Q fever is a disease caused by certain bacteria (Coxiellen). These bacteria are very resistant, their spores can survive in the environment for up to two years.

Q fever is distributed worldwide with the exception of New Zealand and Antarctica

Sheep, goats, cattle, wild mammals, ticks

In natural herds, C. burnetii circulates between wild mammals, birds and ticks. Coxiellen can be transmitted from animals to humans by direct contact or via the respiratory tract by inhalation of dust or droplets containing Coxiella.

2 to 3 weeks in humans

Infected animals are usually not or only severely recognizably diseased. In sheep, goats and cattle, infection causes abortions and the newborn lambs are often weak and barely viable. In humans, the disease can vary greatly in severity and duration. In the majority of infected people, the infection runs its course without any signs of illness. When ill, Q fever usually progresses with the appearance of pneumonia, accompanied by severe headache and muscle pain.

Drug treatment of Q fever is done with certain antibiotics, if necessary.

The control of Q fever in livestock focuses on preventive measures

In Austria, the occurrence of Q fever in animals is not notifiable.

Q fever was first described in Queensland, Australia in 1935. The causative agent of Q fever is a pleomorphic (rod-shaped, coccoid to lanceolate), 0.2-1 µm long, Gram-negative bacterium called Coxiella burnetii. Previously, C. burnetii was classified in the Rickettsiaceae family; however, molecular biological analyses showed that Coxiella is closely related to Legionella (Runge & Ganter 2008). The bacterium is highly resistant to chemical (e.g. formaldehyde) and physical influences (UV radiation, elevated temperature, desiccation). The ability to form permanent forms in the form of spores and the high resistance to desiccation allow it to survive outside organisms in dust, on hay, wool, etc. for years. The survival time of C. burnetii (Runge & Ganter 2008) is:

• in dust and wool at 20 °C storage 7-9 months, at 4 °C 1-2 years.
• in butter and soft cheese at 20 °C 42 days
• in meat at 4 °C one month
• in raw milk at 4-6 °C 90-273 days
• in dry milk at room temperature 40 months, at -20 °C 2 years, at +70 °C 15 sec., in 70 % ethanol 30 minutes

Coxiellia occur in two forms: the larger vegetative form [L(arge C(ell) V(ariant: in phagolysosomes] and the smaller, very resistant spore-like form[S(mall)CV and Spore-like SCV: in the environment]. The latter develops at the pole ends of the large form. The smaller spore-like forms are primarily responsible for the high tenacity (up to 2 years) of these bacteria. Both forms can reproduce by bipartition. Q fever is a worldwide zoonosis with the exception of New Zealand and Antarctica. The greatest infestation is found in warm, dry and tick-rich regions of Europe. However, Q fever also occurs in tick-free regions of the Alps.

C. burnetii has a broad host spectrum - infection has predominantly been diagnosed in sheep (seroprevalence Ö in 2005: 0.4-9.9 %), goats (seroprevalence Ö in 2005 5.6-34.7 %), cattle and wild ruminants (= main hosts): mostly inapparent, latent colonisation of genitalia and udder, occurrence of population-wise clustered abortions, retentio, metritis. In addition, cats, dogs, rabbits and birds may also be reservoir hosts. Equidae and pigs are rarely affected. Studies in Germany showed an increasing seroprevalence of Q fever infections in cattle herds. In Japan and the USA, a positive seroprevalence in cattle herds has also been confirmed.

Transmission

In natural herds, C. burnetii circulates between wild mammals, birds, and ticks. Ticks are reservoirs and an important vector, but not the main source of infection for livestock. Infected afterbirths following abortions in sheep and goats are considered the main source. Up to 40 tick species have been identified as vectors for Coxiella. Ticks remain infected for life and can also pass on the pathogen to their offspring. In Germany, mainly the sheep tick(Dermacentor marginatus) plays a role by transmission between domestic and wild animals, but it is not a direct source of infection for humans. C. burnetii has also been isolated from lice, flies and, in addition to ticks, from other mites. Two independent infection cycles can be distinguished: the first is a natural infection involving ticks and wild animals, in which infections of domestic animals can occur. This infection cycle is linked to the presence of certain tick species. A cycle develops between the larvae and nymphs of Dermacentor spp. and rodents, affecting larger hosts (e.g. deer, foxes, sheep, goats and cattle) twice a year in Germany (March-April and August-September) when adult ticks occur. Spring and summer-autumn are known as seasonal risk periods in Germany because of host transitions of adult ticks. The second cycle is an arthropod-independent domestic cycle. The chain of infection among warm-blooded animals is maintained in this cycle without an intermediate host. Transmission occurs through abortive material, excreta, and feces; respiratory transmission through dust and droplet aerosols is also possible. In domestic animals, coxial spread can occur either passively via tick feces in the fleece (dark discoloration in deeper fleece) or actively through infection. Infected animals may excrete the pathogen via secretions and excretions (vaginal secretions, urine, feces, saliva). In the animal body, spread occurs via the bloodstream. C. burnetii multiplies in the phagolysosomes of monocytes and macrophages. In cattle, coxiellemia originating from the primary pulmonary focus leads to pathogen colonization in the organs, which is usually only temporary. Coxiellia also reaches the uterus and mammary gland via the bloodstream, where it may persist for months without the infected animal showing symptoms. During gravidity, the infection is reactivated, and the uterus and mammary glands in particular can harbor the pathogen for years. Significant amounts of pathogen are produced and excreted in both organs. Coxiellen are also excreted intermittently with milk. Birth products (e.g. afterbirth, amniotic fluid, lochia) and the newborns contaminated with them are particularly highly infectious. Dried-up fruit skins left on pasture can lead to contamination of the area for months.

Transmission to humans

Q fever can be transmitted from animals to humans by direct contact or via the respiratory tract by inhalation of dust or droplets containing Coxiella (= aerogenic transmission). A classical route of infection for animals but also for humans is transmission through tick faeces, e.g. in sheep wool of infected or uninfected animals. Contaminated clothing also plays a role in indirect transmission. Occupational groups that come into contact with infected animals, such as farmers, veterinary staff, slaughterhouse staff, sheep herders, shearers, but also visitors to farms are at risk. Visitors to farms should therefore be prohibited from entering premises with infected animals in order to minimise the risk of inhaling infected dust. Dust containing C. burnetiican be carried by wind and can endanger people at a distance of several kilometres. Coxiella burnetii has not only been found in herds affected by Q fever, but has also been detected in raw milk and raw milk products (e.g. soft cheese, butter) and in the muscle meat and organs of infected animals. The risk for humans of contracting the disease through a food-borne infection has been documented in individual cases; however, transmission through food plays a rather minor role in the infection process. For precautionary reasons, raw milk from infected herds should always be subjected to heat treatment; raw milk and raw milk products from C. burnettii-positive herds must not be sold to consumers. Pasteurisation reliably destroys the pathogens.

Symptoms

The infected animals are usually only subclinically diseased. In sheep, goats and cattle, infection triggers abortions or the newborn lambs are often weak and barely viable; in cattle in particular, coxials are also the cause of fertility problems.

In the majority of infected individuals, the infection runs its course without any signs of illness. The disease - only about one third of infected persons become visibly ill - begins about 2-3 weeks after infection with chills, headache and feeling of illness. The severity and duration of the disease can vary greatly. In most cases, Q fever progresses with the appearance of pneumonia, accompanied by severe headache and muscle pain. The prognosis is good. Only about 5 percent of those with the disease require hospitalization. However, in isolated cases in which the acute infection was not recognized, chronic disease progression occurs, primarily heart valve inflammation. The medical treatment of Q fever is carried out, if necessary, with certain antibiotics. Pregnant women should be treated with antibiotics until delivery if exposure is confirmed; chronic courses (heart valve inflammations) require even longer-lasting antibiotic therapies (3 years). The mortality rate for Q fever is less than 1% of cases.

Control

The medical control measures recommended by the EU are: antibiotic therapy and vaccination of susceptible animals before the next pregnancy. A French vaccine is available in the veterinary sector. A French combination vaccine against Chlamydia and Coxiellen is available. After vaccination in cattle, there were significant improvements in the incidence of fertility disorders, udder health and pneumonia. Indication in sheep: vaccination to reduce abortions before the next mating season, vaccination of sheep in Q fever epidemic areas. This does not eliminate the pathogen, but significantly reduces the amount shed via infected animals.

Control of Q fever in livestock also focuses on preventive measures. A prerequisite for Q fever prevention and control measures is the timely identification of infections in livestock. Some important recommendations for identifying Q fever outbreaks are to look for the possible sources of infection (sheep, goats, cattle, fallow deer), the presence of lambing/calving, examination for tick infestation (tick faeces in the fleece - dark discolouration in the deeper fleece, skin is inflammatory changed or (tick faeces in the fleece - dark discolouration in the deeper fleece, skin is inflamed or encrusted at the bite sites of the ticks, particles similar to carbon dust are present in the densely covered region between the head ("skull"), neck and withers) and serological and molecular biological examinations to clarify the course of infection (rise in titer); immunohistochemical procedures and microbiological examinations (samples: afterbirths, genital swabs).

Measures to reduce pathogen spread in passive vector function:

• Tick faeces in fleece: disinfection with suitable equipment - in this case it is recommended to involve the sheep association and acaricide treatment before the next tick infestation season.
• Indoor shearing - respiratory protection, hygiene, disposal of contaminated wool by burning.
• Measures to reduce the spread of pathogens when the vector is active
• Control of new arrivals
• Bringing pregnant animals into the barn for lambing or calving: lambing or calving should take place in closed barns at a sufficient distance from residential areas.
• Tetracycline use in high-bearing ewes reduces the abortion rate, but does not eliminate the pathogen from the flock.
• Elimination of afterbirths: contamination of the environment with birth products from infected animals should be minimised to prevent airborne transmission of the pathogen. Afterbirths and stillbirths should be collected in closed, liquid-impermeable containers and disposed of properly. The containers must be properly disinfected afterwards.
• Infected dams and newborn lambs must not be removed from the pens until at least 14 days after birth.
• Professional disinfection of the sheds and equipment affected by the infection: 10-20 % chlorinated lime solution, 1 % lysol solution or 5 % hydrogen peroxide solution. Regular cleaning of the stables should not be carried out with high-pressure jets or steam jets in the first phase, as this promotes the spread of pathogens through aerosols.
• Soiled bedding as well as sheep manure from infected sheds must be piled up in windrows covered with plastic film and stored for 2 years until it can be applied to agricultural land and ploughed under. Transporting animal manure from infected barns is not advisable on windy days due to dust formation
• Persons who are present in stables with infected animals for shearing or other activities should observe the usual hygiene rules (e.g. washing hands several times, wearing protective gloves and their own work clothes) and wear protective masks. Exposure to infectious dust from sheepskin (tick faeces) can be minimised by shearing followed by treatment against ectoparasites
• Controlled acaricide treatment in: a) herds suspected of being infected prior to the next tick infestation season, b) herds in known dermacentor biotopes annually at the beginning of a dermacentor infestation season. Procedure with pyrethroids, combing procedure with organophosphates, injection procedure with macrocyclic lactones. Complete elimination of the causative agent of Q fever in natural herds is not possible because ticks and wildlife are the reservoir of the pathogen. However, by controlling ticks in the affected flocks every year at the beginning of the tick season (February), the spread of the pathogen can be significantly reduced.
• Flocks of sheep and goats should not be moved closer than 500 m to residential areas.
• Preventing public access to sites of increased risk
• Dogs and cats should stay away from pens with infected animals

The diagnosis is generally made by a blood test (detection of specific antibodies).