Q Fever

Infectious Agent

The gram-negative intracellular bacterium Coxiella burnetii .

Transmission

Most commonly through inhalation of aerosols or dust contaminated with dried birth fluids or excreta from infected animals (usually cattle, sheep, or goats). C. burnetii is highly infectious and persists in the environment. Infections via ingestion of contaminated, unpasteurized dairy products and human-to-human transmission via sexual contact have been rarely reported.

Epidemiology

Distributed worldwide; the prevalence is highest in African and Middle Eastern countries. Reported rates of human infection are higher in France and Australia than in the United States. The largest known Q fever outbreak reported to date involved approximately 4,000 human cases and occurred during 2007–2010 in the Netherlands. Travelers who visit rural areas or farms with cattle, sheep, goats, or other livestock may be exposed to Q fever. Occupational exposure to infected animals (such as in farmers, veterinarians, butchers, meat packers, and seasonal or migrant farm workers), particularly during parturition, poses a high risk for disease transmission.

Clinical Presentation

It is estimated that more than half of acute infections are mild or asymptomatic. Incubation period is typically 2–3 weeks but may be shorter after exposure to large numbers of organisms. The most common presentation of acute infection is a self-limiting influenzalike illness, with pneumonia or hepatitis in more severe acute infections. Chronic infections occur primarily in patients with preexisting cardiac valvulopathies, vascular abnormalities, or immunosuppression. Women infected during pregnancy are at risk for adverse pregnancy outcomes unless treated. The most common manifestations of chronic disease are endocarditis and endovascular infections. Chronic infections may become apparent months or years after the initial exposure.

Diagnosis

Serologic evidence of a 4-fold rise in phase II IgG by indirect fluorescent antibody test between paired sera taken 3–4 weeks apart is the gold standard for diagnosis of acute infection. A single high serum phase II IgG titer (>1:128) in conjunction with clinical evidence of infection may be considered evidence of probable acute Q fever.

Chronic Q fever diagnosis requires a phase I IgG titer >1:512 and clinical evidence of persistent infection (for example, endocarditis, infected vascular aneurysm, osteomyelitis). Detection of C. burnetii in whole blood, serum, or tissue samples by PCR, immunohistochemical staining, or isolation can also be used to confirm chronic Q fever. Tests for direct detection of C. burnetii may not be widely available, but the Rickettsial Zoonoses Branch at CDC can provide assistance (www.cdc.gov/qfever/public-health/index.html). Q fever is a nationally notifiable disease.

Treatment

Doxycycline has been used most frequently, although fluoroquinolones remain an alternative. Pregnant women, children aged <8 years with mild illness, and patients allergic to doxycycline may be treated with an antibiotic such as trimethoprim-sulfamethoxazole. Treatment for acute Q fever is not recommended for asymptomatic people or for those whose symptoms have resolved. Chronic C. burnetii infections require long-term combination therapy. The best outcomes are seen with the combination of doxycycline and hydroxychloroquine. Alternatives include trimethoprim-sulfamethoxazole, fluoroquinolones, and rifampin. Treatment of Q fever may also involve surgery.

Prevention

Avoid areas where potentially infected animals are kept, and avoid consumption of unpasteurized dairy products. A human vaccine for Q fever has been developed and used in Australia, but it is not available in the United States.

CDC website: www.cdc.gov/qfever

Bibliography

  1. Anderson A, Bijlmer H, Fournier PE, Graves S, Hartzell J, Kersh GJ, et al. Diagnosis and management of Q fever—United States, 2013: recommendations from CDC and the Q Fever Working Group. MMWR Recomm Rep. 2013 Mar 29;62(RR-03):1–30.
  2. Delord M, Socolovschi C, Parola P. Rickettsioses and Q fever in travelers (2004–2013). Travel Med Infect Dis. 2014 Sep–Oct;12(5):443–58.  [PMID:25262433]
  3. Million M, Thuny F, Richet H, Raoult D. Long-term outcome of Q fever endocarditis: a 26-year personal survey. Lancet Infect Dis. 2010 Aug;10(8):527–35.  [PMID:20637694]
  4. Robyn MP, Newman AP, Amato M, Walawander M, Kothe C, Nerone JD, et al. Q fever outbreak among travelers to Germany who received live cell therapy—United States and Canada, 2014. MMWR Morb Mortal Wkly Rep. 2015 Oct 2;64(38):1071–3.  [PMID:26421460]
  5. Roest HI, Tilburg JJ, van der Hoek W, Vellema P, van Zijderveld FG, Klaassen CH, et al. The Q fever epidemic in The Netherlands: history, onset, response and reflection. Epidemiol Infect. 2011 Jan;139(1):1–12.  [PMID:20920383]

Author

Gilbert J. Kersh