An overview of atypical enteropathogenic<i>Escherichia coli</i>

Hernandes, Rodrigo T.; Elias, Waldir P.; Vieira, MÃ ́nica A.M.; Gomes, Tânia A. T.

doi:10.1111/j.1574-6968.2009.01664.x

Cited by 251 publications

(260 citation statements)

References 129 publications

(168 reference statements)

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“…Although some zoonotic pathogens, such as Campylobacter jejuni, are recognized as the most frequent gastrointestinal bacterial pathogen in humans in industrialized countries (11,12), the contribution of other zoonotic pathogens (such as enteropathogenic E. coli or many strains of Shiga-toxigenic E. coli) to human diarrhea is less understood (13)(14)(15).…”

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confidence: 99%

Detection of Zoonotic Enteropathogens in Children and Domestic Animals in a Semirural Community in Ecuador

Vasco

Graham

Trueba

2016

Appl Environ Microbiol

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Animals are important reservoirs of zoonotic enteropathogens, and transmission to humans occurs more frequently in low-and middle-income countries (LMICs), where small-scale livestock production is common. In this study, we investigated the presence of zoonotic enteropathogens in stool samples from 64 asymptomatic children and 203 domestic animals of 62 households in a semirural community in Ecuador between June and August 2014. Multilocus sequence typing (MLST) was used to assess zoonotic transmission of Campylobacter jejuni and atypical enteropathogenic Escherichia coli (aEPEC), which were the most prevalent bacterial pathogens in children and domestic animals (30.7% and 10.5%, respectively). Four sequence types (STs) of C. jejuni and four STs of aEPEC were identical between children and domestic animals. The apparent sources of human infection were chickens, dogs, guinea pigs, and rabbits for C. jejuni and pigs, dogs, and chickens for aEPEC. Other pathogens detected in children and domestic animals were Giardia lamblia (13.1%), Cryptosporidium parvum (1.1%), and Shiga toxin-producing E. coli (STEC) (2.6%). Salmonella enterica was detected in 5 dogs and Yersinia enterocolitica was identified in 1 pig. Even though we identified 7 enteric pathogens in children, we encountered evidence of active transmission between domestic animals and humans only for C. jejuni and aEPEC. We also found evidence that C. jejuni strains from chickens were more likely to be transmitted to humans than those coming from other domestic animals. Our findings demonstrate the complex nature of enteropathogen transmission between domestic animals and humans and stress the need for further studies. IMPORTANCEWe found evidence that Campylobacter jejuni, Giardia, and aEPEC organisms were the most common zoonotic enteropathogens in children and domestic animals in a region close to Quito, the capital of Ecuador. Genetic analysis of the isolates suggests transmission of some genotypes of C. jejuni and aEPEC from domestic animals to humans in this region. We also found that the genotypes associated with C. jejuni from chickens were present more often in children than were those from other domestic animals. The potential environmental factors associated with transmission of these pathogens to humans then are discussed. Diarrheal diseases are a major cause of illness and death in lowand middle-income countries (LMICs), where there are over 1.5 billion diarrhea cases that occur annually among children less than 5 years old, resulting in nearly 700,000 deaths (1). Although the contribution of zoonotic pathogens to human diarrheal disease is significant (2), these pathogens are often overlooked, and their detection may be hindered by patterns of seasonality (3). Zoonotic enteropathogens comprise a large and diverse range of microorganisms that could be transmitted to humans by consumption of meat or dairy products, by direct contact with animals (or their feces) in the environment, or by consumption of food or water contaminated with animal f...

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Detection of Zoonotic Enteropathogens in Children and Domestic Animals in a Semirural Community in Ecuador

Vasco

Graham

Trueba

2016

Appl Environ Microbiol

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“…The results clearly demonstrated a delay in bacterial adhesion and formation of actin-rich pedestals in aEPEC, in comparison to that observed with tEPEC strains. There are some factors that could explain these results, such as the absence of BFP and Per, both located in pEAF (11). In fact, all aEPEC strains of this study lack the perABC sequences (data not shown).…”

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confidence: 73%

“…On the other hand, aEPEC strains frequently display a localized adherence-like (LAL) pattern, in which the compact clusters are not observed (19). In contrast to the LA pattern, which can be observed after 3 h of bacterium-eukaryotic cell contact (17), the LAL pattern is expressed after 6 h of interaction (11). Consequently, the A/E lesions can be detected in tEPEC after 3 h of interaction, while in aEPEC this phenotype is delayed and not detected until after 6 h (20)(21)(22)(23)(24).…”

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confidence: 87%

“…EPEC strains are currently classified as typical (tEPEC) if they harbor the E. coli adherence plasmid (pEAF) or atypical (aEPEC) if they lack that plasmid (10,11). pEAF contains the bfp operon, encoding the bundle-forming pilus (BFP), and per (plasmid-encoded regulator) operon, which encodes the regulator proteins PerA, PerB, and PerC, involved in the regulation of BFP, LEE genes, and per itself (12)(13)(14).…”

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Late Establishment of the Attaching and Effacing Lesion Caused by Atypical Enteropathogenic Escherichia coli Depends on Protein Expression Regulated by Per

et al. 2015

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c Enteropathogenic Escherichia coli (EPEC) is classified as typical (tEPEC) or atypical (aEPEC) based on the presence or absence of the E. coli adherence factor plasmid (pEAF), respectively. The hallmark of EPEC infection is the formation of the attaching and effacing (A/E) lesions on the gut mucosa. We compared the kinetics of A/E lesion formation induced by aEPEC and tEPEC. The examination of infected HEp-2 cells clearly demonstrated delayed A/E lesion formation by aEPEC in comparison to tEPEC. This delay was associated with the expression of locus of enterocyte effacement (LEE)-encoded virulence factors (i.e., intimin and EspD). Indeed, the insertion of a plasmid containing perABC, a transcriptional regulator of virulence factors involved in A/E formation, into aEPEC strains increased and accelerated the formation of A/E lesions. Interestingly, the enhanced expression and translocation of LEE-encoded proteins, such as those expressed in LEE5 (intimin) and LEE4 (EspD), in aEPEC (perABC) was independent of bacterial adhesion. The secretion kinetics of these two proteins representing LEE5 and LEE4 expression correlated with A/E lesion formation. We conclude that the lack of Per in the regulation network of virulence genes is one of the main factors that delay the establishment of A/E lesions induced by aEPEC strains.

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“…aEPEC has phenotypic and genotypic properties different from those of typical enteropathogenic E. coli (tEPEC), which causes diarrhea mainly in children Ͻ2 years old (4). The frequency of aEPEC strains has increased in both diarrheic and nondiarrheic children to the point that tEPEC strains are often outnumbered in regions where diarrhea due to E. coli is endemic (5,6). The main difference between aEPEC and tEPEC is the absence of the EPEC adherence factor plasmid (pEAF) in the former group (4,7).…”

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Flagellar Cap Protein FliD Mediates Adherence of Atypical Enteropathogenic Escherichia coli to Enterocyte Microvilli

et al. 2016

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The expression of flagella correlates with different aspects of bacterial pathogenicity, ranging from adherence to host cells to activation of inflammatory responses by the innate immune system. In the present study, we investigated the role of flagella in the adherence of an atypical enteropathogenic Escherichia coli (aEPEC) strain (serotype O51:H40) to human enterocytes. Accordingly, isogenic mutants deficient in flagellin (FliC), the flagellar structural subunit; the flagellar cap protein (FliD); or the MotAB proteins, involved in the control of flagellar motion, were generated and tested for binding to differentiated Caco-2 cells. Binding of the aEPEC strain to enterocytes was significantly impaired in strains with the fliC and fliD genes deleted, both of which could not form flagella on the bacterial surface. A nonmotile but flagellated MotAB mutant also showed impaired adhesion to Caco-2 cells. In accordance with these observations, adhesion of aEPEC strain 1711-4 to Caco-2 cells was drastically reduced after the treatment of Caco-2 cells with purified FliD. In addition, incubation of aEPEC bacteria with specific anti-FliD serum impaired binding to Caco-2 cells. Finally, incubation of Caco-2 cells with purified FliD, followed by immunolabeling, showed that the protein was specifically bound to the microvillus tips of differentiated Caco-2 cells. The aEPEC FliD or anti-FliD serum also reduced the adherence of prototype typical enteropathogenic, enterohemorrhagic, and enterotoxigenic E. coli strains to Caco-2 cells. In conclusion, our findings further strengthened the role of flagella in the adherence of aEPEC to human enterocytes and disclosed the relevant structural and functional involvement of FliD in the adhesion process.

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An overview of atypical enteropathogenicEscherichia coli

Cited by 251 publications

References 129 publications

Detection of Zoonotic Enteropathogens in Children and Domestic Animals in a Semirural Community in Ecuador

Detection of Zoonotic Enteropathogens in Children and Domestic Animals in a Semirural Community in Ecuador

Late Establishment of the Attaching and Effacing Lesion Caused by Atypical Enteropathogenic Escherichia coli Depends on Protein Expression Regulated by Per

Flagellar Cap Protein FliD Mediates Adherence of Atypical Enteropathogenic Escherichia coli to Enterocyte Microvilli

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