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Review
. 2023 Nov 14;23(1):796.
doi: 10.1186/s12879-023-08789-6.

Acinetobacter spp. bloodstream infection in hematological patients: a 10-year single-center study

Jia Li  1   2 , Xiaomeng Feng  1   2 , Jieru Wang  1   2 , Qingsong Lin #  1   2 , Yizhou Zheng  1   2 , Fengkui Zhang  1   2 , Yingchang Mi  1   2 , Xiaofan Zhu  1   2 , Erlie Jiang  1   2 , Zhijian Xiao  1   2 , Jianxiang Wang  1   2 , Sizhou Feng #  3   4
Affiliations
Review

Acinetobacter spp. bloodstream infection in hematological patients: a 10-year single-center study

Jia Li et al. BMC Infect Dis. .

Abstract

Purpose: This study investigated the clinical and antimicrobial characteristics of Acinetobacter spp. bloodstream infection (BSI) in hematological patients. Risk factors for 30-day mortality and carbapenem-resistant Acinetobacter spp. (CRA) BSI acquisition were also identified.

Methods: We reviewed forty hematological patients with Acinetobacter spp. BSI in a large Chinese blood disease hospital between 2013 and 2022. The remaining CRA isolates were subjected to whole-genome sequencing.

Results: The 30-day mortality rate was high at 35%. Hematological patients with Acinetobacter spp. BSI often presented with severe conditions and co-infections at multiple sites. All strains were colistin-susceptible and 40.0% were CR. Multivariate analysis identified several risk factors associated with CRA BSI acquisition, including previous exposure to carbapenems within 30 days and CRA colonization. Very severe aplastic anaemia, tetracycline-resistant Acinetobacter spp. BSI, and unresolved neutropenia after infection were closely associated with 30-day mortality. Non-survivors often presented with higher median PCT and CRP levels and severe complications, such as intracranial infection, cardiac dysfunction, respiratory failure, and severe sepsis or septic shock. Our study also identified inappropriate empirical antibiotic therapy as an independent predictor of 30-day mortality (OR: 11.234, 95% CI: 1.261-20.086, P = 0.030). This study was the first to report A. oleivorans as a human pathogen, and to identify its unique oxacillinase, OXA-325.

Conclusion: An environment-originated non-pathogenic species can become pathogenic when the body's immunity is compromised. Our results also highlighted the importance of improving neutropenia after infection, treating severe organ dysfunction, and administering appropriate empirical antibiotic therapy to reduce mortality in this patient population.

Keywords: Acinetobacter; Bloodstream Infection; Outcome; Risk factors; Treatment.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Distribution of drug resistance according to carbapenem-resistant (CR) and multidrug-resistant (MDR) stratifications. CAR, carbapenems; FQs, fluoroquinolones; AGs, aminoglycosides; CSL, cefoperazone-sulbactam; TZP, piperacillin-tazobactam; TMP-SMZ, trimethoprim-sulfamethoxazole; TCY, tetracycline; CST, colistin
Fig. 2
Fig. 2
Kaplan-Meier curves of the 30-day probability of survival for patients with and without (A) appropriate empirical therapy, (B) resolved neutropenia after infection, (C) tetracycline-resistant Acinetobacter spp. BSI, and (D) cardiac dysfunction
Fig. 3
Fig. 3
The vital virulence factors (A) and drug-resistance genes (B) of the remaining Acinetobacter strains isolated from the bloodstream. The text above represents the types of genes, and the text below represents the names of genes. Blue squares indicate gene positives, while white squares indicate gene negatives. OMP, outer membrane proteins; LPS, lipopolysaccharide; PD, phospholipase D; QS, quorum-sensing system; PNAG, beta-1-6-linked poly-N-acetyl glucosamine; PBPs, penicillin-binding proteins; FQs, fluoroquinolones; Ms, macrolides; TCs, tetracyclines; A, ambler class A of β-lactams antibiotics
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