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Shannon Manning - Michigan State University. East Lansing, MI, US

Shannon Manning Shannon Manning

Foundation Professor of Molecular Biology and Epidemiology | Michigan State University

East Lansing, MI, UNITED STATES

Expert in E. coli outbreaks

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Biography

My laboratory studies the molecular epidemiology and evolutionary genetics of infectious diseases, namely those caused by diarrheagenic Escherichia coli and Streptococcus agalactiae. We apply molecular biology, epidemiological and evolutionary methods to answer questions about pathogenesis, emergence, virulence, evolution, and transmission of pathogens in human and animal populations. Our studies of both Shiga toxin-producing E. coli (STEC) O157:H7 and S. agalactiae are similar in that the phylogenetic analysis of genomic data and the subsequent epidemiological analysis identified specific strain types to be more important for disease. Most of our current and future research projects are associated with these key findings that will ultimately enhance our understanding of how genetic variation contributes to clinical illness.

We also manage and curate the STEC Center, which serves as a repository for STEC and other enteric pathogens.

Industry Expertise (4)

Education/Learning Laboratory Services Research Biotechnology

Areas of Expertise (6)

Molecular Biology Epidemiology Microbiology E. Coli Outbreaks Molecular Genetics Agriculture and Natural Resources

Accomplishments (1)

Grant - E. Coli Research (professional)

From the U.S. Department of Agriculture

Education (2)

University of Michigan: Ph.D., Molecular Epidemiology 2001

University of Michigan: M.P.H., Hospital and Molecular Epidemiology 1998

News (4)

A Safer Tomorrow

MSU Today  

2016-08-10

One of the biggest challenges in the fight against infectious diseases—caused by pathogens like bacteria and viruses—is that pathogens constantly change, evolve, or acquire new characteristics. In an evolutionary arms race at the molecular level, Michigan State University microbiology and molecular genetics researcher Shannon Manning and her team are finding ways to protect people with new vaccines and treatments by predicting how these pathogens will change...

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Researchers and Farmers Collaborate to Prevent E. Coli

MSU Today  

2016-07-05

“Reducing STEC colonization and shedding in cattle can decrease the likelihood of these bacterial pathogens from entering the food supply and causing foodborne infections in people,” said Shannon Manning, MSU molecular biologist and principal investigator of the study. “By understanding specific factors that increase the risks of STEC shedding in cattle, new management strategies, such as the isolation of high-risk animals, can be developed to limit transmission."...

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Controlling Levels of Specific Gut Bacteria Could Prevent Severe Diarrhea

MSU Today  

2015-11-10

In the MSU study, most of the patients had an increase in the level of Escherichia, bacteria that are commonly found in the intestines that can sometimes be pathogenic, said Shannon Manning, MSU Foundation Professor of microbiology and molecular genetics and leader of the study.

“Compared to the uninfected patients in the study, the patients who were infected with four different diarrheal pathogens – Salmonella, Shiga toxin-producing E. coli, Campylobacter and Shigella – all had increased levels of Escherichia,” she said. “In addition, patients had a decrease in the Escherichia population after they recovered.”...

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Shannon Manning: Decoding deadly E. coli

MSU Today  

2015-01-05

Shannon Manning is an AgBioResearch microbiologist and molecular geneticist. Her research focuses on applying molecular and evolutionary approaches to study the virulence, epidemiology and evolution of bacterial pathogens to better understand pathogenesis, emergence, and transmission in human and animal populations...

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Journal Articles (5)

Contribution of the RgfD quorum sensing peptide to rgf regulation and host cell association in group b Streptococcus Genes

2017

Streptococcus agalactiae (group B Streptococcus; GBS) is a common inhabitant of the genitourinary and/or gastrointestinal tract in up to 40% of healthy adults; however, this opportunistic pathogen is able to breach restrictive host barriers to cause disease and persist in harsh and changing conditions. This study sought to identify a role for quorum sensing, a form of cell to cell communication, in the regulation of the fibrinogen-binding (rgfBDAC) two-component system and the ability to associate with decidualized endometrial cells in vitro. To do this, we created a deletion in rgfD, which encodes the putative autoinducing peptide, in a GBS strain belonging to multilocus sequence type (ST)-17 and made comparisons to the wild type. Sequence variation in the rgf operon was detected in 40 clinical strains and a non-synonymous single nucleotide polymorphism was detected in rgfD in all of the ST-17 genomes that resulted in a truncation. Using qPCR, expression of rgf operon genes was significantly decreased in the ST-17 ΔrgfD mutant during exponential growth with the biggest difference (3.3-fold) occurring at higher cell densities. Association with decidualized endometrial cells was decreased 1.3-fold in the mutant relative to the wild type and rgfC expression was reduced 22-fold in ΔrgfD following exposure to the endometrial cells. Collectively, these data suggest that this putative quorum sensing molecule is important for attachment to human tissues and demonstrate a role for RgfD in GBS pathogenesis through regulation of rgfC.

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Multilocus sequence types associated with neonatal group B streptococcal sepsis and meningitis in Canada Journal of Clinical Microbiology

2009

Group B streptococci (GBS), a leading cause of neonatal sepsis and meningitis, are transferred to neonates from colonized mothers during childbirth. Prior studies using multilocus sequence typing (MLST) have found specific GBS clones (e.g., sequence type 17 [ST-17]) to be associated with neonatal disease in several geographic locations. Few population-based studies, however, have been conducted to determine the frequency of disease caused by specific GBS clones. MLST was used to assess the genetic diversity of 192 GBS strains from neonates and young children identified by population-based surveillance in Alberta, Canada, from 1993 to 2002. Comparisons were made to 232 GBS strains collected from colonized pregnant women, and all strains were characterized for one of nine capsule (cps) genotypes. A total of 47 STs were identified, and more than 80% of GBS strains were represented by 7 STs that have been shown to predominate in other populations. ST-17 and ST-19 were more prevalent in strains causing early onset disease (EOD) and late onset disease (LOD) than from pregnant women, whereas STs 1, 12, and 23 were more common in pregnant women. In addition, ST-17 strains and close relatives more frequently caused meningitis than sepsis and LOD versus EOD in this population of neonates. Further research is required to better understand why strains belonging to the ST-17 phylogenetic lineage are more likely to cause both LOD and meningitis and may provide clues into the pathogenesis of these conditions.

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Variation in virulence among clades of Escherichia coli O157: H7 associated with disease outbreaks Proceedings of the National Academy of Sciences of the United States of America

2008

Escherichia coli O157:H7, a toxin-producing food and waterborne bacterial pathogen, has been linked to large outbreaks of gastrointestinal illness for more than two decades. E. coli O157 causes a wide range of clinical illness that varies by outbreak, although factors that contribute to variation in disease severity are poorly understood. Several recent outbreaks involving O157 contamination of fresh produce (e.g., spinach) were associated with more severe disease, as defined by higher hemolytic uremic syndrome and hospitalization frequencies, suggesting that increased virulence has evolved. To test this hypothesis, we developed a system that detects SNPs in 96 loci and applied it to >500 E. coli O157 clinical strains. Phylogenetic analyses identified 39 SNP genotypes that differ at 20% of SNP loci and are separated into nine distinct clades. Differences were observed between clades in the frequency and distribution of Shiga toxin genes and in the type of clinical disease reported. Patients with hemolytic uremic syndrome were significantly more likely to be infected with clade 8 strains, which have increased in frequency over the past 5 years. Genome sequencing of a spinach outbreak strain, a member of clade 8, also revealed substantial genomic differences. These findings suggest that an emergent subpopulation of the clade 8 lineage has acquired critical factors that contribute to more severe disease. The ability to detect and rapidly genotype O157 strains belonging to such lineages is important and will have a significant impact on both disease diagnosis and treatment guidelines.

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Variation in virulence among clades of Escherichia coli O157: H7 associated with disease outbreaks Proceedings of the National Academy of Sciences

2008

Escherichia coli O157:H7, a toxin-producing food and waterborne bacterial pathogen, has been linked to large outbreaks of gastrointestinal illness for more than two decades. E. coli O157 causes a wide range of clinical illness that varies by outbreak, although factors that contribute to variation in disease severity are poorly understood. Several recent outbreaks involving O157 contamination of fresh produce (e.g., spinach) were associated with more severe disease, as defined by higher hemolytic uremic syndrome and hospitalization frequencies, suggesting that increased virulence has evolved. To test this hypothesis, we developed a system that detects SNPs in 96 loci and applied it to >500 E. coli O157 clinical strains. Phylogenetic analyses identified 39 SNP genotypes that differ at 20% of SNP loci and are separated into nine distinct clades. Differences were observed between clades in the frequency and distribution of Shiga toxin genes and in the type of clinical disease reported. Patients with hemolytic uremic syndrome were significantly more likely to be infected with clade 8 strains, which have increased in frequency over the past 5 years. Genome sequencing of a spinach outbreak strain, a member of clade 8, also revealed substantial genomic differences. These findings suggest that an emergent subpopulation of the clade 8 lineage has acquired critical factors that contribute to more severe disease. The ability to detect and rapidly genotype O157 strains belonging to such lineages is important and will have a significant impact on both disease diagnosis and treatment guidelines.

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Repeated evolution of an acetate-crossfeeding polymorphism in long-term populations of Escherichia coli Molecular Biology and Evolution

1998

Six out of 12 independent replicate populations of Escherichia coli maintained in long-term glucose-limited continuous culture for up to approximately 1,750 generations evolve polymorphisms maintained by acetate crossfeeding. In all cases, the acetate-crossfeeding phenotype is associated with semiconstitutive overexpression of acetyl CoA synthetase, which allows for the enhanced uptake of low levels of exogenous acetate. Mutations in the 5' regulatory region of the acetyl CoA synthetase locus are responsible for all the acetate crossfeeding phenotypes found. These changes were either transposable-element insertions or a single T-->A nucleotide substitution at position -93 relative to the acs gene translation start site.

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