Q FEVER (Coxiella burnetii infection)

I.          IDENTIFICATION

A.        CLINICAL DESCRIPTION: An acute febrile zoonotic disease caused by the rickettsial organism Coxiella burnetii.  The incubation period is typically two to three weeks.  Onset may be sudden with rigors, severe retrobulbar headache, weakness, malaise, anorexia, severe sweats and other nonspecific systemic symptoms. Pneumonia, meningoencephalitis, gastroenteritis and hepatitis have also been described.  Pregnant women are at risk for fetal death and abortion.
The chronic form of Q fever is uncommon but is a much more serious disease.  Endocarditis is the major manifestation of chronic Q fever, which is characterized by infection that persists for more than 6 months.  Chronic hepatitis or osteomyelitis may also occur, as well as infections of aneurysms and of vascular prostheses.  Infection of humans usually occurs by inhalation of these organisms from air that contains airborne barnyard dust contaminated by dried placental material, birth fluids, and excreta of infected herd animals.  Ingestion of contaminated milk is a less common mode of transmission.  Human to human transmission occurs rarely, if ever.

B.        REPORTING CRITERIA: Confirmatory or supportive laboratory findings in an individual with a clinically compatible illness.

            NOTE that there are two separate case definitions for Acute Q fever and Chronic Q fever.  Coxiella burnetii occurs in two antigenic phases called phase I and phase II.  This antigenic difference is important in diagnosis.  In acute cases of Q fever, the antibody level to phase II is usually higher than that to phase I, often by several orders of magnitude, and generally is first detected during the second week of illness.  In chronic Q fever, the reverse situation is true (i.e., phase I titers are higher than phase II).  Thus, high levels of antibody to phase I in later specimens in combination with constant or falling levels of phase II antibodies and other signs of inflammatory disease suggest chronic Q fever.   Antibodies to phase I and II antigens have been known to persist for months or years after initial infection.

C.        ACUTE Q FEVER:
           1. LABORATORY CRITERIA FOR CONFIRMATION (acute Q Fever):

1. A fourfold change in IgG antibody titer to C. burnetii phase II antigen by IFA in paired serum samples, OR
2. A positive PCR assay for C. burnetii, OR
3. Demonstration of C. burnetii in a clinical specimen by immunohistochemical methods (IHC), OR
4. Isolation of C. burnetii from a clinical specimen by culture.

2. LABORATORY SUPPORTIVE EVIDENCE (acute Q fever):

1. A single supportive IFA IgG titer of ≥1:128 to phase II antigen (phase I titers may be elevated as well),  OR
2. Serologic evidence of elevated phase II IgG or IgM antibody reactive with C. burnetii antigen by enzyme-linked immunosorbent assay (ELISA), dot-ELISA, or latex agglutination.

3. CLINICAL CRITERIA FOR ACUTE Q FEVER:  Acute fever and at least one of the
    following: rigors, severe retrobulbar headache, acute hepatitis, pneumonia, or elevated
    liver enzyme levels.

4. WISCONSIN CASE DEFINITION – ACUTE Q FEVER

1. CONFIRMED ACUTE Q FEVER:  A laboratory confirmed case that either meets clinical case criteria or is epidemiologically linked to a lab-confirmed case.
2. PROBABLE ACUTE Q FEVER:  A clinically compatible case of acute illness (meets clinical evidence criteria for acute Q fever illness) that has laboratory supportive results for past or present acute disease (antibody to Phase II antigen) but is not laboratory confirmed.

D.        CHRONIC Q FEVER:
            1. LABORATORY CRITERIA FOR CONFIRMATION (chronic Q Fever):

1. Serological evidence of IgG antibody to C. burnetii phase I antigen ≥ 1:800 by IFA (while phase II IgG titer will be elevated as well; phase I titer is higher than the phase II titer), OR
2. Detection of C. burnetii DNA in a clinical specimen via amplification of a specific target by PCR assay, OR
3. Demonstration of C. burnetii antigen in a clinical specimen by IHC, or
4. Isolation of C. burnetii from a clinical specimen by culture.

            2. LABORATORY SUPPORTIVE EVIDENCE (chronic Q fever):

• An antibody titer to C. burnetii phase I  IgG antigen ≥1:128 and < 1:800 by IFA.

            3. CLINICAL CRITERIA FOR CHRONIC Q FEVER:  Newly recognized, culture-negative
                endocarditis, particularly in a patient with previous valvulopathy or compromised immune
                system; suspected infection of a vascular aneurysm or vascular prosthesis; or chronic
                hepatitis, osteomyelitis, osteoarthritis, or chronic hepatitis, osteomyelitis, osteoarthritis, or
                pneumonitis in the absence of other known etiology.

            4. WISCONSIN CASE DEFINITION – CHRONIC Q FEVER

1. CONFIRMED CHRONIC Q FEVER:  A clinically compatible case of chronic illness (meets clinical criteria for chronic Q fever) that is laboratory confirmed for chronic infection.
2. PROBABLE CHRONIC Q FEVER:  A clinically compatible case of chronic illness (meets clinical evidence criteria for chronic Q fever) that has laboratory supportive results for past or present chronic infection (antibody to Phase I antigen).

II.        ACTIONS REQUIRED / PREVENTION MEASURES

1. WISCONSIN DISEASE SURVEILLANCE CATEGORY II: Report to the patient's local health officer on an Acute and Communicable Disease Case Report (DPH 4151) or other means within 72 hours of the identification of a case or suspected case.

2. EPIDEMIOLOGY REPORTS REQUESTED:
   1. Acute and Communicable Diseases Case Report  (DPH 4151).
   2. Q Fever Case Report – CDC 55.1 (Rev. 2/2008)
      
      
3. PUBLIC HEALTH INTERVENTIONS:
   1. Educate persons in high-risk occupations (sheep and dairy farmers, veterinarian researchers) on the sources of infection and the necessity for adequate disinfection and infection control measures.
   2. Appropriately dispose of placenta, birth products, fetal membranes, and aborted fetuses at facilities housing sheep and goats.
   3. Restrict access to barns and laboratories used in housing potentially infected animals.
   4. Use only pasteurized milk and milk products.
   5. Use appropriate procedures for bagging, autoclaving, and washing of laboratory clothing.
   6. Vaccinate (where possible) individuals engaged in research with pregnant sheep or live C. burnetii. Vaccine not available to the general public in the United States.
   7. Counsel persons at highest risk for developing chronic Q fever, especially persons with pre-existing cardiac valvular disease or individuals with vascular grafts.
   8. DPH recommendations exist for workers on farms where Q fever has been diagnosed in livestock.  Call the State Public Health Veterinarian for these

4. BIOTERRORISM CONSIDERATIONS:
   Coxiella burnetii is a highly infectious agent that is relatively resistant to heat and drying.  It can become airborne and inhaled by humans. A single organism may cause disease in a susceptible person.  This agent could be developed for use in biological warfare and is considered a potential terrorist threat.

III.       CONTACTS FOR CONSULTATION

A.        DPH REGIONAL STAFF: See Epinet Introduction: “REGIONAL OFFICE CONTACTS”.

B.        BCD / COMMUNICABLE DISEASE EPIDEMIOLOGY SECTION:  (608) 267-7321.

C.        WSLH / VIRAL AND RICKETTSIAL SEROLOGY:  (608) 262-0248.

IV.       RELATED REFERENCES

1.         Heymann DL, ed. Q Fever. In: Control of Communicable Diseases Manual. 18th ed. Washington, DC: American Public Health Association, 2004:434-438.

2.         Pickering LK, ed. Q fever. In: Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, IL: American Academy of Pediatrics, 2006:550-552.