Swine and Poultry Pathogens: the Complete Genome Sequences of Two Strains ofMycoplasma hyopneumoniaeand a Strain ofMycoplasma synoviae

Abstract

This work reports the results of analyses of three complete mycoplasma genomes, a pathogenic (7448) and a nonpathogenic (J) strain of the swine pathogen Mycoplasma hyopneumoniae and a strain of the avian pathogen Mycoplasma synoviae; the genome sizes of the three strains were 920,079 bp, 897,405 bp, and 799,476 bp, respectively. These genomes were compared with other sequenced mycoplasma genomes reported in the literature to examine several aspects of mycoplasma evolution. Strain-specific regions, including integrative and conjugal elements, and genome rearrangements and alterations in adhesin sequences were observed in the M. hyopneumoniae strains, and all of these were potentially related to pathogenicity. Genomic comparisons

Comparative proteomics of two Mycoplasma hyopneumoniae strains and Mycoplasma flocculare identified potential porcine enzootic pneumonia determinants

“…M. hyopneumoniae pathogenic strain 7448 was isolated from an infected swine from Lindóia do Sul (SC, Brazil) [7]. M. hyopneumoniae non-pathogenic strain J (ATCC 25,934), and the non-pathogenic M. flocculare (ATCC 27,716) were acquired from American Type Culture Collection by the Empresa Brasileira de Pesquisa Agropecuária-Centro Nacional de Pesquisa de Suínos e Aves (EMBRAPA-CNPSA, Concórdia, SC, Brazil).…”

“…Despite the pathogenic nature of M. hyopneumoniae , there are some strains that vary in their virulence levels, or even are avirulent, such as M. hyopneumoniae J, which has reduced adhesion capacity to porcine cilia [6]. Comparisons between the genomes of M. hyopneumoniae pathogenic and non-pathogenic strains (7448 and J, respectively) revealed no extensive genomic differences [7]. Moreover, previous comparative phylogenetic and phylogenomic studies provided evidences of the close relationship of M. hyopneumoniae and M. flocculare [7–9], which share most of the known virulence-related genes [10].…”

“…Comparisons between the genomes of M. hyopneumoniae pathogenic and non-pathogenic strains (7448 and J, respectively) revealed no extensive genomic differences [7]. Moreover, previous comparative phylogenetic and phylogenomic studies provided evidences of the close relationship of M. hyopneumoniae and M. flocculare [7–9], which share most of the known virulence-related genes [10]. The differences between M. hyopneumoniae and M. flocculare include the absence, in M. flocculare , of the glpO gene, related to M. hyopneumoniae hydrogen peroxide generation and cytotoxicity [11,12], and differential domains between orthologs from the P97 family of adhesins and from other surface proteins [13].…”

Nested-PCR for the detection of Mycoplasma hyopneumoniae in bronchial alveolar swabs, frozen tissues and formalin-fixed paraffin-embedded swine lung samples: comparative evaluation with immunohistochemical findings and histological features

“…The formaldehyde initiates DNA denaturation (interchain hydrogen bonds break and bases unstacking) at the AT-rich regions of double-stranded DNA creating sites for chemical interaction (Srinivasan et al 2002). The Mycoplasma hyopneumoniae genome presents a high A+T content of about 70% (Vasconcelos et al 2005) thereby the effects of ϐixatives produce greater damages on its DNA, making its extraction and manipulation a major challenge. Ha et al (2005), found a 100% agreement between seminested PCR on formalin-ϐixed and fresh lung tissues.…”

Detection, quantification and genetic variability of Mycoplasma hyopneumoniae from apparently healthy and pneumonic swine

“…All samples were firstly analyzed using a Mollicutes-PCR (KUPPEVELD et al, 1994). Afterwards, all Mollicutes positive samples were used for M. hyopneumoniae detection using the following DNA amplification assays: A multiplex PCR described by Yamaguti (2008), directed to the multiple detection of M. hyopneumoniae, M. hyorhinis and M. flocculare (data not published), a real-time PCR (STRAIT et al, 2008) and an assay based in the amplification of 4 VNTR containing regions (VRANCKX et al, 2011).…”