Coxiella burnetii - Q-Fever

  • Diagnosis
  • Monitoring
  • Background
  • Lab Tests
  • References
  • Related Topics

Indications for Testing

Laboratory Testing

  • CDC laboratory confirmation of C. burnetii
  • Nonspecific testing – acute disease
    • CBC – thrombocytopenia common
    • Serum transaminases – moderately elevated in many patients
    • Patients with endocarditis
  • Antibody titers by IFA, ELISA
    • Acute disease
      • Perform phase I and II IgG and IgM antibody testing
      • Results
        • Phases I and II – IgM increased
        • Phase II, IgG increased
        • May take 2-4 weeks after onset of symptoms for increased titers
        • May be detected up to 12 weeks after illness onset
  • Chronic disease
    • Phase I – IgG persistently increased
    • Endocarditis – IgG titer ≥1:800 is diagnostic
  • PCR – helpful in patients where disease is suspected and titers are low
    • Can be performed on tissue fluids (eg, CSF, pleural)
    • Most sensitive in first week of illness
    • Sensitivity rapidly diminishes with antibiotic therapy
  • Immunohistochemical staining – not widely available
  • Culture tests – not recommended
    • Lack sensitivity
    • Available only in research laboratories due to extreme infectivity


Imaging Studies

  • Echocardiogram
  • IgG phase I – monitor treatment efficacy; expect decreased IgG in successful therapy
  • May want to consider repeat serum testing using IgG phase I in patients with known valvular abnormalities, if initial testing was negative
  • Follow-up testing recommended for all patients with acute disease
    • Antibody titers
    • Echocardiogram

Q-fever, a worldwide zoonosis, is caused by Coxiella burnetii and is named for a 1985 disease outbreak in Queensland, Australia.


  • Incidence – <50/year in U.S.
  • Age – highest prevalence in 30s-60s
  • Sex – M>F
    • Women and children more commonly asymptomatic
  • Transmission
    • Important reservoirs of C. burnetii include cattle, sheep, and goats, as well as the rodents, cats, and birds that feed on them
    • Infection in these animals is enzootic and usually asymptomatic
    • Bacteria infects humans via
      • Inhaling contaminated dust particles and aerosols
      • Handling/ingesting infected raw meat or milk


  • Gram-negative coccobacillus
  • Obligate intracellular bacterial pathogen (family Coxiellaceae; order Legionellales) with worldwide distribution
  • Classified as a class B bioterrorism agent

Risk Factors

  • Occupational – farmers, veterinarians, abattoir workers, military personnel
  • Ingestion of unpasteurized dairy products
  • Underlying valve disease – risk factor for endocarditis


  • C. burnetii exists in two antigenic phases (phases I and II) – antigenic difference is important to diagnosis
    • Antibodies to both phase I and II antigens may persist for months or years after initial infection
  • Acute disease
    • Antibody levels to phase II antigens are usually higher (often by several orders of magnitude) than those for phase I antigens and are usually detected during the second week of symptoms
  • Chronic disease
    • Subsequent testing shows high antibody levels to phase I antigens and constant or decreasing levels of antibodies to phase II antigens
      • Because antibodies to phase I antigens generally require longer to appear, consistent high levels may indicate continued exposure to the bacteria
    • Signs and symptoms of inflammatory disease

Clinical Presentation

  • Incubation period – ~2-6 weeks
  • Acute disease symptoms
    • Most cases are self-limiting, flu-like illnesses
      • Fever peaks in 2-4 days near 40°C, then gradually declines over period of 1-2 weeks
    • Constitutional – malaise, anorexia, myalgias, weakness, intense headache
    • Pneumonia or bronchitis – tachypnea, rales, rhonchi, cough, wheezing
    • Hepatitis – nausea, vomiting, diarrhea, anorexia, elevated transaminases, rarely jaundice
    • Myocarditis, pericarditis
    • During pregnancy – abortion, prematurity, low birth weight
  • Chronic disease symptoms – rare (<1%)
    • Defined as infection lasting >6 months
    • Presence of endocarditis – pathognomonic for chronic disease
    • Occurs in patients with pre-existing heart valve damage (usually aortic and mitral valves), immunosuppression, or chronic renal disease
    • May result in culture-negative endocarditis
    • Symptoms – low-grade fever, cardiac failure, hepatosplenomegaly, clubbing of digits
    • Other organs may be involved – hepatitis, vascular infection, osteomyelitis, lymphadenitis
Tests generally appear in the order most useful for common clinical situations. Click on number for test-specific information in the ARUP Laboratory Test Directory.

Coxiella burnetii (Q-Fever) Antibodies, IgG and IgM, Phase I and II with Reflex to Titer 2012634
Method: Semi-Quantitative Indirect Fluorescent Antibody

Coxiella burnetii (Q-Fever) Antibody IgG, Phase I and II with Reflex to Titer 2012625
Method: Semi-Quantitative Indirect Fluorescent Antibody


Initial testing may not be helpful; treatment should be based on clinical and other laboratory assessment


American Society for Clinical Pathology. Choosing Wisely - Five Things Physicians and Patients Should Question. An initiative of the ABIM Foundation. [Last revision Feb 2015; Accessed: Jan 2016]

General References

Cutler SJ, Bouzid M, Cutler RR. Q fever. J Infect. 2007; 54(4): 313-8. PubMed

Gikas A, Kokkini S, Tsioutis C. Q fever: clinical manifestations and treatment. Expert Rev Anti Infect Ther. 2010; 8(5): 529-39. PubMed

Hartzell JD, Wood-Morris RN, Martinez LJ, Trotta RF. Q fever: epidemiology, diagnosis, and treatment. Mayo Clin Proc. 2008; 83(5): 574-9. PubMed

Parker NR, Barralet JH, Bell AM. Q fever. Lancet. 2006; 367(9511): 679-88. PubMed

Terheggen U, Leggat PA. Clinical manifestations of Q fever in adults and children. Travel Med Infect Dis. 2007; 5(3): 159-64. PubMed

Tissot-Dupont H, Raoult D. Q fever. Infect Dis Clin North Am. 2008; 22(3): 505-14, ix. PubMed

Medical Reviewers

Last Update: September 2016