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Bacterium

Acinetobacter baumannii

Harmful Systemic Other Skin Respiratory tract Wounds Gut
Harmful
Effect
Systemic
Impact
Other, Skin, Respiratory tract, Wounds, Gut
Location
Common
Prevalence

Overview

Acinetobacter baumannii is a Gram-negative, aerobic, non-fermenting coccobacillus and one of the most clinically significant opportunistic pathogens in healthcare settings. Designated as a WHO priority pathogen for new antibiotic development, it is a member of the notorious ESKAPE pathogens and causes up to 1.4 million hospital-acquired infections annually.[1]

Key Characteristics

A. baumannii possesses several distinctive features that contribute to its success as a nosocomial pathogen:

  • Morphology: Pleomorphic coccobacilli appearing in pairs or chains
  • Environmental persistence: Survives for weeks to months on dry hospital surfaces
  • Biofilm formation: Forms robust biofilms on medical devices and surfaces
  • Genomic plasticity: Contains numerous mobile genetic elements facilitating resistance gene acquisition
  • Natural competence: Capable of DNA uptake through horizontal gene transfer
  • Metabolic versatility: Utilizes various carbon and energy sources

Antibiotic Resistance Mechanisms

A. baumannii has developed an alarming array of resistance mechanisms making it increasingly difficult to treat:[2]

β-Lactamases

  • Produces all four Ambler classes of β-lactamases
  • OXA-type carbapenemases (OXA-23, OXA-24, OXA-51, OXA-58) are predominant
  • Metallo-β-lactamases (NDM, IMP, VIM) increasingly reported

Efflux Pumps

  • AdeABC: Primary efflux pump conferring multidrug resistance
  • AdeFGH and AdeIJK: Additional RND-family pumps
  • Up-regulation contributes to tigecycline and colistin resistance

Other Mechanisms

  • Decreased membrane permeability through porin loss (CarO, OprD)
  • Target site modifications (lipid A modifications for colistin resistance)
  • Homologous recombination for acquiring resistance traits[3]

Virulence Factors

The pathogen employs a "persist and resist" strategy through diverse virulence factors:[6]

Adhesion and Biofilm

  • Outer membrane proteins (OmpA, CarO, Omp33): Facilitate host cell attachment
  • CsuA/BABCDE pili: Essential for abiotic surface attachment
  • Bap (Biofilm-associated protein): Critical for biofilm maturation

Immune Evasion

  • Capsular polysaccharides: Protect against complement and phagocytosis
  • LPS modifications: Alter host immune recognition
  • Type VI secretion system: Delivers effectors to competing bacteria and host cells

Metal Acquisition

  • Acinetobactin: Primary siderophore for iron acquisition
  • ZnuABC: Zinc transport system
  • Sophisticated systems for manganese acquisition

Clinical Significance

Infections and Mortality

A. baumannii causes severe healthcare-associated infections with mortality rates of 43-84% in ICU settings:

  • Ventilator-associated pneumonia (VAP): Most common manifestation
  • Bloodstream infections: Often catheter-related with high mortality
  • Wound infections: Particularly in trauma and burns
  • Meningitis: Following neurosurgical procedures
  • Urinary tract infections: Catheter-associated

Risk Factors

  • Mechanical ventilation
  • Prolonged ICU stay
  • Prior antibiotic therapy
  • Invasive devices (central lines, urinary catheters)
  • Immunosuppression
  • Combat-related injuries ("Iraqibacter")

Treatment Options

Current therapeutic strategies for carbapenem-resistant A. baumannii (CRAB) infections are limited:[4]

First-Line Options

  • Sulbactam-durlobactam with carbapenem: Preferred therapy for CRAB
  • High-dose ampicillin-sulbactam (6-9g daily): Backbone of many regimens
  • Polymyxin B: Favored over colistin due to better pharmacokinetics

Alternative Agents

  • High-dose tigecycline (100mg q12h): For non-pulmonary infections
  • Cefiderocol: Emerging option, especially for MDR strains
  • Minocycline (200mg q12h): Alternative for susceptible strains

Emerging Therapies

  • Bacteriophage therapy
  • Antimicrobial peptides
  • CRISPR-Cas systems for sequence-specific targeting
  • Artilysins (engineered endolysins)

Gut Colonization and Microbiome Interactions

Recent research has revealed important aspects of A. baumannii gut colonization:[5]

  • Ornithine metabolism: Uses ornithine succinyltransferase (AstO) to compete with gut microbiota
  • Dietary influence: Dietary ornithine supplementation promotes colonization
  • Infant colonization: Significantly higher in formula-fed versus breastfed infants
  • Reservoir function: Gut serves as metabolic reservoir for antimicrobial-resistant strains
  • Commensal inhibition: Produces acinetobactin to outcompete skin and respiratory commensals

One Health Perspective

A. baumannii is increasingly recognized as a One Health pathogen found in companion animals, livestock, wildlife, food, and aquatic environments. Direct transmission between human and non-human populations has been documented, with resistance increasing in populations with closer human contact.

References

  1. Lee CR, Lee JH, Park M, et al. Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options. Frontiers in Cellular and Infection Microbiology. 2017;7:55. doi:10.3389/fcimb.2017.00055

  2. Vrancianu CO, Gheorghe I, Czobor IB, Chifiriuc MC. Antibiotic Resistance Profiles, Molecular Mechanisms and Innovative Treatment Strategies of Acinetobacter baumannii. Microorganisms. 2020;8(6):935. doi:10.3390/microorganisms8060935

  3. Cain AK, Hamidian M. Portrait of a killer: Uncovering resistance mechanisms and global spread of Acinetobacter baumannii. PLOS Pathogens. 2023;19(8):e1011520. doi:10.1371/journal.ppat.1011520

  4. Kubin CJ, Garzia C, Uhlemann AC. Acinetobacter baumannii treatment strategies: a review of therapeutic challenges and considerations. Antimicrobial Agents and Chemotherapy. 2025;69(8):e01063-24. doi:10.1128/aac.01063-24

  5. Ren X, Clark RM, Bansah DA, et al. Amino acid competition shapes Acinetobacter baumannii gut carriage. Cell Host & Microbe. 2025;33(8):1396-1411.e9. doi:10.1016/j.chom.2025.07.003

  6. Mea HJ, Yong PVC, Wong EH. An overview of Acinetobacter baumannii pathogenesis: Motility, adherence and biofilm formation. Microbiological Research. 2021;247:126722. doi:10.1016/j.micres.2021.126722

  7. Zhang S, Di L, Qi Y, Qian X, Wang S. Treatment of infections caused by carbapenem-resistant Acinetobacter baumannii. Frontiers in Cellular and Infection Microbiology. 2024;14:1395260. doi:10.3389/fcimb.2024.1395260

  8. Shadan A, Pathak A, Ma Y, et al. Deciphering the virulence factors, regulation, and immune response to Acinetobacter baumannii infection. Frontiers in Cellular and Infection Microbiology. 2023;13:1053968. doi:10.3389/fcimb.2023.1053968

Associated Conditions

→ Pneumonia → Sepsis → Wound infections → Urinary tract infections → Meningitis → Ventilator-associated pneumonia

Research References

  1. Lee CR, Lee JH, Park M, et al.. Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options. Frontiers in Cellular and Infection Microbiology. 2017. doi:10.3389/fcimb.2017.00055
  2. Vrancianu CO, Gheorghe I, Czobor IB, Chifiriuc MC. Antibiotic Resistance Profiles, Molecular Mechanisms and Innovative Treatment Strategies of Acinetobacter baumannii. Microorganisms. 2020. doi:10.3390/microorganisms8060935
  3. Cain AK, Hamidian M. Portrait of a killer: Uncovering resistance mechanisms and global spread of Acinetobacter baumannii. PLOS Pathogens. 2023. doi:10.1371/journal.ppat.1011520
  4. Kubin CJ, Garzia C, Uhlemann AC. Acinetobacter baumannii treatment strategies: a review of therapeutic challenges and considerations. Antimicrobial Agents and Chemotherapy. 2025. doi:10.1128/aac.01063-24
  5. Ren X, Clark RM, Bansah DA, et al.. Amino acid competition shapes Acinetobacter baumannii gut carriage. Cell Host & Microbe. 2025. doi:10.1016/j.chom.2025.07.003
  6. Mea HJ, Yong PVC, Wong EH. An overview of Acinetobacter baumannii pathogenesis: Motility, adherence and biofilm formation. Microbiological Research. 2021. doi:10.1016/j.micres.2021.126722