Both Col‐ and ColV, I‐K94+ strains of Escherichia coli, grown at pH 7–0, failed to grow after relatively short periods of exposure to pH 3·0 or 3·5. After growth in exposure medium initially at pH 5·0, both strains were almost unaffected by exposure to such acid pH values. Addition of catalase to nutrient agar only slightly increased plating efficiency after acid treatment and very slightly reduced the difference in survival, after acid treatment, between organisms grown from pH 5·0 and those grown from pH 7·0. Accordingly, acid resistance of organisms grown from pH 5·0 is not chiefly due to greater resistance to hydrogen peroxide already present in nutrient media.

The findings reviewed here overturn a major tenet of bacterial physiology, namely that stimuli which switch-on inducible responses are always detected by intracellular sensors, with all other components and stages in induction also being intracellular. Such an induction mechanism even applies to quorum-sensed responses, and some others which involve functioning of extracellular components, and had previously been believed to occur in all cases. In contrast, for the stress responses reviewed here, triggering is by a quite distinct process, pairs of extracellular components being involved, with the stress sensing component (the extracellular sensing component, ESC) and the signalling component, which derives from it and induces the stress (the extracellular induction component, EIC), being extracellular and the stimulus detection occurring in the growth medium. The ESCs and EICs can also be referred to as extracellular sensing and signalling pheromones, since they are not only needed for induction in the stressed culture, but can act as pheromones in the same region activating other organisms which fail to produce the extracellular component (EC) pair. They can also diffuse to other regions and there act as pheromones influencing unstressed organisms or those which fail to produce such ECs. The cross-talk occurring due to such interactions, can then switch-on stress responses in such unstressed organisms and in those which cannot form the ESC/EIC pair. Accordingly, the ESC/EIC pairs can bring about a form of intercellular communication between organisms. If the unstressed organisms, which are induced to stress tolerance by such extracellular components, are facing impending stress challenge, then the pheromonal activities of the ECs provide an early warning system against stress. The specific ESC/EIC pairs switch-on numerous responses; often these pairs are proteins, but non-protein ECs also occur and for a few systems, full induction needs two ESC/EIC pairs. Most of the above ECs needed for response induction are highly resistant to irreversible inactivation by lethal agents and conditions and, accordingly, many killed cultures still contain ESCs or EICs. If these killed cultures come into contact with unstressed living organisms, the ECs again act pheromonally, altering the tolerance to stress of the living organisms. It has been claimed that bacteria sense increased temperature using ribosomes or the DnaK gene product. The work reviewed here shows that, for thermal triggering of thermotolerance and acid tolerance in E. coli, it is ESCs which act as thermometers.

A study of the conjugal transfer of ColV,I-K94 tn 10 from acid-treated donors suggested that acid-habituated recipients repair acid-damaged plasmid DNA better than those that are not habituated. The presence of an increased repair activity for acid-damaged DNA in habituated cells was confirmed by isolating pBR322 from acid-treated organisms; habituated cells produced more transformants when transformed by it than did non-habituated ones. Additionally, agarose gel electrophoretic studies of pBR322 DNA isolated from acid-damaged cells and tests of its transforming activity both indicated that plasmid DNA in habituated cells is less damaged by extreme acidity than is that in non-habituated organisms.

Escherichia coli grown in broth initially at pH 5.0 (pH 5.0‐grown organisms) survived exposure to inorganic acid or to acid pH plus organic acid which prevented subsequent growth by pH 7.0‐grown organisms. This resistance of pH 5.0‐grown organisms to organic acids was observed at acid pH with lactic, propionic, benzoic, sorbic, trans‐cinnamic and acetic acids. Such resistance might allow acid‐habituated organisms to survive in acid foods or at body sites such as the urinary tract where organic acids are present at acid pH.

The lethal effects of inorganic acid on phoE+ Escherichia coli strains, grown at neutral pHo, were enhanced by chloramphenicol, apparently because some organisms acquire acid tolerance (habituate) during challenge and chloramphenicol stops this. Phosphate (and/or polyphosphate) present during challenge prevented killing and damage by acid to outer membranes, DNA and cellular enzymes but did not prevent acid pHo enhancing novobiocin activity. To reverse acid effects, phosphate must interact with or cross the outer membrane but need not enter the cytoplasm; it is probable that it competes with H+ (or protonated anions) for passage through the PhoE pore. Phosphate also prevented induction of beta-galactosidase in a strain with the cadA promoter fused to lacZ. Four unc mutants showed essentially normal acid sensitivity and habituation; the same was true for strains with lesions in fur, oxyR, katF, phoP, cadA and hycB. In contrast, deletion of rpoH led to slightly increased acid sensitivity for cells grown at pHo 7.0, although habituation was relatively normal.