Q fever pathophysiology: Difference between revisions
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==Overview== | |||
Q fever is a disease caused by C. brutenii, an intracellular gram negative bacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism. | |||
==Pathophysiology== | ==Pathophysiology== | ||
===Transmission:=== | ===Transmission:=== | ||
The organism is transmitted through:<ref name="pmid17423643">{{cite journal |vauthors=Marrie TJ |title=Q fever - a review |journal=Can. Vet. J. |volume=31 |issue=8 |pages=555–63 |year=1990 |pmid=17423643 |pmc=1480833 |doi= |url=}}</ref> | The organism is transmitted through:<ref name="pmid17423643">{{cite journal |vauthors=Marrie TJ |title=Q fever - a review |journal=Can. Vet. J. |volume=31 |issue=8 |pages=555–63 |year=1990 |pmid=17423643 |pmc=1480833 |doi= |url=}}</ref> | ||
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*Vertical (mother to fetus) transmission has been reported | *Vertical (mother to fetus) transmission has been reported | ||
*Parentral | *Parentral | ||
* | *Through tick bites | ||
===Pathogenesis:=== | ===Pathogenesis:=== |
Revision as of 17:08, 8 June 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Overview
Q fever is a disease caused by C. brutenii, an intracellular gram negative bacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism.
Pathophysiology
Transmission:
The organism is transmitted through:[1]
- Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission.
- Ingestion of raw dairy products
- Vertical (mother to fetus) transmission has been reported
- Parentral
- Through tick bites
Pathogenesis:
C. Brutenii has the ability to exist in 2 forms:
Small cell form:[2] Often described as the spore form of C. Brutenii Resists the external environmental factors as heat, pressure and dissinfectants for long periods
Large cell form: The active form of the organism Large cell form persists in the macrophages inside acidic vacuoles.
Small and large cell forms are antigenically different and this plays a role in the virulence of the organism. The genome of C. Brutenii has been analysed in 1995. Multiple genes encoding for Na/ ion proton exchanger have been discovered and this explains the ability of the organism to survive in low PH.
The infection has 2 phases that correlate with changes in the lipopolysaccharide of C. Brutenii:[3] Phase I: characterized by smooth lipopolysacharide capsule. Despite being less efficient in invasion of host cells, antibodies against phase I is always isolated from acute Q fever patients.
Phase II: characterized by rough lipopolysacharide capsule and antibodies against phase II have been isolated from chronic Q fever patients.
Q fever as a biological weapon:
C. Brutenii is an extremely virulent organism.
According to WHO estimates[4], an amount of 50 kg of C. Brutenii if spread in an area of 2 square kilometers is capable of:
- Infecting 500,000 humans
- Killing 150 individuals
- Causing acute illness in 125,000 individuals
- Causing chronic illness in 9,000 individuals
Microscopic pathology:
- C. Brutenii is a gram negative polymorphic intracellular organism.[5]
- It was previously classified as a ricketsia, but now is considered a proteobacterium.
References
- ↑ Marrie TJ (1990). "Q fever - a review". Can. Vet. J. 31 (8): 555–63. PMC 1480833. PMID 17423643.
- ↑ "Diagnosis of Q Fever".
- ↑ Choyce DP (1992). "Anterior chamber lens exchange". J Cataract Refract Surg. 18 (5): 537. PMID 1489455.
- ↑ "apps.who.int" (PDF).
- ↑ "Q Fever on JSTOR".