Phenylacetic acid mediates Acinetobacter baumannii entry into a viable but non-culturable state

TL;DR

The study shows that phenylacetic acid helps Acinetobacter baumannii survive dry conditions by entering a non-growing but alive state.

Contribution

The paper identifies phenylacetic acid catabolism as a novel regulator of desiccation tolerance and VBNC state in A. baumannii.

Findings

Phenylacetic acid catabolism is essential for desiccation tolerance in Acinetobacter baumannii.

Deletion of the paa operon eliminates clonogenicity of desiccated cells but allows survival in a VBNC state.

PAA catabolism mediates biofilm regulation and entry into VBNC state under desiccation.

Abstract

Desiccation tolerance is central to the pathogenic success of the opportunistic pathogen Acinetobacter baumannii, allowing its survival on hospital surfaces in the absence of water and nutrients for months at a time, compromising surface decontamination and aiding cross-contamination between staff and patients. Despite the importance of desiccation tolerance, the regulation underpinning this behaviour remains largely elusive. In this work, transcriptomic analyses of desiccated cells revealed phenylacetic acid (PAA) catabolism as an essential mediator of desiccation tolerance. We subsequently demonstrate that deletion of the paa operon abolished the clonogenicity of desiccated cells. Strikingly, these A. baumannii cells remained viable by entering the viable but non-culturable (VBNC) state, a means to survive extreme stressors like antibiotic exposure. Furthermore, we uncover that PAA catabolism is necessary to mediate PAA-driven biofilm regulation. These findings highlight PAA catabolism as a modulator of biofilm formation and a key pathway for entry into the VBNC state in response to desiccation. This reveals PAA catabolism as a target for novel infection prevention strategies.

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