The Yersinia Type III Secretion System

Welcome to this week’s #micromeded! This week, we are exploring the type 3 secretion system (T3SS) expressed in pathogenic Yersiniae (plural form, describing multiple Yersinia species). The main pathogenic Yersiniae in humans are Y. pestis (etiologic agent for black plague), Y. enterocolitica, and Y. pseudotuberculosis. In order for a strain to be fully pathogenic, the strain needs to contain the virulence plasmid which can be assessed either through PCR or by growing the organism on CR-MOX agar—an agar that assess both the ability of the organism to absorb Congo Red and grow in higher concentrations of calcium. CR-MOX is more commonly used to assess the pathogenicity of Y. enterocolitica (see image to the left from Farmer II, et al.), but since enteropathogenic Yersiniae (Y. enterocolitica and Y. pseudotuberculosis) are commonly overwhelmed by other enterics in culture, the isolation of this microbe is becoming increasingly more uncommon. One of the possible ways to enrich Yersiniae in mixed stool culture is through cold enrichment since Yersinia spp. are psychrotolerant (able to grow at lower temperatures, unlike other enteric bacteria).

Each of the pathogenic Yersiniae have their own pathogenic plasmid detailed to the right from Hu et al. (Y. pestis = pCD1 = outermost, Y. pseudotuberculosis = pIB1 = middle, and Y. enterocolitica = pYVe = innermost). These plasmids contain many of the same genes which are responsible for coding for the T3SS in the above image. By convention, the genes that code for the T3SS are named ysc and the effector proteins that are imported into the host cell are named yop. The T3SS must penetrate the inner and outer membrane of the bacterium as well as the human membrane. Once the T3SS is formed, the Yop effector proteins can be transported into the host cell via an ATP-dependent transport mechanism. The Yop effectors can then cause downstream changes to the host cell (typically a macrophage) where the bacterium can resist the formation of the phagolysosome, macrophage apoptosis, and immune signaling. These effects enable long-term survival and dissemination of the bacterium throughout the body and evasion of the immune system.