Q-fever, a worldwide zoonoses, is caused by Coxiella burnetii.

Epidemiology

• Incidence - <50/year in U.S.
• Transmission
  • Important reservoirs of C. burnetii include cattle, sheep and goats as well as rodents and cats that feed on them
  • Infection in these animals is enzootic and usually asymptomatic
  • Bacteria infects humans via:
    • Inhalation of contaminated dust particles and aerosols
    • Handling/ingesting infected raw meat or milk

Organism

• Gram-negative coccobacillus
• Obligate intracellular parasite (family Rickettsia) with worldwide distribution

Risk Factors

• Occupational - farmers, veterinarians, abattoir workers, military personnel
• Ingestion of unpasteurized dairy products

Pathophysiology

• Coxiella burnetii exists in two antigenic phases -- phase I and phase II
• Acute disease
  • Antibody level to phase II is usually higher than that to phase I, often by several orders of magnitude,
  • Antibody level is generally detected during the second week of illness
• Chronic disease
  • Antibodies to phase I antigens generally require longer to appear and indicate continued exposure to the bacteria

Clinical Presentation

• Incubation period about 2-6 weeks
• Symptoms
  • Most cases are self-limiting febrile 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
  • Pneumonitis or bronchitis - tachypnea, rales, rhonchi, cough, wheezing
  • Hepatitis - nausea, vomiting, diarrhea,  anorexia, elevated transaminases, rarely jaundice
• Chronic disease rare (<1%)
  • The presence of endocarditis is pathognomonic for chronic disease
    • Occurs in patients with pre-existing heart valve damage, 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

Treatment

• Treatment is curative; monitor titers to assess treatment success

Diagnosis

• Indications for testing - febrile illness with appropriate risk factors
• Laboratory testing
  • Antibody titers by IFA, ELISA
    • Acute disease -Phase I and II IgM increased, Phase II IgG increased
      • May take 3-4 weeks after onset of illness to rise
    • Chronic disease - Phase I IgG and IgA increased  
  • DNA testing
  • Immunohistochemical staining
  • Culture tests are not recommended; available only in research laboratories

Disease Monitoring

• IgG Phase I - use to monitor treatment efficacy except a decrease in successful therapy