Q fever pathophysiology: Difference between revisions
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Large cell form persists in the macrophages inside acidic vacuoles. | 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. | *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 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:<ref name="pmid1489455">{{cite journal |vauthors=Choyce DP |title=Anterior chamber lens exchange |journal=J Cataract Refract Surg |volume=18 |issue=5 |pages=537 |year=1992 |pmid=1489455 |doi= |url=}}</ref> | The infection has 2 phases that correlate with changes in the lipopolysaccharide of C. Brutenii:<ref name="pmid1489455">{{cite journal |vauthors=Choyce DP |title=Anterior chamber lens exchange |journal=J Cataract Refract Surg |volume=18 |issue=5 |pages=537 |year=1992 |pmid=1489455 |doi= |url=}}</ref> | ||
*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 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. | **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:=== | ===Q fever as a biological weapon:=== | ||
Revision as of 17:26, 8 June 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Q fever Microchapters |
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Diagnosis |
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Treatment |
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Case Studies |
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Q fever pathophysiology On the Web |
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American Roentgen Ray Society Images of Q fever pathophysiology |
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Risk calculators and risk factors for Q fever pathophysiology |
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.
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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".