Q-Fever

“Q-Fever” means “Query Fever”. Click on article name to display it:

First described in Australia in 1935, Q-fever is a disease with acute and chronic stages. 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. The incidence of Q-fever is underreported due to the mildness of many cases. Because the disease is underreported, scientists cannot reliably assess how many cases of Q-fever have actually occurred worldwide.

Infection of humans usually occurs by inhalation of the bacteria from air that contains airborne barnyard dust contaminated by dried placental material, birth fluids, and excreta of infected herd animals. Airborne particles containing organisms may be carried downwind for a considerable distance (one-half mile or more). Direct contact with infected animals and other contaminated materials, such as wool, straw fertilizer and laundry also occurs. Other modes of transmission to humans, including tick bites and human to human transmission, are rare. Humans are often very susceptible to the disease, and very few organisms may be required to cause infection.
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. C. 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.

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 C. burnetii antigens. In the past, the microagglutination (MA) assay and the complement fixation (CF) test were mainly used to detect antibodies to C. burnetii. These tests are still widely used in the veterinary medicine as they do not require a sophisticated laboratory equipment and the CF test is often used as a golden standard in detecting antibodies to C. burnetii. Recently, an enzyme-linked immunosorbent assay (ELISA) and an indirect immunofluorescence assay (IFA) have found a wide application as they are much more sensitive than the preceeding tests. IFA is simple, very economical in the use of reagents and became a method of choice for a large number of sera to be screened. However, the data obtained are highly subjective and the results may vary considerably from laboratory to laboratory. Thus, it appears that ELISA is the most reliable serological method in diagnosing Q-fever. Our recent studies, have demonstrated that it gave the best sensitivity and specificity in detecting not only IgG but also IgM and IgA classes of antibodies.
C. burnetii may also be identified in infected tissues by using immunohistochemical staining and DNA detection methods.
C. 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.
Our recent studies an those of others 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.

• Educate the persons in high risk occupations sources of infection, and adequate disinfection procedures.
• 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.
• Pasteurize all 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 and goats or live C. burnetii.
• Quarantine imported animals.
• Ensure that holding facilities for sheep and goats 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.