Yersinia and Shigella

Types of Yersinia

Main pathogenic species are Y. pestis, Y. entericolitica Y. pseudotuberculosis

Plague

Transmitted to human host by bite of infected fleas, associated with rodents that carry fleas

Three forms: Bubonic, Pneumonic, Septicemic

Three great pandemics across history (most common is Black Death)

Bubonic Plague

Bacteria invade macrophage and accumulates in lymph nodes

Lymph nodes swell greatly and can burst (buboes)

Not typically transmitted host to host

Flea bite of infected human can pass bacteria

Pneumonic Plague

Most dangerous form of the plague

Bacteria infect alveolar macrophage of the lung

Causes damage to lung tissue

Coughing up blood and bacteria

Can be transmitted by host to host and spreads quickly through communities

Septicemic Plague

Infection of blood stream

Causes clotting and vascular damage leading to tissue necrosis (gangrene)

Black color of necrotic tissue gave name black death

Other Yersinia Manifestations

Y. Enterocolitcia: Enterocolitis frequently in children that mimics appendicitis

Y. Pseudotuberculosis: Rare in humans, usually causes disease in immunocompromised

Virulence Factors

All three species have large 70-75 kbp plasmid that carries general virulence

Pestis has two additional plasmids

YST produced by enterocolitica similar to ETEC

Y. pestis Virulence Factors

110 kbp Fra-antiphagocytic surface protein forms a protein capsule

9.5 kbp plasminogen activator protease which degrades complement

Also survives neutrophils (PMN) using Yop, Yad LcrV

Yop H and E injected into host directly by Type III secretion system (molecular syringe built by bacterium and allows direct injection of bacterial protein into host)

Yop E stops actin polymerization

Yop H is a protein kinase that interferese with signal transduction

Type III Secretion System

Similar to flagellum

Typically injects material from the cytoplasm inside the inner membrane

Sometimes opening in structure allow injection of molecules located in periplasmic space or even in gap between bacteria and host cells

Temperature and Virulence

Y. pestis always ready to go enterocolitica and pseudotuberculosis are temperature regulated

Causes the lag in ramping up virulence

Shigella

Extremely close relative to E. coli

Causes dyentery and hemolytic uremic syndrome

ID50 of 100-200 cells and as few as 6 will work

S. flexneri, S. boydii, S. sonnei, S. dysenteriae, all cause disease

HUS

Just like EHEC Shigella produce Shiga toxin that can spread through body

AB toxin where A blocks translation

Kidney damage in children

Toxin also damages intestines

Dysentery

Direct pathology

Like Listeria but IpaD (attachment), IpaB (internalization) IpaC (lyse of vesicles) IcsA (polymerize actin) IcsB (lyse double vessicle)

Kill mucosal cells by competition for micronutrients

Tissue damages to host by inflammation and cell death

Can spread by infecting macrophages similar to Salmonella (invade M cells and then underlying macrophage)