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Q fever
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comprehensive CDC information about bioterrorism and related issues,
please visit http://www.bt.cdc.gov.
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Overview
Q fever is a zoonotic disease caused by
Coxiella burnetii, a species of bacteria that is distributed globally.
In 1999, Q fever became a notifiable disease in the United States but
reporting is not required in many other countries. Because the disease is
underreported, scientists cannot reliably assess how many cases of Q fever
have actually occurred worldwide. Many human infections are inapparent.
Cattle, sheep, and goats are the primary
reservoirs of C. burnetii. Infection has been noted in a wide
variety of other animals, including other breeds of livestock and in
domesticated pets. Coxiella burnetii does not usually cause clinical
disease in these animals, although abortion in goats and sheep has been
linked to C. burnetii infection. Organisms are excreted in milk,
urine, and feces of infected animals. Most importantly, during birthing the
organisms are shed in high numbers within the amniotic fluids and the
placenta. The organisms are resistant to heat, drying, and many common
disinfectants. These features enable the bacteria to survive for long
periods in the environment. Infection of humans usually occurs by
inhalation of these organisms from air that contains airborne barnyard dust
contaminated by dried placental material, birth fluids, and excreta of
infected herd animals. Humans are often very susceptible to the disease,
and very few organisms may be required to cause infection.
Ingestion of contaminated milk, followed by
regurgitation and inspiration of the contaminated food, is a less common
mode of transmission. Other modes of transmission to humans, including tick
bites and human to human transmission, are rare.
Signs and Symptoms in Humans
Only about one-half of all people infected
with C. burnetii show signs of clinical illness. Most acute cases of
Q fever begin with sudden onset of one or more of the following: high fevers
(up to 104-105° F), severe headache, general
malaise,
myalgia, confusion, sore throat, chills, sweats, non-productive cough,
nausea, vomiting, diarrhea, abdominal pain, and chest pain. Fever usually
lasts for 1 to 2 weeks. Weight loss can occur and persist for some time.
Thirty to fifty percent of patients with a symptomatic infection will
develop pneumonia. Additionally, a majority of patients have abnormal
results on liver function tests and some will develop
hepatitis. In general, most patients will recover to good health within
several months without any treatment. Only 1%-2% of people with acute Q
fever die of the disease.
Chronic Q fever, characterized by infection
that persists for more than 6 months is uncommon but is a much more serious
disease. Patients who have had acute Q fever may develop the chronic form as
soon as 1 year or as long as 20 years after initial infection. A serious
complication of chronic Q fever is
endocarditis, generally involving the aortic heart valves, less commonly
the mitral valve. Most patients who develop chronic Q fever have
pre-existing valvular heart disease or have a history of vascular graft.
Transplant recipients, patients with cancer, and those with chronic kidney
disease are also at risk of developing chronic Q fever. As many as 65% of
persons with chronic Q fever may die of the disease.
The
incubation period for Q fever varies depending on the number of
organisms that initially infect the patient. Infection with greater numbers
of organisms will result in shorter incubation periods. Most patients
become ill within 2-3 weeks after exposure. Those who recover fully from
infection may possess lifelong
immunity against re-infection.
Diagnosis
Because the signs and symptoms of Q fever
are not specific to this disease, it is difficult to make an accurate
diagnosis without appropriate laboratory testing. Results from some types of
routine laboratory tests in the appropriate clinical and epidemiologic
settings may suggest a diagnosis of Q fever. For example, a platelet count
may be suggestive because persons with Q fever may show a transient
thrombocytopenia. Confirming a diagnosis of Q fever requires
serologic testing to detect the presence of
antibodies to Coxiella burnetii antigens. In most laboratories,
the
indirect immunofluorescence assay (IFA) is the most dependable and
widely used method. Coxiella burnetii may also be identified in
infected tissues by using
immunohistochemical staining and DNA detection methods.
Coxiella burnetii
exists in two antigenic phases called phase I and phase II. This antigenic
difference is important in diagnosis. In acute cases of Q fever, the
antibody level to phase II is usually higher than that to phase I, often by
several orders of magnitude, and generally is first detected during the
second week of illness. In chronic Q fever, the reverse situation is true.
Antibodies to phase I antigens of C. burnetii generally require
longer to appear and indicate continued exposure to the bacteria. Thus,
high levels of antibody to phase I in later specimens in combination with
constant or falling levels of phase II antibodies and other signs of
inflammatory disease suggest chronic Q fever. Antibodies to phase I and II
antigens have been known to persist for months or years after initial
infection.
Recent studies have shown that greater
accuracy in the diagnosis of Q fever can be achieved by looking at specific
levels of classes of antibodies other than IgG, namely IgA and IgM.
Combined detection of IgM and IgA in addition to IgG improves the
specificity of the assays and provides better accuracy in diagnosis. IgM
levels are helpful in the determination of a recent infection. In acute Q
fever, patients will have IgG antibodies to phase II and IgM antibodies to
phases I and II. Increased IgG and IgA antibodies to phase I are often
indicative of Q fever endocarditis.
Treatment
Doxycycline is the treatment of choice for
acute Q fever. Antibiotic treatment is most effective when initiated within
the first 3 days of illness. A dose of 100 mg of doxycycline taken orally
twice daily for 15-21 days is a frequently prescribed therapy. Quinolone
antibiotics have demonstrated good in vitro activity against C. burnetii
and may be considered by the physician. Therapy should be started again if
the disease relapses.
Chronic Q fever endocarditis is much more
difficult to treat effectively and often requires the use of multiple drugs.
Two different treatment protocols have been evaluated: 1) doxycycline in
combination with quinolones for at least 4 years and 2) doxycycline in
combination with hydroxychloroquine for 1.5 to 3 years. The second therapy
leads to fewer relapses, but requires routine eye exams to detect
accumulation of chloroquine. Surgery to remove damaged valves may be
required for some cases of C. burnetii endocarditis.
Prevention
In the United States, Q fever outbreaks
have resulted mainly from occupational exposure involving veterinarians,
meat processing plant workers, sheep and dairy workers, livestock farmers,
and researchers at facilities housing sheep. Prevention and control efforts
should be directed primarily toward these groups and environments.
The following measures should be used in
the prevention and control of Q fever:
- Educate the public on sources of
infection.
- Appropriately dispose of placenta, birth
products, fetal membranes, and aborted fetuses at facilities housing sheep
and goats.
- Restrict access to barns and
laboratories used in housing potentially infected animals.
- Use appropriate procedures for bagging,
autoclaving, and washing of laboratory clothing.
- Vaccinate (where possible) individuals
engaged in research with pregnant sheep or live C. burnetii.
- Quarantine imported animals.
- Ensure that holding facilities for sheep
should be located away from populated areas. Animals should be routinely
tested for antibodies to C. burnetii, and measures should be
implemented to prevent airflow to other occupied areas.
- Counsel persons at highest risk for
developing chronic Q fever, especially persons with pre-existing cardiac
valvular disease or individuals with vascular grafts.
A vaccine for Q fever has been developed
and has successfully protected humans in occupational settings in Australia.
However, this vaccine is not commercially available in the United States.
Persons wishing to be vaccinated should first have a skin test to determine
a history of previous exposure. Individuals who have previously been exposed
to C. burnetii should not receive the vaccine because severe
reactions, localized to the area of the injected vaccine, may occur. A
vaccine for use in animals has also been developed, but it is not available
in the United States.
Significance for Bioterrorism
Coxiella burnetii
is a highly infectious agent that is rather resistant to heat and drying. It
can become airborne and inhaled by humans. A single C. burnetii
organism may cause disease in a susceptible person. This agent could be
developed for use in biological warfare and is considered a potential
terrorist threat.
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