Gram-negativeBacilliNon-fermenters

Acinetobacter baumannii

Aerobic, non-fermenting Gram-negative coccobacillus that is a leading cause of multidrug-resistant nosocomial infections, particularly ventilator-associated pneumonia, bloodstream infections, and wound infections in critically ill and immunocompromised patients.

Organism Card

DomainMust know
Identity
  • Gram-negative coccobacillus (short, plump rods often appearing as diplococci) [1][2]
  • Strictly aerobic, non-fermenting
  • Family Moraxellaceae; may be confused with Neisseria on Gram stain due to coccobacillary shape
  • One of the most important MDR/XDR nosocomial pathogens worldwide [1][3]
Lab discriminator
  • Oxidase-NEGATIVE (key discriminator vs Pseudomonas which is oxidase +) [1][2]
  • Non-motile (vs Pseudomonas which is motile)
  • Grows on MacConkey agar (lactose non-fermenter → colourless colonies)
  • Catalase positive
  • Can survive on dry surfaces for weeks → facilitates hospital outbreaks [1][4]
Reservoir / transmission
  • Ubiquitous in the hospital environment: survives on dry surfaces, ventilator tubing, bed rails, hands of HCWs [1][4]
  • Predominantly healthcare-associated transmission; ICU is the highest-risk setting
  • Community-acquired infections rare; described in warm humid climates
  • HK relevance: important cause of nosocomial outbreaks in local ICUs; notifiable as MDR organism under CHP surveillance [4]
Key virulence
  • Biofilm formation on medical devices (ETT, catheters) → persistence + resistance [1]
  • Outer membrane protein OmpA → adhesion, invasion, apoptosis of host cells
  • Lipopolysaccharide (LPS) → septic shock
  • Remarkable ability to acquire resistance genes (e.g. OXA-type carbapenemases, NDM-1 metallo-β-lactamases) [1][3]
  • Desiccation tolerance → survives weeks on surfaces, driving outbreaks [4]
Clinical syndromes
  • Ventilator-associated pneumonia (VAP) — most important syndrome; ICU patient on prolonged mechanical ventilation [1][2]
  • Bacteraemia / catheter-related bloodstream infection — high mortality [1]
  • Wound / burn infections — especially combat/trauma wounds
  • Nosocomial UTI (catheter-associated)
  • Nosocomial meningitis (post-neurosurgical)
  • Predominantly affects immunocompromised / critically ill / ICU patients with prolonged hospitalisation & prior broad-spectrum antibiotics [1][2][3]
Diagnosis
  • Specimen: blood culture, sputum/BAL, wound swab, urine, CSF as appropriate
  • Gram stain: G−ve coccobacilli (can be misread as Neisseria) [2]
  • Culture on blood agar / MacConkey; MALDI-TOF MS for rapid ID
  • Always perform susceptibility testing — resistance pattern dictates therapy [1][3]
  • Pitfall: colonisation vs true infection — must correlate with clinical signs, especially for respiratory isolates
Treatment
  • Empirical choice depends on local antibiogram; resistance to almost all β-lactams, fluoroquinolones, and aminoglycosides is common [1][3]
  • Carbapenem-susceptible: meropenem or imipenem (doripenem also active) [3]
  • Carbapenem-resistant (CR-AB): options include colistin (polymyxin E), high-dose ampicillin-sulbactam, tigecycline, or combinations [1][3]
  • Sulbactam has intrinsic activity against Acinetobacter (unique among β-lactamase inhibitors) [3]
  • Colistin is often the drug of last resort for XDR strains; nephrotoxicity is the main concern [1][3]
  • Source control essential: remove/replace infected lines, devices
  • Newer agents: cefiderocol; combination therapy preferred for XDR strains [3]
Prevention
  • Contact precautions for MDR/XDR strains: gown + gloves; single room or cohorting [4]
  • Strict hand hygiene (alcohol-based handrub effective) and environmental disinfection are critical [4]
  • Surveillance cultures in outbreak settings
  • Antibiotic stewardship to limit selection pressure for resistant strains [1][3][4]
  • No vaccine available
  • CHP Hong Kong surveillance: CRE/MDRO alert organism — lab notification triggers infection control measures [4]
Classic traps
  • Don't confuse with Pseudomonas: both are G−ve non-fermenters, but Acinetobacter is oxidase −, non-motile; Pseudomonas is oxidase +, motile, produces pigments [1][2]
  • Don't confuse with Neisseria on Gram stain: both appear as G−ve diplococci/coccobacilli, but Acinetobacter is oxidase − and grows on MacConkey; Neisseria is oxidase + and requires enriched media [2]
  • Vignette clue: ICU patient, prolonged ventilation, prior broad-spectrum antibiotics, multidrug-resistant G−ve coccobacillus → think A. baumannii [1]
  • Sulbactam activity is unique — if an exam question asks which β-lactamase inhibitor has intrinsic anti-Acinetobacter activity, answer is sulbactam [3]

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