Typhus pathophysiology

Jump to navigation Jump to search

Typhus Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Typhus from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Chest X Ray

Other Diagnostic Studies

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Typhus pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Typhus pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Typhus pathophysiology

CDC on Typhus pathophysiology

Typhus pathophysiology in the news

Blogs on Typhus pathophysiology

Directions to Hospitals Treating Typhus

Risk calculators and risk factors for Typhus pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Overview

Pathophysiology

Transmission

  • Rickettsial pathogens are harboured by parasites such as fleas, lice, mites, and ticks.
  • Organisms are transmitted by the bites from these parasites or by the inoculation of infectious fluids or feces from the parasites into the skin.
  • Inhaling or inoculating conjunctiva with infectious material also causes infection.
Type of Infection Spread
Epidemic typhus Body louse
Trench fever Body louse
Murine typhus Flea infested rats
Cat flea rickettsioses Flea infested dogs and cats
Scrub typhus Mites
Tick borne rickettsiosis Ticks
Rickettsialpox Mites
Anaplasmosis Ixodes tick
Ehrlichiosis Lone star tick
Q fever Infected veterinary animals
Cat scratch disease Infected cats
Oroya fever Sandflies

Incubation

  • Incubation period of Typhus fever varies from one to two weeks.

Dissemination

  • Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. On ingestion, they replicate intracellularly inside the lysed cells and disseminate systemically.

Pathogensis

  • The major pathology is caused by a vasculitis and its complications.
  • On transmission, Rickettsia is actively phagocytosed by the endothelial cells of the small venous, arterial, and capillary vessels.
  • It is followed by systemic hematogenous spread resulting in multiple localizing vasculitis.
  • This process may cause result in occlusion of blood vessels and initiates inflammatory response (aggregation of leukocytes, macrophages, and platelets) resulting in small nodules.
  • Occlusion of supplying blood vessels may cause gangrene of the distal portions of the extremities, nose, ear lobes, and genitalia.
  • This vasculitic process causes destruction of the endothelial cells and leakage of the blood leading to volume depletion with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure.
  • Endotheleal damage also leads to activation of clotting system (DIC).

Immune response

Genetics

There is no known genetic association to Typhus fever.

References


Template:WH Template:WS