Q Fever
My-Dog.info > Dog Diseases, Bites, Worms & Ticks
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 species 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 only pasteurized milk and milk products.
- 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.
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