Typhus pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathophysiology of typhus fever can be described in the following steps:<ref name="pmid22449515">{{cite journal |vauthors=Rajapakse S, Rodrigo C, Fernando D |title=Scrub typhus: pathophysiology, clinical manifestations and prognosis |journal=Asian Pac J Trop Med |volume=5 |issue=4 |pages=261–4 |year=2012 |pmid=22449515 |doi=10.1016/S1995-7645(12)60036-4 |url=}}</ref> | |||
===Transmission=== | ===Transmission=== | ||
*Rickettsial pathogens are harboured by parasites such as fleas, lice, mites, and ticks. | *Rickettsial pathogens are harboured by parasites such as fleas, lice, mites, and ticks. | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]
Overview
Typhus is a zoonotic disease, humans are infected by the bites from parasites such as fleas, lice, mites, and ticks or by the inoculation of infectious fluids or feces from the parasites into the skin. The incubation period of Typhus fever varies from one to two weeks. Following transmission, rickettsia are ingested by macrophages and polymorphonuclear cells. The major pathology is caused by a vasculitis and its complications. This process may cause result in occlusion of blood vessels and initiates inflammatory response (aggregation of leukocytes, macrophages, and platelets) resulting in small nodules. 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.
Pathophysiology
The pathophysiology of typhus fever can be described in the following steps:[1]
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
- 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
- ↑ Rajapakse S, Rodrigo C, Fernando D (2012). "Scrub typhus: pathophysiology, clinical manifestations and prognosis". Asian Pac J Trop Med. 5 (4): 261–4. doi:10.1016/S1995-7645(12)60036-4. PMID 22449515.