Q fever in Small Ruminants (Query fever; Coxiella burnetii
Coxiella burnetii organisms (red) within infected placenta cells (blue)
The Washington Animal Disease Diagnostic Laboratory at Washington State
University (WSU-WADDL) has
received an increased number of inquiries about Q fever over the past few years.
The questions fall into three
distinct areas and include: testing of dairy goats for the infection in order to
be in compliance with the
Washington State requirements placed on raw milk dairies (RCW 16.36.040);
testing of goats and sheep prior to
sale, and/or breeding (biosecurity profiling); and disease investigation to
determine the cause(s) of pregnancy
loss or low reproductive performance. This information sheet is intended to
answer some of the most common
questions about Q fever. Where appropriate, there are web links to specific
Click on a question or
Query or Queensland fever (Q fever) is a bacterial infection affecting a variety of animal species as well as
human beings. Q fever is caused by Coxiella burnetii
, an obligate, intracellular, rickettsial organism that can
survive in a dried condition for extended periods.
infection of sheep and goats is nearly worldwide in geographical distribution and is thought to
be endemic in most continents. C. burnetii
cycles in a wide variety of wildlife species and their ectoparasites.
The true incidence of Q Fever infection is unknown in the Pacific Northwest region of the USA. WSUWADDL
is currently conducting a research study to determine the geographic distribution and herd prevalence
of C. burnetii
infection in goats in Washington state.
In livestock the disease is usually subclinical. However, occasional abortion outbreaks caused by C. burnetii
have been reported in goats and, less commonly, in sheep. Susceptible pregnant females develop necrotizing
placentitis (inflammation and necrosis of the placenta), which results in abortion, whereas non-pregnant females
do not develop clinical signs. Some ewes and does abort without apparent clinical signs, whereas others show
anorexia and depression 1 to 2 days before aborting. After the initial abortions or infections, animals become
immune to abortion but can remain subclinically infected. After the infection is established, the female can
carry the organism indefinitely, sporadically shedding it in milk and at parturition.
In the susceptible animal host, the bacterium has an affinity for placenta, and high concentrations
(approximately 100 million infectious particles) have been reported per gram of placental tissue. The agent is
shed in birthing fluids and membranes, as well as milk, urine and feces. C. burnetii
is typically acquired by
susceptible animals and humans through inhalation of the organism in fine-particle aerosols. Contact with
droplets or fomites (inanimate objects, such as gloves, coveralls, rags, etc) may also result in transmission.
Ingestion has been proposed as a route of spread, particularly through the consumption of contaminated,
unpasteurized dairy products. Although direct exposure to parturient animals or their birthing products poses the
highest risk for infection, the organism’s ability to persist in the environment may result in a continued risk for
infection weeks to months after the birthing event. Grazing contaminated pastures and tick bites are other
possible sources of infection.
Q fever can be transmitted to human beings primarily by inhalation of dessicated aerosol particles from the
environment, and through contact with infected animals, particularly placentas and birthing fluids but also other
animal products like wool. Disease in human beings is characterized by influenza-like symptoms. The majority
of human cases have a history of contact with infected sheep or goats. The organism is killed by pasteurization
but can be transmitted in non-pasteurized milk. All persons should wear masks and gloves when removing
manure from the barn, assisting with lambing and kidding, and handling aborted fetuses.
Although human and animal vaccines for C. burnetii
have been developed, none are commercially available for
use in the United States. Also, lack of knowledge on shedding patterns among ruminants makes definitive
determination of Q fever shedding status difficult. Therefore, prevention efforts must focus on minimizing
contact with animals that may be shedding C. burnetii
in body secretions and excretions. Although it may not
be practical or possible to eliminate the risk of Q fever in a typical farm setting, the risk for spread can be
decreased by 1) proper sanitation – good hygiene, especially when working with parturient animals; 2)
segregated kidding/lambing areas; 3) removal of risk material from birthing areas (birthing products/fluids,
contaminated bedding, manure); 4) good manure management; 5) control of ticks on livestock; and 6)
restriction of moving peri-parturient animals (close to birthing or giving birth within the past two weeks) off the
For more information on "Best Practices to Control Q Fever" visit the Washington State Department of
Agriculture website at:
Diagnosis of Q Fever abortion requires laboratory testing of aborted fetuses and placenta from aborting does or
ewes. Diagnosis is based on identification of lesions in the placenta (gross and microscopic pathology) together
with identification of the organism by non-culture methods. Culturing of C. burnetii
in the laboratory is not
feasible because of the particularly contagious potential of the organism in laboratory cultures to laboratory
technicians. Therefore diagnosis of Q Fever abortion at WSU-WADDL is based upon special non-culture
methods such as immunohistochemistry, to visually identify C. burnetii
under the microscope within the
formalin fixed infected placenta (Figure 1) or molecular diagnostic polymerase chain reaction (PCR) methods
that uses amplification of C. burnetii
DNA directly from infected placenta (formalin-fixed or fresh).
Instructions on the optimal tissues to submit to WADDL for diagnosis of Q-fever abortion, or other causes of
abortion are available at:
Figure 1. Coxiella burnetii
organisms (red) within infected placenta cells (blue).
There are a number of serology tests for Q Fever in animals that identify a host immune response (antibodies) to
infection indicative of a previous or current infection. However, serology tests do not indicate
whether or not an infected ewe or doe may be shedding organisms. Also, serological assays are most suitable
for screening herds or flocks, but the interpretation of individual animal level is difficult.
WSU-WADDL uses a commercially available ELISA for Q Fever serology ("CHEKIT-Q-FEVER"; IDEXX
Laboratories). Q fever ELISA tests are preferred for practical reasons (ease of use and commercially
availability of test kits) and for their higher sensitivity compared to other tests, such as complement fixation test
(CFT). The supplier gives ELISA test kit cut offs. For the IDEXX CHEK-Q-FEVER test values are normalized
to a kit positive control (to decrease test variability) and values less than 30% are considered negative, values
greater than or equal to 40% are considered positive, and values between 30% and 40% are considered suspect.
If a sample is suspect it is recommended to collect a new sample from the animal and retest. If the sample
remains suspect after 2 separate test, then retest by another method (such as CFT) and investigation of the
epidemiological situation in the herd should be considered. Also, remember that serological assays are designed
for herd or flock use and some scientific publications advocate interpretation of serological tests with a
minimum of 6 animals tested.
On selected cases (usually retests) WADDL may also send samples to a USDA national reference laboratory,
which uses the complement fixation test (CFT)) assay. CF antibody titers between 1:10 and 1:40 are
characteristic of past infection while titers of 1:80 or more (from a group of at least 5 animals) indicate active
Highly sensitive PCR tests (that amplify organism DNA) are currently in use at WSU-WADDL and can be used
to diagnose C. burnetii
shedding in body fluids on subclinically infected animals. However, since shedding is
sporadic (does not occur at all times) a negative PCR tests cannot rule out C. burnetii
Bjorka, Anderson A. Notes from the field: Q fever outbreak associated with goat farms – Washington and
Montana, 2011. CDC MMWR 60(40): 1393-94, 2011.
Bottcher J. et al. Insights into the dynamics of endemic Coxiella burnetii
infection in cattle by application of
phase –specific ELISA’s in an infected dairy herd. Vet Microbiol 151: 291-300, 2011.
Guatteo R, et al. Prevalence of Coxiella burnetii
infection in domestic ruminants: a critical review. Vet
Microbiol 149: 1-16, 2011.
Horigan MW, Bell MM, Pollard, TR, Sayers AR, Pritchard GC. Q fever diagnosis in domestic ruminants:
comparison between complement fixation and commercial enzyme-linked immunosorbent assays. J Vet Diag
Invest 23(5): 924-931, 2011
Q fever. Chapter 2.1.12. In OlE Manual of Diagnostic Tests and Vaccines for Terrestrial Animals 7th ed. P 1-13,
Rousset E, et al. Comparative diagnostic potential of three serological tests for abortive Q fever in goat herds.
Vet Microbiol 124: 286-297, 2007.
If additional questions arise,
contact the Consulting Microbiologist at WADDL @ 509-335-9696
Dr. James Evermann, Dr. Tim Baszler, Dr. Kerry Sondgeroth