Some aspects of development of typhoid fever and persistent brucellosis infection

Abstract

Bacterial vacuolated intracellular parasites, such as Salmonella spp. and Brucella spp., possess the ability to cause persistent, long-life chronic infection during which the microbe continues to replicate inside the host organism in spite of the development of an immune response. Such bacteria develop a strategy to evade the immune response, which plays a key role in the development of chronic infection. The implementation of this strategy is aimed at inhibiting the action of factors of innate immunity. In brucella, this process is mediated by the noncanonical structure of lipopolysaccharide (LPS), as a result of which the pathogen is not recognized by the cells of innate immunity, as well as by the functioning of T4CC, the effector proteins of which block the development of the inflammatory response. The strategy of S. Typhi is realized via the expression of genes of pathogenicity island 7 encoding Vi-antigen and genotoxin. Vi-antigen inhibits recognition of the microbe by cells of the innate immune system. Typhoid genotoxin causes the death of immune cells. Brucella realizes this strategy via the noncanonical structure of LPS and T4SS, effector proteins of which block the development of inflammation. Alternative activated macrophages appear during chronic infection caused by both pathogens. These microbes are able to regulate the metabolism of macrophages according to their needs while persisting in them. A review of the sources of information on this problem allows us to conclude that both the causative agent of typhoid fever S. Typhi and the causative agents of brucellosis use the same strategies for the development of a chronic infectious process, but the implementation of these strategies is carried out specifically.