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Case Reports
. 2025 Apr 30;7(3):dlaf067.
doi: 10.1093/jacamr/dlaf067. eCollection 2025 Jun.

AMRrounds: Carbapenem-resistant Acinetobacter baumannii in the intensive care unit-when resistance meets severity

Davide Mangioni  1 , Chiara Abbruzzese  2 , Antonio Teri  3 , Chiara Bonaiuto  4   5 , Alessandro Pecere  6 , Claudia Alteri  3   7 , Ciro Canetta  8 , Antonio Muscatello  1 , Gian Maria Rossolini  4   5 , Annapaola Callegaro  3 , Giacomo Grasselli  2   9 , Marcello Sottocorno  6 , Mauro Panigada  2 , Alessandra Bandera  1   9
Affiliations
Case Reports

AMRrounds: Carbapenem-resistant Acinetobacter baumannii in the intensive care unit-when resistance meets severity

Davide Mangioni et al. JAC Antimicrob Resist. .
No abstract available

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Figures

Figure 1.
Figure 1.
Chest X-ray performed at hospital admission (a) (no pathological findings) and 7 days later at the onset of respiratory failure and septic shock (b), which shows extensive lung consolidations in the lower right lobe and in the upper and lower left lobes.
Figure 2.
Figure 2.
Antibiotic susceptibility profile of the isolates corresponding to the clinical case. aRelevant resistome from WGS analysis for the ST369 isolate: blaOXA-66 (up-regulated by upstream insertion of ISAba1), blaADC-30 (up-regulated by upstream insertion of ISAba1), blaOXA-23, ftsIN392T, ΔpirA, parCS84L, gyrAS81L. Resistome analysis was carried out using the ResFinder (https://github.com/cadms/resfinder), NCBI AMRFinderPlus (https://github.com/ncbi/amr) and Comprehensive Antibiotic Resistance Database (CARD) (https://card.mcmaster.ca/) platforms. The presence of IS elements in the 500 bp region upstream of the resistance genes was determined using the ISfinder tool (https://www-is.biotoul.fr/). Variant calling was performed using snippy (https://github.com/tseemann/snippy) using CP091345 as reference. Only resistance mechanisms deemed to be potentially relevant to the observed resistance phenotypes are indicated. bRelevant resistome from WGS analysis: blaOXA-66, blaADC-73 (up-regulated by upstream insertion of ISAba1), blaOXA-23, blaTEM-1, ftsIA515V, armA, parCS84L, gyrAS81L. Resistome analysis was carried out as described in footnote a. Only resistance mechanisms deemed to be potentially relevant to the observed resistance phenotypes are indicated. cDetermined by broth microdilution, using iron-depleted medium for cefiderocol testing (EUCAST 15.0, 2025). dAccording to CLSI standard M100, 35th Edition (2025). eAccording to EUCAST 15.0 clinical breakpoints (2025). fAccording to EUCAST 15.0 clinical breakpoints (2025), the MIC value indicates the absence of phenotypically detectable resistance mechanisms. In this case, EUCAST warns against using this agent as monotherapy due to lack of clinical evidence, while the agent could be used in combination with other effective measures. gAccording to EUCAST guidance on ‘When there are no breakpoints in breakpoint tables?’ (September 2024), when there is a ‘dash’ instead of numerical values the microbe can be reported as resistant without further testing. hAccording to EUCAST 15.0 clinical breakpoints (2025), the in vitro activity of cefiderocol for Acinetobacter spp. is comparable to the activity of the agent for Enterobacterales and there are also animal data to suggest efficacy. However, there are insufficient clinical data to determine a clinical breakpoint. Isolates with MIC values of ≤0.5 mg/L are mostly devoid of resistance mechanisms. Isolates with MICs of 1–2 mg/L have acquired resistance mechanisms that may result in impaired clinical response. Isolates with MIC values of >2 mg/L will likely be resistant. iAccording to EUCAST guidance on ‘When there are no breakpoints in breakpoint tables?’ (September 2024), for the treatment of Gram-negative aerobic bacteria the clinical use of ampicillin/sulbactam should be discouraged when MIC values are higher than 8 mg/L.
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References

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