Evasive strategies by the organism

It is only in recent years that the molecular basis of virulence and the genetic determinants of pathogenicity which allow salmonellae to invade and multiply in the hostile environment of the host have begun to be elucidated. As S. typhi does not infect conventional laboratory rodents, much of the information is gained from animal models (mouse typoid) and cell culture systems. Invasive salmonellae penetrate through the epithelial cells and M cells of the distal ileum and Peyer's patches; the brush border degenerates and the organisms pass through the cell enclosed in a membrane to exit through the basal pole to the submucosa. Flagella, motility, chemotaxis and smooth LPS contribute to invasion. Salmonella inva-sins and a cytotoxin have been described; invasion of and replication within epithelial cells are under separate genetic control. In gastroenteritis bacterial multiplication does not proceed beyond the intestine; some but not all strains will cause fluid accumulation in the rabbit ileal loop model. The precise mechanism of fluid loss remains unclear.

In invasive disease (e.g. enteric fevers) bacteria disseminate to the liver, spleen and bone marrow, grow within and kill hepatocytes. They also grow inside macrophages in vitro and can kill them, and the ability of salmonellae to grow inside cultured mouse macrophages correlates with mouse virulence. However, the ability of salmonellae to grow inside macrophages in the tissues is debated, as macrophages in lesions have been seen to contain mainly dead salmonellae. Polymorphs are prominent in the early stages of infection and may contribute to the lysis of infected hepatocytes. In chickens purulent pericarditis caused by, for example, S. enteritidis is not uncommon. The precise mechanisms of survival within macrophages are still unclear; resistance to lysosomal enzymes and inhibition of phagolysosome fusion have been described, with the Vi antigen increasing the resistance of S. typhi to killing by leukocytes. Transposon-generated macrophage-sensi-tive mutants were found to be auxotrophic or sensitive to serum or oxidative stress. Mutations in genes which respond to environmental changes affect survival in macrophages; ompR regulates expression of outer membrane porins in respons to osmolarity changes (ompR mutations are attenuating), while the phoP phoQ operon responds to phagolysosomal signals (low pH, cationic peptides), increasing resistance to phagocyte defensins. The large serotype specific ('cryptic') plasmid present in some but not all salmonellae (absent in S. typhi) affects serum resistance and persistence and growth in the tissues.

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