Physiology of Yersinia pestis.

Abstract

This chapter outlines the physiology of Yersinia pestis with emphasis on identifying unique functions required for tissue invasion and acute disease. These activities are opposed to often incompatible processes expressed by very closely related Yersinia pseudotuberculosis, which causes localized gastrointestinal infection. Gain of new information in Y. pestis entailed lateral transfer of plasminogen activator and anti-phagocytic capsular antigen via the plasmids pPCP and pMT, respectively, and derepression of the pigmentation locus facilitating colonization of the flea vector. The ability to survive in austere natural environments became unnecessary following mastery of the closed flea-rodent-flea life cycle permitting concomitant chromosomal degeneration (large and small deletions, additions, inversions, translocations, transposon inserts, and single base substitutions causing nonsense and missense mutations). Consequently, modern Y. pestis lacks a functional pentose-phosphate pathway, glyoxylate bypass, and is unable to directly catabolize L-aspartate and close metabolic derivatives directly via the tricarboxylic acid cycle. The missing gene products accounting for these and numerous other metabolic lesions are now well-established. This group includes formyltetrahydrofolate deformylase (PurU) required for synthesis of glycine. This deficiency is associated with a dramatic ability of Y. pestis to catabolize L-serine, required by the host to initiate methylation of DNA (necessary in turn to initiate successful innate immune processes leading to delayed-type hypersensitivity).