Acinetobacter baumannii complex

INITIAL APPROACH

• Isolate significance: Respiratory and wound isolates from ventilated or severely injured patients frequently represent colonisation. A positive culture alone does not justify a toxic multidrug regimen. Treatment recommendations for invasive carbapenem-resistant A. baumannii (CRAB) apply to infection, not carriage. [12]
• Parallel workstreams: Clinical assessment of the source, laboratory confirmation of identity and relevant resistance, and an infection prevention and control (IPC) assessment should proceed together. The AMRHAI reference unit provides identification, resistance confirmation, typing and outbreak advice and is an appropriate resource when routine results or treatment options are problematic. [8]
• Jurisdiction: The treatment hierarchy below reflects US guidance (IDSA 2026) and is not UK formulary advice. A UK authorisation or routine NHS supply route for sulbactam-durlobactam has not been established, and neither should be inferred from US approval.

MICROBIOLOGY AND NOMENCLATURE

Morphology. Acinetobacter species are non-fermenting Gram-negative coccobacilli. Growing cultures show plump rods, and stationary-phase cultures show coccoid forms, often in pairs. Some isolates destain poorly and appear Gram-variable. Colonies are smooth, non-pigmented and sometimes mucoid. The organisms lack flagella (twitching motility can occur) and are oxidase negative. These features support preliminary recognition but do not establish a species. [1]

Nomenclature. Genomic species 3 is now A. pittii, and genomic species 13TU is A. nosocomialis. Both names are validly published (Nemec et al., 2011), and descriptions of them as proposed names are out of date. [2]

Reporting. The EUCAST organism table is written for Acinetobacter spp., because the studies underlying its breakpoints could not reliably distinguish species. A laboratory report of complex and a study with molecular speciation therefore differ in taxonomic resolution. [11]

EPIDEMIOLOGY

United Kingdom. UKHSA identifies pneumonia, bloodstream infection, wound infection and urinary infection as the principal presentations, mainly in patients who are already unwell in hospital. The UKHSA overview describes the genus in environmental sources; this does not provide a prevalence estimate for A. baumannii carriage or environmental occupancy. [3]

England bacteraemia, 2020 (historical data, not a current incidence estimate). The species table records 882 Acinetobacter spp. bloodstream episodes. [5]

Shares are calculated from the report’s counts. A genus-level bloodstream total is therefore not an A. baumannii count. The report also notes that changing identification methods alter species distributions. No current UK-wide, species-confirmed incidence figure is available.

Europe. The ECDC/WHO Europe report on 2024 invasive isolates describes wide geographic variation and high carbapenem resistance among Acinetobacter spp. in many participating countries. These genus-level data on sampled invasive isolates are not a measure of admission risk or a UK empirical susceptibility estimate. [6]

Risk factors and transmission. Ventilation, catheters, open surgical wounds, intensive care stay and prolonged admission are the main healthcare exposures. Transmission occurs through contaminated hands, equipment and surfaces, and carriage without infection is common. When healthcare acquisition is suspected, both patient contacts and shared equipment warrant assessment. [4]

CLINICAL MANIFESTATIONS

Healthcare-associated disease. Bloodstream, pulmonary, urinary and wound infections are the recognised syndromes. In a colonised patient, the specimen site and the clinical picture must be interpreted together. A respiratory isolate does not establish that each episode of deterioration is Acinetobacter pneumonia, and a wound isolate does not automatically indicate invasive disease. [4]

Community-onset pneumonia. This has a distinct evidence base. An Australian prospective series (1997 to 2012) described 41 bacteraemic episodes. Of 37 isolates with molecular speciation, 35 were A. baumannii and 2 were A. nosocomialis. Hazardous alcohol use was present in 82% of patients, 80% required intensive care, and 28-day mortality was 11%. All patients received appropriate antibiotics within 24 hours. Because this was an observational regional cohort, the low mortality cannot be attributed causally to early active therapy, and its susceptibility data should not be applied to UK empirical prescribing. [7]

Central nervous system infection. Healthcare-associated ventriculitis guidance addresses Acinetobacter specifically. Relevant settings include recent neurosurgery, head trauma and CSF hardware. The guideline emphasises CSF culture, clinical assessment and device management, and notes that normal CSF indices do not reliably exclude infection. [19]

Interpretation of mortality data. Mortality in treatment trials is all-cause mortality in selected populations. ATTACK enrolled mainly pneumonia, with bloodstream infection a small minority, so its mortality estimate is not an attributable-mortality estimate for every Acinetobacter syndrome. [13]

LABORATORY DIAGNOSIS

Identification. UK SMI ID 17 places validated MALDI-TOF MS at the centre of non-glucose-fermenter identification. The instrument instructions are followed, the identification database is maintained, and inconsistent results are resolved by another method or reference referral. Gram appearance and oxidase reaction are supportive observations and do not replace validated identification. ID 17 does not provide an AST standard. [1]

Reference laboratory referral. AMRHAI provides Acinetobacter identification, susceptibility investigation, molecular resistance confirmation and typing, and advises on transmission pathways, treatment options and public health risk. Referral should state the clinical syndrome and the question asked, for example uncertain identification, unexpected susceptibility, suspected acquired carbapenemase or linked isolates. Not every isolate requires every test. [8] UKHSA also requests that Acinetobacter isolates suspected of carrying an acquired carbapenemase be sent to AMRHAI for confirmation. [22]

Genomics. Genomic data answer a different question from routine identification. In a Birmingham outbreak, whole-genome sequencing assigned 74 isolates from 49 patients to the outbreak and excluded 18 others. Combined with temporal and location data, it linked clinical and environmental isolates and traced a contaminated bed and a burns theatre. The study also demonstrated within-host diversity, so a single colony may not represent all diversity present, and related genomes still require epidemiological interpretation. [21]

Not addressed. The sources reviewed describe no universal Acinetobacter serological test, screening specimen set or clearance protocol. This does not establish that no specialised assay exists, and any such addition requires its own validated purpose and current reference laboratory instructions.

PATHOGENESIS

In strain AB5075, deletion of the capsule-associated gene wzc, with complementation to confirm the effect, increased susceptibility to the tested disinfectants, lysozyme and desiccation. Capsule also contributed to survival in a mouse lung model. These findings support a causal role for capsule in those strain and model outcomes. [9]

The clinical interpretation is bounded. Environmental persistence and host interaction have experimentally demonstrable bacterial determinants, but a mouse phenotype does not predict individual patient mortality. The study did not show significant protection against every host antimicrobial tested, so findings should not be summarised as capsule protecting against all immune killing or taken to indicate that a disinfectant regimen is ineffective in practice. [9]

SUSCEPTIBILITY AND RESISTANCE

Mechanisms. Sulbactam has direct antibacterial activity through Acinetobacter penicillin-binding proteins (PBP1 and PBP3 per the US label), and durlobactam protects it against relevant serine beta-lactamases. The US label states that the combination is not active against isolates producing Ambler class B metallo-beta-lactamases or carrying modification of the sulbactam target PBPs. [14] A primary study of contemporary isolates identified metallo-beta-lactamases and PBP3 changes as the main drivers of reduced activity. Not every PBP3 substitution was sufficient: the common A515V change did not independently reproduce the resistant phenotype, and AdeIJK-mediated efflux contributed in a subset of experiments. [10]

Carbapenem resistance therefore does not predict susceptibility to sulbactam-durlobactam, and neither does any single sequence variant. The phenotype should be confirmed, and a genetic result interpreted in its biological context. The study combined surveillance, genomic and laboratory experiments and is not a clinical outcomes trial.

EUCAST interpretive criteria (version 16.1, valid from 24 June 2026). [11]

CLSI categories should not be substituted when reporting under EUCAST.

Activity versus clinical benefit. CREDIBLE-CR was a descriptive, open-label trial in heterogeneous carbapenem-resistant infections. End-of-study deaths in the safety population were 34/101 with cefiderocol and 9/49 with best available therapy (difference 15.3%, 95% CI -0.2 to 28.6, per the UK SmPC). The excess occurred principally in patients with Acinetobacter infections. These figures are not Acinetobacter-only mortality fractions and do not establish that the drug caused the difference, but they make unqualified claims of clinical equivalence inappropriate. [16] The SmPC states that the cause of the mortality difference has not been established. [15]

ANTIMICROBIAL THERAPY

Carbapenem-resistant A. baumannii: current hierarchy (US guidance, IDSA 2026). [12]

1. For invasive CRAB infection, sulbactam-durlobactam combined with imipenem or meropenem is preferred.
2. If sulbactam-durlobactam is not immediately available, high-dose ampicillin-sulbactam (9 g/day of the sulbactam component) plus at least one other agent (for example cefiderocol, minocycline or polymyxin B) may be used as a temporary bridge only, until sulbactam-durlobactam can be started.
3. If the isolate is resistant to sulbactam-durlobactam, the 2026 update describes two non-sulbactam agents, or sulbactam-durlobactam plus cefiderocol.
4. Clinical outcome data for cefiderocol in CRAB remain inconclusive.

Metallo-beta-lactamase production or changes in the sulbactam target alter this approach. These are US expert suggestions, not UK formulary instructions. IDSA also advises against meropenem or imipenem for CRAB except alongside sulbactam-durlobactam, and against rifamycins and nebulised antibiotics.

Evidence for sulbactam-durlobactam. ATTACK compared sulbactam-durlobactam with colistin, and both arms also received imipenem-cilastatin. In the carbapenem-resistant efficacy population, day-28 deaths were 12/63 (19%) versus 20/62 (32%), a difference of -13.2 percentage points (95% CI -30.0 to 3.5). The trial met its prespecified non-inferiority criterion (margin 20 percentage points). Because the confidence interval includes zero, the result does not establish superior survival. Nephrotoxicity occurred in 12/91 (13%) versus 32/85 (38%). Because both arms received imipenem, the trial does not isolate the contribution of imipenem. [13]

Label scope. The US label covers adults with hospital-acquired or ventilator-associated bacterial pneumonia (HABP/VABP) caused by susceptible A. baumannii-calcoaceticus complex. Use at bloodstream or other sites follows IDSA guidance rather than the label. [14]

Sulbactam-durlobactam dosing (US label; not a UK authorisation statement). Each dose contains sulbactam 1 g plus durlobactam 1 g, infused intravenously over 3 hours. Creatinine clearance is estimated using Cockcroft-Gault. [14]

Doses on haemodialysis days are given after dialysis. The labelled HABP/VABP duration is 7 to 14 days, guided by clinical status. Severe hypersensitivity to either component or to other beta-lactams is a contraindication. The label provides no CRRT regimen.

Cefiderocol dosing (UK SmPC). Cefiderocol is licensed for infections due to aerobic Gram-negative organisms in adults with limited treatment options and should be used only after consultation with a physician experienced in infectious diseases. All doses are intravenous infusions over 3 hours, with creatinine clearance by Cockcroft-Gault. [15]

Duration follows the site of infection: 7 to 14 days for HAP/VAP, and up to 21 days may be required. Safety and efficacy under 18 years are not established. Contraindications include cephalosporin hypersensitivity and severe hypersensitivity to other beta-lactams, and avoidance in pregnancy is preferred. The table provides no CRRT dose and does not establish activity against an individual isolate.

Colistimethate sodium dosing (UK Colomycin SmPC). Doses are specified in international units of colistimethate sodium, not milligrams of colistin base, and a dose from an international paper should not be used until its chemical form and unit are confirmed. The SmPC recommends 9 million IU/day in 2 or 3 divided doses, with a 9 million IU loading dose in critically ill patients. This is based on limited population pharmacokinetic data in critically ill patients, and up to 12 million IU may be needed in some patients with good renal function. Maintenance is adjusted for renal function. [17] The EUCAST reference regimen for its breakpoints is 4.5 MU twice daily after a 9 MU load, the same 9 MU/day. [11]

Syndrome-specific considerations.

• Susceptible HAP/VAP: Older ATS/IDSA guidance (2016) supports a susceptible carbapenem or ampicillin-sulbactam. Seven days is the default duration, extended or shortened according to response. This is syndrome-based guidance and does not require stopping at 7 days when a deep focus is uncontrolled. For CRAB drug selection, it should be read alongside the 2026 guidance rather than the older colistin-centred hierarchy. [18]
• Ventriculitis and meningitis: The 2017 IDSA guideline recommends meropenem for susceptible Acinetobacter and intravenous plus intraventricular polymyxin for carbapenem-resistant infection, with removal of infected CSF hardware. It predates sulbactam-durlobactam and does not validate newer regimens or their CNS dosing. Treatment requires joint planning by microbiology or infectious diseases, neurosurgery and pharmacy. No well-supported newer-agent CNS regimen is established. [19]
• Bloodstream, bone, endovascular and deep wound infection: No single organism-wide dose and duration table exists. The syndrome and source-control requirement are defined before treatment is chosen, and a pneumonia course should not be extrapolated to these presentations. Pregnancy, neonates, CRRT and drug access require case-specific verification.

MONITORING OF THERAPY

• Colistimethate: Renal function is measured at baseline and regularly during treatment, and maintenance dosing is revised against creatinine clearance. Hypovolaemia and other nephrotoxic drugs increase risk. Neurotoxicity, including neuromuscular effects, is particularly relevant with excess exposure or impaired renal clearance, so interacting nephrotoxic and neurotoxic medicines are reviewed rather than monitoring creatinine alone. [17]
• Cefiderocol: The SmPC advises regular renal function monitoring because dose adjustment may be needed during therapy. It also warns of seizures (adjust the dose for renal function or discontinue), Clostridioides difficile-associated diarrhoea and positive Coombs tests. [15]
• CSF infection: Clinical response is followed and, when infection is treated with an external drainage device in place, CSF cultures are repeated until negative. Routine daily cultures of an external drain placed for another indication are not recommended unless clinically indicated. [19]
• Pneumonia: Duration is guided by the trajectory of clinical, respiratory and laboratory findings. Radiographic infiltrates can persist beyond clinical resolution, and continuing treatment solely because an image has not normalised risks confusing delayed radiological clearing with microbiological failure. [18]

A suggested review record documents the working syndrome, the chosen active regimen, the dose calculation, the source-control decision, the observed response, adverse effects and the next review date. This is an editorial checklist to make decisions reviewable and not a validated response score.

VACCINES

No UK-licensed Acinetobacter vaccine and no UK vaccination recommendation were identified in the authoritative sources reviewed, and no schedule is provided. Preclinical vaccine research exists, but its efficacy claims are not covered here. This does not establish that no programme exists elsewhere.

ADJUNCTIVE THERAPY

Bacteriophage therapy. A case report described personalised intravenous and intracavitary bacteriophages in a patient with necrotising pancreatitis and disseminated resistant Acinetobacter infection who had deteriorated despite previous treatment. Improvement and clearance followed. This uncontrolled single case cannot separate the contribution of phages from concurrent treatment and provides no response rate. It supports further investigation rather than a standard regimen. A later erratum concerns phage provenance. [24] [25]

Other adjuncts. The evidence reviewed supports no pathogen-specific immunotherapy, steroid regimen or other non-antimicrobial adjunct. Use of an investigational intervention requires separate assessment of current evidence, governance and availability, and laboratory synergy or a favourable individual report does not establish clinical efficacy.

PREVENTION AND OUTBREAK INVESTIGATION

Immediate IPC measures. NHS Scotland’s National Infection Prevention and Control Manual (NIPCM) recommends single-room placement for infections spread by contact, with isolation decisions documented and reviewed. When single rooms are limited, cohorting requires IPC involvement, and patients with different agents or strains are not mixed. Reusable care equipment is dedicated where possible and decontaminated before reuse. Isolation and cohort areas require at least daily environmental decontamination, increased on IPC advice, following product instructions for preparation and contact time. This is Scottish national guidance, and the relevant national and local policy applies in other UK settings. [20]

Cluster investigation. Epidemiological and microbiological data are assessed together. The Birmingham investigation showed that genomic data can exclude apparently related isolates as well as link clinical and environmental isolates. Specimen dates, patient locations, shared equipment and isolate relationships are reviewed together. This is an operational interpretation of one study and not a universal genomic-distance threshold for transmission. [21]

Screening. The ECDC CRAB survey protocol collects specimen, patient and hospital data and distinguishes colonisation from infection, and its errata include a correction to a colonisation-sampling box. A survey design is not a validated clinical screening or decolonisation protocol, and no universal staff-screening, decolonisation or clearance regimen is established. [26]

Reporting in England. Since 1 October 2020, diagnostic laboratories in England have been required to notify acquired carbapenemase-producing Gram-negative organisms from human samples through SGSS. [22] This is a mechanism-based requirement. It is not a notification requirement for every Acinetobacter isolate and should not be assumed to apply in the other UK nations. The latest UKHSA quarterly CPO update should be consulted for current figures.

Withdrawn guidance. The 2006 UK working party Acinetobacter outbreak document is marked withdrawn on GOV.UK and is not used as current authority. [23]

INTERPRETATION OF FINDINGS

Dosing tables are provided under ANTIMICROBIAL THERAPY. The matrix below identifies the decision each type of evidence can support.

ILLUSTRATIVE CASES

These hypothetical cases illustrate interpretation of the evidence and do not describe actual patients.

Respiratory isolate. A ventilated patient has Acinetobacter complex in a tracheal aspirate, with unchanged oxygen requirements and observations. This does not by itself establish ventilator-associated pneumonia. Colonisation is recognised, and invasive CRAB treatment advice is not intended for carriage. The clinical syndrome is reassessed before prescribing, and the case provides insufficient evidence to diagnose infection. [12]

Interpretation of a trial result. ATTACK is sometimes described as proving that sulbactam-durlobactam reduces mortality compared with colistin. The prespecified primary conclusion was non-inferiority. The mortality difference favoured sulbactam-durlobactam numerically, but its confidence interval included zero, so proven superiority overstates the result. [13]

Suspected equipment reservoir. Two patients with resistant Acinetobacter shared equipment and have similar routine antibiograms. Transmission is not established by this alone. The link is treated as a hypothesis and examined with location and timing data and, where appropriate, higher-resolution typing. In the Birmingham study, genomics both confirmed environmental links and excluded isolates initially considered part of the outbreak. [21]

EVIDENCE GAPS

Version changes. IDSA replaced its antimicrobial-resistance guidance in summer 2026, and EUCAST version 16.1 has been valid since 24 June 2026. Earlier recommendations require rechecking against both. [12] [11]

Unresolved questions (not filled by extrapolation):

• Species-confirmed UK incidence
• Routine UK access and authorisation for sulbactam-durlobactam
• Validated universal screening and clearance schedules
• Comparative newer-agent CNS treatment
• Comprehensive paediatric, pregnancy and CRRT regimens
• A current verified UK vaccine recommendation

These define questions for a focused update or for case-specific specialist advice.

Evidence hierarchy. Randomised treatment results, observational outbreak findings, experimental mechanisms and expert guidance answer different questions. Evidence quality is best described for the underlying claim rather than assigning one grade to the whole organism topic.

Sources

Numbers match the citations in the text.