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 agents are usually not transmissible directly from person to person except by blood transfusion or organ transplantation, although sexual and placental transmission has been proposed for Coxiella.
  • Transmission generally occurs via an infected arthropod vector or through exposure to an infected animal reservoir host.
  • 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 also results in loss of intravascular volume with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure.

Immune response

  • Higher-affinity leucocyte integrins (LFA-1 and Mac-1) binding to members of the immunoglobulin (Ig) mediate initial leucocyte contact with EC by capturing them from the bloodstream
  • Cytokines like tumour necrosis factor-alpha, interleukin (IL)-1beta and IL-6 up-regulate cellular adhesion molecules (CAMs) on the surface of host leucocytes and endothelial cells (EC)
  • CAMs help in leucocyte transmigration across the endothelium.[1]
  • This is followed by characteristic rolling and firm tethering to the endothelium and enabling subsequent leucocyte diapedesis.
  • Tumor necrosis factor α (TNF-α) produce on activation of cell mediated immunity, stimulates T lymphocytes and macrophages, which help in eliminating intracellular rickettsia. Virulent rickettsia tend to suppress the activity of tumor necrosis factor α (TNF-α) and IFN-gamma.
  • Cytokines such as interleukin (IL) 12 promote production of Interferon γ (IFN-γ) responses. IFN-γ, which drives TH1-type responses and stimulates macrophage activation. Cytokines, which include , IL-6, IL-4and IL-10, down-regulate the protective response.

Genetics

There is no known genetic association to Typhus fever.

References

  1. Lasky LA (1995). "Selectin-carbohydrate interactions and the initiation of the inflammatory response". Annu. Rev. Biochem. 64: 113–39. doi:10.1146/annurev.bi.64.070195.000553. PMID 7574477.


Template:WH Template:WS