Public health priority:
Case management: Q fever cases can be treated with appropriate antibiotics. All notifications should be followed up to ascertain the most likely source of infection, and to determine if there are any other linked cases.
Management of co-exposed persons: Whilst person-to-person transmission is rare, there may be individuals who have been exposed to a common source (co-exposed). Identify co-exposed individuals (e.g. those at the same workplace), and advise them of the early signs and symptoms of Q fever to aid early diagnosis and treatment. In responses to Q fever linked to workplace/occupational settings, [SafeWork NSW] should be involved, as [should] [NSW Department of Primary Industries] (if relevant); workers should be assessed for immunity. Non-immune workers should not perform work that exposes them to Q fever risks until at least 15 days after vaccination against Q fever.
The infectious agent is Coxiella burnetii, an obligate intracellular Gram negative coccobacillus. It is a highly infective and efficient pathogen, with an extremely long biological half-life.1 The disease was first described as Q (for query) fever in 1937 by Edward Derrick in Queensland,2 with the organism subsequently identified through culture almost simultaneously by Cox3 in the US and Burnet4 in Australia. The organism has since been found around the world (with the exception of Antarctica and possibly New Zealand).5
Cattle, sheep, and goats are the primary reservoirs for C. burnetii,6,7 but a wide range of domestic8,9 and wild animals can be infected,10 including camels, llamas, alpacas, rodents, cats, dogs, horses, rabbits, pigs, buffalo, foxes, some birds, bandicoots, and kangaroos. Ticks are an important vector in the transmission cycle in reservoir species.11
Clinical signs in animals include abortion, stillbirth, retention of fetal membranes, endometritis, infertility, and pneumonia. Cattle are usually asymptomatic. Most wildlife species do not exhibit clinical signs of infection.12 Shedding of high numbers of organisms from infected animals occurs particularly with birth products (e.g. placental tissue and birth fluids).12 C. burnetii also can be shed in the urine, faeces, and milk of infected animals. Animals may eat the placenta after giving birth, and C. burnetii can survive digestion and pass through an animal’s intestine, leading to the organism being discharged with the faeces. With transport of manure this can lead to the organism being spread widely in the environment.13,14
C. burnetii not only exists in a variety of domestic and wild animal species, but also in the general environment (e.g. dust and soil).15 It is resistant to a variety of harsh environmental conditions, including elevated temperatures, desiccation, osmotic shock, UV light, and chemical disinfectants.16 It can survive as an infectious agent on wool at 15–20oC for 9 months and on fresh meat in cold storage for more than a month.
Considering the major transmission routes of C. burnetii to humans, Q fever is not only thought to be a disease of occupational hazard (e.g. for farmers/abattoir workers), but also an environmental disease.27
C. burnetii has been listed as a Category B bioterrorism agent by the US Centers for Disease Control and Prevention,12,28 due to its ease of production, survival in desiccation, and transmission through inhalation.
Typically, the incubation period is 2–3 weeks, depending on the size of the infecting dose (range 4 days to 6 weeks).7
Person-to-person spread rarely occurs. Immunity following recovery from clinical illness may be life-long,12 with cell-mediated immunity lasting longer than humoral immunity. Antibodies are detectable for three to five years, but may persist for as long as 15 years.
Following infection with C. burnetii, the majority of cases (60%) will be asymptomatic/subclinical infections.19 Q fever may be present as an acute or chronic illness.
A person with acute Q fever can present with a variety of symptoms. The most common manifestation is an influenza-like illness which might occur in conjunction with hepatitis and/or pneumonia.5 Commonly reported signs and symptoms include fever, chills, sweats, severe headache (especially behind the eyes), photophobia, weakness, anorexia, nausea, myalgia, cough, and weight loss. Patients can present with mild hepatitis associated with C. burnetii infection, which is more frequently acquired in sheep and goat-breeding areas.6
Pneumonia is an important manifestation of acute Q fever, ranging from mild to severe. Q fever pneumonia can, however, appear similar to other aetiologies of atypical pneumonia, such as those associated with Legionella or Mycoplasma, requiring consideration of differential diagnoses. Pneumonia is less common in Australian than European cases, and upper respiratory tract involvement and tracheobronchitis seen with influenza are not typical features of Q fever.
A minority of infected cases (≤1%) may develop pericarditis, myocarditis,29 or neurologic complications (e.g. meningoencephalitis, encephalomyelitis).5 Infection in pregnant women (symptomatic or not) can lead to abortion, premature delivery, or low birth weight.30 The case fatality rate for untreated acute cases is usually less than 1%.12
Chronic Q fever can occur from one month to several years after acute illness, and sometimes without a history of acute illness, as a result of persistence of C. burnetii infection in the host after a primary infection.
Chronic Q fever may present as one of three major forms according to the focus of infection:
Q fever fatigue syndrome (QFS) refers to systemic symptoms that fail to recover more than 12 months after the acute illness. Typical features of QFS include profound fatigue, arthralgia, myalgia, concentration and memory problems, sleeping problems, sweats, and headaches.33 QFS is the most common sequela following acute infection in Australia, occurring in approximately 10–15% of patients with acute Q fever.19
At-risk occupational groups (including contractors within the industries) are those with contact of high-risk animals or animal products,19 including:
Other people at risk of Q fever through non-occupational, environmental exposures include:
Persons at increased risk for chronic Q fever after experiencing an acute infection include:29, 31
Q fever is a zoonotic disease that occurs around the world. The true incidence of disease is greater than that reported because of subclinical infection, as well as limited clinical suspicion and testing.
In Australia, there were around 500–800 notifications (2.5–5.0 per 100,000 population) annually in the 1990s.37 During 2001–2006, an Australian Government funded National Q Fever Management Program was implemented in Australia, which provided subsidised vaccination to at-risk groups, initially to abattoir workers, contractors working in abattoirs, and sheep shearers; and subsequently to sheep, dairy, and beef cattle farmers, and their employees and family members working on farms.38 The program was concluded in late 2006. This program led to a substantial decrease in national Q fever notifications over the period and beyond, from 792 cases (4.0 per 100,000 population) in 2002 to a nadir of 314 cases (1.4 per 100,000 population) in 2009. However, since cessation of the program there has been a gradual increase in annual Q fever notifications after 2010, reaching 551 cases (2.3 per 100,000 population) in 2016.37 Q fever notification rates are relatively high in Australia compared with European countries (0.18 per 100,000 population in 2014)39 and the US (0.04 per 100,000 population per year).40
The majority of Australian Q fever notifications have been reported from Queensland and New South Wales, which accounted for 48% and 39% of total national notifications, respectively, during 2011–2015.37 The notification rate remains highest in south west/central west Queensland and northwest New South Wales,38 generally reflecting the intensity of local cattle, sheep, and goat husbandry, and associated processing industries.
Q fever outbreaks have been reported occasionally in Australia, generally related to occupational and/or environmental exposures (Table 1).The largest reported Q fever outbreak in the world occurred in the Netherlands from 2007 to 2010, involving over 4,000 cases (including 28 deaths reported).41, 42 The outbreak was linked to dairy goat farms situated in and around densely populated areas. In the context of this large outbreak, the Q fever notification rate peaked at 9.8 per 100,000 population per year in the Netherlands in 2009.43
Abattoir in Victoria44
Q fever vaccine (Q-VAX®) has been available in Australia since 1989, with efficacy estimated at 83-100%.19 The vaccine is recommended for those at risk of infection with C. burnetii.
Immunisation of those in high risk occupational groups is the most effective preventive measure against Q fever. This includes everyone whose work exposes them to cattle, sheep, goats, kangaroos, camels, and other high risk animals and animal products (including products of conception). See Section 1 (Persons at increased risk of disease) for details of the at-risk occupations. In addition, people who are at risk of Q fever through non-occupational, environmental exposures (see Section 1) are also recommended for vaccination.
Work health and safety legislation places duties on employers to ensure the health and safety of their workers, so far as is reasonably practicable. Ideally, vaccination should occur at least 15 days before the person starts working in an at-risk environment. People who visit high risk workplaces (even occasionally), such as tradespeople, labour hire workers, or occupational health staff, should also be vaccinated.
Pre-vaccination testing is imperative as a hypersensitivity reaction to the vaccine can result from previous (possibly unrecognised) exposure to the organism. A stringent pre-vaccination protocol must be followed, which includes skin testing for cellular immunity, serological testing for humoral immunity, and a detailed history looking for previous laboratory-confirmed Q fever disease and previous vaccination. Persons who have worked for some time in the livestock or meat industries or another high risk occupational group should be questioned particularly carefully. Pre-vaccination screening tests require expertise in both administration and interpretation. See the online version of the Australian Immunisation Handbook for current, detailed recommendations for pre-vaccination screening and vaccination.54
The lower acceptable age limit for Q fever vaccination is not known; however, it is not currently recommended for use in anyone aged less than 15 years. Q fever vaccination is not recommended during pregnancy. In general, Q fever skin testing and vaccination should be avoided in individuals with impaired immunity – if exposure is unavoidable or highly likely, expert advice on vaccination should be sought for these cohorts.
The Australian Q fever register is owned and funded by the Australian Meat Processor Corporation (AMPC). It was established in 2001 to store information about Q fever vaccination status of people who have agreed to provide information (www.qfever.org). This website has a link to lists of Q fever vaccine service providers and a searchable database of the immune status of individuals who choose to submit their details.
As well as vaccination as a preventive measure, individuals, companies and employers, and government agencies can take steps to reduce the risk of exposure to Q fever through workplace design, safe work practices and town planning.
Engineering and design controls can be used in Q fever high risk areas (e.g. kill floors, offal rooms, slink rooms, yards, and pens) to minimise exposure, for example:
Town planning should consider the potential for windborne spread of Q fever and limit the encroachment of residential dwellings on existing likely sources of Q fever, including abattoirs, tanneries, stockyards, and land that has historically been used for these purposes. Dust contaminated by the organisms can be carried downwind for several kilometres.7 In the Q fever outbreak settings in the Netherlands, the population risk of infection was substantially higher within five kilometres of infected dairy goat farms.57
Within 5 working days of notification, enter cases onto the [NSW Notifiable Conditions Information Management System (NCIMS)]. In an outbreak setting, data should be entered within 3 working days following notification.
No evidence of reinfection has been documented, and full recovery from an acute Q fever infection usually confers life-long immunity. Chronic manifestations of Q fever following a primary infection are not considered as reinfection. As such, there should be no second notification of Q fever from the same person.
Public Health Units work collaboratively with healthcare providers and patients to ascertain Q fever cases, complete the case investigation, identify further cases of similar exposures, and provide information and education on Q fever prevention and control (see 8 for details).
In the context of responding to a Q fever outbreak or cases occurring in workplace settings, the following jurisdictional government agencies should be included for information sharing and joint investigation (see Section 12 for details):
The case definition may have been updated since the publication of this guideline. Please check the case definitions on the Australian Department of Health’s website for the latest version.
Only confirmed cases should be notified.
A confirmed case requires either:
Detection of specific IgM in the absence of recent Q fever vaccination.
A clinically compatible disease.
The most recent Australian national notifiable diseases case definition for Q fever can be found at the Department of Health website.
Please note, the above Q fever case definition does not differentiate between acute and chronic Q fever, and potentially excludes some chronic Q fever cases due to exclusion of serology testing for antibodies to Phase I antigen in the definition.
A series of blood specimens should be requested if acute Q fever infection is suspected and should include:
The steps for laboratory diagnosis are illustrated in Appendix 4. Further detail on tests and interpreting results is provided below, as well as on Public Health Laboratory Network (PHLN) laboratory case definitions website.
Consideration should also be given toward other zoonotic diseases based on risk exposures.
In acute Q fever cases, the organism may be detected in blood up to 2 weeks after illness onset. If the patient presents within this period, unclotted blood or serum should be submitted for PCR (and possible culture – see below). Whilst PCR offers a highly sensitive method for detecting both live and dead C. burnetii, a negative result alone does not exclude a Q fever diagnosis, and serological testing should be completed for all cases.
In chronic Q fever cases, C. burnetii DNA may be detected by PCR in peripheral blood mononuclear cells or in biopsy specimens from focally infected tissue (e.g. heart valves, bone, synovium). The sensitivity of PCR in serum in patients with endocarditis or vascular infection is low to modest, in the order of 23–67%.58
PCR positive with negative serology results confirm acute Q fever, and theoretically convalescent serology is not indicated, however it is useful if serial testing is performed at intervals to screen for chronic infection.
Indirect immunofluorescence assay (IFA) is the reference method, but the complement fixation test (CFT) and enzyme immunoassays (EIA) are also used to support diagnoses. For the diagnosis and follow up of C. burnetii infection, IFA to both phase I and phase II antigens for subclasses IgM, IgG, and IgA is recommended.
It is important to note that single serology tests (EIA, CFT, or IFA) are unable to distinguish between acute, past and chronic infections, and antibody detection is highly dependent on the timing of specimen collection. Two serum/clotted blood samples should, therefore, always be collected if Q fever is suspected — one at presentation, and another 2–3 weeks later, even if the patient has since recovered. Seroconversion usually occurs within 7–15 days after exposure, and ninety per cent (90%) of cases have seroconverted by the third week after exposure.
Significant antibody titres may take 3–4 weeks from illness onset to appear in some cases. In cases not definitively confirmed by other means, a third sample is recommended, which should be collected 3–4 weeks after fever onset.
The interpretation of Q fever serology results can be challenging. There are different patterns of antibody response during the course of acute Q fever and chronic Q fever, specifically in terms of antibody subclasses to Phase I and Phase II antigens.19 For example, in acute Q fever cases, IgM to Phase II antigen tends to rise first, followed by rise of IgG and IgA to Phase II antigen as detected by IFA at various times after the onset of disease.59 In contrast, for chronic Q fever (e.g. endocarditis), IgG, with or without IgA to Phase I antigen, is present at high titre.19,60 A chart and reference tables are provided at Appendix 5 to assist in interpreting serology results. Where required, Public Health Units should seek expert guidance in interpreting these results.
Management of acute Q fever includes the measurement of serial antibody titres over time. This can aid in identifying those at risk of developing chronic Q fever, and allow early interventions. It is preferable that confirmed cases have testing undertaken at a laboratory with such capacity.
Isolation of C. burnetii by culture can only be performed by vaccinated staff in an appropriate physical containment level 3 (PC3) facility.61 For this reason, culture is strongly discouraged except where appropriate facilities and training exist – currently culture is only performed at the Australian Rickettsial Reference Laboratory (ARRL), Geelong, Victoria.
Public Health Unit staff carry out case investigation in collaboration with the case’s treating doctor and the case.
Complete relevant sections of the Q fever Case Investigation Form (Appendix 3) with treating doctor to:
Complete relevant sections of the Q fever Case Investigation Form (Appendix 3) with the case (or carer) to:
Commence empiric treatment if Q fever is clinically suspected. Do not wait for laboratory results. Refer to latest edition of the Therapeutic Guidelines: Antibiotic.
A two week course of oral doxycycline is generally used to treat acute Q fever.
Trimethoprim+sulfamethoxazole is recommended for pregnant women until 32 weeks of gestation, even if recovered, to prevent fetal and maternal complications.34
After treatment of C. burnetii primary infection, it is recommended to screen for risk factors of chronic Q fever infection, including pre-existing valvular heart disease/valvular prosthesis, vascular aneurysms/vascular grafts, and immunosuppression.29 A cardiac assessment, which may include echocardiography, is recommended to assess whether there are underlying abnormalities of the heart valves. Those who are at higher risk of chronic Q fever should be monitored serologically and clinically at 3, 6, 9, 12, 18, and 24 months after acute infection. There is a body of evidence to suggest antibiotic prophylaxis for 12 months in case of cardiac valve problems/valvular prosthesis may be of benefit.29
In chronic disease (e.g. endocarditis), prolonged combination therapy (with addition of hydroxychloroquine) and cardiac surgery may be required. Expert advice from an infectious diseases physician and other specialist physicians should be sought as appropriate.
The case should be advised of the nature of the infection and its mode of transmission, and of appropriate precautions necessary to prevent others from becoming infected from exposure to the same source. The case should also be advised about seeking medical care if symptoms do not resolve following completion of treatment, or new symptoms develop that may indicate a complication or a chronic Q fever infection (Appendix 1: Q fever Factsheet).
Exclusion of infected persons is not required. Q fever is rarely transmissible from person to person.
See Section 12 for active case finding in special situations.
C. burnetii is highly resistant to desiccation and may remain viable in dust for more than a year. It is killed by heat (>63 degrees Celsius for 30 minutes), and some disinfectants including hydrogen peroxide, sodium hypochlorite (at concentrations of greater than 5 per cent), and 2 per cent formaldehyde. A 1:100 dilution of household bleach is also an effective solution.29
Appropriate animal and environmental management plays an important role in reducing transmission of C. burnetii to humans. Lessons and experience drawn from Q fever outbreaks in Victoria13 and the Netherlands,14 which were linked to goat dairy farms, point to effective measures in reducing Q fever risk, including:
In occupational settings and outbreaks, active case finding among identified co-exposed persons should be considered (Section 12). The aim of identifying co-exposed persons is to alert them to the possibility that they could develop disease due to a common source exposure.
A co-exposed person is defined as anyone who may have experienced the same occupational, animal, or environmental exposures as the case, or who may have been exposed to contaminated items associated with the case (e.g. clothing/boots). Person-to-person transmission is extremely unlikely. Co-exposed persons may include people at the workplace (including those without direct contact with animals or animal products) and home.
Vaccination during the incubation period does not prevent the disease. Post-exposure antibiotic prophylaxis is not recommended.
Q fever information (Appendix 1) should be provided to co-exposed persons with advice to seek medical attention should they develop symptoms. Q fever vaccination should be recommended to all non-immune workers in high-risk occupations.
Those workers/co-exposed persons with the same exposure that do not have immunity to Q fever through natural infection or vaccination should not visit the setting, enter high risk workplaces or perform work that exposes them to Q fever risks without wearing a properly fitted particulate respirator (e.g. disposable P2 respirator).
In addition to the generic case and co-exposed person follow-up requirements described above, further actions are required in the following instances:
Q fever case investigation may identify a plausible link with a workplace (such as an abattoir or dairy farm). Two cases or more within a three-month period in an at-risk workplace is considered a workplace outbreak.
Responses to cases occurring in workplace settings (including outbreaks) need to be carried out in collaboration between the Public Health Unit, [SafeWork NSW], and the [NSW Department of Primary Industries] if relevant. Unvaccinated Public Health Unit staff are not to be exposed to Q fever risks as part of the disease investigation and response.
Immediate responses include working with the employer and management to:
The role of [SafeWork NSW] is to investigate and identify unsafe working conditions, and to monitor and enforce compliance. This may involve a site visit and discussions with the employer. [SafeWork NSW] may, in consultation with the health department and [NSW Department of Primary Industries], provide information and advice to the employer.
The term ‘cluster’ is taken to mean the occurrence of more cases than expected in the community, where sources of infection are not apparent. For example, the year to date number of Q fever notifications from a region is over 2 standard deviations more than the previous five year mean over the same period.
The goal of community cluster detection is to further explore potential sources of infection and risk factors for Q fever in a broader community context, thereby informing public health action to interrupt transmission and prevent further cases.
Elements of the cluster response include:
Links to State and Territory Public Health Legislation, the Biosecurity Act 2015 and the National Health Security Act 2007.