Q fever is a zoonotic infection caused by Coxiella burnetii — an obligate intracellular bacterium that is one of the most infectious organisms known (as few as one organism can cause disease). The primary reservoir is sheep, goats and cattle — which shed massive numbers of organisms in placental material, urine, feces and milk during parturition. Humans are infected predominantly by inhaling contaminated aerosols. Q fever presents as a febrile illness, pneumonia or hepatitis acutely, and — in a small percentage of patients — chronic infection (most commonly Q fever endocarditis).

How is Q fever transmitted?

Primary route: inhalation of contaminated dust/aerosols — when infected sheep, goat or cattle give birth, aerosols containing C. burnetii spread considerable distances downwind (documented outbreaks from kilometres away from infected farms). Secondary routes: ingestion of contaminated raw milk; tick bites (ticks are the amplifying vector in nature, not important for human disease). C. burnetii is extremely environmentally resistant — survives drying and sunlight for weeks to months in soil and dust.

What are the symptoms of Q fever?

Acute Q fever: approximately 50-60% are asymptomatic or have mild illness. Symptomatic: sudden high fever, severe headache, myalgia, fatigue — lasting 2-3 weeks. Three main clinical presentations: self-limiting febrile illness (most common); pneumonia (approximately 35% of symptomatic cases — typically mild, atypical pneumonia); hepatitis (approximately 40% — typically anicteric, abnormal liver enzymes). Chronic Q fever: Q fever endocarditis (most common — approximately 60-70% of chronic cases) — subacute onset months to years after acute infection, in patients with pre-existing heart valve disease. Other chronic: vascular infection, osteomyelitis, chronic hepatitis.

Why is Q fever so underdiagnosed?

Q fever is called "the forgotten fever" because: it mimics many common conditions (influenza, community-acquired pneumonia, hepatitis, viral syndrome); the diagnosis requires specific serology (Phase I/II IgG by IFA) not performed in routine clinical workup; blood cultures are always negative (C. burnetii is an obligate intracellular organism); most clinicians do not consider it in the differential unless there is a clear animal exposure history; and many cases are self-limiting (the patient recovers before testing). The result: most Q fever cases in the world go undiagnosed.

What is Q fever endocarditis and how is it managed?

Q fever endocarditis occurs in approximately 1% of acute Q fever cases — but in patients with pre-existing valvular disease, vascular grafts or immunosuppression, the risk is dramatically higher. It presents subacutely (months to years after exposure) with fever, weight loss, hepatosplenomegaly and embolic phenomena. It is the most common cause of blood culture-negative endocarditis in endemic areas. Diagnosis: Phase I IgG titre ≥1:800 is the hallmark. Echocardiography typically shows vegetations. Treatment: doxycycline (100mg BD) + hydroxychloroquine (200mg TDS) for minimum 18 months — with Phase I IgG monitoring. Surgery may be required for valve destruction.

Is Q fever present in Georgia?

The South Caucasus — including Georgia — has a substantial livestock (sheep, goat, cattle) farming sector, making Q fever a plausible occupational risk for farmers, veterinarians and rural communities. C. burnetii seroprevalence studies in animals and humans in the region suggest circulation. Q fever should be considered in any occupationally exposed patient with prolonged fever, atypical pneumonia or hepatitis of uncertain cause, and in all blood culture-negative endocarditis cases. PHIG monitors zoonotic diseases including Q fever.

How does GMJ News cover Q fever?

GMJ News covers WHO Q fever data, the Netherlands 2007-2010 mega-outbreak, Q fever endocarditis diagnosis and treatment, occupational exposure prevention, reproductive complications, and the South Caucasus relevance. Q fever exemplifies One Health — human disease driven by animal reservoir management — directly relevant to PHIG's zoonotic disease programme.

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Q Fever

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Q fever — caused by the obligate intracellular bacterium Coxiella burnetii — is a zoonosis transmitted primarily through inhalation of dust or aerosols contaminated by infected sheep, goats and cattle (particularly from parturition products) that causes an estimated 200,000 cases per year globally — massively underreported because it mimics influenza, pneumonia, hepatitis and other conditions (WHO). The most serious manifestation — Q fever endocarditis (chronic Q fever in patients with pre-existing valvular disease) — is a life-threatening infection requiring 18+ months of doxycycline + hydroxychloroquine and causes up to 60-70% of chronic Q fever mortality if missed. The 2007-2010 Netherlands outbreak (approximately 4,000 human cases from dairy goat farms) was the largest Q fever outbreak ever recorded.

Key messages

200,000+ cases/year — massively underdiagnosed

Q fever affects an estimated 200,000+ people per year globally — but is profoundly underdiagnosed because it mimics many other febrile illnesses (pneumonia, hepatitis, influenza) and laboratory confirmation requires specialist tests unavailable in most clinical settings (WHO).

Inhaling dust from infected livestock

Coxiella burnetii is transmitted primarily by inhalation of contaminated aerosols from parturition products (placenta, amniotic fluid), feces, urine, or milk of infected sheep, goats and cattle. A single inhaled organism can cause infection.

Q fever endocarditis — the deadly chronic form

Q fever endocarditis — occurring in patients with pre-existing valvular heart disease or vascular grafts — is a life-threatening chronic infection that may manifest months to years after the acute illness. It carries high mortality if missed and requires ≥18 months of doxycycline + hydroxychloroquine.

Doxycycline is first-line for acute disease

Doxycycline (100mg twice daily for 14+ days) is the first-line treatment for acute Q fever. Early treatment reduces illness duration and may prevent chronic Q fever.

Occupational disease of the farming community

Q fever predominantly affects farmers, shepherds, veterinarians, abattoir workers and laboratory personnel handling infected animal products. Seasonal peaks coincide with animal lambing/kidding seasons when infected placental material is most abundant.

Netherlands 2007-2010 mega-outbreak

The Netherlands experienced the largest Q fever outbreak ever recorded (2007-2010): approximately 4,000 human cases and 25 deaths from intensive dairy goat farms. The outbreak forced massive culling of pregnant goats and vaccination of all dairy goats in affected areas.

Key statistics

~200K+

estimated Q fever cases/year globally (massively underreported)

WHO

~4K

cases in Netherlands 2007-2010 outbreak

ECDC/WHO

60-70%

of chronic Q fever cases are Q fever endocarditis

WHO/ESCMID

18+ months

doxycycline + hydroxychloroquine treatment duration for endocarditis

WHO/ESCMID

1 organism

sufficient to cause human infection (extreme infectivity)

WHO

Category B

CDC bioterrorism classification (aerosolisable)

CDC

Q fever clinical spectrum — approximate frequency of manifestations

Source: WHO/ESCMID. Most infections are self-limiting; chronic Q fever endocarditis is rare but lethal if missed.

Glossary of key terms

Coxiella burnetii
WHOAn obligate intracellular Gram-negative bacterium (now reclassified to Gammaproteobacteria after molecular analysis). Produces two antigenic phases: Phase II (virulent — shed by animal sources); Phase I (avirulent — found in chronic human infection). Highly resistant to desiccation and environmental degradation.

Phase I vs Phase II antibodies
WHO/ESCMIDThe Phase I/Phase II IgG serology is central to distinguishing acute from chronic Q fever: Acute Q fever: Phase I IgG <1:800 (typically Phase II dominant). Chronic Q fever (endocarditis): Phase I IgG ≥1:800 (a diagnostic criterion). A Phase I IgG titre ≥1:800 warrants investigation for chronic Q fever in any patient with fever, valvular disease or a vascular prosthesis.

Q fever endocarditis
WHO/ESCMIDChronic C. burnetii infection of heart valves — occurring in patients with pre-existing valvular abnormalities, vascular prostheses or immunosuppression. Subacute presentation: prolonged fever, weight loss, night sweats, clubbing, hypergammaglobulinaemia. Culturally negative endocarditis — Q fever serology essential in all blood culture-negative endocarditis. Treated with doxycycline + hydroxychloroquine ≥18 months.

Doxycycline + hydroxychloroquine
ESCMID/WHOThe combination for Q fever endocarditis: hydroxychloroquine alkalinises the phagolysosome (where C. burnetii resides), potentiating doxycycline's bactericidal activity. Required for ≥18 months (Phase I IgG <1:200 as treatment endpoint). Doxycycline monotherapy is inadequate for endocarditis — higher relapse rate.

Blood culture-negative endocarditis (BCNE)
ESC/ESCMIDEndocarditis where conventional blood cultures are negative — accounting for approximately 5-10% of endocarditis. Major causes: prior antibiotics; intracellular organisms (Coxiella burnetii — Q fever; Bartonella; Tropheryma whipplei). Q fever serology and 16S rRNA PCR on valve material should be part of all BCNE investigations.

Reproductive consequences in women
WHOQ fever in pregnant women can cause miscarriage (approximately 25%), intrauterine growth restriction, preterm birth and placentitis. Pregnant women exposed to infected animals are at higher risk of obstetric complications. Doxycycline is contraindicated in pregnancy; TMP-SMX is used instead.