Q fever pathophysiology: Difference between revisions
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===Transmission:=== | ===Transmission:=== | ||
The organism is transmitted through: | 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> | ||
*Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission. | *Aerosoloes: Inhalation of contaminated aerosoles is the main mode of transmission. | ||
*Ingestion of raw dairy products | *Ingestion of raw dairy products | ||
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C. Brutenii has the ability to exist in 2 forms: | C. Brutenii has the ability to exist in 2 forms: | ||
Small cell form: | Small cell form:<ref name="urlDiagnosis of Q Fever">{{cite web |url=http://jcm.asm.org/content/36/7/1823.short |title=Diagnosis of Q Fever |format= |work= |accessdate=}}</ref> | ||
Often described as the spore form of C. Brutenii | Often described as the spore form of C. Brutenii | ||
Resists the external environmental factors as heat, pressure and dissinfectants for long periods | Resists the external environmental factors as heat, pressure and dissinfectants for long periods | ||
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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 | 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. | ||
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==Microscopic pathology:== | ==Microscopic pathology:== | ||
*C. Brutenii is a gram negative polymorphic intracellular organism. | *C. Brutenii is a gram negative polymorphic intracellular organism.<ref name="urlQ Fever on JSTOR">{{cite web |url=http://www.jstor.org/stable/4458369?seq=1#page_scan_tab_contents |title=Q Fever on JSTOR |format= |work= |accessdate=}}</ref> | ||
*It was previously classified as a ricketsia, but now is considered a proteobacterium. | *It was previously classified as a ricketsia, but now is considered a proteobacterium. | ||
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Revision as of 17:01, 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
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".