Chapter 3Infectious Diseases Related To Travel
Alicia Anderson, Jennifer McQuiston
Q fever is caused by the organism Coxiella burnetii, which is an obligate intracellular bacterium.
MODE OF TRANSMISSION
Q fever is a zoonotic disease that is often associated with exposure to cattle, sheep, and goats. The most common mode of transmission to humans is inhalation of aerosols or dust contaminated with dried birth fluids or excreta from infected animals. Direct animal contact is not required for transmission to occur. Infections via ingestion of contaminated dairy products and human-to-human transmission via sexual contact or during parturition have been rarely reported.
Q fever is found worldwide. Human cases of Q fever have been reported from across the United States and are most commonly reported in those who are occupationally exposed to livestock. The average annual reported incidence of Q fever in the United States is 0.28 cases per million population per year, with an estimated national seroprevalence of 3.1%. The incidence in the United Kingdom also appears to be low (2 cases per million), whereas the reported incidence in France (500 cases per million) and Australia (38 cases per million) is much higher. Q fever is believed to be underdiagnosed and underreported throughout the world, so the number of reported cases likely does not reflect the true incidence of disease.
The largest outbreak of Q fever ever reported is ongoing in the Netherlands. From 2007 through 2009, more than 3,500 cases were reported: most in the southern region, although cases have been confirmed throughout the country. Cases have continued throughout 2010.
Travelers who visit rural areas or farms with cattle, sheep, goats, or other livestock may be exposed to Q fever. Transmission is also possible by drinking unpasteurized milk. 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. Recent cases of Q fever in military personnel returning from deployments to Iraq and Afghanistan should alert clinicians to consider this diagnosis among people presenting with compatible symptoms.
Approximately half of infected people are asymptomatic. Symptomatic illness typically occurs within 2–3 weeks after exposure. Variable incubation periods may be dose-dependent, with shorter incubation periods after exposure to high organism numbers. The most common presentation is a mild and self-limiting influenzalike illness. Other potential manifestations include pneumonia, hepatitis, myocarditis, encephalitis, osteomyelitis, and miscarriage in pregnant women. Chronic Q fever is uncommon (<1% of acutely infected patients). Most chronic cases (60%–70%) present as culture-negative endocarditis in patients with a preexistent valvulopathy. Pregnant women and immunosuppressed people are also considered at high risk for developing chronic Q fever.
Serologic evidence of a 4-fold rise in phase II IgG by indirect immunofluorescent assay (IFA) between paired sera taken 2–4 weeks apart is the gold standard for diagnosis of acute infection. A single high serum phase II IgG titer (higher than 1:128) by IFA may be considered evidence of probable infection.
C. burnetii may be detected in infected tissues by using immunohistochemical staining, DNA detection methods, or by direct isolation of the agent via culture. PCR assays may be used on whole blood samples in the early stages of illness and before initiation of antibiotic therapy.
Chronic Q fever may occur months or years after an acute infection and is typically diagnosed based on the presence of a rising phase I IgG titer (typically 1:800 or higher) that is most often higher than phase II IgG and an identifiable nidus of infection (such as endocarditis, vascular infection, osteomyelitis, chronic hepatitis). Treatment for chronic Q fever should not be given on the basis of elevated serologic titers alone without clinical manifestation of persistent infection.
Doxycycline is the treatment of choice for acute Q fever. Pregnant women, children aged <8 years with mild illness, and patients allergic to doxycycline may be treated with other antibiotics. Treatment should not be delayed while awaiting laboratory results, and consultation with an infectious diseases physician is recommended. Treatment for acute Q fever is not recommended for asymptomatic people or for those whose symptoms have resolved. Chronic Q fever endocarditis is more difficult to treat effectively and typically requires long-term combination therapy.
Prophylactic treatment for chronic Q fever endocarditis should be considered on the basis of a rising phase I IgG titer (typically 1:800 or higher) that is most often higher than phase II IgG and preexisting valvular heart disease (such as a history of a valvular graft, prosthetic heart valve, or congenital heart defect). Additional information can be found on the CDC website at emergency.cdc.gov/agent/qfever.
PREVENTIVE MEASURES FOR TRAVELERS
A human vaccine for Q fever has been developed and used successfully in Australia. No vaccine is commercially available in the United States. No drugs for preventing infection are available, and doxycycline is not recommended as prophylaxis after a known Q fever exposure, because it will not prevent infection. Preventive measures are aimed at restricting access to areas where potentially infected animals are kept and at properly disposing birth products from livestock. People at highest risk for developing chronic Q fever (pregnant women, people with preexisting valvulopathy, and immunosuppressed people) should be educated on the risks and sources of infection. Travelers should also avoid consumption of unpasteurized dairy products.
- Anderson AD, Kruszon-Moran D, Loftis AD, McQuillan G, Nicholson WL, Priestley RA, et al. Seroprevalence of Q fever in the United States, 2003–2004. Am J Trop Med Hyg. 2009 Oct;81(4):691–4.
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- Gleeson TD, Decker CF, Johnson MD, Hartzell JD, Mascola JR. Q fever in US military returning from Iraq. Am J Med. 2007 Sep;120(9):e11–2.
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- McQuiston JH, Childs JE, Thompson HA. Q fever. J Am Vet Med Assoc. 2002 Sep 15;221(6):796–9.
- McQuiston JH, Holman RC, McCall CL, Childs JE, Swerdlow DL, Thompson HA. National surveillance and the epidemiology of human Q fever in the United States, 1978–2004. Am J Trop Med Hyg. 2006 Jul;75(1):36–40.
- Schimmer B, Morroy G, Dijkstra F, Schneeberger PM, Weers-Pothoff G, Timen A, et al. Large ongoing Q fever outbreak in the south of The Netherlands, 2008. Euro Surveill. 2008 Jul 31;13(31).
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