The Interplay between the Microbiota and Enterohemorrhagic
            <i>Escherichia coli</i>

Pifer, Reed; Sperandio, Vanessa

doi:10.1128/microbiolspec.ehec-0015-2013

Cited by 29 publications

(27 citation statements)

References 92 publications

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“…Owning farm animals was a risk factor for detecting STEC in children, and summertime was a risk factor for both STEC and EPEC. It is known that ruminants and, specifically, cattle are the main reservoir for STEC [15]. In summer, outdoor keeping of dairy cattle is common and beef calving season is ongoing.…”

Section: Discussionmentioning

confidence: 99%

Potential causative agents of acute gastroenteritis in households with preschool children: prevalence, risk factors, clinical relevance and household transmission

Heusinkveld

Mughini‐Gras

Pijnacker

et al. 2016

Eur J Clin Microbiol Infect Dis

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Acute gastroenteritis (AGE) morbidity remains high amongst preschool children, posing a significant societal burden. Empirical data on AGE-causing agents is needed to gauge their clinical relevance and identify agent-specific targets for control. We assessed the prevalence, risk factors and association with symptoms for enteropathogens in households with preschool children. A monthly-repeated cross-sectional survey of enteropathogens in households with preschool children was performed. A parent-child pair per household (n = 907 households) provided faecal samples and reported their symptoms and potential risk exposures. Samples were tested by multiplex reverse transcription polymerase chain reaction (RT-PCR) for 19 enteropathogens. Associations were assessed using logistic regression. 28.3 % of children (n = 981) and 15.6 % of parents (n = 971) carried pathogenic bacteria and/or Escherichia coli-associated pathogenicity genes, and 6.5 % and 3.3 % carried viruses, respectively. Giardia lamblia (4.6 % of children, 2.5 % of parents) and Dientamoeba fragilis (36 %, 39 %, respectively) were the main parasites, and were associated with pet exposure. Living in rural areas was associated with carriage of pathogenic E. coli, norovirus I and D. fragilis. Pathogenic E. coli was associated with summertime and livestock exposure. Attending day-care centres increased the risk of carrying norovirus, sapovirus and G. lamblia. Viruses occurred mainly in winter and were associated with AGE symptoms. Child-parent associations were found for bacterial pathogenicity genes, viruses, G. lamblia and D. fragilis. Enteropathogens spread widely in households with preschool children, particularly viruses, which more often cause symptoms. While bacteria predominate during summer and in those exposed to livestock, viruses predominate in wintertime and, like G. lamblia, are widespread amongst day-care centre attendees.

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Section: Discussionmentioning

confidence: 99%

Potential causative agents of acute gastroenteritis in households with preschool children: prevalence, risk factors, clinical relevance and household transmission

Heusinkveld

Mughini‐Gras

Pijnacker

et al. 2016

Eur J Clin Microbiol Infect Dis

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“…Finally, QseC also regulates the expression of a second TCS, QseEF, which is essential for pedestal formation and the formation of attaching and effacing (A/E) lesions (Reading et al ., ). Indeed, as discussed in greater detail below, QseBC initiates a complex signaling cascade that integrates both positive and negative controls of EHEC virulence factors (Hughes et al ., ; Pifer & Sperandio, ). In uropathogenic E. coli , deletion of qseC resulted in reduced bladder titers and decreased formation of intracellular bacterial communities in a mouse acute infection model (Kostakioti et al ., ), and a decreased ability to establish chronic cystitis (Kostakioti et al ., ).…”

Section: Functional Outcomes Of Qsebc Activation: Biofilms and Virulencementioning

confidence: 99%

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

Weigel

Demuth

2015

Molecular Oral Microbiology

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SummaryThe QseBC two‐component system (TCS) is associated with quorum sensing and functions as a global regulator of virulence. Based on sequence similarity within the sensor domain and conservation of an acidic motif essential for signal recognition, QseBC is primarily distributed in the Enterobacteriaceae and Pasteurellaceae. In Escherichia coli, QseC responds to autoinducer‐3 and/or epinephrine/norepinephrine. Binding of epinephrine/norepinephrine is inhibited by adrenergic antagonists; hence QseC functions as a bacterial adrenergic receptor. Aggregatibacter actinomycetemcomitans QseC is activated by a combination of epinephrine/norepinephrine and iron, whereas only iron activates the Haemophilus influenzae sensor. QseC phosphorylates QseB but there is growing evidence that QseB is activated by non‐cognate sensors and regulated by dephosphorylation via QseC. Interestingly, the QseBC signaling cascades and regulons differ significantly. In enterohemorrhagic E. coli, QseC induces expression of a second adrenergic TCS and phosphorylates two non‐cognate response regulators, each of which induces specific sets of virulence genes. This signaling pathway integrates with other regulatory mechanisms mediated by transcriptional regulators QseA and QseD and a fucose‐sensing TCS and likely controls the level and timing of virulence gene expression. In contrast, A. actinomycetemcomitans QseC signals through QseB to regulate genes involved in anaerobic metabolism and energy production, which may prime cellular metabolism for growth in an anaerobic host niche. QseC represents a novel target for therapeutic intervention and small molecule inhibitors already show promise as broad‐spectrum antimicrobials. Further characterization of QseBC signaling may identify additional differences in QseBC function and inform further development of new therapeutics to control microbial infections.

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“…Many enteric pathogens exploit this intestinal chemistry to recognize the environment and gauge host physiology. These pathogens are crafty in recognizing different microbiota as well as host derived signals and nutrients to coordinate expression of their virulence traits, and adjust their metabolism to ensure successful competition for nutrients and a colonization niche (Hughes and Sperandio, 2008; Pifer and Sperandio, 2014). …”

Section: Introductionmentioning

confidence: 99%

Frenemies: Signaling and Nutritional Integration in Pathogen-Microbiota-Host Interactions

Cameron

Sperandio

2015

Cell Host & Microbe

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Summary The mammalian gastrointestinal (GI) microbiota is highly adapted to thrive in the GI environment and performs key functions related to host nutrition, physiology, development, immunity, and behavior. Successful host-bacterial associations require chemical signaling and optimal nutrient utilization and exchange. However, this important balance can be severely disrupted by environmental stimuli, with one of most common insults upon the microbiota being infectious diseases. Although the microbiota acts as a barrier towards enteric pathogens, many enteric pathogens exploit signals and nutrients derived from both the microbiota and host to regulate their virulence programs. Here we review several signaling and nutrient recognition systems employed by GI pathogens to regulate growth and virulence. We discuss how shifts in the microbiota composition change host susceptibility to infection, and how dietary changes or manipulation of the microbiota could potentially prevent and/or ameliorate GI infections.

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The Interplay between the Microbiota and Enterohemorrhagic Escherichia coli

Abstract: The gastrointestinal tract of mammals is home to a plethora of microbial species that comprise the microbiota.

Cited by 29 publications

References 92 publications

Potential causative agents of acute gastroenteritis in households with preschool children: prevalence, risk factors, clinical relevance and household transmission

Potential causative agents of acute gastroenteritis in households with preschool children: prevalence, risk factors, clinical relevance and household transmission

QseBC, a two‐component bacterial adrenergic receptor and global regulator of virulence in Enterobacteriaceae and Pasteurellaceae

Frenemies: Signaling and Nutritional Integration in Pathogen-Microbiota-Host Interactions

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