Q fever

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Q fever is caused by infection with Coxiella burnetii. This organism is uncommon but may be found in cattle, sheep, goats and other domestic mammals, including cats and dogs. The infection results from inhalation of contaminated particles in the air, and from contact with the vaginal mucus, milk, feces, urine, or semen of infected animals. The incubation time is 9-40 days. It is considered to be possibly the most infectious disease in the world, as a human being can be infected by a single bacterium.^[1]

The disease was first described by Edward Holbrook Derrick in Australia and the pathogen was first described in 1937 by Frank Macfarlane Burnet.

According to the onset of symptoms, Q fever can be classified as acute or chronic.

Q fever is a disease caused by C. burnetii, an intracellular, gram-negative proteobacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism.

Q fever is caused by the bacteria C. burnetii, which lives in domestic animals such as cattle, sheep, goats, birds, and cats. Some wild animals and ticks also carry the bacteria. Q fever may be contracted through drinking raw (unpasteurized) milk, or after inhaling dust or droplets in the air that are contaminated with animal feces, blood, or birth products.

Q fever must be differentiated from other diseases that cause atypical pneumonia such as Mycoplasma pneumonia and legionellosis.

C. brutenii is found everywhere except Antarctica and New Zealand. The disease is slightly more prevalent in the elderly and in the male population.

The organism is present mainly in the secretions of cattle and sheep. Any occupation that involves contact with cattle and sheep increases the risk of contracting the disease.

Acute Q fever has a good prognosis even without treatment. Chronic Q fever has a less favorable prognosis.

Acute Q fever presents with flu-like symptoms, pneumonia, and hepatitis. Chronic Q fever almost always presents with endocarditis and sometimes gives musculoskeletal and vascular manifestations.

Patients with Q fever usually appear ill. Physical examination of patients with Q fever is usually remarkable for fever, pneumonia, and hepatomegaly.

Laboratory findings consistent with the diagnosis of Q fever include positive serology for antibodies (especially indirect immunofluorescence (IIF), positive PCR, and elevated liver enzymes.

On chest X-ray, Q fever is characterized by either signs of atypical pneumonia (hazy, nonlocalized airspace opacities) or it may show signs of typical pneumonia (lobar consolidation and occasional pleural effusions) in few patients.

Chest CT scan may be helpful in the diagnosis of Q fever. Findings on CT scan suggestive of Q fever include scattered consolidation and opacities or lobar consolidation in one specific lobe.

There are no additional MRI findings associated with Q fever. Chest X-ray and CT are usually sufficient to diagnose Q fever.

There are no other specific imaging findings for Q fever.

There are no additional diagnostic findings for Q fever.

The mainstay of therapy for Q fever is doxycycline. The chronic form is more difficult to treat and can require up to two years of treatment with doxycycline and hydroxychloroquine. Q fever in pregnancy is especially difficult to treat because doxycycline is contraindicated in pregnancy and so preferred treatment is trimethoprim/sulfamethoxazole.

Surgical intervention is not recommended for the management of Q fever.

Effective measures for the primary prevention of Q fever include educating the public on sources of infection, appropriate disposal of the placenta, birth products, fetal membranes, and aborted fetuses at facilities housing sheep and goats and restricting access to barns and laboratories used in housing potentially infected animals.

There are no secondary preventive measures available for Q fever.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Q fever was first described by Edward Holbrook Derrick in Australia and the pathogen was first described in 1937 by Frank Macfarlane Burnet.

• Q fever was first described by Edward Holbrook Derrick in abattoir workers in Brisbane, Queensland, Australia.^[1]
• The “Q” stands for “query” and was applied at a time when the causative agent was unknown; it was chosen over suggestions of “abattoir fever” and “Queensland rickettsial fever” to avoid directing negative connotations at either the cattle industry or the state of Queensland.^[2]
• The pathogen causing Q fever was discovered in 1937 when Frank Macfarlane Burnet and Mavis Freeman isolated the bacterium from one of Derrick’s patients.^[3]
• It was originally identified as a species of the genus Rickettsia. H. R. Cox and Gordon Davis isolated it from ticks in Montana, USA, in 1938.^[4] It is a zoonotic disease whose most common animal reservoirs are cattle, sheep, and goats. Coxiella burnetii is no longer regarded as closely related to Rickettsiae, but as similar to Legionella and Francisella, and is a proteobacterium.

• Q fever has been described as a possible biological weapon.^[5]
• The United States investigated Q fever as a potential biological warfare agent in the 1950s, with eventual standardization as agent OU. At Fort Detrick and Dugway Proving Ground, human trials were conducted on whitecoat volunteers to determine the median infective dose (18 MICLD₅₀/person i.h.) and the course of infection.
• As a standardized biological, it was manufactured in large quantities at Pine Bluff Arsenal, with 5,098 gallons in the arsenal in bulk at the time of demilitarization in 1970.
• Q fever is a category “B” agent.^[6] It can be contagious, and is very stable in aerosols in a wide range of temperatures. Q fever microorganisms may survive on surfaces for up to 60 days.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Q fever may be classified according to the course of the disease as acute or chronic. Acute Q fever has a very rapid onset and resolves within 6 months of onset. Chronic Q fever persists for more than six months and is associated with a poorer prognosis.

Q fever may be classified according to the course of the disease as follows:

• Characterized by a very rapid onset of flu-like symptoms, pneumonia, and hepatitis.
• Resolution of infection in less than 6 months.

• Characterized by persistence of infection (clinically or serologically) for more than six months.^[1]
• Chronic Q fever almost always leads to endocarditis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Q fever is a disease caused by C. burnetii, an intracellular, gram-negative proteobacterium. The disease can have a wide range of clinical presentations and affect many organ systems due to the unique virulence factors of the organism.

The organism is transmitted through:^[1]

• Aerosols: Inhalation of contaminated aerosols is the main mode of transmission
• Ingestion of raw dairy products
• Vertical (mother to fetus) transmission has been reported
• Parenteral
• Tick bites

The infection has two phases, which correlate to changes in the lipopolysaccharide of C. burnetii:^[2]

• Phase I: Characterized by a smooth lipopolysaccharide capsule. Despite being less efficient in the invasion of host cells, antibodies against phase I are always isolated from acute Q fever patients.
• Phase II: Characterized by a rough lipopolysaccharide capsule. Antibodies against phase II have been isolated from chronic Q fever patients.

C. burnetii can exist in two forms: the small cell form and the large cell form. The small and large cell forms are antigenically different, which plays a role in the virulence of the organism.

The small cell form is often described as the spore form of C. burnetii. It can resist external environmental factors such as heat, pressure, and disinfectants for long periods of time.

The large cell form is the active form of the organism. It persists in macrophages inside acidic vacuoles.

• The genome of C. burnetii was analyzed in 1995. Multiple genes encoding for Na+ ion proton exchange have been discovered, explaining the ability of the organism to survive in a low pH environment.

• There is a delay between the entry of the organism into the host cell and the fusion with lysosomes. This delay is thought to be due to the transformation from the small cell variant into the large cell variant.
• The acidic environment inside the lysosome has little effect on the large cell form of the organism.

• The lipopolysaccharide capsule is one of the most important virulence factors of the organism.

• The different phases of infection are associated with changes in the lipopolysaccharide capsule.

• Lipopolysaccharide phase I (smooth polysaccharide) is associated with protection against the host’s immune response.
• Lipopolysaccharide phase II (rough polysaccharide) is isolated from avirulent, non-infectious host cells and is not associated with protection of the virus from the host cell.

• Both humoral and cell mediated immunity are involved in the immune response against C. burnetii. However, cell mediated immunity is more important in defending against the organism and people with deficient cell mediated immunity are more susceptible to developing chronic infection.

• Because of its route of infection, C. burnetii can be used as a biological warfare agent.
• Q-fever is a category “B” agent. It is highly contagious and very stable in aerosols at a wide range of temperatures.
• Just 1-2 particles are enough to infect an individual.
• Q-fever microorganisms can survive on surfaces up to 60 days (like sporulating bacteria).
• According to WHO estimates, 50 kg of C. burnetii, if spread in an area of 2 square kilometers, is capable of:^[4]

• Infecting 500,000 humans
• Killing 150 individuals
• Causing acute illness in 125,000 individuals
• Causing chronic illness in 9,000 individuals

• C. burnetii is a gram negative, polymorphic, intracellular organism.^[5]
• It was previously classified as a Rickettsia, but now is considered a proteobacterium.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Coxiella burnetii is an obligate intracellular bacterial pathogen, and is the causative agent of Q fever. The genus Coxiella is morphologically similar to Rickettsia, but with a variety of genetic and physiological differences. C. burnetii is a small Gram-negative bacterium that is highly resistant to environmental stresses such as high temperature, osmotic pressure, and ultraviolet light. These characteristics are attributed to a small cell variant form of the organism that is part of a biphasic developmental cycle, including a more metabolically and replicatively active large cell variant form.^[1] It can survive standard disinfectants, and is resistant to many other environmental changes like those presented in the phagolysosome.^[2]

The ID₅₀ (the dose needed to infect 50% of experimental subjects) is one via inhalation; i.e., inhalation of one organism will yield disease in 50% of the population. This is an extremely low infectious dose (only 1-10 organisms required), making C. burnetii one of the most infectious known organisms.^[3][4] Disease occurs in two stages: an acute stage that presents with headaches, chills, and respiratory symptoms, and an insidious chronic stage.

While most infections clear up spontaneously, treatment with tetracycline or doxycycline appears to reduce the symptomatic duration and reduce the likelihood of chronic infection. A combination of erythromycin and rifampin is highly effective in curing the disease, and vaccination with Q-VAX vaccine (CSL) is effective for prevention of it. [Source?]

The bacteria use a Type IVB secretion system known as Icm/Dot to inject effector proteins called Ank proteins into the host. These effectors increase the bacteria‘s ability to survive inside the host cell. In Legionella pneumophila, which uses the same secretion system and also injects Ank proteins, survival is enhanced because these Ank proteins interfere with fusion of the bacteria-containing vacuole with the host’s degradation endosomes.^[5]

There are currently at least 5 completely sequenced genomes of Coxiella burnetti ^[6] which contain about 2.1 Mbp of DNA each and encode around 2,100 open reading frames. 746 (or about 35%) of these genes have no known function.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Q fever is more prevalent in the elderly and in males. It has been a notifiable disease in the US since 1999. Q fever is underreported, thus scientists cannot reliably assess its incidence.^[1]

• Q fever is slightly more prevalent in elderly people; however, it is often seen in various age groups.
• Q fever is occasionally seen in children, especially those who live on a farm.
• In infected children younger than 3 years old, Q fever usually presents as pneumonia.^[2]

• Due to differing employment rates in typical professions that predispose people to contracting Q fever, men are more often affected than women.^[3]

• In 1999, Q fever became a notifiable disease in the United States but reporting is not required in many other countries.
• In Europe, Q fever often presents as hepatitis rather than pneumonia as it does in the United States.^[1]

• C. burnetii is found everywhere except in Antarctica and New Zealand.
• Q fever infections are often subclinical.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

C. burnetii, the organism that causes Q fever, is present mainly in the secretions of cattle and sheep. Any occupation that involves contact with cattle and sheep increases the risk of the disease.

Risk factors for developing Q fever include drinking raw (unpasteurized) milk or inhaling dust or droplets in the air that are contaminated with animal feces, blood, or birth products.^[1][2] These risks may be attributed to different employment rates in typical professions. “At risk” occupations include, but are not limited to:^[3][4]

• Animal transporters
• Farmers
• Hide (tannery) workers
• Laboratory workers handling potentially infected veterinary samples or visiting abattoirs
• People who cull and process kangaroos
• Shearers
• Stockyard workers
• Veterinary personnel

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]

Acute Q fever has a good prognosis even without treatment. Chronic Q fever has a less favorable prognosis.

If left untreated, most patients will recover within several months.^[1]

If left untreated, chronic Q fever is usually deadly. However, with appropriate treatment, the case fatality rate is around 10%.^[1]

• Atypical pneumonia
• Acute respiratory distress syndrome (ARDS) in rare cases

• Endocarditis
• Pericarditis or myocarditis
• Pericardial effusion

• Hepatic fibrosis and cirrhosis

• Osteomyelitis
• Arthritis

• Abortion
• IUGR
• Intrauterine fetal death

• Acute Q fever is responsive to treatment and even without treatment, mortality rate is 1-2%.

• Chronic Q fever is more serious, with a case fatality rate of 10% after treatment.^[2]

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