The pathogenic rickettsial agent was identified by Harold Cox and MacFarlane Burnet in 1935, which lends explanation to the proper name for Q-fever becoming Coxiella burnetti. Coxiella burnetti is a gram negative coccobacillus that lives and replicates within host monocytes and macrophages. Since the identification of C. burnetti as the causative agent for Q-fever, exposure and disease has, as of the year 2002, been reported in every country except New Zealand.
Q-fever is an important zoonotic disease for several reasons. There are multiple sources of exposure, human infection with C. burnetti may result in clinical signs ranging from headache to death, and animals with C. burnetti are seemingly normal, with the exception of occasional abortion storms occurring in the herd. Finally, culturing the organism from tissues of suspected animals is difficult, making serology necessary for diagnosis. Considering all of these factors, it is clear that measures for monitoring prevalence, risk assessment and active prevention protocols should be in place for all individuals at risk for exposure to C. burnetti.
Sources of exposure to C. burnetti include, but are not exclusive, to slaughterhouses, farms, research institutions and veterinary facilities. People have also acquired Q-fever following contact with urine, milk and feces from infected animals. In Idaho, people with no animal contact but who lived within a mile of an abattoir which frequently processed sheep from a research institution, were diagnosed with Q-fever. Awareness of zoonotic risk is especially important for abattoir workers, farmers, veterinarians, research employees and veterinary students due to their increased contact with animals, animal tissues and fluids and animal waste. However, all individuals exposed to C. burnetti are susceptible to infection.
A broad spectrum of clinical signs in humans with Q-fever has been reported since the earliest identified case. Clinical signs range from mild self-limiting fever, headache, nausea, eye pain, shaking, chills, anorexia, nausea, arthralgia, myalgia and non-productive cough, to pulmonary disease, meningitis, pericarditis and valvular endocarditis. Meningoencephalitis and myocarditis have occurred with C. burnetti infection. Individuals with valvular heart conditions or susceptible immune status are at increased risk for development of more severe clinical signs if infected with C. burnetti. Up to ˝ of exposed individuals will seroconvert without having exhibited any clinical illness. Others will experience a variable incubation period anywhere from one to three weeks before onset of clinical signs. While mild forms of infection resolve spontaneously, treatment with doxycylcine will shorten the course of disease. If cardiac involvement occurs, doxycycline and hydroxychloroquine are administered long term. Valvular replacement may be required if severe valvular disease occurs.
Species of interest in the transmission of C. burnetti are primarily the bovine, caprine and ovine. However, felids and canids have been associated with human infection. In the host animal, whatever the species, the C. burnetti organisms concentrate in fetal/placental fluids and tissues. The concentration may exceed one billion times the ID50 (the dose of enough quantity to infect 50% of exposed people). Animals and people alike acquire the infection by contacting these infected tissues, or contacting contaminated items. Coxiella burnetti organisms have two life cycle stages: the large-cell variant (LCV) and the small cell variant (SCV). The LCV is the vegatative form seen in infected monocytes and macrophages. The SCV is seen extracellularly and is presumed to be the infectious form of the organism. When the environment is contaminated with these organisms, via contact with infected tissues and fluids, the SCV variant survives exposure to physical and chemical disruption. Inhalation of the aerosolized organism is the most common route of infection.
There are two primary ways to diagnose Q-fever in humans and animals: isolation of the organism and serologic testing. Organism isolation requires laboratories with established biosafety level 3 conditions and the use of tissue culture, lab animals or embryonated eggs. Serologic testing can be performed using indirect fluorescent antibody (IFA), enzyme immunoassay, and complement fixation. Antigenic detection assays, immunohistochemical staining (IHC), nucleic acid detection assays and polymerase chain reaction (PCR) are also available testing.
Because of the ease of sampling and assaying, serologic testing is the preferred method to diagnose Q-fever in humans and animals. Two antigenic forms of C. burnetti are important for serologic diagnosis: avirulent smooth lipopolysaccharide microorganism (S-LPS) phase I antigen and avirulent rough lipopolysaccharide microorganism (R-LPS) phase II antigen. Currently, the Centers for Disease Control are responsible for maintaining epidemiologic surveys of disease in the United States. Case reporting is the limiting factor to valid epidemiologic distribution of a disease. With the serologic assays available and the relative ease of accessing laboratories for performing these assays, monitoring the prevalence of Q-fever would not be an overwhelming task. In addition, the potential life-threatening outcome for some individuals when infected with Q-fever substantiates the importance of monitoring prevalence and establishing risk.
The total number of cases of a specific disease in a given population at a certain time is the prevalence of that disease. Prevalence of Q-fever can be established through serologic monitoring. The number of new cases of a specific disease during a fixed time is the incidence of that disease. Incidence of Q-fever can be established through serologic monitoring. Risk is defined as the chance of an unfavorable event occurring. In this instance, that event would be exposure to or contraction of Q-fever. Risk can be assessed by examining prevalence and incidence.
Prevention is defined as "measures designed to prevent the introduction of a disease in the areas where it does not already exist and improve the resistance of the population and decrease the chances of the infection from spreading when it already exists in the population". The introduction of Q-fever is prevented from entering the population, the herd, by purchasing animals from serologically negative herds. Improving the resistance in the population, humans, is possible by vaccination. Vaccination is currently reserved for individuals considered at greatest risk of exposure, such as biosafety-3 level laboratory workers. Isolating or depopulating affected animals and taking personal protective measures when working with suspected or confirmed infected animals or contaminated materials will decrease the chance of spread of Q-fever. Personal protective measures include masking, gowning, gloving, and wearing protective eye gear during high-risk exposure. High-risk exposure can include examining aborted materials, aiding in dystocia, cesarean section or necropsy of pregnant cows, goats, sheep, etc, and working in abattoirs, laboratories housing Q-fever infected animals or tissues. The objective of the personal protective measure is to decrease exposure to infective organisms by providing a physical barrier and minimizing environmental contamination and eventual aerosolization by discarding all contaminated items immediately following use. As mentioned previously, the organism is persistent in the environment. This should be considered when re-populating or isolating a herd.
Q-fever is an historical and persistent zoonotic disease. It is required in the state of Indiana to report cases of Q-fever in animals. For additional information about reportable diseases, visit www.cdc.gov or contact the Indiana State Veterinarians Office at http://www.in.gov/boah/.
-by Sherry Walters, Class of 2004
-edited by Dr. Leon Thacker, ADDL Director
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