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Typhus fever

Typhus is defined as a group of diseases caused by bacteria that are spread to humans by fleas, lice, and chiggers.
Typhus fevers include scrub typhus, murine typhus, and epidemic typhus.
Chiggers spread scrub typhus, fleas spread murine typhus, and body lice spread epidemic typhus.
The most common symptoms are fever, headaches, and sometimes rash.

Most rickettsial pathogens are transmitted by ectoparasites such as fleas, lice, mites, and ticks.
Organisms can be transmitted by bites from these ectoparasites or by the inoculation of infectious fluids or feces from the ectoparasites into the skin. *Inhaling or inoculating conjunctiva with infectious material may also cause infection for some of these organism
The arthropod vector of epidemic typhus is the body louse (Pediculus corporis).
This is the only vector of the typhus group.
Rickettsia prowazekii,is the etiologic agent of typhus, lives in the alimentary tract of the louse.

A Rickettsia- harboring louse bites a human to engage in a blood meal and causes a pruritic reaction on the host's skin.
The louse defecates as it eats.
Scratching a louse-bite site allows the rickettsia-laden excrement to be inoculated into the bite wound.
The Rickettsia travel to the bloodstream and rickettsemia develops.

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

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.
On entry into the body, the organisms multiply in the endothelial cells, which 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 may also result in loss of intravascular colloid with subsequent hypovolemia and decreased tissue perfusion and, possibly, organ failure.