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Coxiella Burnetii

Summary

Coxiella burnetii is an intracellular pathogen with a slow replication rate that belongs to the Coxiellaceae family and is responsible for causing an arthropods-transmitted disease known as Q fever [1].

Coxiella burnetii is an intracellular pathogen with a slow replication rate that belongs to the Coxiellaceae family and is responsible for causing an arthropods-transmitted disease known as Q fever [1].

Staining and microbiological features:  

  • C. burnetti is an obligate intracellular pathogen [2] and requires host cells to replicate [1].

Transmission electron microscopic (TEM) image, revealed ultrastructural details exhibited by numerous, Coxiella burnetii bacteria, which cause the worldwide disease known, as Q fever. Original image sourced from US Government department: Public Health Image Library, Centers for Disease Control and Prevention. Under US law this image is copyright free, please credit the government department whenever you can”. by Centers for Disease Control and Prevention is marked with CC0 1.0.

  • Although it has a gram-negative cell wall, it stains poorly with gram staining [1].
  • Unlike many rickettsial organisms, Coxiella burnetii does not require an arthropod vector for transmission [3]. 
  • Domestic animals, particularly cattle, sheep, and goats, are common reservoirs for Coxiella burnetii [3].

Virulence:

  • The presence of its endospore form confers resistance to heat and drying and facilitates the organism to survive in the extracellular environment [4].
  • It has the ability to endure and thrive in the acidic pH (4.5) environment of phagolysosomes [3]. 
  • Since it exclusively thrives within host cells [5], it must evade the apoptosis process of the host cells. Therefore, it has developed mechanisms to interfere with host cell signaling and delay apoptosis. Interferon-γ facilitates the fusion of phagosomes and lysosomes, leading to the demise of phagocytosed bacteria. However, during Coxiella infection, host cells may occasionally overproduce IL-10. This excess IL-10 disrupts the phagosome-lysosome fusion, promoting the intracellular survival of Coxiella burnetii and leading to chronic infection [1].
  • A small infectious dose of 10 bacteria or fewer is adequate to induce infection [1].

Transmission:

  • Airborne transmission can occur in individuals engaged in handling contaminated animal products such as dried placenta [3].
  • Transmission is also possible through Unpasteurized milk contaminated with C. burnetii [3].

Diseases and complications:   

  • Q fever: The patient can present with flu-like symptoms, including fever, headache, muscle pain, and fatigue. However, the rash is absent (unlike Rickettsia) [1,3]. Involvement of the lungs and liver can lead to pneumonia and granulomatous hepatitis, respectively. Some patients can also develop culture-negative endocarditis [6]. Immunocompromised patients or those with valvular heart disease can develop chronic Q fever [5].

Diagnostic testing:   

  • The preferred diagnostic approach is serology (particularly indirect immunofluorescence) [7]. Serological tests such as microagglutination tests, indirect immunofluorescence antibody tests, and ELISA can detect rising antibody titers [8].
  • Culture (not routinely done) [8
  • PCR is helpful in patients with culture-negative endocarditis [7].

References:

  1. Medical Microbiology by Patrick R. Murray Ph.D., Ken Rosenthal Ph.D., Michael A. Pfaller MD, 8th edition (page no: 346)
  2. USMLE Step 1 Lecture Notes: Microbiology / Immunology (Kaplan Medical), 2020 (page no: 264)
  3. CMMRS edition 6, 2016-17 (page no: 126)
  4. CMMRS edition 6, 2016-17 (page no: 120)
  5. Jawetz, Melnick, & Adelberg’s Medical Microbiology Twenty-Seventh Edition (page no: 346)
  6. CMMRS edition 6, 2016-17 (page no: 121)
  7. Jawetz, Melnick, & Adelberg’s Medical Microbiology Twenty-Seventh Edition (page no: 347)
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