Yersiniosis

Spread spoil food products. even with a slit contamination it could still grow in host. it could spread systemically causing lymphadenitis.

Facultative anaerobic, they grow at room temp and time in extreme conditions. It can identify whether in the human host or outside it. when in the host it changes shape and turns on transcription to protect itself from the macrophage.

became pathogenic because it uses plasmid to replicate and infect the host.

reductive evolution and causing many form of diseases

burst and release bacteria in the bloodstream or end up directly in the lungs and cause Pneumonic plague.

Septicemic plague when bubo relased in the bloodstream.

Y. pestis lack pMT1 + pPLA plasmid

down-regulate anti-bacterial responses that constrict bacterial survival in the host.

allowing extracellular Yersinia adhering at the surface of a target cell to inject an array of bacterial effectors into cytosol.

resist phagocytosis by peritoneal macrophages.

promotes the disruption of actin filaments, cell rounding and blockage of phagocytosis.

As a cysteine protease to cleave Rho family GTPases.

- Iron acquisition for pathogens in the low iron conditions of the host.

- Yersiniabactin-Fe³⁺ recognizes TonB-dependent receptor

- Ybt, provides the bacteria to multiply in the host

Inhibits GDI and Locks GTPase in GDP form

- inhibits the host immune response

- blocking multiple signaling pathways

- MAPK and NFkappaB pathways in the infected cell

Y. pestis expressing stimulatory hexa-acylated LPS activates TLR4 and induces inflammation and adaptive immune response