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.

1. Summary, 678 2. Introduction 2.1. Chemical and biological stress agents affecting enterobacteria, 678 2.2. Sensing of chemical and biological stress stimuli, 678 2.3. Intracellular sensors detect intracellularly‐produced chemical stressing agents, 679 2.4. Intracellular sensors and intracellular induction components could delay response induction by extracellular chemical or biological stress agents, 680 2.5. Extracellular sensors and EICs give early warning of stress, 681 2.6. Disadvantages of extracellular components being needed for stress response induction, 682 2.7. Extracellular sensors and EICs allow stressed cells to warn unstressed ones, 682 2.8. A second role for some extracellular stress sensors, 683 3. Responses switched on by extracellular sensors and EICs 3.1. Involvement of EICs and ESCs in acid tolerance induction at pH 5·0 and at other mildly acidic pH values, 683 3.2. Further evidence for the obligate involvement of extracellular sensors and EICs in acid tolerance induction at pH 5·0, 684 3.3. On the nature of the acid pH tolerance‐inducing ESC and EIC, 686 3.4. The acid tolerance ECs and their relation to other extracellular response‐inducing components, 686 3.5. Extracellular components are needed for other inducible acid tolerance responses, 687 3.6. Involvement of EICs and extracellular sensors in acid tolerance in E. coli O157, 687 3.7. EICs involved in acid tolerance induction are diffusible, 687 4. Acid sensitization at alkaline pH and the role of extracellular sensor and EIC(s), 688 5. Responses affecting tolerance to alkali 5.1. Alkali sensitization at acidic pH, 688 5.2. Induced alkali tolerance at pH 9·0 and role of extracellular components, 688 6. Inducible tolerance to alkylhydroperoxides, 689 7. Are extracellular sensors and extracellular induction components needed for all stress responses?, 689 8. Altered responsiveness of extracellular sensors depending on growth conditions, 691 9. Protection of living cells from chemical stress by dead cultures, 691 10. How can intracellular levels of stress be detected?, 692 11. Are Nikolaev’s extracellular ‘protectants’ and similar components related to EICs?, 693 12. Conclusions, 693 13. References, 694

In a comparative study of different Salmonella enteritidis phage type 4 isolates we found that those isolates with enhanced heat tolerance also survived better than isolates that were heat sensitive either at pH 2.6, in 10 mM H 2 O 2 , or on surfaces. Culture to the stationary phase increased the heat tolerance of all isolates and the acid and H 2 O 2 tolerance of heat-tolerant isolates. With heat-sensitive isolates, however, extended culture had no impact on survival in H 2 O 2 and only a marginal impact on acid tolerance. The growth phase had no appreciable impact on the surface survival of any of the isolates.

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.

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