Biology subjects

Baby, V.

Publications and source records attributed to Baby, V..

3 recordsLinked to original sources

bioRxiv2023

Comparative genomics of Mycoplasma feriruminatoris, a fast-growing pathogen of wild Caprinae

Mycoplasma feriruminatoris is a fast-growing Mycoplasma species isolated from wild Caprinae and first described in 2013. M. feriruminatoris isolates have been associated with arthritis, keratoconjunctivitis, pneumonia and septicemia, but were also recovered from apparently healthy animals. To better understand what defines this species, we performed a genomic survey on 14 strains collected from free-ranging or zoo-housed animals between 1987 and 2017. The average chromosome size of the M. feriruminatoris strains was 1,040 {+/-} 0,024 kbp, with 24% G+C and 852 {+/-} 31 CDS. The core genome and pan-genome of the M. feriruminatoris species contained 628 and 1,312 protein families, respectively. The M. feriruminatoris strains displayed a relatively closed pan-genome, with many features and putative virulence factors shared with species from the M. mycoides cluster, including the MIB-MIP Ig cleavage system, a repertoire of DUF285 surface proteins and a complete biosynthetic pathway for galactan. M. feriruminatoris genomes were found to be mostly syntenic, although repertoires of mobile genetic elements, including Mycoplasma Integrative and Conjugative Elements, insertion sequences, and a single plasmid varied. Phylogenetic- and gene content analyzes confirmed that M. feriruminatoris was closer to the M. mycoides cluster than to the ruminant species M. yeatsii and M. putrefaciens. Ancestral genome reconstruction showed that the emergence of the M. feriruminatoris species was associated with the gain of 17 gene families, some of which encode defense enzymes and surface proteins, and the loss of 25 others, some of which are involved in sugar transport and metabolism. This comparative study suggests that the M. mycoides cluster could be extended to include M. feriruminatoris. We also find evidence that the specific organization and structure of the DnaA boxes around the oriC of M. feriruminatoris may contribute to drive the remarkable fast growth of this minimal bacterium.

microbiology↗

bioRxiv2023

Evolution of the CRISPR-Cas9 defence system following a bacterial host shift

CRISPR-Cas systems are bacterial defences that target bacteriophages and mobile genetic elements. How these defences evolve in novel host environments remains, however, unknown. We studied the evolution of the CRISPR-Cas system in Mycoplasma gallisepticum, a bacterial pathogen of poultry that jumped into a passerine host [~]30 years ago. Over the decade following the host shift, all isolates displayed a functional CRISPR-Cas system were found not only to harbour completely new sets of spacers, but the DNA protospacer adjacent motif (PAM) recognised by the main effector MgCas9 was also different. These changes in CRISPR-Cas diversity and specificity are consistent with a change in the community of phages and mobile elements infecting M. gallisepticum as it colonised the novel host. In the years following the host shift, we also detected a gradual rise in isolates displaying non-functional MgCas9. After 12 years, all circulating isolates harboured inactive forms only. This loss of CRISPR-Cas function comes at a time when the passerine host is known to have evolved widespread resistance, which in turn drove the evolution of increasing M. gallisepticum virulence through antagonistic coevolution. Such striking concordance in the rise of inactivated forms of CRISPR-Cas and the evolution of host resistance suggests that inactivation of the CRISPR-Cas system was necessary for enabling adaptive bacterial responses to host-driven selection. We highlight the need to consider both host and pathogen selection pressures on bacteria for understanding the evolution of CRISPR-Cas systems and the key factors driving the emergence of a pathogenic bacterium in a novel host. Data summaryThe authors confirm all supporting data and protocols have been provided within the article or through supplementary data files available in the online version of this article. GenBank accession numbers of all publicly available M. gallisepticum genomes are listed in Table S3. Sequences of the CRISPR locus of other strains are also provided in Table S3. Impact statementMycoplasma are minimal bacteria involved in many diseases affecting humans and a wide diversity of animals. In this paper, we report the evolution of the Type II CRISPR-Cas system of the bird pathogen, Mycoplasma gallisepticum, following an host jump from its original poultry host into its novel house finch host in the early 90s. Instances in which bacterial pathogens have been documented to jump into and subsequently adapt to a new host are rare, and the well documented case of M. gallisepticum is a unique model to evaluate the effect of any dramatic host environmental change on bacterial CRISPR-Cas defence systems. First, we performed in silico analyses on an extended set of 98 M. gallisepticum genomes to better understand the evolution of the CRISPR-Cas9 system in the novel finch host. We documented several evolutionary events leading to the drastic divergence of spacer sets present in poultry and house finch arrays, as well as the progressive inactivation of the CRISPR-Cas system after 12 years in the novel finch host. Second, using in vitro and in vivo assays, we demonstrated that the evolution of the MgCas9 PI domain, involved in the protospacer adjacent motif (PAM) recognition has led to a major change in the defence system, with a modification of the recognized PAM in the novel host. Such radical change in the CRISPR-Cas defence system of M. gallisepticum may have implications for the its rapid adaptation to its novel host. Together, our results highlight the need to consider not only the host-driven selection pressures a bacterium experiences, but also the complex interplay between phages and defence systems for better understanding the key factors driving the emergence of a pathogenic bacterium in a novel host.

microbiology↗

bioRxiv2022

Molecular epidemiology of carbapenemase-producing Acinetobacter spp. from Israel, 2001-2006: earliest report of blaNDM predating the oldest known blaNDM-positive strains

BackgroundCarbapenem-resistant Acinetobacter baumannii (CRAb) is a WHO priority 1 critical pathogen. Despite early emergence of elevated CRAb rates in Israel, limited molecular data from this location are available. We searched for carbapenemases among 198 clinical Acinetobacter spp. from Israel between 2001 and 2006. MethodsStrains from 3 archives underwent whole-genome sequencing (Illumina NovaSeq on all, MinION on a subset) and computational analyses: assembly (Unicycler), annotation (prokka), identification (Kraken, rpoB similarity), search for carbapenemases (ResFinder, BLDB curation). FindingsA. baumannii (Ab) represented 179 (90{middle dot}4%) Acinetobacter spp. Eighty-four Ab (46{middle dot}9%) carried a carbapenemase: 38 (45{middle dot}2%) blaOXA-72 (blaOXA-24-like); 28 (33{middle dot}3%) blaOXA-23-like (20 blaOXA-23 and 8 blaOXA-225); 18 (21{middle dot}5%) blaOXA-58 (16 from 2001-2). Carbapenemase rates increased yearly from 2002 (32%) to 2006 (67%). Eight species of non-baumannii Acinetobacter (NbA) accounted for 19 isolates (9{middle dot}6%). Two of three A. junii contained blaOXA-58, one of which, Ajun-H1-3, isolated in January 2004, also possessed blaNDM-1. The pNDM-Ajun-H1-3 plasmid matched numerous NDM-positive plasmids reported from 2005 onwards in Acinetobacter spp. as well as Enterobacterales. InterpretationWe assessed carbapenemase diversity among Acinetobacter spp. in Israel from 2001-2006. Findings in Ab predate observations elsewhere: rapidly rising carbapenemase rates, driven by blaOXA-23-like and blaOXA-24-like genes replacing blaOXA-58. Among NbA, an A. junii isolated in 2004 carried blaNDM-1, making it the earliest NDM-positive isolate reported to date, preceding those from 2005 in India. Further research into blaNDMs emergence is warranted, in order to shed light on the evolution and spread of this and other antibiotic-resistance genes. FundingCentre de recherche Charles-Le Moyne; Department of Microbiology and Infectious Diseases, Faculty of Medicine and Health Sciences, Universite de Sherbrooke; Fonds de recherche du Quebec - Sante; New Frontiers in Research Fund Grant NFRFE-2019-00444; CIFAR-Azrieli Global Scholars Program.

microbiology↗