Q fever pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Ahmed Younes (talk | contribs) |
Ahmed Younes (talk | contribs) |
||
| Line 29: | Line 29: | ||
*Small and large cell forms are [[Antigen|antigenically different]] and this plays a role in the [[virulence]] of the [[organism]]. | *Small and large cell forms are [[Antigen|antigenically different]] and this plays a role in the [[virulence]] of the [[organism]]. | ||
*The [[genome]] of ''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'' has been analyzed in 1995. Multiple [[genes]] encoding for Na/ ion proton exchanger have been discovered and this explains the ability of the organism to survive in [[PH|low PH]]. | *The [[genome]] of ''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'' has been analyzed in 1995. Multiple [[genes]] encoding for Na/ ion proton exchanger have been discovered and this explains the ability of the organism to survive in [[PH|low PH]]. | ||
The infection has 2 phases that correlate with changes in the [[lipopolysaccharide]] of ''[[Coxiella burnetii|C.]] [[Coxiella burnetii|burnetii]]'':<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 [[lipopolysaccharide]] capsule. Despite being less efficient in the invasion of host cells, [[antibodies]] against phase I is always isolated from acute Q fever patients. | |||
:*Phase II: characterized by rough [[lipopolysaccharide]] capsule and [[antibodies]] against phase II have been isolated from chronic Q fever patients. | |||
* There is a delay between the entry of the organism into the host cell and the fusion with lysosomes. This delay is thought to be due to the transform from the small cell variant into the large cell variant. | |||
* The acidic environment inside the lysosome has a little effect on the large cell form of the organism. | |||
====Virulence factors==== | |||
*Lipopolysaccharide capsule is one of the most important virulence factors of the organism. | |||
*The different phases of infection is associated with changes in the polysaccharide capsule. | |||
:*Lipopolysaccharide phase I (smooth polysaccharide) is associated with protection against the host immune response | |||
:*Lipopolysaccharide phase 2 (rough) is isolated from avirulent non infectious host cells and is not associated with protection of the virus from the host cell. | |||
*Both humoral and cell mediated immunity are involved in the immune response against C.brutenii. However, cell mediated immunity is more important in the defense against the organism and people with deficient cell mediated immunity is more susceptible develop chronic infection. | |||
===Q fever as a biological weapon=== | ===Q fever as a biological weapon=== | ||
Revision as of 14:20, 30 July 2017
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
|
Q fever Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Q fever pathophysiology On the Web |
|
American Roentgen Ray Society Images of Q fever pathophysiology |
|
Risk calculators and risk factors for Q fever pathophysiology |
Overview
Q fever is a disease caused by C.burnetii, an intracellular gram-negative proteobacterium. 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
- tick bites
Pathogenesis
C. burnetii has the ability to exist in 2 forms:
Small cell form[2]
Often described as the spore form of C. burnetii Resists the external environmental factors as heat, pressure and disinfectants 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. burnetii has been analyzed 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. burnetii:[3]
- Phase I: characterized by smooth lipopolysaccharide capsule. Despite being less efficient in the invasion of host cells, antibodies against phase I is always isolated from acute Q fever patients.
- Phase II: characterized by rough lipopolysaccharide capsule and antibodies against phase II have been isolated from chronic Q fever patients.
- There is a delay between the entry of the organism into the host cell and the fusion with lysosomes. This delay is thought to be due to the transform from the small cell variant into the large cell variant.
- The acidic environment inside the lysosome has a little effect on the large cell form of the organism.
Virulence factors
- Lipopolysaccharide capsule is one of the most important virulence factors of the organism.
- The different phases of infection is associated with changes in the polysaccharide capsule.
- Lipopolysaccharide phase I (smooth polysaccharide) is associated with protection against the host immune response
- Lipopolysaccharide phase 2 (rough) is isolated from avirulent non infectious host cells and is not associated with protection of the virus from the host cell.
- Both humoral and cell mediated immunity are involved in the immune response against C.brutenii. However, cell mediated immunity is more important in the defense against the organism and people with deficient cell mediated immunity is more susceptible develop chronic infection.
Q fever as a biological weapon
- Because of its route of infection it can be used as a biological warfare agent.
- Q-fever is category "B" agent. It is highly contagious and very stable in aerosols in a wide range of temperatures.
- Just 1-2 particles are enough to infect an individual.
- Q-fever microorganisms may survive on surfaces up to 60 days (like sporulating bacteria).
- According to WHO estimates[4], an amount of 50 kg of C. burnetii 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. burnetii is a gram negative polymorphic intracellular organism.[5]
- It was previously classified as a rickettsia, 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".