Coxiella burnetii

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

Coxiella burnetii, a bacterium of the family Coxiellaceae in the order Legionellales is a worldwide, gram-negative, obligate intracellular, immotile, pleomorphic rod. Size 0.2-0.4 µm × 0.4-1 µm. Coxiella burneti is a member of the Coxiellaceae family (previously assigned to the Rickettsiaceae family) and is the causative agent of Q fever.

C. burnetii has two antigenic phases (phase I and II), which is comparable to the smooth and rough growth forms, respectively, 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 survivable and highly infectious.
• Large cell variants (LCV): SCVs become large cell variants (LCV), intracellular vegetative stages in the organism.

Transmission to humans occurs in particular through inhalation of dust (faeces of the tick) or through contact with contaminated products such as wool, milk or meat. Ticks can also transmit the pathogen to other animals (and humans). In Slovenia, Coxiella antigen was detected in 2.5% of ticks (Knap N et al. 2019)! Human-to-human transmission seems to be extremely rare.

Due to the formation of the spore-like SCV, a high resistance to desiccation, heat, cold, sunlight and many disinfectants exists. Years of survival in soil or dust are possible. The pathogen can be spread aerogenically over several kilometres.

Incubation period: 2-3 weeks. Q fever caused by Coxiella burneti is a notifiable disease (§ 7 IfSG: notification by name also in the case of direct or indirect evidence of acute infection). Q fever is a zoonosis in which humans become infected via aerogenic inhalation of infected sheep tick faeces. Particularly at risk are e.g. farmers, shepherds and abattoir workers through infected stable animals, hay, wool, etc. The infection is asymptomatic in animals. In humans, natural infections are also inapparent or subclinical in 50-70% of cases.

Acute Q fever: The following triad occurs in severe cases of the disease:

Sudden fever with chills and severe feeling of illness and arthralgias. Fever may persist for 1-3 weeks.

Headache (retrobulbar)

Atypical pneumonia (in about 50% of cases) with continuous or remitting fever up to 40°C for several weeks. Transaminase rise only slight, rarely gastrointestinal symptoms or jaundice.

Furthermore:

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

Detection of C. burnetii DNA; pathogen isolation

Antibody detection

C. burnetii has been studied in bioweapons programmes in several countries. It is important as a BT agent because it can be spread as an aerosol, because of its environmental stability and because of its high infectivity as an aerosol (it is possible that a single inhaled germ can cause the disease). C. burnetii has only a low lethality (< 2 %).

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

1. Eldin C et al. (2017) From Q fever to Coxiella burnetii infection: a paradigm shift. Clin Microbiol Rev 30:115-190.
2. Knap N et al. (2019) The prevalence of Coxiella burnetii in ticks and animals in Slovenia. BMC Vet Res 15:368.
3. Morroy G et al (2016) Fatigue following Acute Q fever: A Systematic Literature Review. PLoS One 1:e0155884.
4. Reimer LG (1993) Q fever. Clin Microbiol Rev 6:193-198.