1887

Abstract

To study the possible mechanism of extracellular resistance to phagocytes developed by in the early stage of plague infection, the behaviour of two strains, the vaccine EV-76 and fully virulent 231 (LD, 10 c.f.u.), was studied in-depth after cultivation at the host temperature in conditions simulating the bloodstream environment of mammals. For this, two standard basal media supplemented with calcium and glucose in appropriate concentrations were employed: Hottinger broth, routinely used for growth of , and RPMI 1640, simulating human extracellular fluid. Although both media permitted to achieve the resistant state, RPMI enabled significantly higher bacterial proliferation and increased modifications in the production of the principal surface antigens that affect the relevant phenotype characteristics. In general, our results indicate that the bacteria in the resistant state do not produce species-specific antigens, i.e. fraction 1 or F1, ‘murine’ toxin or Ymt, plasminogen activator (Pla) and any surface-specific polysaccharides, resulting in unmasking of the cross-reactive epitopes of lipid A in reduced lipopolysaccharide. This may produce mimicry by of some human tissue and blood cell components, with no immune response and inflammation at the site of infection at the early stage, which enables to survive, extensively multiply and spread into the circulation.

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2005-05-01
2019-11-13
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