Q Fever: Etiology, general properties, pathogenesis and laboratory diagnosis

Q fever is a zoonotic disease with worldwide distribution having both acute and chronic stages. Q fever is caused by the intracellular bacterium Coxiella burnetii and is endemic in nearly every country in the world.

General properties of Coxiella burnetii

  1. Gram negative, pleomorphic coccobacilli
  2. Obligate intracellular pathogen

Mode of transmission

Q fever is usually transmitted to humans after contact with infected animals or exposure to contaminated environments such as through aerosolization of the bacteria from animal products; person-to-person transmission is rare.  Drinking infected milk can transmit infection.
Cattle, sheep, and goats are the primary reservoirs of Coxiella burnetii although a variety of species may be infected. Organisms are excreted in milk, urine, and feces of infected animals.

Laboratory diagnosis of Q Fever

Sample: Blood (Microscopy and culture), Serum (for serological testing)

Culture: Isolation of the coxiella from blood, sputum or other clinical specimens is possible but not recommended due to hazards of laboratory infection.  Please remember that Coxiella burnetii is a category B bioterrorism

Polymerase chain reaction (PCR) assay

During the acute phase of illness, a sample of whole blood can be tested by polymerase chain reaction (PCR) assay to determine if a patient has Q fever.  This method is most sensitive in the first week of illness but sensitivity decreases rapidly following the administration of appropriate antibiotics.

Although a positive PCR result is helpful, a negative result does not rule out the diagnosis.

Serological studies

Antibodies to C. burnetii, with detectable antibody titers usually observed by 7-10 days after the onset of illness.

There are two distinct antigenic phases to which humans develop antibody responses.

Acute infection:  an antibody response to C. burnetii Phase II antigen is predominant and is higher than Phase I antibody response;

Chronic infection the reverse is true in chronic infection which is associated with a rising Phase I IgG titer (according to current U.S. case definitions >1:800) that is often much higher than Phase II IgG. 

Serological tests such as microagglutination, complement fixation, immunofluorescence and enzyme linked immunosorbent assay using phase I and phase II antigens are commonly performed.

The gold standard serologic test for diagnosis of acute Q fever is the indirect  immunofluorescence assay (IFA) using C. burnetii antigen, performed on paired serum samples to demonstrate a significant (four-fold) rise in antibody titers. The first sample should be taken as early in the disease as possible, preferably in the first week of symptoms, and the second sample should be taken 2 to 4 weeks later.

Paired samples taken 2-3 weeks apart demonstrating a significant (four-fold) rise in antibody titer provides the best evidence for a correct diagnosis of acute Q fever.


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