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Acinetobacter baumannii

Acinetobacter baumannii is a Gram-negative, aerobic, non-motile, pleomorphic bacillus belonging to the genus Acinetobacter, recognized as an opportunistic pathogen that primarily causes nosocomial infections in healthcare settings. It is ubiquitous in the environment, commonly found in soil and water, and can colonize human skin, respiratory tract, and oropharynx in low numbers without causing disease in healthy individuals. However, in vulnerable patients, it leads to severe infections such as pneumonia, bloodstream infections, urinary tract infections, and wound infections, with transmission occurring via contaminated surfaces, medical equipment, or person-to-person contact, often through unwashed hands. The bacterium's notoriety stems from its remarkable ability to acquire multidrug resistance, including to , making it a key member of the group of , a threat, and a critical according to the , with mortality rates for resistant strains ranging from 30% to 75%. Resistance mechanisms encompass degradation enzymes, efflux pumps, altered drug targets, and reduced outer membrane permeability, often carried on like resistance islands. High-risk groups include those in intensive care units, on mechanical ventilators, with indwelling catheters or open wounds, prolonged hospital stays, weakened immune systems, chronic lung disease, or . A. baumannii enhances its pathogenicity through formation on medical devices, which promotes persistence and evasion of defenses, and virulence factors like the outer membrane protein A (OmpA), which induces . Its shows increasing prevalence in high-density healthcare environments, particularly in regions with heavy use, such as parts of , underscoring the need for stringent control, , and emerging therapies like to mitigate outbreaks.

Taxonomy and Characteristics

Classification and Etymology

Acinetobacter baumannii is a within the Acinetobacter, which belongs to the Moraxellaceae, order Pseudomonadales, class , phylum Proteobacteria, and kingdom . This taxonomic placement reflects its as a Gram-negative, aerobic bacterium based on phylogenetic analyses of 16S rRNA sequences and other molecular markers. The genus name Acinetobacter derives from the Greek words a-kinētos, meaning "non-motile," referring to the organism's lack of flagella and inability to move. The species epithet baumannii honors the American microbiologists Paul and Linda Baumann, who contributed significantly to the of non-fermentative . This naming was formalized in 1986 by Bouvet and Grimont, who recognized A. baumannii as a distinct through and DNA hybridization studies. The history of A. baumannii traces back to 1911, when microbiologist Martinus Willem Beijerinck first isolated a similar from and described it as Micrococcus calcoaceticus due to its ability to oxidize calcium acetate. In 1954, Brisou and Prévot proposed the genus to encompass non-motile, oxidase-negative coccobacilli previously classified under various names. The species A. baumannii was specifically delineated in the 1960s and formally named in 1986, distinguishing it from other Acinetobacter genomospecies based on phenotypic and genotypic characteristics. The type strain of Acinetobacter baumannii is ATCC 19606, originally isolated from human urine before 1948 and deposited in culture collections such as CIP 70.34 and NCTC 12156. This strain serves as the reference for identification and has been extensively sequenced to support genomic studies.

Morphology and Physiology

Acinetobacter baumannii is a Gram-negative, strictly aerobic, non-fermentative characterized by its short, plump rod shape, typically measuring 0.6–1.0 μm in width and 1.5–2.5 μm in length. These cells often appear pleomorphic and can be difficult to decolorize during Gram staining, occasionally leading to misidentification as cocci. The bacterium does not produce spores and generally lacks a prominent capsule, contributing to its robust environmental persistence. Physiologically, A. baumannii is catalase-positive and oxidase-negative, enabling it to thrive in oxygen-rich environments through oxidative metabolism. It exhibits optimal growth at temperatures between 20°C and 44°C, with a preference for 37°C, and tolerates a pH range of 5.5–8.0, allowing adaptation to diverse niches including hospital settings. The organism utilizes a wide variety of carbon sources, such as acetate, supporting its non-fastidious nature and ability to colonize varied substrates. On solid media like sheep blood agar or tryptic soy agar, A. baumannii forms smooth, grayish-white colonies, sometimes mucoid, reaching 1–2 mm in diameter after 24 hours of incubation at 37°C. Although non-motile and lacking flagella, it demonstrates twitching motility facilitated by type IV pili, which aids in surface translocation and initial without true capability.

Genome and Proteins

The of Acinetobacter baumannii consists of a single circular with a size typically ranging from 3.9 to 4.0 and a G+C content of approximately 39%. For instance, the of strain ATCC 19606 measures 3,981,941 bp with 39.15% G+C content. Plasmids are commonly present and can reach sizes up to 100 kb or more, often harboring genes that confer resistance, such as those encoding aminoglycoside-modifying enzymes or sulfonamide resistance determinants. The encodes approximately 3,800 protein-coding sequences (), along with genes including transfer RNAs and ribosomal RNAs, contributing to the bacterium's metabolic versatility and adaptability. In strain V15, for example, the chromosome contains 3,610 predicted with 38.5% G+C content, while associated s encode additional , such as 87 on a 68-kb . These plasmids facilitate , enhancing the pathogen's resistance profile across diverse environments. A key outer membrane protein in A. baumannii is OmpA, a porin with a molecular weight of approximately 38 kDa that forms a β-barrel structure featuring four extracellular loops essential for interactions. OmpA functions in to cells and confers resistance to complement, contributing to the bacterium's potential. Other notable proteins include the AdeRS two-component system, which regulates the expression of the AdeABC to modulate multidrug efflux and maintain cellular under stress. Additionally, some strains possess CRISPR-Cas systems, primarily type I-F variants, that provide adaptive immunity against bacteriophages by acquiring and utilizing spacer sequences to target invading viral DNA.

Habitat and Ecology

Natural Reservoirs

Acinetobacter baumannii is commonly found in and water environments, where it thrives in moist conditions. The bacterium has been isolated from agricultural soils in at a prevalence of 41% and in , often as multidrug-resistant strains. In aquatic settings, it persists in freshwater bodies, , and plants; for example, 98 isolates were recovered from South Africa's , with 53.1% showing multidrug resistance, and high resistance rates (up to 86%) have been reported in Croatian wastewater treatment plants. These habitats underscore its ubiquity outside clinical contexts, contributing to environmental dissemination. Animal reservoirs play a key role in the ecology of A. baumannii, with detections in the gastrointestinal tracts and other sites of such as (7.0% isolation from associated samples in ) and (32.5% from chicken meat in ). The pathogen is also present in companion animals including dogs, cats, and horses, as well as wildlife like white storks, where isolation rates reached 30% in nestlings. In healthy humans, carriage remains low, typically 3-10% on and in the oropharynx, distinguishing it from higher rates for other species. Associations with plants further expand its natural niches, as A. baumannii has been detected on and crops, particularly those irrigated with contaminated . For instance, 5% of vegetable samples in Eastern harbored the bacterium, and it has been identified in irrigated farmlands via bird feces contamination, posing risks to produce safety. Such findings highlight fresh produce as a potential vector for environmental transmission. Key persistence factors allow A. baumannii to endure , surviving on dry surfaces for weeks to over 90 days in some strains, far exceeding the few days for desiccation-sensitive variants. This tolerance is mediated by the two-component regulator BfmR, which controls stress responses, and is enhanced by formation, enabling prolonged viability in arid conditions.

Environmental Distribution

Acinetobacter baumannii is frequently detected in air and dust within healthcare and community settings, facilitating through fomites and contaminated particles. The bacterium demonstrates remarkable persistence on dry surfaces, remaining viable for periods extending up to four months under ambient conditions, which contributes to its environmental dispersal and role in nosocomial outbreaks. This survival capability is enhanced by its formation of biofilms on such surfaces, allowing it to withstand and mechanical stress. In aquatic environments, A. baumannii commonly contaminates plumbing systems, where it colonizes and fixtures, posing risks to vulnerable patients. It has also been isolated from potable water supplies and plants, highlighting its adaptability to chlorinated and nutrient-limited conditions in these systems. The bacterium enters the through contamination of raw vegetables, , and during and , with isolates recovered from these sources showing genetic similarities to clinical strains. This presence raises concerns for potential foodborne transmission, particularly in regions with inadequate . A. baumannii thrives in warm and humid climates, with higher environmental prevalence observed in tropical regions, though it is detected globally across temperate and tropical zones. Seasonal variations in its abundance correlate with warmer temperatures, influencing its ecological distribution and infection rates.

Pathogenesis and Virulence

Virulence Factors

_Acinetobacter baumannii employs a range of virulence factors that facilitate adhesion, immune evasion, toxin production, and host tissue invasion, enabling its persistence and pathogenicity in immunocompromised hosts. These molecular mechanisms allow the bacterium to colonize surfaces, evade innate immune responses, acquire essential nutrients, and disseminate systemically. Key adhesins, such as Type IV pili and the CsuA/B chaperone-usher system, promote initial attachment to host cells and abiotic surfaces, initiating infection. Adhesins play a critical role in host cell attachment. Type IV pili mediate twitching motility and direct bacterial adhesion to epithelial cells, enhancing colonization and facilitating for genetic exchange. The CsuA/B chaperone-usher system assembles fimbriae-like structures that bind to hydrophobic surfaces via the CsuE subunit's exposed loops, promoting stable attachment and early initiation on medical devices. For immune evasion, capsular form a protective layer that inhibits by macrophages and complement activation, with the capsular type conferring high serum resistance. Outer membrane protein A (OmpA) induces in host epithelial and immune cells by translocating to mitochondria, triggering production and activation, thereby suppressing inflammatory responses. Toxins further contribute to tissue damage and nutrient acquisition. Cytotoxic phospholipases C (Plc1 and Plc2) hydrolyze host phospholipids, causing membrane disruption and cytolysis in lung epithelial cells, with mutants exhibiting reduced virulence in murine models. Siderophores, particularly acinetobactin, enable iron scavenging in iron-restricted host environments by chelating ferric iron with high affinity, supporting bacterial growth and persistence during sepsis; acinetobactin biosynthesis is essential for full virulence in Galleria mellonella and vertebrate infection models. Regarding invasion, lipid A modifications, such as hepta-acylation mediated by LpxM acyltransferase, strengthen the outer membrane against cationic antimicrobial peptides, enhancing bacterial survival in bloodstream and facilitating systemic infections.

Biofilm Formation

Acinetobacter baumannii forms biofilms as structured communities of bacterial cells embedded in a self-produced extracellular polymeric substance (EPS) matrix, which protects the organism from environmental stresses and host defenses. These biofilms typically develop on abiotic surfaces such as medical catheters and biotic surfaces like host tissues, contributing to the persistence of infections in healthcare settings. The process of biofilm formation occurs in distinct stages. Initial attachment involves reversible adhesion to surfaces mediated by type IV pili, particularly the Csu pilus system (CsuA/BABCDE), which enables the bacteria to colonize substrates like polystyrene or host epithelia. This is followed by irreversible attachment and microcolony formation, where cells produce adhesins and begin synthesizing EPS components. Maturation then ensues, with proliferation of cells forming multilayered, three-dimensional structures encased in EPS composed of polysaccharides (e.g., poly-N-acetylglucosamine [PNAG]), proteins (e.g., biofilm-associated protein [Bap]), lipids, and extracellular DNA, creating a protective barrier. Finally, dispersal occurs through the production of surfactants or in response to nutrient limitation, allowing cells to disseminate and initiate new infections. Regulatory pathways tightly control these stages. Quorum sensing via the AbaI/AbaR system, which produces N-(3-hydroxydodecanoyl)-L-homoserine lactone (3-OH-C12-HSL), coordinates population density-dependent behaviors, including enhanced formation by upregulating production and assembly. Additionally, cyclic di-GMP signaling modulates and synthesis; elevated levels of this second messenger promote stability by activating diguanylate cyclases that regulate expression and PNAG production. Clinically, A. baumannii biofilms enhance bacterial survival in nutrient-poor environments, such as those encountered during prolonged hospital stays. Biofilms in general are associated with 65–80% of chronic bacterial infections, and A. baumannii biofilms particularly contribute to persistent nosocomial infections, including and . This architecture not only shields cells from antibiotics but also facilitates chronic colonization, complicating treatment efforts.

Host Interaction

_Acinetobacter baumannii primarily enters the human host through opportunistic routes, exploiting breaches in natural barriers such as wounds, invasive medical devices like ventilation tubes and urinary catheters, or direct bloodstream invasion during nosocomial transmission. This bacterium is particularly adept at infecting immunocompromised individuals, including those in intensive care units with underlying conditions like , burns, or prolonged hospitalization, where it colonizes mucosal surfaces in the respiratory and gastrointestinal tracts via mechanisms. As an opportunistic , it rarely causes disease in healthy hosts but thrives in those with weakened defenses, facilitating initial attachment and invasion through a zipper-like process involving host cell . Upon entry, A. baumannii elicits a robust yet dysregulated , often culminating in a characterized by elevated levels of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β, primarily triggered via (TLR4) signaling on host cells. Neutrophils represent the primary cellular effectors against the infection, deploying (ROS) and (NETs) for bacterial clearance; however, their efficacy is significantly impaired by the bacterium's polysaccharide capsule, which shields surface antigens and promotes immune evasion in virulent strains. This capsule, along with other factors like outer membrane protein A (OmpA), contributes to persistent inflammation and host tissue damage without effective resolution. The pathogen exhibits distinct tissue , favoring sites that support its survival and dissemination, such as the lungs where it causes by invading alveolar epithelial cells, the bloodstream leading to and bacteremia, and the central nervous system resulting in , particularly in neonates or trauma patients. A. baumannii demonstrates remarkable persistence within host macrophages, where it survives intracellularly by modulating phagosomal maturation and evading lysosomal degradation, thereby establishing a for prolonged . This intracellular niche enhances its ability to disseminate systemically from initial colonization sites. A. baumannii can establish latency as an colonizer. Acinetobacter species can colonize the skin or mucous membranes of up to 40% of healthy adults, though A. baumannii rates are generally low (e.g., 1-5% in community settings), particularly in hospital environments, without clinical manifestations. Reactivation occurs upon host , such as during or critical illness, transforming commensal into active through mechanisms that exploit the pre-existing bacterial .

Antibiotic Resistance

Resistance Mechanisms

Acinetobacter baumannii exhibits intrinsic to multiple through physiological barriers and active expulsion mechanisms. The outer serves as a primary barrier due to its low permeability, primarily mediated by selective porins such as OmpA and CarO, which restrict the entry of hydrophilic drugs like . Reduced expression or mutations in these porins further diminish antibiotic influx, contributing to baseline against beta-lactams and other agents. Additionally, constitutive efflux systems actively pump out from the cell, enhancing tolerance to a broad spectrum of compounds including tetracyclines and aminoglycosides. Acquired resistance in A. baumannii arises primarily through and , enabling rapid to selective pressures. Plasmids and integrons facilitate the of resistance determinants across bacterial populations, allowing the acquisition of that confer protection against various drug classes. For instance, in the gyrA alter the target, leading to against fluoroquinolones by preventing drug binding. These mechanisms, often combined with , promote the evolution of highly resistant strains in clinical settings. Small non-coding RNAs (sRNAs) play a crucial role in of resistance genes in A. baumannii. For example, the sRNA AbsR25 negatively regulates the expression of the A1S_1331 transporter, a major facilitator superfamily protein involved in efflux-mediated drug expulsion; under stress conditions like exposure to , reduced AbsR25 levels increase transporter expression, bolstering resistance. Such sRNAs enable fine-tuned responses to antibiotics by modulating transporter and other resistance-related genes, enhancing survival in hostile environments. Multi-drug resistant (MDR) strains of A. baumannii, defined as resistant to at least one agent in three or more categories, pose a significant global challenge, with resistance reported in up to 90% of isolates in regions like parts of and as of 2020-2023. Recent data as of 2024 indicate resistance exceeding 90% in many and Asian countries, with rates approaching 100% in parts of and , underscoring the pathogen's adaptability and the urgent need for novel therapeutics. formation further exacerbates resistance by providing a protective that limits penetration. A. baumannii also develops resistance to , the last-resort polymyxin antibiotic, primarily through modifications to (LPS). The PmrAB two-component system upregulates phosphoethanolamine transferase (EptA, also known as PmrC) to add phosphoethanolamine to , reducing the net negative charge and electrostatic binding of colistin. Complete loss of LPS via mutations in lpx genes or enhanced efflux via pumps like AdeIJK also contributes to resistance, with global prevalence increasing to 1-10% among CRAB isolates as of 2024.

AbaR Resistance Islands

AbaR resistance islands are genomic islands in Acinetobacter baumannii that serve as harboring multiple antibiotic genes, primarily associated with global clone 1 (GC1) strains. These islands contribute significantly to the multidrug phenotype by integrating into the bacterial and facilitating the acquisition and dissemination of determinants. Structurally, AbaR islands vary in size from ~20 to 86 kb and exhibit a transposon-like , often bounded by inverted repeats and insertion sequences such as ISAba125. They typically integrate into the at a specific site adjacent to the tniA gene of a Tn7-like backbone, disrupting the comM gene in most cases to avoid excision by host genome maintenance mechanisms. The core structure includes a variable "cargo" region flanked by transposon modules, allowing for modular assembly of genes through recombination events. The islands carry a diverse array of resistance genes, with representative examples including tet(A) for tetracycline efflux, aadB (also known as ant(2″)-Ia) for aminoglycoside adenylylation, and cat (or catA1) for chloramphenicol acetylation. Other common genes encompass aphA1b and aacC1 for additional aminoglycoside resistance, sulI for sulfonamide resistance, and blaTEM for beta-lactam resistance, enabling broad-spectrum multidrug resistance. These gene clusters vary across subtypes, reflecting ongoing genetic plasticity. The archetype AbaR1 was first described in 2006 in the epidemic French clinical AYE of GC1 A. baumannii. Their traces back to the mid-1970s, originating from an ancestral AbaR0 island that acquired resistance genes via horizontal transfer, likely from other . Over time, more than 31 subtypes (AbaR1 to AbaR31) have been characterized, differing in gene content and arrangement due to insertions, deletions, and transposition events mediated by mobile elements. This diversification has driven the epidemic spread of resistant s. Prevalence of AbaR islands varies by region and clone but is estimated at 20-50% among clinical A. baumannii isolates globally, with higher rates (up to 66%) in GC1 and GC2 lineages from settings. They are particularly common in multidrug-resistant strains from , , and , underscoring their role in facilitating outbreaks.

Efflux Pumps and Beta-Lactamases

Acinetobacter baumannii employs several s as key mechanisms for expelling antibiotics, contributing significantly to its multidrug resistance profile. The AdeABC , belonging to the resistance-nodulation-division () family, is a comprising the inner transporter AdeB, the outer channel AdeA, and the fusion protein AdeC; it actively exports a broad spectrum of substrates, including beta-lactams such as and cephalosporins, as well as quinolones like and . The expression of AdeABC is tightly regulated by the AdeRS two-component , where AdeS acts as the sensor and AdeR as the response , enabling the bacterium to sense environmental cues and modulate activity in response to antibiotic exposure. Overexpression of AdeABC, often resulting from point mutations in the adeRS genes—such as substitutions in the of AdeR or the A domain of AdeS—has been observed in a high proportion of multidrug-resistant clinical isolates, leading to elevated minimum inhibitory concentrations (MICs) for multiple drug classes. In addition to AdeABC, A. baumannii possesses other RND efflux pumps that confer to specific . The AdeFGH pump primarily expels , tetracyclines, and , with overexpression linked to reduced susceptibility to these agents in clinical strains, particularly in regions with high usage. Similarly, the AdeIJK pump targets , tetracyclines, and aminoglycosides, contributing to against these compounds; its inactivation has been shown to restore and alter bacterial , underscoring its in both and . These pumps collectively enhance the bacterium's ability to survive in -rich environments, such as settings, by reducing intracellular drug accumulation. Complementing efflux mechanisms, A. baumannii produces beta-lactamases that hydrolyze , further bolstering resistance. Intrinsically, the bacterium expresses an Acinetobacter-derived cephalosporinase (), an AmpC-type encoded by the bla_ADC , which efficiently hydrolyzes cephalosporins and provides baseline resistance to these agents; variations in ADC alleles, such as ADC-25 and ADC-56, exhibit functional diversity that influences the level of resistance to expanded-spectrum cephalosporins like cefepime. Acquired resistance is primarily mediated by OXA-type carbapenem-hydrolyzing class D beta-lactamases (CHDLs), including OXA-23 and OXA-58, which are - or chromosome-borne and confer resistance to such as imipenem and . OXA-23, first identified in the early , is the most prevalent CHDL in A. baumannii and hydrolyzes imipenem with a catalytic (k_{cat}/K_m) of approximately 10^4 M^{-1} s^{-1}, enabling weak but clinically significant degradation of this last-resort . OXA-58, another key , shares similar hydrolytic activity but is often associated with distinct clones, highlighting the diversity of these acquired resistance determinants in driving global outbreaks of carbapenem-resistant A. baumannii.

Clinical Manifestations

Signs and Symptoms

_Acinetobacter baumannii infections primarily manifest in hospitalized patients, particularly those in intensive care units (ICUs) with compromised immune systems or invasive devices, leading to a range of severe clinical presentations. The most common sites of infection include the , bloodstream, and soft tissues, , and urinary tract, with symptoms varying by the affected organ system. Ventilator-associated pneumonia is a frequent manifestation, especially in mechanically ventilated ICU patients, characterized by fever, dyspnea, and production of purulent sputum. This form of pneumonia often develops as a nosocomial infection and is associated with high mortality rates ranging from 40% to 60%. The pathogen's ability to form biofilms on endotracheal tubes contributes to persistent colonization and progression to invasive disease. Bacteremia caused by A. baumannii typically presents as in ICU patients, with symptoms including chills, fever, and , often originating from indwelling catheters or secondary to other infections like or wound sites. This condition is particularly severe, leading to in up to one-third of cases and mortality rates of 20% to 60%. Wound and skin infections, common in or surgical patients, may progress to , featuring localized swelling, , purulent discharge, and severe pain. These infections are notable in military populations with combat injuries, where environmental exposure exacerbates tissue invasion. Less common presentations include , which manifests with , , fever, and altered mental status, primarily as a nosocomial complication in neurosurgical patients, carrying a mortality of 20% to 30%. Urinary tract infections, often catheter-associated, typically present with , fever, and suprapubic pain, though they may remain in some cases.

Diagnosis

Diagnosis of Acinetobacter baumannii infections relies on confirmation through and from clinical specimens such as , respiratory secretions, , and swabs, combined with susceptibility testing to guide management. Traditional culture-based methods remain the cornerstone, supplemented by molecular techniques for rapid and specific detection, particularly in cases of suspected multidrug-resistant strains. Serological approaches play a minor role due to inherent limitations, while resistance profiling is essential for characterizing the isolate's pattern.

Culture

Acinetobacter baumannii is isolated using standard microbiological culture techniques on non-selective media like blood agar, where it forms smooth, opaque, non-hemolytic colonies, and selective media such as MacConkey agar, on which it appears as pale or colorless non-lactose-fermenting colonies. Growth typically occurs within 24-48 hours of incubation at 35-37°C, allowing for preliminary identification based on colony morphology and Gram stain characteristics revealing Gram-negative coccobacilli. Species-level identification is achieved using commercial biochemical systems like the API 20NE strip, which analyzes enzymatic reactions and carbon source utilization to differentiate A. baumannii from other non-fermentative Gram-negative bacteria. These methods provide a turnaround time of 24-48 hours but may require confirmation in complex cases due to phenotypic similarities with other Acinetobacter species.

Molecular

Molecular diagnostics enable faster and more precise identification of A. baumannii, particularly in outbreak settings or for detecting carbapenem-resistant strains. (PCR) targeting the intrinsic blaOXA-51-like is a standard confirmatory test, as this carbapenemase-encoding sequence is unique to A. baumannii and distinguishes it from closely related species with high specificity. For broader taxonomic resolution, 16S rRNA sequencing compares amplicons against reference databases, offering reliable species identification even for atypical isolates. (MALDI-TOF MS) provides rapid results within minutes from cultured colonies by generating protein spectra matched to spectral libraries, achieving over 95% accuracy when using expanded databases that include entries. These techniques can be applied directly to clinical specimens in some protocols, reducing diagnostic delays compared to culture alone.

Serology

Serological tests for A. baumannii are limited in clinical practice due to frequent with other species and environmental , which complicates interpretation and reduces diagnostic specificity. Antigen-based assays, such as those employing monoclonal antibodies against the O-antigen component of , are primarily used for epidemiological purposes like capsule serotyping and strain delineation rather than routine diagnosis. These methods can differentiate serovars in settings but lack the and speed required for acute .

Resistance Profiling

Antimicrobial susceptibility testing is performed on confirmed A. baumannii isolates to identify resistance patterns, guiding empirical therapy in infections often involving multidrug-resistant strains. Disk diffusion, following Clinical and Laboratory Standards Institute (CLSI) guidelines, measures inhibition zone diameters around antibiotic-impregnated disks on Mueller-Hinton agar, providing categorical interpretations (susceptible, intermediate, resistant) for common agents like and aminoglycosides. determines minimum inhibitory concentrations (MICs) by serial dilutions in 96-well plates, offering quantitative data essential for agents with variable breakpoints, such as , and is considered the gold standard for accuracy per CLSI protocols. Both methods typically require 18-24 hours of incubation post-isolation and are crucial for detecting extensively drug-resistant phenotypes prevalent in hospital settings.

Treatment and Prevention

Therapeutic Approaches

The treatment of Acinetobacter baumannii infections, particularly those caused by multidrug-resistant (MDR) or strains, is complicated by extensive antibiotic resistance mechanisms, necessitating tailored antimicrobial strategies based on susceptibility testing. For , sulbactam-durlobactam (2 g intravenously every 6 hours) combined with a such as is the preferred regimen per IDSA 2024 guidelines, showing efficacy against resistant isolates. or polymyxin B is an alternative option, often administered intravenously, due to their activity against many resistant isolates, though and limit their use. is preferred for infections, leveraging its bacteriostatic activity and favorable in tissues, with high-dose regimen for at 200 mg loading followed by 100 mg every 12 hours. Combination therapies are frequently employed to enhance efficacy and mitigate resistance, especially in severe cases like bacteremia or . Sulbactam, acting as both a beta-lactamase inhibitor and direct against A. baumannii, is combined with such as for synergistic effects, showing reduced mortality in retrospective studies. Aminoglycosides like are added to regimens for their concentration-dependent killing, particularly in polymyxin-based combinations, where dual active agents improve outcomes in . Emerging antibiotics offer hope for infections, with eravacycline demonstrating clinical utility in real-world cases of and , achieving 30-day mortality rates around 24% in observational data and showing activity against resistant strains, though limited data and higher mortality in some studies warrant caution. , a approved by the FDA in for complicated urinary tract infections and expanded in 2020 for hospital- and , exhibits potent activity against A. baumannii by exploiting iron uptake pathways, with rates exceeding 90% in global surveillance. , using lytic bacteriophages targeted to A. baumannii, is under investigation in preclinical models and early-phase trials as of 2025, demonstrating clearance of infections in animal and models without significant adverse effects. Supportive measures are integral to management, particularly for , where supports and improves oxygenation in critically ill patients. Source control through surgical is essential for wound or abscess-related infections to reduce bacterial burden and facilitate penetration. Overall, therapy selection relies on local resistance patterns and patient factors, with infectious disease consultation recommended for optimization.

Infection Control Measures

Infection control measures for Acinetobacter baumannii in healthcare settings emphasize preventing transmission through standardized protocols that target healthcare worker practices, patient management, and environmental persistence. These strategies, recommended by authorities, have demonstrated effectiveness in reducing nosocomial infections, particularly for multidrug-resistant strains like carbapenem-resistant A. baumannii (CRAB). Hand hygiene remains the most critical intervention, as healthcare worker hands are a primary for in 20-40% of nosocomial cases. Protocols mandate cleaning hands with alcohol-based rubs (preferred for efficiency) or and before and after patient contact, aseptic tasks, or handling invasive devices. Specifically, 70% ethyl alcohol reduces A. baumannii counts on contaminated hands by 98%, outperforming other agents like in some studies, while and is essential when hands are visibly soiled to ensure mechanical removal of transient . Adherence rates, though variable (30-100%), improve outcomes when directly observed, particularly in intensive care units where compliance is often lower. Patient isolation under contact precautions is essential to limit spread, involving placement in single rooms or cohorting with similarly colonized patients, alongside mandatory use of gowns and gloves by staff during care. These measures, including proper donning and doffing of to avoid self-contamination, have successfully contained outbreaks in facilities by interrupting direct and indirect transmission. Enhanced barrier precautions may apply in , with dedicated equipment for affected patients to minimize cross-contamination. Environmental disinfection addresses A. baumannii's ability to survive on dry surfaces for extended periods, including biofilms that enhance persistence. Daily cleaning of areas (e.g., bed rails, ) with EPA-registered sporicidal agents like () or accelerated , ensuring proper dilution and contact time, is standard. Terminal room disinfection using vapor or UV-C light achieves near-100% inactivation in controlled settings, outperforming manual methods where <50% of surfaces may be adequately cleaned otherwise. A. baumannii biofilms on surfaces contribute to environmental reservoirs, but rigorous disinfection protocols mitigate this risk. Active surveillance via screening high-risk patients (e.g., those in ICUs or with recent exposure) using rectal or swabs detects early, with and rectal sites showing sensitivities of 50-80% or higher in studies. Results guide and inform facility-wide responses, supported by like the CDC's Laboratory for free testing. Complementing this, stewardship programs restrict broad-spectrum agents like to curb resistance selection, integrating education to sustain overall compliance.

Epidemiology

Hospital-Acquired Infections

Acinetobacter baumannii is a major cause of hospital-acquired infections, particularly in intensive care units (ICUs), where it accounts for approximately 1.5-2.4% of nosocomial globally. The incidence is notably higher among mechanically ventilated patients, comprising up to 12.8% of cases according to surveillance data. These infections often manifest as , , urinary tract infections, or wound infections in vulnerable patients. Key risk factors for nosocomial A. baumannii infections include prolonged hospitalization, which increases exposure to the hospital environment; use of invasive devices such as central venous catheters, endotracheal tubes, and urinary catheters; and prior therapy, which disrupts normal flora and selects for resistant strains. Patients in ICUs are especially susceptible due to these factors combined with underlying comorbidities like or chronic illnesses. Transmission primarily occurs through person-to-person contact via contaminated hands of healthcare workers, as well as via contaminated medical such as ventilators and surfaces in the hospital setting. The bacterium's ability to persist on dry surfaces for extended periods facilitates this spread in healthcare environments. Attributable mortality from nosocomial A. baumannii infections ranges from 20% to 50%, with rates often higher (35-70%) in cases of , particularly among patients with multidrug-resistant strains, as reported in studies from the 2020s. Effective control measures, such as hand and equipment sterilization, are essential to mitigate these risks.

Outbreaks in Military Populations

A significant surge in Acinetobacter baumannii infections occurred among during the and conflicts from 2003 to 2011, with over 1,000 cases documented across military treatment facilities. These infections predominantly affected service members with traumatic injuries, particularly soil-contaminated wounds caused by (IED) detonations, which introduced environmental reservoirs of the bacterium into open injuries. The implicated strains were typically multidrug-resistant clones, exemplified by the international clone II (ST2 Pasteur lineage), which exhibit enhanced through high production that facilitates adherence to surfaces and evasion of host defenses. These characteristics contributed to persistent infections in combat-related extremity . Evacuation pathways amplified risks, as wounded personnel received initial in contaminated hospitals before to the in , where a significant proportion of among Iraq and Afghanistan casualties were identified as A. baumannii. A. baumannii often complicated infections in these populations, particularly in cases involving amputations. Among survivors, long-term sequelae included chronic , highlighting ongoing challenges in veteran care, as reported in Department of surveillance data.

Global Incidence Trends

Acinetobacter baumannii, particularly its carbapenem-resistant strains (), has emerged as a significant global since the early 2000s, with incidence rising due to international travel, , and healthcare-associated transmission. The designated carbapenem-resistant A. baumannii as a critical in 2017 to prioritize of new antibiotics. Globally, A. baumannii causes approximately 1 million infections annually (predominantly hospital-acquired), with being a significant resistant subset associated with an estimated 57,700 attributable deaths in 2019 alone. These trends reflect the bacterium's adaptability in intensive care units (ICUs) and its association with high-mortality infections in vulnerable populations. As of 2024, the Centre for Prevention and Control (ECDC) reports continued disparities in incidence across . Regional variations in prevalence are stark, with higher rates in compared to . In the region, pooled carbapenem resistance rates reached 71.7% from 2012 to 2019, exceeding 87% in and 70-80% in during similar periods. In contrast, reports much lower carbapenem non-susceptibility at around 2.8%, while Southern and see rates above 50% in countries like and . The 2023 incidence of bloodstream infections was 2.98 per 100,000 population, highlighting ongoing disparities driven by differences in antibiotic use and infection control. The have seen further escalation, particularly post-COVID-19, with a 78% increase in hospital-onset CRAB infections from 2019 to , rising from 6,000 to 7,500 cases. Similar surges occurred in ICUs, where CRAB colonization and infection rates increased up to 7.5-fold during early compared to 2019. underscores clonal expansion of the ST2 Pasteur (international clone 2), which comprises 57% of over 15,000 analyzed global genomes and is linked to high gene carriage. At-risk groups include the elderly, where advanced age elevates infection risk, and diabetics, who face heightened acquisition and mortality from CRAB due to impaired immune responses.