Q fever pathophysiology: Difference between revisions
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The active form of the [[organism]] | The active form of the [[organism]] | ||
large cell form persists in the [[macrophages]] inside acidic vacuoles. | |||
*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]]. | ||
Revision as of 16:33, 27 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 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
- 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 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. Brutenii 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. Brutenii:[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.
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. 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 rickettsia, 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".