Q fever A78.x

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

Balkan fever; Q-fever; Queryfever

History
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The disease was first scientifically described in 1937 by Edward Holbroock Derrick among slaughterhouse workers in Brisbane, Queensland, Australia as a disease of unknown cause, which led to the name Q fever (from "query" for "questionable").

Definition
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Notifiable worldwide, triggered by Coxiella burneti (§ 7 IfSG: reporting by name even in case of direct or indirect evidence with reference to acute infection). zoonosis. Humans become infected in particular via aerogenic inhalation of infected sheep tick faeces. Particularly at risk are e.g. farmers, shepherds and slaughterhouse workers through infected stable animals, hay, wool etc. The infection is asymptomatic in animals.

Pathogen
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The pathogen, Coxiella burneti is a worldwide occurring, gram-negative, obligate intracellular, immobile, pleomorphic rod. Size 0.2-0.4 µm × 0.4-1 µm.

C. burnetii has two antigen phases (phase I and II), which are comparable to the smooth and rough growth form of the lipopolysaccharides of Enterobacteriaceae.

Coxiella burneti can exist in 2 forms:

  • Small cell variants (SCV), spore-like stages with high tenacity. This form is extremely viable and highly infectious.
  • Large cell variants (LCV): SCVs become large cell variants (LCV), intracellular, vegetative stages in the organism.

The host spectrum includes sheep ticks, rodents, wild animals, cattle, sheep, goats, other mammals and birds. Q-fever is a zoonosis that occurs worldwide, except in New Zealand. Q-fever also (rarely) leads to outbreaks in Germany. Here the sheep tick is the main vector for the infection of sheep. In addition to a basal infection cycle between ticks and rodents, an infection cycle exists between ticks and domestic animals such as sheep and cattle.

Transmission to humans occurs in particular through inhalation of dust (excrement of the coloured tick) or through contact with contaminated products such as wool, milk or meat. Ticks can also transmit the pathogen to other animals. A transmission from person to person seems to be extremely rare.

Incubation period: 2-3 weeks

Due to the formation of SCV, there is a high resistance to dehydration, heat, cold, sunlight and many disinfectants. Years of survival in soil or dust are possible. The pathogen can be spread over several kilometres by anaerobic means.

Occurrence/Epidemiology
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The range of hosts includes sheep ticks, rodents, wildlife, cattle, sheep, goats, other mammals and birds. Q-fever is a zoonosis that occurs worldwide - except for New Zealand. Q-fever also (rarely) leads to outbreaks in Germany. Here the sheep tick is the main vector for the infection of sheep. In addition to a basal infection cycle between ticks and rodents, an infection cycle exists between ticks and domestic animals such as sheep and cattle.

Clinical features
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Natural infections are inapparent or subclinical in 50-70 % of cases.

Acute Q-fever: The following triad occurs in severe cases of illness:

  1. Sudden fever with chills and severe illness and arthralgia. Fever may persist for 1-3 weeks.
  2. Headache (retrobulbar)
  3. Atypical pneumonia (in about 50% of cases) with continuous or remitting fever up to 40°C for several weeks. Transaminase increase only slight, rarely gastrointestinal symptoms or jaundice.

Furthermore:

  • exanthema, conjunctivitis, cough, chest pain.
  • Granulomatous hepatitis (30% of cases); often asymptomatic course


In case of infections during pregnancy: miscarriage, premature birth or reduced birth weight possible.

Chronic courses: Endocarditis is the most frequent and dangerous late complication of Q fever.

Laboratory
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No leukocytosis but left shift

CRP ↑ BSG ↑ possibly transaminsaen ↑

Detection of C.burnetii DNA; pathogen isolation

Antibody detection

Diagnosis
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A human Q fever infection is usually diagnosed by serological methods. It should be noted that serological detection of antibodies is only possible 1-2 weeks after clinical manifestation. The most important parameter for the early detection of acute Q-fever diseases are anti-phase 2 IgM antibodies. The following clinical examination materials should be used for diagnosis:

  • blood
  • Serum
  • Bioptates (bone marrow, tissue samples)
  • Sputum
  • Urine

CBC against phase 2 becomes positive at the earliest 2-3 weeks after the onset of symptoms. In contrast, IgM antibodies against phase 2 are usually detectable by ELISA and IIFT in acute Q-fever as early as 7-15 days after the onset of the disease.

In the further course of the acute infection, phase 2 IgG antibodies appear a few days later. The highest phase 2 IgG antibody titers are reached during convalescence about 8 weeks after clinical symptoms.

Pathogen detection: a well-founded suspected diagnosis from clinical material can be expected within 24 h depending on the method (EM: 90 min - with fixed sample 20 min, PCR 4-24 h). In an accumulation of human cases of illness with clinical suspicion of Q fever, direct pathogen detection by means of PCR from blood is recommended due to the delayed antibody response.

Consiliary laboratories:

  • LGA Baden-Württemberg Department 93: Hygiene and infection control Nordbahnhofstr. 135
  • Robert Koch Institute Centre for Biological Safety Nordufer 20 13353 Berlin Friedrich-Loeffler-
  • Institute Federal Research Institute for Animal Health Institute for Epidemiology Seestr. 55 16868 Wusterhausen

Complication(s)
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Neurological (cerebral) manifestations are impressive as aseptic meningoencephalitis with retrobulbar headache, aphasia, hemiparesis, confusion and visual disturbances.

Rare is a persistent course of infection with endocarditis and chronic granulomatous hepatitis (months to years after infection).

The occurrence of chronic fatigue syndrome (CSF) is possible.

Therapy
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An antibiotic therapy should be carried out when the disease is confirmed because of the risk of a chronic course.

Acute course:

  • Doxycycline 2 × 100 mg/d p. o. for 14-21 days.
  • Alternatively: fluoroquinolones, e.g. ciprofloxacin, levofloxacin.

Chronic course:

  • Doxycycline 2 × 100 mg/day p. o. and chloroquine 1-3 × 200 mg/day for at least 18 months.
  • Alternatively, success has also been achieved with doxycycline + fluoroquinolones or rifampicin or TMP/SMZ.

Pregnant women and children:

  • Cotrimoxazole or Clarithromycin.
  • Alternatively, the combination of ciprofloxacin/ doxycycline or ciprofloxacin/rifampicin is only recommended with reservations during pregnancy.

Active immunisation of exposed individuals (Q-Vax® - a Q-fever vaccine consisting of inactivated phase I pathogens): This vaccine is not approved in Germany! Q-Vax® is available in Australia. Due to moderate tolerance and the risk of severe hyperallergic reactions, especially in asymptomatic infections, its use is currently not justified.

General therapy
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Eliminate the sources of infection!

Possible industrial safety measures (wear masks)

Since human-to-human transmission has been described only very sporadically, no special isolation measures are necessary.

Progression/forecast
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Untreated: Total lethality < 2 %.

Inapparente/subclinical courses usually self-limiting.

Coxial endocarditis: fatal in 4 % of cases within 3 years.

Treatment: Post-Q fever fatigue syndrome (general feeling of weakness, easy fatigue and reduced physical performance - often convalescence of several months necessary).

Prophylaxis
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Post-exposure prophylaxis (PEP): Post-exposure prophylaxis should be started at the latest between the 8th and 12th day after a suspected (B) exposure to Coxielles:

  • doxycycline 2 × 100 mg/day p. o. for 7 days
  • Alternatively: erythromycin 4 × 500 mg/day p. o. for 7 days.

Note(s)
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C. burnetii has been the subject of research in biological weapons programmes in various countries. It is important as a BT agent because of its potential for aerosol application, its environmental stability and its high infectivity as an aerosol (possibly a single inhaled germ can cause the disease). C. burnetii has only a low lethality (< 2%).

In 2001, a major endemicity occurred in the Lahn-Dill district, in 2003 in Soest. In 2005, about 300 persons with the diagnosis Q fever were registered in the urban area of Jena. The trigger was a flock of sheep grazing in the area of the residential area.

Literature
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  1. Eldin C et al (2017) From Q Fever to Coxiella burnetii Infection: a Paradigm Change. Clin Microbiol Rev 30:115-190.
  2. Morroy G et al (2016) Fatigue following Acute Q-Fever: A Systematic Literature Review. PLoS One 1:e0155884.
  3. Reimer LG (1993) Q fever. Clin Microbiol Rev 6:193-198.

Disclaimer

Please ask your physician for a reliable diagnosis. This website is only meant as a reference.

Authors

Last updated on: 29.10.2020