Rickettsia rickettsii - Pathogenesis, Virulence Factor, Actin bases Motility

Virulence Factor of Rickettsia rickettsii

The virulence factor of Rickettsia rickettsii includes:

1. actin-based motility for cell spread

2. induced phagocytosis

3. phospholipase

4. hemolysin C

Pathogenesis of Rickettsia rickettsii

• Pathogenic effects were seen when it invades the endothelial lining of the vascular system within various organs

• infection occurs via the bite of a hard-shelled tick

• Rickettsia rickettsii attaches to endothelial cells via Rickettsial outer membrane protein A (rOmp A), rOmp B, and Mammalian receptor Ku70

• Rickettsia is phagocytosed by the host cell into the cytoplasm. But it escapes from the phagosome before the formation of the phagolysosome using membranolytic enzymes (phospholipase A2 and hemolysin C)

• Replication by binary fission occurs in the cytoplasm or also may occur in the host cell nucleus

• cell-to-cell spread occurs by actin-based motility

• the host cell is damaged due to the rupture of vascular endothelial cells leading to inflammation and blood leakage. Endothelial cells are injured due to toxic reaction

• O2 and N species, damage to cell membrane on rickettsial exit, Tc- induced apoptosis of infected host cell

• cause vasculitis and vascular lesion found in the skin, liver, heart, CNS, and adrenal gland

• cytokines (IFN-γ) are also induced

Actin based motility of Rickettsia rickettsii

Rickettsia rickettsii uses host cell actin cytoskeleton to promote intracellular mobility and cell-to-cell spread by the assembly of a distinctive “comet tail’ that consists of long, unbranched actin filaments.

Bacterial protein Rick A assembles branched actin networks.

Host Arp 2/3 complex is involved in actin-based motility are activated by the pathogen itself.