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Coxiella burnetii

I. General Information

1. NCBI Taxonomy ID:

2. Disease:

Q fever

3. Introduction

Coxiella burnetii is an intracellular organism that causes Q fever. Unlike other rickettisiae, however, C. burnetii, multiplies in the phagolysosomal vacuoles and remains in the vacuoles throughout its life cycle (Burton et al., 1971; Burton et al., 1978; Ormsbee, 1969). The microorganism is able to survive under the hostile conditions within the phagolysosomes (Akporiaye and Baca, 1983). C. burnetii also has two phases (phase I and phase II) based on the pathways involved and the cell coating (Mege et al., 1997; Capo et al., 1999). Phase I organisms are more virulent and have complete smooth-type lipopolysaccharide (LPS) while phase II organisms are avirulent and have incomplete rough-type LPS (Hackstadt et al., 1985) . Due to highly resistance to chemical agents and hostile environments, and the low number of C. burnetii required for an infection through inhalation, Coxiella burnetii is listed CDC category B priority agent. Common symptoms for Q fever include fever, headache, malaise, and myalgia.

4. Microbial Pathogenesis

C. burnetii is found in large numbers in birth fluids of goat and cows (Stoker and Marmion, 1955). Humans are then infected by inhaling from the infected aerosols or dust particles with the contaminated birth fluids. Approximately only 10 microorganisms are needed to infect humans (Tigertt et al., 1961). Based on animal models, C. burnetii is first engulfed by macrophages after inital infection in the lungs (Burton et al., 1971; Burton et al., 1978). The microorganism grows within the acidic environment, with a pH around 4.7 - 4.8 (Ohkuma and Poole, 1978), in the phagolysosome and eventually rupture the host cells and infect other neighboring cells (Hackstadt and Williams, 1981; Burton et al., 1971). C. burnetii suppresses the host immune responses and avoids host cell activation (avoid recognition by TLR). As a result, the microogranism is able to persist within phagolysosome (Zamboni et al., 2004; Shannon et al., 2005).

Link to pathogenesis of Coxiella burnetii in HazARD.

5. Host Ranges and Animal Models

Several species are infected by C. burnetii. However, the disease seems to be more severe in human beings (Waag, 2007). C. burnetii has also been found to cause abortions in humans, goats, sheeps, and cattles (Langley et al., 2003; Palmer et al., 1983; Waldhalm et al., 1978). C. burnetii can be cultured and isolated using chicken embryo yolk sacs. Model organisms normally use for infection research include mice and guinea pigs, and sheeps (Williams and Thompson, 1991).

6. Host Protective Immunity

Antibodies produced by the immune system is not the primary mechanism used for resistance. Studies have shown that the activation of monocytes and macrophages by gamma interferon results in the production of active nitrogen and oxygen intermediates. This mechanism results in the killing of C. burnetii (Brennan et al., 2004; Turco et al., 1984). However, C. burnetii minimizes detection by the host cell, thereby minimizes the killing by the intermediates (see Microbial Pathogensis for more information).

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