(1):e3-e16. doi: 10.1093/infdis/jiaf099. Epub [PubMed PMID: 40037395]
Sinha R, Ottosen EN, Ngwaga T, Shames SR, DiRita VJ. Carbapenem-Resistant Enterobacter hormaechei Uses Mucus Metabolism to Facilitate Gastrointestinal Colonization. bioRxiv : the preprint server for biology. 2024 Sep 25:():. pii: 2024.09.25.615021. doi: 10.1101/2024.09.25.615021. Epub 2024 Sep 25 [PubMed PMID: 39386425]
Zeng Z, Wei Y, Ye C, Jiang Y, Feng C, Guo T, Song M, Ding Y, Zhan P, Liu J. Carbapenem-Resistant Enterobacter cloacae Complex in Southwest China: Molecular Characteristics and Risk Factors Caused by NDM Producers. Infection and drug resistance. 2024:17():1643-1652. doi: 10.2147/IDR.S447857. Epub 2024 Apr 29 [PubMed PMID: 38707989]
Husna A, Rahman MM, Badruzzaman ATM, Sikder MH, Islam MR, Rahman MT, Alam J, Ashour HM. Extended-Spectrum β-Lactamases (ESBL): Challenges and Opportunities. Biomedicines. 2023 Oct 30:11(11):. doi: 10.3390/biomedicines11112937. Epub 2023 Oct 30 [PubMed PMID: 38001938]
Gomez-Simmonds A, Annavajhala MK, Seeram D, Hokunson TW, Park H, Uhlemann AC. Genomic epidemiology of carbapenem-resistant Enterobacterales at a New York City hospital over a 10-year period reveals complex plasmid-clone dynamics and evidence for frequent horizontal transfer of bla (KPC). Genome research. 2024 Nov 20:34(11):1895-1907. doi: 10.1101/gr.279355.124. Epub 2024 Nov 20 [PubMed PMID: 39366703]
Lumbreras-Iglesias P, de Toro M, Vázquez X, García-Carús E, Rodicio MR, Fernández J. High-risk international clones ST66, ST171 and ST78 of Enterobacter cloacae complex causing blood stream infections in Spain and carrying bla(OXA-48) with or without mcr-9. Journal of infection and public health. 2023 Feb:16(2):272-279. doi: 10.1016/j.jiph.2022.12.015. Epub 2022 Dec 26 [PubMed PMID: 36621205]
Li X, Wang Q, Huang J, Zhang X, Zhou L, Quan J, Wang Z, Zhou H, Li R, Tu Y. Clonal outbreak of NDM-1-producing Enterobacter hormaechei belonging to high-risk international clone ST78 with the coexistence of tmexCD2-toprJ2 and mcr-9 in China. International journal of antimicrobial agents. 2023 Jun:61(6):106790. doi: 10.1016/j.ijantimicag.2023.106790. Epub 2023 Mar 15 [PubMed PMID: 36924803]
Chen CM, Tang HL, Chen YT, Ke SC, Lin YP, Chen BH, Teng RH, Chiou CS, Lu MC, Lai YC. Emergence and transmission of the high-risk ST78 clone of OXA-48-producing Enterobacter hormaechei in a single hospital in Taiwan. Emerging microbes & infections. 2024 Dec:13(1):2404165. doi: 10.1080/22221751.2024.2404165. Epub 2024 Sep 22 [PubMed PMID: 39258852]
Emeraud C, Girlich D, Deschamps M, Rezzoug I, Jacquemin A, Jousset AB, Lecolant S, Locher L, Birer A, Naas T, Bonnin RA, Dortet L. IMI-Type Carbapenemase-Producing Enterobacter cloacae Complex, France and Overseas Regions, 2012-2022. Emerging infectious diseases. 2024 Jun:30(6):1279-1282. doi: 10.3201/eid3006.231525. Epub [PubMed PMID: 38782383]
Karlsson M, Lutgring JD, Ansari U, Lawsin A, Albrecht V, McAllister G, Daniels J, Lonsway D, McKay L, Beldavs Z, Bower C, Dumyati G, Gross A, Jacob J, Janelle S, Kainer MA, Lynfield R, Phipps EC, Schutz K, Wilson L, Witwer ML, Bulens SN, Walters MS, Duffy N, Kallen AJ, Elkins CA, Rasheed JK. Molecular Characterization of Carbapenem-Resistant Enterobacterales Collected in the United States. Microbial drug resistance (Larchmont, N.Y.). 2022 Apr:28(4):389-397. doi: 10.1089/mdr.2021.0106. Epub 2022 Feb 16 [PubMed PMID: 35172110]
Matsuo A, Matsumura Y, Mori K, Noguchi T, Yamamoto M, Nagao M. Molecular epidemiology and β-lactam resistance mechanisms of Enterobacter cloacae complex isolates obtained from bloodstream infections, Kyoto, Japan. Microbiology spectrum. 2025 Apr:13(4):e0248524. doi: 10.1128/spectrum.02485-24. Epub 2025 Mar 10 [PubMed PMID: 40062888]
Liu Y, Li F, Fang Y, Zhong Q, Xiao Y, Zheng Y, Zhu J, Zhao C, Cao X, Xiong J, Hu L. Clinical Characteristics, Prognosis and Treatment of Bloodstream Infections with Enterobacter Cloacae Complex in a Chinese Tertiary Hospital: A Retrospective Study. Infection and drug resistance. 2024:17():1811-1825. doi: 10.2147/IDR.S460744. Epub 2024 May 9 [PubMed PMID: 38741943]
Level 2 (mid-level) evidenceHan M, Hua M, Xie H, Li J, Wang Y, Shen H, Cao X. Clinical Characteristics and Risk Factors for Multidrug-Resistant Enterobacter cloacae Complex Bacteremia in a Chinese Tertiary Hospital: A Decade Review (2013-2022). Infection and drug resistance. 2025:18():427-440. doi: 10.2147/IDR.S502509. Epub 2025 Jan 22 [PubMed PMID: 39867289]
Bayrakçi S, Åžahin A, Bayrakçi O, Aslan S. Characteristics of ventilator-associated pneumonia due to Gram-negative bacteria in the intensive care unit: A single-center experience. Medicine. 2025 Jun 27:104(26):e42946. doi: 10.1097/MD.0000000000042946. Epub [PubMed PMID: 40587686]
Elbehiry A, Al Shoaibi M, Alzahrani H, Ibrahem M, Moussa I, Alzaben F, Alsubki RA, Hemeg HA, Almutairi D, Althobaiti S, Alanazi F, Alotaibi SA, Almutairi H, Alzahrani A, Abu-Okail A. Enterobacter cloacae from urinary tract infections: frequency, protein analysis, and antimicrobial resistance. AMB Express. 2024 Feb 8:14(1):17. doi: 10.1186/s13568-024-01675-7. Epub 2024 Feb 8 [PubMed PMID: 38329626]
García Cardona C, Bernaus Johnson MC, Martínez Ros J, Hernández-Gonzalez N, Auñon Rubio Á, Anglès Crespo F, Arteagoitia-Colino I, Coifman-Lucena I, Esteban-Moreno J, Moral Escudero E, Gómez García L, Nóvoa Martínez R, Ortega Columbrans A, Veloso Duran M, Font-Vizcarra L. Enterobacter cloacae Infection After Surgical Treatment of Ankle Fractures, a Multicenter Observational Study. Foot & ankle international. 2023 May:44(5):424-430. doi: 10.1177/10711007231157688. Epub 2023 Mar 15 [PubMed PMID: 36923994]
Level 2 (mid-level) evidenceMoriyama K, Ando T, Kotani M, Tokumine J, Nakazawa H, Motoyasu A, Yorozu T. Risk factors associated with increased incidences of catheter-related bloodstream infection. Medicine. 2022 Oct 21:101(42):e31160. doi: 10.1097/MD.0000000000031160. Epub [PubMed PMID: 36281147]
Haddadin Y, Annamaraju P, Regunath H. Central Line–Associated Blood Stream Infections. StatPearls. 2026 Jan:(): [PubMed PMID: 28613641]
Pallitto CR, Feuerstein JL, Baer AZ, Bishara JD, Bhavsar SM. Enterobacter cloacae Complex Meningitis in a Full-term Neonate. Clinical pediatrics. 2023 Oct:62(10):1150-1154. doi: 10.1177/00099228231155391. Epub 2023 Mar 12 [PubMed PMID: 36908064]
Ioannou P, Vamvoukaki R, Kofteridis DP. Infective endocarditis by Enterobacter cloacae: a systematic review and meta-analysis. Journal of chemotherapy (Florence, Italy). 2022 Feb:34(1):1-8. doi: 10.1080/1120009X.2021.1959786. Epub 2021 Aug 9 [PubMed PMID: 34369324]
Level 1 (high-level) evidenceIseri Nepesov M, Kilic O, Sali E, Yesil E, Akar A, Kaman A, Metin Akcan O, Kilic Cil M, Ozlu C, Lacinel Gurlevik S, Ulusoy E, Cetin BS, Akici N, Cakir D, Uslu Aygun FD, Hancerli CO, Tekin Yilmaz A, Alkan G, Uygun H, Bucak IH, Bursal B, Celik T, Sutcu M, Oz FN, Gayretli Aydin ZG, Karbuz A, Akturk H, Kepenekli E, Emiroglu M, Oncel S, Nuhoglu C, Korucu IH, Incesu M, Kaya A, Bombaci H, Dinleyici M, Carman KB, Duman M, Turel O, Yilmaz D, Alabaz D, Belet N, Tanir G, Turgut M, Celebi S, Kuyucu N, Arisoy ES, Durmaz G, Kaya M, Kara A, Dinleyici EC. Pathogens in Pediatric Septic Arthritis: A Multi-Center Study in Turkiye (PEDSART Study). Children (Basel, Switzerland). 2024 Jan 22:11(1):. doi: 10.3390/children11010134. Epub 2024 Jan 22 [PubMed PMID: 38275444]
Kvopka M, Kingston E, Nguyen DDH, Tong JY, Kirk HL, Whyte CM, Dalgliesh JD, Danks JJ. Multi-resistant Enterobacter cloacae dacryocystitis and preseptal cellulitis: case and review of literature. Orbit (Amsterdam, Netherlands). 2023 Aug:42(4):441-444. doi: 10.1080/01676830.2022.2026417. Epub 2022 Jan 25 [PubMed PMID: 35075984]
Level 3 (low-level) evidenceBennett W, Mende K, Campbell WR, Beckius M, Stewart L, Shaikh F, Rahman A, Tribble DR, Yabes JM. Enterobacter cloacae infection characteristics and outcomes in battlefield trauma patients. PloS one. 2023:18(8):e0290735. doi: 10.1371/journal.pone.0290735. Epub 2023 Aug 29 [PubMed PMID: 37643169]
Cruz R, López E, Meneses C, Alegría Y. [Enterobacter cancerogenus bacteremia in a patient with pelvic trauma]. Revista chilena de infectologia : organo oficial de la Sociedad Chilena de Infectologia. 2022 Apr:39(2):218-220. doi: 10.4067/S0716-10182022000200218. Epub [PubMed PMID: 35856997]
Yan S, Zhu X, Yu T, Li D, Li S, Xue L. Characterization of pathogenic microorganisms in diabetic foot infections and development of a risk prediction model. Scientific reports. 2025 Jul 2:15(1):23553. doi: 10.1038/s41598-025-07092-5. Epub 2025 Jul 2 [PubMed PMID: 40604114]
Yang S, Hu L, Zhao Y, Meng G, Xu S, Han R. Prevalence of multidrug-resistant bacterial infections in diabetic foot ulcers: A meta-analysis. International wound journal. 2024 Apr:21(4):e14864. doi: 10.1111/iwj.14864. Epub [PubMed PMID: 38619084]
Level 1 (high-level) evidenceEkwall-Larson A, Yu D, Dinnétz P, Nordqvist H, Özenci V. Single-Site Sampling versus Multisite Sampling for Blood Cultures: a Retrospective Clinical Study. Journal of clinical microbiology. 2022 Feb 16:60(2):e0193521. doi: 10.1128/JCM.01935-21. Epub 2021 Dec 1 [PubMed PMID: 34851687]
Level 2 (mid-level) evidenceEvans L, Rhodes A, Alhazzani W, Antonelli M, Coopersmith CM, French C, Machado FR, Mcintyre L, Ostermann M, Prescott HC, Schorr C, Simpson S, Wiersinga WJ, Alshamsi F, Angus DC, Arabi Y, Azevedo L, Beale R, Beilman G, Belley-Cote E, Burry L, Cecconi M, Centofanti J, Coz Yataco A, De Waele J, Dellinger RP, Doi K, Du B, Estenssoro E, Ferrer R, Gomersall C, Hodgson C, Møller MH, Iwashyna T, Jacob S, Kleinpell R, Klompas M, Koh Y, Kumar A, Kwizera A, Lobo S, Masur H, McGloughlin S, Mehta S, Mehta Y, Mer M, Nunnally M, Oczkowski S, Osborn T, Papathanassoglou E, Perner A, Puskarich M, Roberts J, Schweickert W, Seckel M, Sevransky J, Sprung CL, Welte T, Zimmerman J, Levy M. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive care medicine. 2021 Nov:47(11):1181-1247. doi: 10.1007/s00134-021-06506-y. Epub 2021 Oct 2 [PubMed PMID: 34599691]
Tripathi N, Zubair M, Sapra A. Gram Staining. StatPearls. 2025 Jan:(): [PubMed PMID: 32965827]
Jung B, Hoilat GJ. MacConkey Medium. StatPearls. 2025 Jan:(): [PubMed PMID: 32491326]
Ashurst JV, Dawson A. Klebsiella Pneumonia. StatPearls. 2025 Jan:(): [PubMed PMID: 30085546]
Munguia-Ramos D, Xancal-Salvador LF, Esteban-Kenel V, Ortiz-Conchi N, Jaimes-Aquino RA, Mendoza-Rojas M, Cervantes-Sánchez A, Méndez-Ramos S, Rivera-Villegas HO, Rajme-Lopez S, Tamez-Torres KM, Roman-Montes CM, Martínez-Gamboa A, Bobadilla Del-Valle M, Sifuentes-Osornio J, Ponce-de-Leon A, Gonzalez-Lara MF, Martinez-Guerra BA. Rapid Detection of Carbapenemases Using NG-Test(®) CARBA 5 in Positive Blood Cultures: A Diagnostic Test Study. Antibiotics (Basel, Switzerland). 2024 Nov 20:13(11):. doi: 10.3390/antibiotics13111105. Epub 2024 Nov 20 [PubMed PMID: 39596798]
Campos AF, Arantes T, Cambiais AMVB, Cury AP, Tiroli CG, Rossi F, Malbouisson LMS, Costa SF, Guimarães T. Impact of an Antimicrobial Stewardship Program Intervention Associated with the Rapid Identification of Microorganisms by MALDI-TOF and Detection of Resistance Genes in ICU Patients with Gram-Negative Bacteremia. Antibiotics (Basel, Switzerland). 2022 Sep 9:11(9):. doi: 10.3390/antibiotics11091226. Epub 2022 Sep 9 [PubMed PMID: 36140007]
Ji Y, Wang P, Xu T, Zhou Y, Chen R, Zhu H, Zhou K. Development of a One-Step Multiplex PCR Assay for Differential Detection of Four species (Enterobacter cloacae, Enterobacter hormaechei, Enterobacter roggenkampii, and Enterobacter kobei) Belonging to Enterobacter cloacae Complex With Clinical Significance. Frontiers in cellular and infection microbiology. 2021:11():677089. doi: 10.3389/fcimb.2021.677089. Epub 2021 May 18 [PubMed PMID: 34095000]
Halder G, Chaudhury BN, Mandal S, Denny P, Sarkar D, Chakraborty M, Khan UR, Sarkar S, Biswas B, Chakraborty A, Maiti S, Dutta S. Whole genome sequence-based molecular characterization of blood isolates of carbapenem-resistant Enterobacter cloacae complex from ICU patients in Kolkata, India, during 2017-2022: emergence of phylogenetically heterogeneous Enterobacter hormaechei subsp. xiangfangensis. Microbiology spectrum. 2024 Apr 2:12(4):e0352923. doi: 10.1128/spectrum.03529-23. Epub 2024 Feb 22 [PubMed PMID: 38385742]
Perera V, Silva N, Jayatilleke K, Silva S, Corea E. Performance of Phenotypic Tests to Detect β-Lactamases in a Population of β-Lactamase Coproducing Enterobacteriaceae Isolates. Journal of laboratory physicians. 2023 Mar:15(1):117-125. doi: 10.1055/s-0042-1760399. Epub 2023 Jan 18 [PubMed PMID: 37064978]
Saito K, Mizuno S, Nakano R, Tanouchi A, Mizuno T, Nakano A, Suzuki Y, Kakuta N, Yano H. Evaluation of NG-Test CARBA 5 for the detection of carbapenemase-producing Gram-negative bacilli. Journal of medical microbiology. 2022 Jun:71(6):. doi: 10.1099/jmm.0.001557. Epub [PubMed PMID: 35671202]
Peri AM, Chatfield MD, Ling W, Furuya-Kanamori L, Harris PNA, Paterson DL. Rapid Diagnostic Tests and Antimicrobial Stewardship Programs for the Management of Bloodstream Infection: What Is Their Relative Contribution to Improving Clinical Outcomes? A Systematic Review and Network Meta-analysis. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2024 Aug 16:79(2):502-515. doi: 10.1093/cid/ciae234. Epub [PubMed PMID: 38676943]
Level 1 (high-level) evidenceGajic I, Kabic J, Kekic D, Jovicevic M, Milenkovic M, Mitic Culafic D, Trudic A, Ranin L, Opavski N. Antimicrobial Susceptibility Testing: A Comprehensive Review of Currently Used Methods. Antibiotics (Basel, Switzerland). 2022 Mar 23:11(4):. doi: 10.3390/antibiotics11040427. Epub 2022 Mar 23 [PubMed PMID: 35453179]
Humphries RM, Miller L, Zimmer B, Matuschek E, Hindler JA. Contemporary Considerations for Establishing Reference Methods for Antibacterial Susceptibility Testing. Journal of clinical microbiology. 2023 Jun 20:61(6):e0188622. doi: 10.1128/jcm.01886-22. Epub 2023 Mar 27 [PubMed PMID: 36971571]
Lawrence J, O'Hare D, van Batenburg-Sherwood J, Sutton M, Holmes A, Rawson TM. Innovative approaches in phenotypic beta-lactamase detection for personalised infection management. Nature communications. 2024 Oct 21:15(1):9070. doi: 10.1038/s41467-024-53192-7. Epub 2024 Oct 21 [PubMed PMID: 39433753]
Tops SCM, Schapendonk CEP, Coolen JPM, Tenover FC, Tickler IA, Melchers WJG, Wertheim HFL. The diagnostic accuracy of the GeneXpert ESBL-ampC prototype assay for rapid PCR-based detection of extended-spectrum beta-lactamase genes directly from urine. Microbiology spectrum. 2023 Dec 12:11(6):e0311623. doi: 10.1128/spectrum.03116-23. Epub 2023 Nov 14 [PubMed PMID: 37962375]
Lee I, Jo JW, Woo HJ, Suk KT, Lee SS, Kim BS. Proton pump inhibitors increase the risk of carbapenem-resistant Enterobacteriaceae colonization by facilitating the transfer of antibiotic resistance genes among bacteria in the gut microbiome. Gut microbes. 2024 Jan-Dec:16(1):2341635. doi: 10.1080/19490976.2024.2341635. Epub 2024 Apr 18 [PubMed PMID: 38634770]
Willems RPJ, Schut MC, Kaiser AM, Groot TH, Abu-Hanna A, Twisk JWR, van Dijk K, Vandenbroucke-Grauls CMJE. Association of Proton Pump Inhibitor Use With Risk of Acquiring Drug-Resistant Enterobacterales. JAMA network open. 2023 Feb 1:6(2):e230470. doi: 10.1001/jamanetworkopen.2023.0470. Epub 2023 Feb 1 [PubMed PMID: 36821114]
Herrmann J, Burgener-Gasser AV, Goldenberger D, Roth J, Weisser M, Tamma PD, Tschudin-Sutter S. Cefepime versus carbapenems for treatment of AmpC beta-lactamase-producing Enterobacterales bloodstream infections. European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology. 2024 Feb:43(2):213-221. doi: 10.1007/s10096-023-04715-5. Epub 2023 Nov 23 [PubMed PMID: 37993680]
Cheo HM, Ho DYK, Koh LP, Koh MCY, Ngiam JN, Lye DCB. Cefepime Versus Carbapenem Therapy for the Treatment of Invasive Infections With Inducible Chromosomal AmpC-Producing Enterobacterales: A Systematic Review and Meta-analysis. Open forum infectious diseases. 2025 Jul:12(7):ofaf413. doi: 10.1093/ofid/ofaf413. Epub 2025 Jul 14 [PubMed PMID: 40718546]
Level 1 (high-level) evidenceChen L, Hua J, He X. Cefepime versus carbapenem for treating complicated urinary tract infection caused by cefoxitin-nonsusceptible ESCPM organisms: a multicenter, real-world study. BMC infectious diseases. 2025 Mar 31:25(1):439. doi: 10.1186/s12879-025-10850-5. Epub 2025 Mar 31 [PubMed PMID: 40165096]
Zilberberg MD, Nathanson BH, Redell MA, Sulham K, Shorr AF. Comparative Outcomes of Meropenem-Vaborbactam vs. Ceftazidime-Avibactam Among Adults Hospitalized with an Infectious Syndrome in the US, 2019-2021. Antibiotics (Basel, Switzerland). 2025 Jan 3:14(1):. doi: 10.3390/antibiotics14010029. Epub 2025 Jan 3 [PubMed PMID: 39858315]
Level 2 (mid-level) evidenceGupta N, Boodman C, Prayag P, Manesh A, Kumar TP. Ceftazidime-avibactam and aztreonam combination for Carbapenem-resistant Enterobacterales bloodstream infections with presumed Metallo-β-lactamase production: a systematic review and meta-analysis. Expert review of anti-infective therapy. 2024 Apr:22(4):203-209. doi: 10.1080/14787210.2024.2307912. Epub 2024 Feb 8 [PubMed PMID: 38258529]
Level 1 (high-level) evidenceEngers DW, Tamma PD, Fiawoo S, Fong K, Jariwala R, Jenkins TC, Kendall RE, Lee JH, McCreary EK, Patel PK, Shihadeh KC, Slish J, Van Schooneveld TC, Malani AN. Transition to Oral Antibiotic Therapy for Hospitalized Adults With Gram-Negative Bloodstream Infections. JAMA network open. 2024 Jan 2:7(1):e2349864. doi: 10.1001/jamanetworkopen.2023.49864. Epub 2024 Jan 2 [PubMed PMID: 38165674]
Subramanian A. Emerging roles of bacteriophage-based therapeutics in combating antibiotic resistance. Frontiers in microbiology. 2024:15():1384164. doi: 10.3389/fmicb.2024.1384164. Epub 2024 Jul 5 [PubMed PMID: 39035437]
Ali SF, Teh SH, Yang HH, Tsai YC, Chao HJ, Peng SS, Chen SC, Lin LC, Lin NT. Therapeutic Potential of a Novel Lytic Phage, vB_EclM_ECLFM1, against Carbapenem-Resistant Enterobacter cloacae. International journal of molecular sciences. 2024 Jan 10:25(2):. doi: 10.3390/ijms25020854. Epub 2024 Jan 10 [PubMed PMID: 38255926]
Palma M, Qi B. Advancing Phage Therapy: A Comprehensive Review of the Safety, Efficacy, and Future Prospects for the Targeted Treatment of Bacterial Infections. Infectious disease reports. 2024 Nov 28:16(6):1127-1181. doi: 10.3390/idr16060092. Epub 2024 Nov 28 [PubMed PMID: 39728014]
Level 2 (mid-level) evidenceMergulhão P, Pereira JG, Fernandes AV, Krystopchuk A, Ribeiro JM, Miranda D, Castro H, Eira C, Morais J, Lameirão C, Gomes S, Leal D, Duarte J, Pássaro L, Froes F, Martin-Loeches I. Epidemiology and Burden of Ventilator-Associated Pneumonia among Adult Intensive Care Unit Patients: A Portuguese, Multicenter, Retrospective Study (eVAP-PT Study). Antibiotics (Basel, Switzerland). 2024 Mar 22:13(4):. doi: 10.3390/antibiotics13040290. Epub 2024 Mar 22 [PubMed PMID: 38666966]
Level 2 (mid-level) evidenceMiron M, Blaj M, Ristescu AI, Iosep G, Avădanei AN, Iosep DG, Crișan-Dabija R, Ciocan A, Perțea M, Manciuc CD, Luca Ș, Grigorescu C, Luca MC. Hospital-Acquired Pneumonia and Ventilator-Associated Pneumonia: A Literature Review. Microorganisms. 2024 Jan 20:12(1):. doi: 10.3390/microorganisms12010213. Epub 2024 Jan 20 [PubMed PMID: 38276198]
Miftode IL, Vâță A, Miftode RȘ, Parângă T, Luca MC, Manciuc C, Èšimpău AS, Radu V, RoÈ™u MF, Stămăteanu LO, Leca D, Anton-Păduraru DT, Miftode EG. The Impact of Urinary Catheterization on the Antibiotic Susceptibility of ESBL-Producing Enterobacterales: A Challenging Duo. Antibiotics (Basel, Switzerland). 2024 May 17:13(5):. doi: 10.3390/antibiotics13050462. Epub 2024 May 17 [PubMed PMID: 38786190]
Maraolo AE, Licciardi F, Gentile I, Saracino A, Belati A, Bavaro DF. Stenotrophomonas maltophilia Infections: A Systematic Review and Meta-Analysis of Comparative Efficacy of Available Treatments, with Critical Assessment of Novel Therapeutic Options. Antibiotics (Basel, Switzerland). 2023 May 15:12(5):. doi: 10.3390/antibiotics12050910. Epub 2023 May 15 [PubMed PMID: 37237813]
Level 1 (high-level) evidenceCheng LS, Chau SK, Chan WS, Chen JH, Wong BK, Fung KS. An outbreak of Burkholderia cepacia complex exit site infection among peritoneal dialysis patients caused by contaminated spray dressing. Infection prevention in practice. 2024 Jun:6(2):100359. doi: 10.1016/j.infpip.2024.100359. Epub 2024 Mar 16 [PubMed PMID: 38559368]
Azerefegne EF, Tasamma AT, Demass TB, Tessema AG, Degu WA. Prevalence of multidrug resistant gram-negative bacteria and associated factors among gram-negative blood culture isolates at Tikur Anbessa Specialized Hospital: a retrospective study. BMC infectious diseases. 2025 Aug 8:25(1):1006. doi: 10.1186/s12879-025-11328-0. Epub 2025 Aug 8 [PubMed PMID: 40781593]
Level 2 (mid-level) evidenceNasr J, Abdessamad H, Mina J, Haykal T, Jamil Y, Abboud E, Mahdi A, Asmar R, Abi Assaad R, Alameddine D, Bourji A, Mahdi M, Abdulaal R, Tomassian S, El Ahmadieh H, Azzam W, Mokhbat JE, Moghnieh R, Rodriguez-Morales AJ, Husni R. The epidemiology of gram-negative bacteremia in Lebanon: a study in four hospitals. Annals of clinical microbiology and antimicrobials. 2024 Oct 9:23(1):90. doi: 10.1186/s12941-024-00740-0. Epub 2024 Oct 9 [PubMed PMID: 39385237]
Calderaro A, Chezzi C. MALDI-TOF MS: A Reliable Tool in the Real Life of the Clinical Microbiology Laboratory. Microorganisms. 2024 Feb 3:12(2):. doi: 10.3390/microorganisms12020322. Epub 2024 Feb 3 [PubMed PMID: 38399726]
Wei M, Chen X, Liu J, Li T, Wang P, Wang S, Wang J, Gu L. Development and Validation of a Novel Multiplex Real-Time PCR Assay for Rapid Detection of Carbapenemase Genes in Carbapenem-Resistant Enterobacterales Isolates and Clinical Samples. Infection and drug resistance. 2024:17():3451-3462. doi: 10.2147/IDR.S475630. Epub 2024 Aug 9 [PubMed PMID: 39139626]
Level 1 (high-level) evidenceFernández-Cuenca F, Delgado-Valverde M, Guridi-Fernández P, Gimeno-Cardona C, Hidalgo-Díaz C, Pascual Á. Reporting antimicrobial susceptibility and detection of carbapenemase production in single and double carbapenemase-producing Gram-negative clinical isolates: a nationwide proficiency study. Frontiers in microbiology. 2025:16():1605590. doi: 10.3389/fmicb.2025.1605590. Epub 2025 Jun 10 [PubMed PMID: 40556889]
Tamma PD, Doi Y, Bonomo RA, Johnson JK, Simner PJ, Antibacterial Resistance Leadership Group. A Primer on AmpC β-Lactamases: Necessary Knowledge for an Increasingly Multidrug-resistant World. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2019 Sep 27:69(8):1446-1455. doi: 10.1093/cid/ciz173. Epub [PubMed PMID: 30838380]
De Waele JJ. Importance of timely and adequate source control in sepsis and septic shock. Journal of intensive medicine. 2024 Jul:4(3):281-286. doi: 10.1016/j.jointm.2024.01.002. Epub 2024 Feb 27 [PubMed PMID: 39035625]
Riccobene T, Ye G, Lock J, Yu KC, Ai C, Gregory S, Gupta V. Outcomes of inadequate empiric therapy and timing of newer antibacterial therapy in hospitalized adults with culture-positive Enterobacterales and Pseudomonas aeruginosa: a multicenter analysis. BMC infectious diseases. 2024 Aug 9:24(1):810. doi: 10.1186/s12879-024-09700-7. Epub 2024 Aug 9 [PubMed PMID: 39123114]
Huespe IA, Huaier Arriazu EF, Sanchez M, Stanek V, Pollán JA, Bauque S, Ávila Poletti D, Monzón V, Novelli Poisson P, Boutet MV, Cunto E, Chediack V, Beloso MT, Rucci V, Lagostena M, Cabrera R, Gutiérrez MJ, Gómez MG, Arias SG, Taffarel C, Ivulich D, Garzón MI, Cornistein W, Gira A, Kriger SG, Duarte L, Estenssoro E, Mirofsky M, Castro MG, Vaena M, Study Group Collaborator. Mortality of metallo-β-lactamase-producing Enterobacterales bacteremias with combined ceftazidime-avibactam plus aztreonam vs. other active antibiotics: a multicenter target trial emulation. Lancet regional health. Americas. 2025 Sep:49():101175. doi: 10.1016/j.lana.2025.101175. Epub 2025 Jul 5 [PubMed PMID: 40688569]
Timsit JF, Wicky PH, de Montmollin E. Treatment of Severe Infections Due to Metallo-Betalactamases Enterobacterales in Critically Ill Patients. Antibiotics (Basel, Switzerland). 2022 Jan 24:11(2):. doi: 10.3390/antibiotics11020144. Epub 2022 Jan 24 [PubMed PMID: 35203747]
Kang CI, Kim SH, Park WB, Lee KD, Kim HB, Oh MD, Kim EC, Choe KW. Bloodstream infections caused by Enterobacter species: predictors of 30-day mortality rate and impact of broad-spectrum cephalosporin resistance on outcome. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. 2004 Sep 15:39(6):812-8 [PubMed PMID: 15472813]
Level 2 (mid-level) evidenceChen Y, Huang J, Dong L, Xu B, Li L, Zhao Z, Li B. Clinical and genomic characterization of carbapenem-resistant Enterobacterales bloodstream infections in patients with hematologic malignancies. Frontiers in cellular and infection microbiology. 2024:14():1471477. doi: 10.3389/fcimb.2024.1471477. Epub 2024 Sep 26 [PubMed PMID: 39391886]
Herrera F, Torres D, Laborde A, Jordán R, Berruezo L, Roccia Rossi I, Mañez N, Tula L, Pereyra ML, Nenna A, Costantini P, Benso J, González Ibañez ML, Eusebio MJ, Baldoni N, Barcán LA, Lambert S, Luck M, Pasterán F, Corso A, Rapoport M, Nicola F, García Damiano MC, Monge R, Carbone R, Reynaldi M, Greco G, Blanco M, Chaves ML, Bronzi M, Carena A, Argentine Group for the Study of Bacteremia in Cancer and Stem Cell Transplant (ROCAS). Epidemiology of Bacteremia in Patients with Hematological Malignancies and Hematopoietic Stem Cell Transplantation and the Impact of Antibiotic Resistance on Mortality: Data from a Multicenter Study in Argentina. Pathogens (Basel, Switzerland). 2024 Oct 26:13(11):. doi: 10.3390/pathogens13110933. Epub 2024 Oct 26 [PubMed PMID: 39599486]
Level 2 (mid-level) evidenceWang L, Zeng C, Li X, Li Y, Liu Z, Hu J. Mortality associated with carbapenem resistance in Klebsiella pneumoniae bloodstream infection: A propensity score-matched study. Infection control and hospital epidemiology. 2024 Jul:45(7):839-846. doi: 10.1017/ice.2024.21. Epub 2024 Mar 15 [PubMed PMID: 38487826]
Ma Z, Lai C, Zhang J, Han Y, Xin M, Wang J, Wu Z, Luo Y. High mortality associated with inappropriate initial antibiotic therapy in hematological malignancies with Klebsiella pneumoniae bloodstream infections. Scientific reports. 2024 Jun 6:14(1):13041. doi: 10.1038/s41598-024-63864-5. Epub 2024 Jun 6 [PubMed PMID: 38844581]
Lumbreras-Iglesias P, Rodrigo-Arrazola E, López-Amor L, Fernández-Suárez J, Rodicio MR, Fernández J. Clinical and Microbiological Risk Factors for 30-Day Mortality of Bloodstream Infections Caused by OXA-48-Producing Klebsiella pneumoniae. Pathogens (Basel, Switzerland). 2023 Dec 21:13(1):. doi: 10.3390/pathogens13010011. Epub 2023 Dec 21 [PubMed PMID: 38276157]
Jeon M, Huh K, Ko JH, Cho SY, Huh HJ, Lee NY, Kang CI, Chung DR, Peck KR. Difference in the Clinical Outcome of Bloodstream Infections Caused by Klebsiella aerogenes and Enterobacter cloacae Complex. Open forum infectious diseases. 2021 Aug:8(8):ofab390. doi: 10.1093/ofid/ofab390. Epub 2021 Jul 20 [PubMed PMID: 34409124]
Level 2 (mid-level) evidenceDhanaraj N, Rowe K, Foppiano Palacios C. Utility of Obtaining Follow-Up Blood Cultures in Gram-Negative Bacterial Bloodstream Infection Among Patients With Hematologic Malignancies. Cureus. 2024 Nov:16(11):e73915. doi: 10.7759/cureus.73915. Epub 2024 Nov 18 [PubMed PMID: 39697922]
Laporte-Amargos J, Sastre E, Bergas A, Pomares H, Paviglianiti A, Rodriguez-Arias M, Pallares N, Badia-Tejero AM, Pons-Oltra P, Carratalà J, Gudiol C. Increasing Gram-Negative Catheter-Related Bloodstream Infection in Cancer Patients. Pathogens (Basel, Switzerland). 2023 Feb 1:12(2):. doi: 10.3390/pathogens12020228. Epub 2023 Feb 1 [PubMed PMID: 36839500]
Buonsenso D, Salerno G, Sodero G, Mariani F, Pisapia L, Gelormini C, Di Nardo M, Valentini P, Scoppettuolo G, Biasucci DG. Catheter salvage strategies in children with central venous catheter-related or -associated bloodstream infections: a systematic review and meta-analysis. The Journal of hospital infection. 2022 Jul:125():1-20. doi: 10.1016/j.jhin.2022.03.010. Epub 2022 Apr 4 [PubMed PMID: 35390396]
Level 1 (high-level) evidenceManyahi J, Joachim A, Msafiri F, Migiro M, Mwingwa A, Kasubi M, Naburi H, Majigo MV. Polymicrobial bloodstream infections a risk factor for mortality in neonates at the national hospital, Tanzania: A case-control study. PloS one. 2024:19(4):e0302076. doi: 10.1371/journal.pone.0302076. Epub 2024 Apr 16 [PubMed PMID: 38625965]
Level 2 (mid-level) evidenceXu J, Yuan Y, Wang B, Zhang Q, Wang J, Wang S, Li Y, Yan W. Microbiological Analysis and Mortality Risk Factors in Patients with Polymicrobial Bloodstream Infections. Infection and drug resistance. 2023:16():3917-3927. doi: 10.2147/IDR.S412669. Epub 2023 Jun 20 [PubMed PMID: 37361937]
Skei NV, Nilsen TIL, Mohus RM, Prescott HC, Lydersen S, Solligård E, Damås JK, Gustad LT. Trends in mortality after a sepsis hospitalization: a nationwide prospective registry study from 2008 to 2021. Infection. 2023 Dec:51(6):1773-1786. doi: 10.1007/s15010-023-02082-z. Epub 2023 Aug 12 [PubMed PMID: 37572240]
Yo CH, Shen YH, Hsu WT, Mekary RA, Chen ZR, Lee WJ, Chen SC, Lee CC. MALDI-TOF mass spectrometry rapid pathogen identification and outcomes of patients with bloodstream infection: A systematic review and meta-analysis. Microbial biotechnology. 2022 Oct:15(10):2667-2682. doi: 10.1111/1751-7915.14124. Epub 2022 Aug 3 [PubMed PMID: 35921430]
Level 1 (high-level) evidence