The Acinetobacter baumannii group:a systemic review

doi:10.5847/wjem.j.issn.1920-8642.2013.03.002

Abstract

Abstract:

BACKGROUND: The Acinetobacter baumannii group, includingAcinetobacter baumannii, Acinetobacter genomospecies 3 and 13TU, is phenotypically indistinguishable and uniformly identified as Acinetobacter baumannii by laboratories of clinical microbiology. This review aimed to demonstrate the differences among them.
METHODS: Literatures associated with the Acinetobacter baumannii group were identified and selected from PubMed databases and relevant journals.
RESULTS: Acinetobacter genospecies 3 and 13TU possess a certain proportion in clinical isolates. There were considerable differences in epidemiologic features, clinical manifestations, antimicrobial resistances and therapeutic options among the Acinetobacter baumannii group. Compared with Acinetobacter genomospecies 3 and 13TU, Acinetobacter baumannii with a higher resistance to antimicrobial agents are easier to be treated inappropriately, and present a worse outcome in patients.
CONCLUSION: The Acinetobacter baumannii group comprises three distinct clinical entities, and their clinical value are not equal.

Key words: Acinetobacter baumannii, Acinetobacter genomospecies 3, Acinetobacter genomospecies 13TU, Difference

Hua-zhong Zhang, Jin-song Zhang, Li Qiao. The Acinetobacter baumannii group:a systemic review[J]. World Journal of Emergency Medicine, 2013, 4(3): 169-174.

Figures/Tables 2

Table 1

Table 2

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Region	A. baumannii group	A. baumannii (%)	Genospecies 3 (%)	Genospecies 13TU (%)
Ireland^[11]	72	25 (34.7)	45 (62.5)	2 (2.8)
Singapore^[12]	193	152 (78.7)	18 (9.3)	23 (11.9)
Korea^[13]	240	127 (52.9)	15 (6.3)	98 (40.8)
USA^[14]	271	187 (69.0)	23 (8.5)	61 (22.5)
Taiwan^[15]	1039	439 (42.3)	133 (12.8)	467 (44.9)
Germany^[16]	1741	335 (19.2)	1053 (60.5)	353 (20.3)

Resistance mechanisms	Antimicrobial agents
Produce antibiotics inactivated enzyme
β-lactamas	β-lactams
Class A: extended-spectrum-β-lactamases (ESBLs): TEM, PER type
Class B: the metallo-lactamases (MBLs): IMP, VIM, SIM type
Class C: AmpC cephalosporinases
Class D: serine carbapenemases (OXA type)
Aminoglycoside-modifying enzymes (AMEs): APHs, AACs	Aminoglycosides
Alter the action sites of antibiotics
Topoisomerase mutations in the genes gyrA and parC	Quinolones
Ribosomal (16S rRNA) methylation: armA	Aminoglycosides
Alteration in penicillin-binding proteins (PBPs)	β-lactams
Reduce the concentration of antibiotics in cells
Decreased permeability of the outer membrane	Multidrug
Efflux pumps
Plasmid-mediated transport protein: TetA, TetB, TetK	Tetracyclines
RND efflux systems: AdeABC, AdeDE, AdeXYZ, AdeIJK	Multidrug
Biofilm formation	Multidrug

[1]	Rui-xue Sun, Priscilla Song, Joseph Walline, He Wang, Ying-chun Xu, Hua-dong Zhu, Xue-zhong Yu, Jun Xu. Morbidity and mortality risk factors in emergency department patients with Acinetobacter baumannii bacteremia [J]. World Journal of Emergency Medicine, 2020, 11(3): 164-168.
[2]	Xiao-fang Cai, Ji-min Sun, Lian-sheng Bao, Wen-bin Li. Risk factors and antibiotic resistance of pneumonia caused by multidrug resistant Acinetobacter baumannii in pediatric intensive care unit [J]. World Journal of Emergency Medicine, 2012, 3(3): 202-207.