![]() Table 1 summarizes the results of susceptibility testing in chick embryos or guinea pigs. Three model systems have been used: chick embryos, guinea pigs, and cell cultures ( 60). Nevertheless, there is a long history of efforts to provide antimicrobial susceptibility data about C. burnetii has been problematic, since it is an intracellular pathogen. Q 212 was isolated from the brachial artery clot of a Nova Scotia, Canada, patient with Q fever endocarditis.ĭetermination of antimicrobial susceptibility of C. Priscilla was isolated from a goat placenta it is a chronic Q fever isolate. Strain Nine Mile was isolated from a tick, Dermacentor sp., collected near Nine Mile creek, Montana in 1935. In many of the in vitro susceptibility studies cited below, three type strains of C. The microorganism proliferates in the lungs and then invades the bloodstream where if uncontrolled by the immune response it can infect heart valves, bone, or liver resulting in chronic disease. The agent may be found in soil, dust, or contaminated environmental products and carried for long distances by wind. Humans acquire the disease by direct contact with parturient animals or their placentas. ![]() The mode of transmission is by inhalation of aerosols containing C. Both acute and chronic infections can also be diagnosed by PCR, immunochemistry, or culture of infected materials. Acute Q fever is characterized by an antibody response to phase II antigen, while chronic Q fever is characterized by a higher response to phase I antigen.Ĭhronic Q fever (endocarditis and granulomatous hepatitis) is confirmed by: a) a complement fixation titer of 1:200 or greater to phase I antigen, or b) IgG antibody titer of 1:800 or greater by microimmunofluorescence. A four-fold rise in antibody titer is considered diagnostic. Since most laboratories do not have the capability to isolate the organism, serologic tests are most common means of diagnosis including complement fixation and indirect fluorescent antibody tests. While still not adequately described in man, it is likely that Q fever during pregnancy results in chronic uterine infection with relapse during subsequent pregnancies as it does in other female mammals ( 27, 42).īecause the illness is often nonspecific in clinical presentation, laboratory testing is necessary to confirm the diagnosis. Chronic Q fever is a much more serious illness and almost always means endocarditis, although infection of an aortic prosthesis or aneurysm is another manifestation of chronic Q fever ( 38). Rarely it is a cause of constrictive pericarditis ( 4). Acute Q fever has a variety of clinical presentations including self-limited febrile illness, pneumonia, hepatitis, meningoencephalitis, and pericarditis. Q fever has two major manifestations in man, acute and chronic infection. In the United States, 71 cases of Q fever were reported to the Centers for Disease Control in 2003. Q fever has been reported from all continents except New Zealand and Antarctica, but the precise incidence is unknown because diagnostic tests are usually not performed and reporting of cases is not required. Cats are the primary reservoir for Q fever in Nova Scotia, Canada and occasional cases have been linked to dogs. The most common animal reservoirs are cattle, sheep and goats. The epidemiology and animal reservoir varies by country. This resulted in three monophyletic groups. ![]() Glazunova et al ( 12) used multispacer sequence typing to characterize 173 isolates. This has led to multiple methods for typing the genome. burnetii may be a relatively recent innovation. The authors concluded that the obligate intracellular life style of C. There are many genes with potential roles in adhesion, invasion, intracellular trafficking, host-cell modulation and detoxification. burnetii strain Nine Mile Phase 1 has now been sequenced ( 52). This phase is much less virulent than phase I. In animals, it exists in phase I and is extremely infectious passage in cell culture or in embryonated eggs results in a change in surface lipopolysaccharides-phase II. burnetii exists in two antigenic phases, phases I and II. It can form a spore, which explains its ability to survive for extended periods in hostile environments and its marked resistance to physiochemical agents. Within these cells it multiplies in an acidic vacuole, pH 4.8. It is a small Gram-negative bacterium that grows only in eukaryotic cells ( 38). Coxiella burnetii is the etiologic agent of Q fever. ![]()
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