Pathogenesis and Clinical Manifestations of Coxiella burnetii

Pathogenesis of Coxiella burnetii

  • Human infection usually follows inhalation of aerosols containing C. burnetii.
  • It is estimated that only between 1 and 10 bacteria are necessary to cause infection.
  • C. burnetii has also been known to enter the body via other mucous membranes, abrasions, and the gastrointestinal tract through consumption of milk from infected animals.
  • C. burnetii exists in two antigenic forms called phase I and phase II.
  • Phase I is the virulent form that is found in humans with Q fever and infected vertebrate animals, and it is the infectious form, whereas Phase II is the avirulent form.
  • Entry into the lungs results in infection of the alveolar macrophages.
Pathogenesis of Coxiella burnetii
Source: Nature Reviews | Microbiology
  • C. burnetii escapes intracellular killing in macrophages by:
    • Inhibiting the final phagosome maturation step (cathepsin fusion)
    • Resistant to the acidic environment of phagolysosome by producing superoxide dismutase.
  • The normal progression after phagocytosis of most organisms is fusion of the phagosome with a series of endosomes (intracellular vesicles), resulting in a drop in intracellular pH, followed by fusion with lysosomes containing hydrolytic enzymes and resultant bacterial death which occurs with C. burnetii if phase II organisms are ingested; however, phase I Coxiella is able to arrest this process before lysosomal fusion.
  • In addition, the organisms require acid pH for their metabolic activities, which, in turn, protects them from the killing activities of most antibiotics.
  • Coxiella is able to regulate the cell signaling pathways in its phagocytic home so that cell death is delayed.
  • The ability of C. burnetii to cause either acute or chronic disease is determined in part by the organism’s ability to survive intracellularly.
  • In acute cases, in the presence of interferon-γ, phagosome–lysosome fusion occurs, leading to bacterial death; however, in chronic infections interleukin-10 is overproduced by the host cell, which interferes with fusion and allows intracellular survival of C. burnetii.
  • Infection with C. bumetii induces autoantibodies, particularly to cardiac and smooth muscles.
  • Chronic form leads to disseminated cases affecting various organs with pathological condition.

Clinical Manifestations of Coxiella burnetii

Query fever (Q fever)

  • The majority of individuals exposed to C. burnetii have an asymptomatic infection, and most symptomatic infections are mild, presenting with nonspecific flulike symptoms with an abrupt onset, high-grade fever, fatigue, headache, and myalgias.
  • The patient may also suffer pneumonitis, hepatic and bone marrow granulomata, and meningoencephalitis.
  • Hepatitis is usually asymptomatic or presents with fever and increase in serum transaminases.
  • Most cases of pneumonia are mild, with a nonproductive cough, fever, and nonspecific findings on chest radiograph.
  • Acute pneumonia and hepatitis are associated with antibodies to phase II antigens.
  • Chronic infections can develop, with the organism persisting in cardiac valves and possibly other foci.
  • Chronic Q fever (symptoms lasting more than 6 months) can develop months to years after the initial exposure and occurs almost exclusively in patients with predisposing conditions, such as underlying valvular heart disease or immunosuppression.
  • Fever is usually absent or of low grade.
  • Reactivation of latent infection may occur during pregnancy, and the organism is shed with the placenta or abortus.
Clinical Manifestations of Coxiella burnetii

About Author

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Sagar Aryal

Sagar Aryal is a microbiologist and a scientific blogger. He is currently doing his Ph.D. from the Central Department of Microbiology, Tribhuvan University in collaboration with Helmholtz-Institute for Pharmaceutical Research Saarland (HIPS), Saarbrucken, Germany. He did his M.Sc. in Microbiology and B.Sc. in Microbiology from St. Xavier’s College, Kathmandu, Nepal. He worked as a Lecturer at St. Xavier’s College, Maitighar, Kathmandu, Nepal, from March 2017 to June 2019. He is interested in research on actinobacteria, myxobacteria, and natural products. He has published more than 15 research articles and book chapters in international journals and well-renowned publishers.

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