Several
C. burnetii strains isolated from animals or humans including patients with acute or persistent focalised Q fever have been used for research
[20]. However, the Nine Mile strain, isolated from the
Dermacentor andersoni tick in Montana in 1938, is to date the strain mostly used in host–pathogen studies
[21]. The lipopolysaccharide (LPS) structure, plasmid, and genotype have been commonly related to the different disease manifestations
[20][22], cytopathic effects in cell cultures
[20], and immune response
[23][24][25][26]. The repeated cultures of
C. burnetii Nile Mile strain result in a truncated LPS (O-antigen modification), which is associated with virulence decrease. This transition from phase I LPS to phase II LPS is related to a ≈26 Kb chromosomal deletion of
C. burnetii genome
[27]. Despite their frequent use in studies, phase II
C. burnetii are not suitable for pathophysiopathological studies.
Generally speaking, placental
C. burnetii isolates appear to be more virulent than other isolates. It has been proposed that the virulence found in the different strains could be due to the variation of LPS but also to the genomic content. Correlations have been found between
C. burnetii genome variations or LPS chemotype and clinical presentations of Q fever
[28][29]. The
C. burnetii RSA493 strain genome was the first strain sequenced in 2003, which led to significant progress in understanding of
C. burnetii pathogenicity
[30]. The genome contains a 1,995,275 bp chromosome and a QpH1 plasmid with 37,393 bp.
C. burnetii virulence appears to be correlated with the expression of certain plasmids. Four different plasmids have been identified among
C. burnetii isolates, including QpH1 (Nine Mile strain), QpRS (Priscilla strain), QpDG (wild rodents), and QpDV
[23].
C. burnetii Nine Mile strain presents the plasmid QpH1, MST16, and GGI
[23]. It was reported that
C. burnetti Nine Mile strain with QpH1 plasmid is the cause of severe
C. burnetii infection in a guinea pig model
[22][24]. Moreover, QpRS and QpDG plasmids have been associated with moderate infection and lack of virulence, respectively
[22][24]. Three of the plasmids identified among
C. burnetii isolates have been found in placental isolates from France and Spain (QpH1, QpRS, and QpDV)
[23]. Obstetric complications are likely to be related to the QpDV plasmid
[23][31]. Indeed, this plasmid has been found in three of six placentas and in placental bacterial strains from abortive women
[23][32]. However, the presence of the QpDV plasmid has also been reported in a healthy woman, and other placental strains of
C. burnetii harbour the QpH1 plasmid (Dutch strains)
[23][33][34].