Pathogenesis and Clinical Manifestations of Coxiella burnetii

Last Updated on January 3, 2020 by Sagar Aryal

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

Pathogenesis and Clinical Manifestations of Coxiella burnetii

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