Q fever is an infectious disease caused by the bacterium Coxiella burnetii. This bacterium is very tough and can survive in harsh conditions. Q fever is a zoonosis, which means it spreads naturally from animals to humans. People usually become infected by inhaling tiny contaminated particles in the air, especially around farm animals such as sheep, goats, and cattle. These particles often come from birth products (like placentas), urine, feces, or milk. The bacteria can also contaminate dust, soil, and farm environments, making airborne infection the most common route. Less often, Q fever can spread through drinking unpasteurized milk, and in rare cases, from person to person through blood transfusion or sexual contact.
In humans, Q fever often looks like the flu, with symptoms such as high fever, tiredness, headache, muscle aches, chills, and sweating. Some people may not show any symptoms at all. In more serious cases, the infection can cause pneumonia (a lung infection), hepatitis (liver inflammation), or a long-term illness known as chronic Q fever. Chronic Q fever can lead to endocarditis, a dangerous infection of the heart’s inner lining, especially in people with heart valve problems or weakened immune systems. This form of the disease can last for months or years and needs long-term antibiotic treatment.
Outbreaks most often occur in farming areas or slaughterhouses (abattoirs). People at higher risk include farmers, veterinarians, slaughterhouse workers, and laboratory staff. While wild animals and pets can carry the bacteria, farm livestock are the main source of human infections.
C. burnetii is known for its ability to survive in the environment. It can form a tough, spore-like stage (called a small cell variant) that resists heat, drying, and many common disinfectants. Because of this, the bacteria can spread over long distances in the air and remain in contaminated areas for a long time, making it difficult to eliminate.
Treatment involves antibiotics, typically doxycycline. Prevention focuses on reducing exposure. This includes good farm hygiene, safe handling of animal births, and careful disposal of materials that might carry the bacteria. In some countries, livestock, especially goats and sheep are vaccinated to reduce the spread. A human vaccine is also available in a few regions, mainly for people at high risk, but it requires careful screening before use and is not widely given due to possible side effects. Other protective steps include wearing protective equipment, improving ventilation in animal housing, and avoiding unpasteurized dairy products.
History and Discovery
Q fever was first identified in 1935 by Australian physician Dr. Edward Holbrook Derrick, following an outbreak of an unexplained febrile illness among abattoir (slaughterhouse) workers in Brisbane, Queensland. Because the cause of the disease was initially unknown, Derrick referred to it as “Q fever,” with “Q” standing for “query.”
In 1937, Australian researchers Frank Macfarlane Burnet and Mavis Freeman succeeded in isolating the bacterium responsible, later named Coxiella burnetii in honor of American bacteriologist Herald Rea Cox, who, around the same time in the United States, also worked on identifying the organism. The classification of C. burnetii as an obligate intracellular bacterium helped distinguish Q fever from other febrile illnesses.
During World War II, Q fever gained further attention when cases were reported among Allied troops stationed in the Mediterranean region, particularly in North Africa and southern Italy, where exposure to contaminated livestock and dust was common. The disease was notable for causing high levels of non-combat illness among soldiers, which highlighted its potential impact on military operations.
Over the following decades, Q fever was recognized as a global zoonosis, with cases reported across Europe, Asia, Africa, and the Americas. Large outbreaks have since been documented, including one of the most significant between 2007 and 2010 in the Netherlands, where over 4,000 human cases were officially reported, linked to intensive goat farming. This outbreak prompted the mass culling of infected animals and the implementation of widespread vaccination programs in livestock.
Differentiation From Similar Diseases
Q fever often resembles other infectious diseases that present with fever and flu-like symptoms, which can make diagnosis challenging. It shares overlapping clinical features with illnesses such as influenza, typhoid fever, brucellosis, tuberculosis, malaria, and rickettsial infections like Rocky Mountain spotted fever. Despite these similarities, several distinguishing features help separate Q fever from other conditions.
- Causative agent: Q fever is caused by the bacterium Coxiella burnetii, an obligate intracellular pathogen. By contrast, typhoid fever is caused by Salmonella enterica serovar Typhi, while brucellosis results from Brucella species, and influenza is caused by viruses.
- Transmission: The primary route of Q fever transmission is inhalation of airborne particles contaminated with C. burnetii, usually from animal birth products or farm dust. This contrasts with typhoid fever, which is waterborne and foodborne, spread through ingestion of contaminated water or food. Brucellosis is generally acquired by direct contact with infected animals or unpasteurized dairy, while influenza spreads through respiratory droplets from human-to-human transmission.
- Clinical course: Q fever may present acutely with fever, headache, chills, and fatigue, but it has a distinct potential to develop into a chronic form, most notably endocarditis (infection of the heart lining and valves). Chronic Q fever is especially associated with patients who have pre-existing heart valve disease or weakened immune systems. This complication is not typically seen with influenza or typhoid fever.
- Organ involvement: While influenza primarily affects the respiratory tract and typhoid fever mainly involves the gastrointestinal system, acute Q fever can manifest as atypical pneumonia or hepatitis, giving it a broader clinical spectrum.
Accurate diagnosis through serologic testing is essential to differentiate Q fever from these diseases and to guide appropriate treatment.
Causes and Transmission
Q fever is caused by a specific bacterial pathogen and involves various animal hosts that carry the bacteria. Transmission to humans occurs mainly through environmental exposure and contact with infected animals or materials.
Causative Agent: Coxiella burnetii
The causative organism is Coxiella burnetii, a small, Gram-negative bacterium that survives and multiplies inside host cells, particularly within macrophages (a type of immune cell).
The bacterium exists in two distinct forms: a small cell variant (SCV), which is spore-like, highly resistant to heat, drying, and many disinfectants, and a large cell variant (LCV), which is the metabolically active form inside host cells.
The SCV allows the bacterium to persist in the environment for months or even years in soil, dust, or contaminated surfaces, contributing to its ability to spread widely and cause outbreaks.
Reservoirs and Carriers
The primary reservoirs of C. burnetii are domestic ruminants, particularly cattle, sheep, and goats. Infected animals often show no clinical symptoms, but they can shed large numbers of bacteria in urine, feces, milk, and especially birth products (placenta, amniotic fluid). The concentration of bacteria in birth products is especially high, making animal birthing a major risk factor for human exposure.
Other animals, including cats, dogs, horses, camels, and wild mammals, as well as birds, have been found to carry the bacterium. Ticks can also act as reservoirs and vectors among animals, although they play only a minor role in transmitting the disease to humans.
Modes of Transmission
- Inhalation of aerosols: The most common mode of human infection is through inhalation of airborne particles contaminated with C. burnetii. These aerosols can originate from dust, hay, straw, or bedding contaminated with animal birth products, feces, or urine.
- Direct contact: People working with infected animals or animal products (wool, hides, manure) may become exposed through skin contact or accidental splashes.
- Ingestion: Drinking unpasteurized milk or dairy products from infected animals has been linked to infection, though this route is less significant than airborne transmission.
- Vector transmission: Tick bites can transmit C. burnetii among animals, but human cases from ticks are rare.
- Human-to-human transmission: This is extremely rare but has been documented in cases involving blood transfusion, sexual contact, or exposure during childbirth.
Geographical Distribution
Q fever occurs worldwide, with cases reported on every continent except Antarctica. The disease is particularly prevalent in regions with large populations of domesticated ruminants. Endemic areas include parts of Australia, Europe (notably the Netherlands and Mediterranean countries), Africa, South America, and North America.
Large-scale outbreaks have been documented in agricultural regions, especially when animal density is high and hygiene practices are insufficient during birthing seasons. One of the largest outbreaks occurred in the Netherlands between 2007 and 2010, linked to goat farms, where thousands of human cases were reported.
The ability of C. burnetii to persist in the environment and spread through airborne particles allows the disease to remain entrenched in rural and farming communities.
Symptoms and Clinical Manifestations
Q fever presents with a range of symptoms depending on its phase. It can manifest as a sudden acute illness or develop into a persistent chronic condition. Some long-term complications may also arise, affecting various organs and systems.
Acute Q Fever Symptoms
Acute Q fever typically has a sudden onset, with symptoms appearing after an incubation period of about two to three weeks following exposure to the bacterium Coxiella burnetii. The disease often resembles influenza in its presentation, with hallmark features such as high fever, sometimes exceeding 39 °C (102 °F), severe headache, fatigue, chills, and diffuse muscle aches. Sweating and malaise are also frequent, adding to the generalized viral-like picture.
Respiratory symptoms are also common in acute infection. Many patients develop a dry cough, which may be accompanied by chest discomfort due to atypical pneumonia. Some individuals experience gastrointestinal disturbances, including nausea, vomiting, diarrhea, and abdominal pain. Liver involvement is another recognized feature, with hepatitis presenting as abdominal discomfort, jaundice, or elevated liver enzymes on blood tests. Though rare, neurological complications such as meningitis or encephalitis have been documented and can pose serious risks.
The duration of acute illness is usually limited to one to two weeks, but the severity can vary significantly. Many recover fully without treatment, although some cases require antibiotics for resolution.
A subset of patients may go on to develop post-Q fever fatigue syndrome, characterized by persistent tiredness, headaches, and mood changes that continue long after the acute infection has resolved.
Chronic Q Fever Presentation
Chronic Q fever is a rare but severe form of the disease, affecting approximately 1–5% of infected individuals. Unlike the acute phase, which resolves within weeks, chronic Q fever can emerge months or even years later. It tends to occur in patients with specific risk factors, such as pre-existing heart valve disease, vascular grafts, compromised immunity, or during pregnancy, when physiological changes heighten vulnerability to persistent infection.
The most critical manifestation of chronic Q fever is endocarditis, a long-term infection of the heart valves that can be life-threatening if untreated. Patients often present with prolonged low-grade fever, night sweats, significant fatigue, and unexplained weight loss. As the condition advances, signs of heart failure may appear, including shortness of breath, swelling of the extremities, and reduced exercise tolerance.
Beyond endocarditis, chronic Q fever can also cause vascular infections, such as infected aneurysms or prosthetic graft infections, which carry a high risk of rupture or systemic spread. In some cases, osteomyelitis or septic arthritis develops, leading to persistent joint or bone pain. Chronic hepatitis may also occur, and though rare, it can progress to cirrhosis with long-term liver damage.
Complications and Long-Term Effects
Endocarditis remains the most significant threat, as it can cause destruction of heart valves, congestive heart failure, or even embolic stroke if infected material dislodges into the bloodstream. Similarly, vascular infections pose a grave danger, with infected aneurysms at risk of catastrophic rupture.
In the liver, chronic Q fever may progress to fibrosis or cirrhosis, contributing to long-term morbidity. Pregnant women face particular risks, with Q fever infection linked to miscarriage, stillbirth, premature birth, and low birth weight in infants. Another common complication is post-infective fatigue syndrome, which can severely impact quality of life. Patients affected by this syndrome may experience persistent exhaustion, impaired concentration, memory difficulties, and muscle weakness for months or years after the initial illness has resolved.
Without intervention, what may begin as a seemingly mild or flu-like illness can progress into a chronic, debilitating, and potentially fatal condition.
Diagnosis of Q Fever
Diagnosing Q fever requires a combination of clinical suspicion, laboratory confirmation, and sometimes imaging studies to establish an accurate picture of the disease. Because Q fever presents with general symptoms like fever, headache, fatigue, and muscle pain, it is often mistaken for other febrile illnesses such as influenza, typhoid, or atypical pneumonia. Accurate diagnosis is essential not only for effective treatment but also to prevent complications like chronic Q fever, which can progress to life-threatening conditions such as endocarditis.
Laboratory Testing Methods
Laboratory confirmation is the cornerstone of Q fever diagnosis. Serological testing, particularly the Indirect Immunofluorescence Assay (IFA), is the gold standard. IFA allows clinicians to measure phase-specific antibodies, with phase II IgM and IgG elevations being indicative of acute infection, while persistent high titers of phase I IgG suggest chronic disease.
Enzyme-linked immunosorbent assays (ELISA) offer a faster and easier option but may lack the specificity required to distinguish between different stages of infection. Molecular testing, especially Polymerase Chain Reaction (PCR), is highly valuable in the early stages of illness, as it can detect C. burnetii DNA in blood or tissue before the immune system has generated detectable antibodies.
However, PCR’s reliability diminishes as the infection progresses. Culture of C. burnetii remains possible but is rarely attempted due to the organism’s highly infectious nature and the requirement for biosafety level 3 facilities, making it impractical for routine diagnostics.
Imaging and Differential Diagnosis
Imaging studies play a supporting role in diagnosing Q fever, particularly in detecting complications. Chest radiographs or CT scans can reveal signs of atypical pneumonia in acute cases, while echocardiography is indispensable for evaluating potential endocarditis in chronic Q fever.
Abdominal ultrasound may also be useful when hepatitis or hepatosplenomegaly is suspected. Because Q fever shares clinical similarities with diseases such as influenza, tuberculosis, viral hepatitis, brucellosis, and atypical pneumonias caused by Mycoplasma pneumoniae or Chlamydophila pneumoniae, a differential diagnosis is essential.
Clinicians must integrate patient history such as occupational or environmental exposure with clinical findings, imaging, and laboratory results to avoid misdiagnosis. Travel history and contact with animals or abattoirs are especially important clues that can point toward Q fever rather than more common respiratory or febrile conditions.
Diagnostic Challenges
One of the most significant obstacles in Q fever diagnosis is its nonspecific presentation. The early symptoms overlap with a wide range of viral and bacterial infections, leading to frequent underdiagnosis or misdiagnosis. In addition, antibody responses often take 7–15 days to develop, meaning serology may be negative during the critical early window.
While PCR testing can fill this gap, its sensitivity declines once antibodies are present, creating a narrow timeframe for optimal use. Chronic Q fever presents even greater challenges, as bacterial loads are low and symptoms such as prolonged fatigue, weight loss, or low-grade fever can be subtle and nonspecific.
Persistent high levels of phase I IgG antibodies remain the most reliable marker of chronic infection, but distinguishing between past exposure and ongoing disease requires careful correlation with clinical signs and imaging.
Treatment and Management
Treatment of Q fever depends on the stage and severity of the infection. Antibiotics are the primary approach, and managing chronic cases requires prolonged therapy and careful monitoring.
Antibiotic Therapy
Doxycycline remains the gold standard for acute Q fever. It is usually prescribed at 100 mg twice daily for 14 days, with early initiation crucial in shortening illness duration and preventing complications such as hepatitis or pneumonia. Patients who begin treatment within the first three days of symptom onset experience faster recovery compared to delayed therapy.
For patients unable to tolerate doxycycline, alternatives such as trimethoprim-sulfamethoxazole or fluoroquinolones may be used, though they are generally less effective. In pregnant women, prolonged courses of co-trimoxazole (throughout pregnancy) are often recommended to reduce the risk of maternal complications and prevent transmission to the fetus.
Management of Chronic Q Fever
Chronic Q fever, most frequently presenting as infective endocarditis or vascular infections is notoriously difficult to treat. It requires long-term combination therapy with doxycycline and hydroxychloroquine for 18 to 24 months. Hydroxychloroquine enhances doxycycline’s bactericidal effect by alkalinizing intracellular vacuoles where Coxiella burnetii resides.
Due to the length of therapy, clinicians must balance efficacy with the risk of side effects. Hydroxychloroquine, for example, carries risks of retinal toxicity, making routine ophthalmologic exams mandatory during treatment. In addition, patients with prosthetic heart valves, aneurysms, or vascular grafts are at significantly higher risk of relapse and often require lifelong follow-up.
If endocarditis causes severe valve destruction, heart failure, or persistent infection despite antibiotic therapy, valve replacement surgery may be necessary. Similarly, vascular infections may require surgical repair or graft replacement in addition to antibiotics. Surgery, when combined with medical therapy, significantly improves survival rates in complicated chronic cases.
Monitoring and Follow-Up
Careful monitoring is essential throughout treatment:
- Serological testing (phase I and II IgG/IgM antibody titers) guides the duration of therapy and confirms treatment response.
- Echocardiography is recommended to detect cardiac involvement early and track changes in patients at risk for endocarditis.
- Liver function tests and complete blood counts are routinely monitored to detect antibiotic-related toxicity.
For chronic Q fever, patients are typically evaluated every 3–6 months during treatment and annually after completing therapy. Lifelong monitoring may be necessary for individuals with prosthetic heart valves or vascular implants.
Prevention and Control
Effective prevention and control of Q fever rely on targeted vaccination, public health measures, and individual protective actions. These strategies reduce transmission, especially in high-risk groups and environments.
Vaccination Strategies
Vaccination remains the most effective method for preventing Q fever in high-risk individuals. The Q-Vax vaccine, developed and licensed in Australia, is the only available vaccine for humans and has proven highly effective in reducing the severity and incidence of disease. However, because individuals previously exposed to Coxiella burnetii may experience severe hypersensitivity reactions if vaccinated, pre-vaccination screening using serological tests and intradermal skin testing is mandatory. This process ensures that only those without prior exposure receive the vaccine safely.
In addition to human vaccination, livestock vaccination programs play a vital role in disease control. Vaccinating sheep and goats, particularly in regions where outbreaks are common, reduces bacterial shedding in birth products such as placenta and amniotic fluid—major environmental sources of infection. By lowering environmental contamination, animal vaccination indirectly protects humans living or working nearby. Sustained vaccine coverage, supported by occupational health policies and ongoing education, ensures long-term protection of at-risk communities.
Public Health Interventions
Public health authorities have a central role in minimizing the spread of Q fever through surveillance, outbreak reporting, and rapid containment measures. Active surveillance programs track cases to identify sources of infection, enabling early intervention to prevent further transmission. When outbreaks occur in agricultural or industrial settings, swift responses such as quarantine of affected herds, disinfection of contaminated facilities, and temporary restrictions on animal movement are essential.
Waste management is another critical element of control. Proper disposal of animal birth materials, manure, and bedding prevents Coxiella burnetii from becoming airborne. Regulations governing abattoirs, dairy farms, and livestock markets enforce biosecurity standards that reduce environmental contamination.
Furthermore, public health education campaigns inform both professionals and the general population about transmission risks, encouraging early diagnosis and reporting. By improving awareness, these campaigns enhance compliance with preventive measures and ultimately limit disease spread.
Personal Protection Measures
For individuals in high-risk occupations, personal protection is indispensable. Wearing personal protective equipment (PPE), including masks, gloves, protective eyewear, and coveralls minimizes the likelihood of inhaling contaminated aerosols or contacting infectious materials. Disinfecting footwear and clothing after working with animals further reduces environmental contamination.
Hygiene practices, particularly thorough handwashing with soap and water after handling animals or animal products, significantly lower the risk of infection. Workers should avoid dusty environments during high-risk activities, such as assisting with animal births or slaughter, since these processes often release large amounts of bacteria into the air. Adequate ventilation systems in barns, abattoirs, and laboratories also help reduce the concentration of airborne particles, offering an additional layer of protection.
Beyond occupational settings, individuals living in rural areas can reduce risk by limiting direct contact with birthing animals, avoiding consumption of raw milk, and maintaining cleanliness around livestock enclosures.
Q Fever in Animals
Q fever primarily affects several animal species that serve as reservoirs or sources of infection. The disease spreads mainly through contact with infected animals or contaminated environments, impacting both animal health and agricultural productivity.
Animal Reservoirs
Coxiella burnetii, the bacterium causing Q fever, is most commonly found in domestic ruminants such as sheep, goats, and cattle. These animals often carry the infection without showing symptoms.
Wild animals, including rodents, birds, and ticks, can also harbor the bacterium but play a less significant role in transmission to humans. In livestock, infection tends to cause reproductive problems like abortions and stillbirths.
Infected animals excrete C. burnetii in birth fluids, milk, urine, and feces. These secretions contaminate the environment and increase the risk of passing the infection to other animals or humans.
Zoonotic Transmission
Transmission occurs when animals shed Coxiella burnetii into the environment, especially during birthing processes. Humans primarily become infected through inhalation of aerosolized particles contaminated with the bacteria.
Contact with contaminated wool, manure, or dust around animal facilities is another important route. Direct handling of birth products from infected animals also poses a high risk.
Ticks can transmit the bacteria between wild animals but rarely infect humans directly. Proper hygiene and protective measures are crucial to minimize zoonotic transmission risks on farms and slaughterhouses.
Impact on Livestock Industry
Q fever causes significant economic losses due to reduced fertility, abortions, and decreased milk production in infected herds. These effects impair farm productivity and animal welfare.
Trade restrictions and quarantine measures may be imposed when Q fever outbreaks occur, further affecting commercial activities. The cost of control and prevention programs, including vaccination and hygiene improvements, adds to financial burdens.
In some regions, Q fever also threatens export markets due to concerns over food safety and animal health certifications. Managing infection in livestock is essential to safeguard industry stability.
Q Fever Outbreaks and Epidemiology
Q fever outbreaks have occurred globally, often linked to livestock exposure. A comprehensive review of 81 human Q fever outbreaks across 27 countries (1990–2022) found outbreaks ranged widely in size (2 to 4,107 cases) and duration (4 to 1,722 days).
The largest recorded outbreak occurred in the Netherlands (2007–2010), with approximately 4,000 confirmed cases, and an estimated over 40,000 people infected. This prompted mass culling of goats of over 62,500 animals across 94 farms and led to dozens of deaths, including fatalities from chronic Q fever.
Another notable outbreak happened in Jena-Winzerla, Germany (2005). Close proximity to a sheep meadow sharply influenced infection risk attack rate (AR) was 11.8% within 50 m, dropping to 1.3% at 350–400 m, indicating an 8.7-fold higher risk nearer the source. Men and adults aged 25–64 had higher attack rates.
A meta-analysis in the Eastern Mediterranean region (2000–2021) revealed a human seroprevalence of 25.5% (95% CI: 16.1–34.9%). In animals it stood at 22.4% (95% CI: 19.8–25.1%), with ticks showing 17.5% positivity.
In rural Australian populations, seroprevalence surveys suggest 1 in 20 people (~5%) have been exposed to Coxiella burnetii.
In Australia, Q fever is endemic. In 2024, there were 878 notified Q fever cases, a notable rise compared to prior years. Cases are reported year-round but peak in warmer, drier months, often aligning with birthing seasons and increased farming activity.
In the state of Victoria (Australia), authorities issued an alert after 77 cases in 2024, marking a sharp increase over the past five years. The alert emphasized risks of long-term complications and promoted vaccination for high-risk occupational groups.
A One Health study during the 2009 Netherlands epidemic used atmospheric dispersion modeling to show that Coxiella concentration in air and environmental factors like vegetation density and soil erosion sensitivity were significantly correlated with incidence rates, enabling the creation of hazard maps for spatial planning.
Q fever can present with mild flu-like symptoms but may also cause more severe forms like atypical pneumonia, granulomatous hepatitis, or—even more rarely—retinal vasculitis. Approximately 50% of infections are asymptomatic. Chronic Q fever may mimic endocarditis and can be fatal if untreated, although appropriate therapy can reduce mortality to around 10%. Some survivors go on to experience Q fever fatigue syndrome, a long-term debilitating condition resembling chronic fatigue syndrome.
At-risk groups include pregnant women, those with heart valve abnormalities or immunosuppression, and certain occupations like farmers, veterinarians, abattoir workers, and laboratory personnel. Infection in pregnancy can result in miscarriage, stillbirth, and other adverse outcomes.