Temperature-inducible surface fibrillae associated with the virulence plasmid of Yersinia enterocolitica and Yersinia pseudotuberculosis

Abstract

When cultivated at 37°C in static broth, human clinical isolates of Yersinia enterocolitica (serogroups 0:3, 0:8, and 0:9) and Yersinia pseudotuberculosis (serogroup 0:11I) produced numerous nonflagellar surface appendages, which appeared as a lawn of fine fibrillae, each having a diameter of 1.5 to 2.0 nm and a length of 50 to 70 nm. Cultivation at 22°C resulted in complete disappearance of the fibrillae. The phenotypic expression of these appendages was correlated with the presence of the 40to 48-megadalton virulence plasmid and was strongly affected by the growth medium. Evidence is presented which suggests that these plasmidmediated, temperature-inducible surface fibrillae are responsible for autoagglutination and are related to production of one prominent, Sarkosyl-insoluble polypeptide of ca. 180 kilodaltons in the bacterial outer membrane.

Analysis of the yopA gene encoding the Yop1 virulence determinants of Yersinia spp.

“…We suggest, on the basis of its small, 2nm diameter (Kapperud et at., 1985), that the fibrillum consists of 4-5 intertwined polypeptide chains, which are anchored to the outer membrane by the hydrophobic carboxy-terminal end. This end of the polypeptide chain resembles the membrane anchorage structure of membrane proteins (Davis and Model, 1985), and could conceivably act as a stop transfer sequence.…”

Genetic evidence that the outer membrane protein YOP1 of Yersinia enterocolitica mediates adherence and phagocytosis resistance to human epithelial cells

“…(b) By introduction of a Yersinia virulence plasmid into a non-cell-adherent Y. enterocolitica strain of serotype 0:5 (aesculin-positive), cell adherence and phagocytosis resistance were transferred concomitantly [10] (aesculin-positive Y. enterocolitica strains are commonly non-cell-adherent [6,14]). A possible candidate responsible for these functions is the large outer membrane protein YOP1, which is known to cover the bacterial surface as a hydrophobic matrix of fibrillae [15,16] and is involved in autoagglutination [17]. Recently, the gene for YOP1 of Y. enterocolitica serotype 0:9 has been located within the BamHI fragment IV (BIV, 8.7 kb) of the 46-MDa virulence plasmid, and has been cloned using the vector pACYC184 [18]).…”

Yersinia pestistargets neutrophils via complement receptor 3

“…In the enteric Yersinia , Ail, YadA and invasin play a prominent role in adhesion, and correspondingly mutants lacking these genes manifest defects in colonization and dissemination during in vivo infections (Miller and Falkow, ; Pepe et al ., ; Marra and Isberg, ; Handley et al ., ; Durand et al ., ; Uliczka et al ., ; Paczosa et al ., ). Adhesion to host cells is necessary for injection of Yop effectors, and in the absence of these adhesins, Yop delivery is compromised (Kapperud et al ., 1985; 1987; Bliska et al ., ; Durand et al ., ; Maldonado‐Arocho et al ., ; Paczosa et al ., ). In particular, Ail and YadA are required for Yop translocation in lungs of infected mice (Paczosa et al ., ), whereas YadA, invasin and Ail each contribute to translocation in spleens of infected mice in a strain‐dependent manner, depending on the relative expression levels of each adhesin (Maldonado‐Arocho et al ., ).…”