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Abstract:

This chapter talks about , Q fever and typing systems. Q fever can be latent and recrudesce during periods of relative immunosuppression, such as late pregnancy, causing fetal infection. Isolation must currently be performed in specialized high-containment biosafety level 3 facilities, as the agent is highly infectious and classified as a select agent and a CDC category B bioterrorism agent. IHC is an excellent method for the detection of antigens in tissue samples particularly cardiac valve tissues that are colonized during chronic Q fever. The detection of antibodies to C. burnetii is the most commonly used and effective method for the diagnosis of Q fever. The primary serologic assays in use today are the indirect immunofluorescent antibody (IFA) assay, the complement fixation (CF) test, and the enzyme-linked immunosorbent assay (ELISA), with the IFA assay being the gold standard and most commonly used method. The diagnosis of chronic Q fever is best performed at reference laboratories that have BSL-3 facilities for the propagation and storage of phase I organisms since is classified as a U.S. category B bioterrorism agent. The recommended treatment for acute Q fever is doxycycline, although strains with partial doxycycline resistance have been reported. Chronic Q fever, especially Q fever endocarditis, requires long-term antibiotics and often valve replacement. Tissue specimens (e.g., heart valve, liver, and bone marrow) are most often positive in chronic Q fever, although peripheral blood leukocytes from such patients can be positive or negative.

Citation: Graves S, Massung R. 2011. , p 1027-1034. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch63

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Image of FIGURE 1
FIGURE 1

Electron micrograph of purified showing both LCV and SVC forms. (Courtesy of Rocky Mountain Laboratories, NIAID, NIH.)

Citation: Graves S, Massung R. 2011. , p 1027-1034. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch63
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Image of FIGURE 2
FIGURE 2

Hematoxylin and eosin stain of liver biopsy in a patient with acute Q fever. A doughnut ring granuloma is shown. Original magnification, ×400. (Courtesy of H. Lepidi, Marseille, France.)

Citation: Graves S, Massung R. 2011. , p 1027-1034. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch63
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Image of FIGURE 3
FIGURE 3

Alkaline phosphatase IHC on the heart valve from a patient with chronic Q fever endocarditis. microorganisms are stained pink within mononuclear cells. Original magnification, ×400.

Citation: Graves S, Massung R. 2011. , p 1027-1034. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch63
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Image of FIGURE 4
FIGURE 4

Identification of C. in shell vial culture at day 6 by the use of specific monoclonal antibody-based direct fluorescent-antibody test. Original magnification, ×1,000.

Citation: Graves S, Massung R. 2011. , p 1027-1034. In Versalovic J, Carroll K, Funke G, Jorgensen J, Landry M, Warnock D (ed), Manual of Clinical Microbiology, 10th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555816728.ch63
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References

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