Q fever pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Q fever Microchapters
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Pathophysiology

Transmission:

The organism is transmitted through:

• 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: 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.

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, 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.
• It was previously classified as a ricketsia, but now is considered a proteobacterium.

References

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