[PubMed] [Google Scholar] 24. of the sequences of the 16S rRNA-encoding gene (195). Another major characteristic of is its antigenic variation, called phase variation. This phenomenon, similar to the rough-smooth variation in enterobacteria, Sorbic acid is due to partial loss of lipopolysaccharide (LPS) (60, 186). The LPS represents a major virulence determinant of (59). When isolated from animals or humans, expresses phase I antigens and is very infectious (a single bacterium may infect a human). Phase I LPS, with its extended carbohydrate structure, sterically blocks access of antibody to surface proteins (59). This may explain, at least in part, why the bacterium persists at unknown sites after recovery from acute cases of Q fever, accompanied by lifelong seropositivity. After subculture in cells or embryonated eggs, modification of the LPS results in an EGR1 antigenic shift to the phase II form, which is less infectious. This LPS modification makes surface proteins accessible for antibodies (59, 186). LPS seems to be the only antigen and immunogen differing between phase I and II in (3). This antigenic peculiarity is extremely valuable for the serological differentiation between acute and chronic Q fever. Open in a separate window FIG. 1 expresses a low degree of genetic heterogeneity among strains. However, variation in the composition of LPS has been demonstrated (60, 185). Moreover, 20 different genotypes have been delineated by pulsed-field gel electrophoresis (65) and/or restriction fragment length polymorphism analysis (178). The 1.6 106-bp genome comprises a chromosome and four copies of a plasmid. Four different plasmids have been described for the Nine Mile strain, and they vary in their size (117, 160, 162, 190). Besides host factors which probably play a major role in the clinical form of the disease (143), the roles of LPS type, plasmid type (161, 173, 177, 203), and the route of infection (111) are still controversial. EPIDEMIOLOGY Q fever is a worldwide zoonosis. The reservoirs are extensive but only partially known and include mammals, birds, and arthropods, mainly ticks. While an important reservoir seems to be small wild rodents, the mostly identified resources of individual infection are plantation animals such as for example cattle, goats, and sheep. Dogs, including felines (67), rabbits, and canines, have got been proven potential resources of metropolitan outbreaks also. Felines are suspected as a significant tank of in cities and may bring on metropolitan outbreaks (90, 108, 118). In Sorbic acid Canada, 6 to 20% of felines have got anti-antibodies (67). Crazy rats have already been suspected as a significant reservoir in the uk (193). Each one of these mammals, when contaminated, shed the desiccation-resistant microorganisms in urine, feces, dairy, and, especially, delivery items (80, 106). Reactivation of an infection occurs in feminine mammals during being pregnant. Q fever causes abortions in goats and, much less often, sheep and causes reproductive complications in cattle (7, 192, 204). Great concentrations of (up to 109 bacterias per g of tissues) are located in the placentas of contaminated animals (4). Because of its level of resistance to physical realtors, linked to its sporulation procedure (89 most Sorbic acid likely, 113), survives for very long periods in the surroundings. In humans, an infection outcomes from inhalation of contaminated aerosols from amniotic placenta or liquid or contaminated wool. As a result, Q fever can be an occupational threat. At most significant risk are people in touch with plantation pets, but also in danger are laboratory workers who use contaminated animals (75). While searching for the foundation of publicity, the investigator should seek out connection with a parturient or newborn pet. Mammals shed in dairy also, and thus, intake of raw dairy is actually a source of an infection (47, 118, 180). Intimate transmitting of Q fever continues to be showed in the mouse (86).