<i>Mycoplasma gallisepticum</i>: influence of cell invasiveness on the outcome of experimental infection in chickens

Much, Peter; Winner, Florian; Stipkovits, L.; Rosengarten, Renate; Citti, Christine

doi:10.1111/j.1574-695x.2002.tb00622.x

Cited by 66 publications

(40 citation statements)

References 25 publications

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“…Mycoplasma gallisepticum high-or low-passaged strains differed significantly in their entry into HeLa cells (Winner et al, 2000). Extension of these findings to the M. gallisepticum chicken infection model demonstrated a correlation between the in vitro invasive potential of specific mycoplasma strains and their mucosal penetration and virulence in vivo (Much et al, 2002). Thomas et al (2003) described varied adherence rates when Mycoplasma bovis isolates that differed in the number of in vitro passages were used to infect a variety of cultured host cells.…”

Section: Discussionmentioning

confidence: 89%

Interaction of Mycoplasma genitalium with host cells: evidence for nuclear localization

et al. 2008

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Mycoplasma genitalium (Mg) is a mollicute that causes a range of human urogenital infections. A hallmark of these bacteria is their ability to establish chronic infections that can persist despite completion of appropriate antibiotic therapies and intact and functional immune systems. Intimate adherence and surface colonization of mycoplasmas to host cells are important pathogenic features. However, their facultative intracellular nature is poorly understood, partly due to difficulties in developing and standardizing cellular interaction model systems. Here, we characterize growth and invasion properties of two Mg strains (G37 and 1019V). Mg G37 is a high-passage laboratory strain, while Mg 1019V is a low-passage isolate recovered from the cervix. The two strains diverge partially in gene sequences for adherence-related proteins and exhibit subtle variations in their axenic growth. However, with both strains and consistent with our previous studies, a subset of adherent Mg organisms invade host cells and exhibit perinuclear targeting. Remarkably, intranuclear localization of Mg proteins is observed, which occurred as early as 30 min after infection. Mg strains deficient in adherence were markedly reduced in their ability to invade and associate with perinuclear and nuclear sites.

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Section: Discussionmentioning

confidence: 89%

Interaction of Mycoplasma genitalium with host cells: evidence for nuclear localization

et al. 2008

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“…Several hypotheses to explain M. synoviae persistence in the treated birds include the following: (i) the possible development of resistance mechanisms as described in vitro [15]; (ii) survival on materials in the animal environment [25] and subsequent natural re-infection of birds; (iii) ability to invade host cells for long periods and reach subcellular fractions where enrofloxacin would not be active or to persist inside the cell [27,39] in a fluoroquinolone-insensitive state, as described for M. penetrans [10]. The presence of a non-or slow-dividing subpopulation named "persisters", as previously described for different bacterial species, may be linked with M. synoviae persistence [1,21].…”

Section: Discussionmentioning

confidence: 99%

Persistence of Mycoplasma synoviae in hens after two enrofloxacin treatments and detection of mutations in the parC gene

et al. 2006

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-The ability of Mycoplasma synoviae, an avian pathogen, to persist despite fluoroquinolone treatments was investigated in hens. Groups of Mycoplasma-free hens were experimentally infected with the M. synoviae 317 strain and treated twice with enrofloxacin at the therapeutic dose. The results show that the two treatments did not have any influence on this strain of M. synoviae recovery from tracheal swabs. Mycoplasmas were isolated from tracheal swab cultures, but not from inner organs such as the liver or spleen, suggesting that this strain of M. synoviae was not able to cross the mucosal barrier to disseminate throughout the host. A significant increase of the resistance level to enrofloxacin of five re-isolated mycoplasma clones, was observed after the second treatment. This increase was associated in two clones to a Ser81→Pro substitution, found in the ParC quinolone-resistance determining region (QRDR) of DNA topoisomerase IV. This is the first time that a mutation in a gene coding for topoisomerase IV is described in M. synoviae after in vivo enrofloxacin treatments in experimentally infected hens.Mycoplasma synoviae / fluoroquinolone / persistence / topoisomerase / poultry

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“…The M. gallisepticum laboratory passages R low and R high used in this study and by others worldwide (6,15,16,23) were kindly provided by S. Levisohn, Kimron Veterinary Institute, Bet Dagan, Israel. R low and R high correspond to the prototype strain R propagated 10 and 160 times in culture medium, respectively (24) and are therefore not clonal populations.…”

Section: Methodsmentioning

confidence: 99%

“…The experimental infection procedure was performed as previously described by our group (6). Briefly, 150 Arbor Acres chickens, 21 days old and certified free of mycoplasmas, were divided into five groups of 30 birds each.…”

Section: Methodsmentioning

confidence: 99%

“…gallisepticum colonizes its host mainly via the mucosal surfaces of the respiratory tract, causing air sacculitis within a few days (6), and disseminates throughout the body. This systemic infection is reflected by the high rate of M. gallisepticum reisolation from inner organs such as the liver, heart, spleen, or kidney (6) and by its detection inside and at the surface of red blood cells of experimentally infected birds (7). Successful infection by M. gallisepticum may rely on two independent phenomena that provide the pathogen with defensive measures against host defenses.…”

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Role of the GapA and CrmA Cytadhesins of Mycoplasma gallisepticum in Promoting Virulence and Host Colonization

Indikova

Much

Stipkovits³

et al. 2013

Infect Immun

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bMycoplasma gallisepticum is an important avian pathogen that commonly induces chronic respiratory disease in chicken. To better understand the mycoplasma factors involved in host colonization, chickens were infected via aerosol with two hemadsorption-negative (HA ؊ ) mutants, mHAD3 and RCL2, that were derived from a low passage of the pathogenic strain R (R low ) and are both deficient in the two major cytadhesins GapA and CrmA. After 9 days of infection, chickens were monitored for air sac lesions and for the presence of mycoplasmas in various organs. The data showed that mHAD3, in which the crmA gene has been disrupted, did not promote efficient colonization or significant air sac lesions. In contrast, the spontaneous HA ؊ RCL2 mutant, which contains a point mutation in the gapA structural gene, successfully colonized the respiratory tract and displayed an attenuated virulence compared to that of R low . It has previously been shown in vitro that the point mutation of RCL2 spontaneously reverts with a high frequency, resulting in on-and-off switching of the HA phenotype. Detailed analyses further revealed that such an event is not responsible for the observed in vivo outcome, since 98.4% of the mycoplasma populations recovered from RCL2-infected chickens still display the mutation and the associated phenotype. Unlike R low , however, RCL2 was unable to colonize inner organs. These findings demonstrate the major role played by the GapA and CrmA proteins in M. gallisepticum host colonization and virulence.

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Mycoplasma gallisepticum: influence of cell invasiveness on the outcome of experimental infection in chickens

Cited by 66 publications

References 25 publications

Interaction of Mycoplasma genitalium with host cells: evidence for nuclear localization

Interaction of Mycoplasma genitalium with host cells: evidence for nuclear localization

Persistence of Mycoplasma synoviae in hens after two enrofloxacin treatments and detection of mutations in the parC gene

Role of the GapA and CrmA Cytadhesins of Mycoplasma gallisepticum in Promoting Virulence and Host Colonization

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