Gram-negativeBacilliEnterobacterales

Klebsiella pneumoniae

Encapsulated, non-motile Gram-negative rod of the Enterobacteriaceae family that is a major cause of nosocomial pneumonia, urinary tract infections, and bacteremia, particularly in immunocompromised and hospitalized patients.

Organism Card

DomainMust know
Identity
  • G−ve, facultative anaerobic rod; Enterobacterales family [1]
  • Non-motile, lactose-fermenting, heavily encapsulated
  • Closely related to other Enterobacterales (E. coli, Enterobacter, Proteus)
Lab discriminator
  • Mucoid colonies on MacConkey agar (lactose fermenter)
  • Prominent polysaccharide capsule → string sign / mucoid appearance [1]
  • Indole −ve (vs E. coli indole +ve); urease +ve; citrate +ve
  • Non-motile (vs motile E. coli, Enterobacter, Proteus)
Reservoir / transmission
  • Normal GI flora; ubiquitous in environment
  • Nosocomial transmission via hands, devices, catheters [1][2]
  • East Asia association: DM + liver abscess → classic HK/Taiwan vignette [3]
Key virulence
  • Thick polysaccharide capsule → anti-phagocytic; serotype K1/K2 most virulent [3]
  • Hypermucoviscosity phenotype (string test +ve > 5 mm) → invasive liver abscess syndrome
  • Siderophores (aerobactin) → iron acquisition
  • LPS endotoxin → sepsis cascade
  • Urease → facilitates UTI persistence
  • Encapsulated organism → dangerous in asplenic patients [4]
Clinical syndromes
  • UTI: 2nd commonest G−ve uropathogen after E. coli; uncomplicated (6%), complicated (8%) [2][5]
  • Pneumonia: classic "currant-jelly sputum", lobar with bulging fissure (upper lobe), CAP in alcoholics/DM; also HAP/VAP [6]
  • Pyogenic liver abscess: classically DM patients in East Asia; may → metastatic endogenous endophthalmitis (60% of endogenous bacterial endophthalmitis in East Asia) [3][7]
  • SBP: common G−ve cause (11% of SBP isolates) in cirrhotic ascites [8]
  • Neonatal meningitis; wound/surgical site infections; bacteraemia
  • PD-related peritonitis: among G−ve causes [9]
  • Ophthalmia neonatorum (less common) [7]
Diagnosis
  • Specimen: urine C/ST, sputum G stain + C/ST, blood culture, ascitic fluid, abscess aspirate
  • G stain: G−ve rods, often with clear capsular halo
  • Culture: mucoid lactose-fermenting colonies on MacConkey
  • Species ID: MALDI-TOF MS (rapid); biochemical panel
  • Liver abscess: USG liver + blood culture; string test for hypermucoviscosity [3]
  • Pitfall: culture-negative SBP still treated as SBP if PMN ≥ 250 [8]
Treatment
  • Empirical: 3rd-gen cephalosporin (cefotaxime / ceftriaxone) for serious infections [8]
  • ESBL-producing Klebsiella: resistant to all β-lactams EXCEPT carbapenems → carbapenems are drug of choice for severe ESBL infections [1]
  • CPE (carbapenemase-producing Enterobacterales): emerging threat; limited options (colistin, ceftazidime-avibactam, tigecycline) [1]
  • Liver abscess: IV antibiotics + percutaneous drainage if ≥ 5 cm
  • UTI: guided by C/ST; nitrofurantoin or TMP-SMX for uncomplicated if susceptible
  • SBP: IV 3rd-gen ceph × 5–7 d; consider carbapenem if severe [8]
Prevention
  • Infection control: hand hygiene, contact precautions for ESBL/CPE colonised patients [1]
  • Antimicrobial stewardship to limit ESBL/CPE emergence [1]
  • Catheter care bundles to prevent nosocomial UTI
  • No vaccine available
  • Asplenic patients: educate re encapsulated organism risk; early Abx for febrile episodes [4]
Classic traps
  • Klebsiella liver abscess + DM + new eye symptoms → endogenous endophthalmitis (consult ophthalmology urgently) [7]
  • Bulging fissure on CXR: think Klebsiella (mucoid exudate) vs S. pneumoniae (also lobar)
  • Mucoid sputum ≠ always Klebsiella; S. pneumoniae is still commonest CAP organism
  • ESBL vs CPE: ESBL still susceptible to carbapenems; CPE is not [1]
  • Encapsulated organism mnemonic: "Some Nasty Killers Have Some Capsule Protection" — includes Klebsiella [4]
  • Non-motile (vs Proteus swarming, Enterobacter motile)

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