A 40-year-old woman who returned from rural Rajasthan develops high fever, headache, and rash 7 days after a tick bite. IgM ELISA for Rickettsia conorii is positive. Which pathophysiological mechanism accounts for the characteristic maculopapular rash and systemic manifestations of Rickettsia?

• A Direct cytotoxic T lymphocyte destruction of endothelial cells carrying rickettsial antigens on MHC class I
• B Platelet aggregation triggered by rickettsial lipopolysaccharide on the endothelial surface
• C IgE-mediated type I hypersensitivity to rickettsial outer membrane proteins
• D Endothelial cell invasion by Rickettsia, causing activated endothelium with increased vascular permeability, coagulopathy, and perivascular inflammation ✓

Explanation

Rickettsia species are obligate intracellular pathogens that specifically target vascular endothelial cells. After tick inoculation, rickettsiae invade endothelial cells and use actin-based motility (ActA/RickA protein activates host Arp2/3 complex) to spread cell-to-cell. Endothelial invasion causes: (1) release of TNF-α, IL-1, and other pro-inflammatory cytokines; (2) upregulation of adhesion molecules; (3) increased vascular permeability causing oedema and rash; (4) activation of coagulation causing microthrombosis. The maculopapular rash (petechial in severe RMSF) reflects widespread endothelial damage. Treatment is doxycycline — a clinical diagnosis should be treated empirically. Indian tick typhus (Mediterranean spotted fever, R. conorii) is treated with doxycycline 100 mg BD for 5–7 days.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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