The genus Yersinia comprises 11 species, three of which have clear etiology for causing human disease (Y. pestis, Y. pseudotuberculosis and Y. enterocolitica). The obligate pathogen Y. pestis is the most infamous of these being the causal agent of plague, a bivalent disease that when left untreated is invariably fatal. The lifecycle of Y. pestis is complex, being dependent on two diverse hosts – the invertebrate flea Xenopsylla cheopis and a mammalian host (usually wild rodents). Although capable of catastrophic consequences, plague in humans is accidental – a consequence of being infected with Y. pestis via the bite of an infected flea that has been forced from its normal rodent host. In brief, the initial stage of disease presents as swollen lymph nodes (buboes) and is termed bubonic plague, whereas the second stage is a more vigorous systemic infection that results in bacterial colonization of multiple tissue organs including the lung. This form of disease is termed pneumonic plague; a highly contagious disease that enables bacteria to rapidly and effectively spread to new hosts via aerosol droplets. In light of this, global health organizations routinely list Y. pestis as a category A biowarfare agent. On the other hand, Y. pseudotuberculosis and Y. enterocolitica are essentially environmental bacteria that are capable of causing spasmodic enteric disease (known as yersiniosis) outbreaks linked to the ingestion of contaminated food or fluids. While these diseases cause gastrointestinal discomfort, they are usually self-limiting and rarely associated with systemic disease. In certain susceptible individuals however, chronic reactive arthritic sequelae can be attributed to these bacteria.
On account of their ability to cause human disease, a prolific amount of information is available that describes these three human pathogens with respect to their ecology, epidemiology and the pathogenesis of disease. In contrast, very little information is available concerning the additional Yersinia species (Y. frederiksenii, Y. intermedia, Y. kristensenii, Y. bercovieri, Y. mollaretii, Y. rohdei, Y. ruckeri, Y. aleksiciae, Y. mexicana and Y. aldovae). However, they might still be clinically relevant given their propensity to harbour a moderate number of genes that encode for products known to be associated with pathogenicity by other non-Yersinia bacteria. It is at least well established that Y. ruckeri is the causative agent of yersiniosis in infected salmonid fish, although the pathogenic mechanisms are comparatively poorly understood.
In the first part of this chapter, the presence of known and suggested protein secretion mechanisms in the Yersiniae are described. Where appropriate, these individual processes are briefly discussed in the context of their contribution to bacterial pathogenesis to help the reader gain an understanding of their physiological importance within the various unique environments of an infected host. As considerably more is known about the pathogenic mechanisms of human pathogenic Yersinia, these examples will dominate the discussion. Then, focus will turn to the consequences of adaptation of pathogenic Yersinia to their surrounding environment. Where possible, emphasis will be given to the crosstalk between metabolism and the temporal and spatial regulatory control of these important secretion systems. This connection ensures that Yersinia conserve their valuable energy reserves to maximize their survival in stressful environments and only synthesize energetically expensive virulence determinants, such as multi-component secretion systems, when they will have utmost benefit during host infections.
United Kingdom: CAB International , 2011, 1. 185-220 p.