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The Diversity of Escherichia coli Pathotypes and Vaccination Strategies against This Versatile Bacterial Pathogen

Pravil Pokharel, Sabin Dhakal, Charles M. Dozois

Microorganisms · 2023 · Review · CC BY

doi:10.3390/microorganisms11020344

Abstract

Escherichia coli (E. coli) is a gram-negative bacillus and resident of the normal intestinal microbiota. However, some E. coli strains can cause diseases in humans, other mammals and birds ranging from intestinal infections, for example, diarrhea and dysentery, to extraintestinal infections, such as urinary tract infections, respiratory tract infections, meningitis, and sepsis. In terms of morbidity and mortality, pathogenic E. coli has a great impact on public health, with an economic cost of several billion dollars annually worldwide. Antibiotics are not usually used as first-line treatment for diarrheal illness caused by E. coli and in the case of bloody diarrhea, antibiotics are avoided due to the increased risk of hemolytic uremic syndrome. On the other hand, extraintestinal infections are treated with various antibiotics depending on the site of infection and susceptibility testing. Several alarming papers concerning the rising antibiotic resistance rates in E. coli strains have been published. The silent pandemic of multidrug-resistant bacteria including pathogenic E. coli that have become more difficult to treat favored prophylactic approaches such as E. coli vaccines. This review provides an overview of the pathogenesis of different pathotypes of E. coli, the virulence factors involved and updates on the major aspects of vaccine development against different E. coli pathotypes.

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From PubMed Central, U.S. National Library of Medicine, as current on Oct 23, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Introduction

1Vaccines are a major asset for the reduction of the burden of infectious diseases worldwide. They can provide long-term immunity, cheaper modalities than diagnosis and treatment of the infections after they have started, and most importantly—can prevent diseases from occurring in susceptible populations or animal species. Despite the potential benefits of vaccines, we do not see much enthusiasm for the development of vaccines against E. coli, particularly for human health. There could be scientific, financial, legal, or political barriers, although increased antimicrobial resistance may promote vaccine development if such pathogens become difficult to treat. Herein, we have summarized aspects of each pathotype of E. coli before presenting vaccine strategies, since different antigens or components (inactivated whole cells, O antigen, fimbriae, adhesins, enterotoxins, outer membrane proteins (OMPs)) have been used against different E. coli pathotypes. Some of the vaccine strategies have been licensed and shown to be efficacious, but most have only been at the developmental stage, as detailed below.

1.1. Escherichia coli

2Escherichia coli (E. coli) is one of the most intensively studied model organisms in microbiology and molecular biology research. E. coli is a well-known commensal bacterium that is among the first colonizing bacteria in the gut after birth. However, in immunosuppressed patients or in healthy individuals whose physical, anatomical and physiological barriers have been compromised, E. coli can cause severe systemic infections. Further, due to the genetic variability some E. coli strains are different from their commensal counterparts and encode specific virulence traits that render them capable of causing disease in a variety of animals. Pathogenic E. coli are broadly divided into two groups, extraintestinal pathogenic E. coli (ExPEC) and intestinal pathogenic E. coli (InPEC). Depending on the presence of specific virulence factors, mechanisms of infection, tissue tropism, interactions with host cells and clinical symptoms, E. coli can be categorized into various pathotypes. These include: (i) Enteropathogenic E. coli (EPEC), a cause of acute and prolonged diarrhea in infants; (ii) Enterohemorrhagic E. coli (EHEC), which can cause hemorrhagic colitis and hemolytic uremic syndrome (HUS); (iii) Enterotoxigenic E. coli (ETEC), a major cause of travelers’ diarrhea; (iv) Enteroaggregative E. coli (EAEC), a cause of acute and chronic diarrhea; (v) Diffusely adherent E. coli (DAEC) which is associated with watery diarrhea in young children; (vi) Enteroinvasive E. coli (EIEC), a cause of dysentery and watery diarrhea; (vii) Adherent-Invasive E. coli (AIEC) which has been associated in the pathogenesis of inflammatory bowel disease (IBD); (viii) Uropathogenic E. coli (UPEC), a common cause of urinary tract infections (UTI); (ix) Neonatal meningitis E. coli (NMEC), a top cause of neonatal meningitis; (x) Septicemia-associated E. coli (SEPEC), which can cause bacteremia and sepsis; (xi) Avian pathogenic E. coli (APEC), which can cause severe respiratory and systemic infections in poultry. E. coli can also be classified into distinct phylogenetic lineages: A, B1, B2, D1, D2, E and clade I. Group A mostly represents non-pathogenic E. coli that reside along the gastrointestinal tract mucosa. Phylogroup B1 contains both commensal and some strains belonging to the EHEC pathotype. D1, D2, and E represent InPEC. Many ExPEC belongs to group B2. E. coli strains that are genetically diverse but phenotypically indistinguishable are grouped into cryptic clade I. Studies indicate that some APEC and ExPEC strains are phylogenetically closely related and share certain virulence genes. APEC and other avian E. coli may cause a wide variety of intestinal and extraintestinal infections, and in some cases, E. coli from poultry may be a reservoir of human ExPEC and InPEC isolates.

3E. coli is one of the most genetically versatile microorganisms and can colonize and persist in primary (bird/animal/human host-associated) and secondary (open or non-host-associated) habitats. The high plasticity of the genome of this bacterial species gives it a tremendous capacity to evolve due to the gain and loss of genes through genetic changes, leading to the emergence of pathogenic strains from the commensal strains. Genomes of pathogenic E. coli strains are generally larger, as the pathogenic strains require additional adaptive features, including virulence factors. Often, virulence genes are located on transmissible genetic elements such as pathogenicity islands (PAIs), bacteriophages, insertion sequences (ISs), integrons, plasmids, or transposons; hence, they can also be horizontally exchanged and may facilitate novel rearrangements among different bacteria. In contrast, commensal bacteria can also become pathogenic by the loss of genes. For example, Shigella became virulent by the loss of E. coli-specific genes—such as cadA and flagellar genes. Shiga toxins, enterohemolysin, cytolethal distending toxins, superoxide dismutase, and some outer membrane proteins (OMPs) are some examples of virulence factors encoded by phages in E. coli strains. The horizontal transfer between different strains favors diversity and versatility, resulting in the creation of new pathogenic strains as well as the dissemination of acquired virulence genes with novel functions outside their clonal lineage. EHEC acquired stx genes (transfer by phages), OI (O-island), and LEE (locus of enterocyte effacement) (PAI) through horizontal gene transfer. EPEC emerged after the acquisition of the LEE island and espC serine protease gene. Likewise, there are many identified PAIs in different E. coli pathotypes which were required via horizontal gene transfer and can contribute to fitness and the colonization of different niches.

4The accumulating genomic sequence data has led to an increased understanding of E. coli virulence factors and mechanisms underlying species diversification and the tracking of foodborne disease outbreaks. In 2011, there was a foodborne outbreak of diarrhea caused by Shiga-toxin-producing Escherichia coli (EHEC-STEC-VTEC) O104:H4 in Germany associated with the consumption of raw fenugreek sprouts. Interestingly, this strain was more virulent than most Shiga-toxin-producing E. coli. DNA sequencing demonstrated that the strain contained toxin-encoding phage similar to the 933W phage found in EHEC and also harbored plasmid-borne virulence factors typically found in EAEC which promote aggregative adherence to intestinal epithelial cells.

5Another example is the STEC/UPEC serotype O2:H6 ST141 strain, a STEC with virulence genes α-hlyA, cnf1, and clb common to UPEC. This hybrid strain can be a melting pot for pathotype conversion of InPEC and ExPEC because it acquired the stx-harboring prophage and ExPEC PAI. It has been also demonstrated that ST141 includes different hybrid versions, namely, UPEC/EAEC, STEC/UPEC/EAEC, and UPEC-Stx/UPEC.

1.2. Phenomenon of Antibiotic Resistance

6It has been shown that E. coli can be highly resistance to many of the antibiotics used by humans since the 1930s. This may be due in part to the high rate of gene acquisition and horizontal transfer capacity of E. coli strains. The emergence of antibiotic resistance might be multifactorial, but it is largely believed to be caused mainly by human activity and increased antibiotic usage for human health, animal health and food production.. The broadly reported multidrug-resistant E. coli ST131 is an example of highly virulent ExPEC associated with urinary and bloodstream infections and has promoted the widespread dissemination of the CTX-M-15 gene. In general, the E. coli strains have evolved to resist major classes of antibiotics such as β-lactams, quinolones, aminoglycosides, sulfonamides and fosfomycin. AmpC-producing E. coli strains are dominant in gut colonization of both animals and humans and environmental contamination in developing countries. As ESBL- and AmpC-producing E. coli are increasingly reported as the cause of severe infections, we are confined to the last resource antibiotic classes such as polymyxins and carbapenems. Additionally, carbapenem-hydrolyzing oxacillinase-48 (Oxa-48) carrying E. coli strains have also been isolated in Europe where 134 cases of E. coli strains carrying the OXA-48 variant OXA-244 were isolated from clinical samples in Germany. This same variant was further identified in 119 E. coli strains isolated from other European countries. Likewise, New Delhi metallo-β-lactamase (NDM-1) and closely related enzymes are a group of zinc-requiring metallo-β-lactamases capable of hydrolyzing a broad range of β-lactams including all penicillins, cephalosporins and carbapenems. Further, resistant strains containing New Delhi metallo-beta-lactamase 1 (NDM-1) as well as over 20 NDM variants have spread and are associated with infections in many parts of the world. With the increase in international travel and trade globalization, resistant bacteria have become a worldwide public health threat. Similarly, there is widespread use of antibiotics in food animals for various reasons, namely, growth promotion or ongoing mass prophylactic medication. In many developing countries, there is widespread use of third- and fourth-generation cephalosporins (ceftiofur and cefquinome) and fluoroquinolones (enrofloxacin) in food animals. The problem is much worse in developing countries due to the increasing number of extended-spectrum β-lactamase-producing and fluoroquinolone-resistant E. coli due to a lack of regulation, resources, controls, and surveillance.

7Thus, to counteract the above-mentioned antibacterial resistance of highly virulent strains, global efforts are needed to ensure the discovery of alternative solutions. Currently, antimicrobial-resistant pathogens are causing 700,000 deaths per year, and 10 million deaths per year are expected by 2050, a number even higher than the 8.2 million caused by cancer today. The development of novel therapeutic approaches will continue to be essential. In addition, alternative sustainable preventive strategies such as vaccination can help in limiting the increase of antibiotic-resistant E. coli. In the following sections of this review, we will summarize the vaccination strategies to prevent diseases caused by different pathotypes of E. coli.

2. Diarrheagenic E. coli Pathotypes

8Diarrhea was responsible for the deaths of at least 370,000 children in 2019; 800,000 fatalities per year according to data from 2013, and the second leading cause of death in children under five years old. Diarrhea is a global problem, but its high morbidity and mortality occur in low-income countries. Most of these are caused by InPEC whose members possess distinct virulence traits, different O:H serotypes and characteristic clinical syndromes even though they share some steps in the mechanism of pathogenesis that include an attachment to the intestinal mucosa and harbor plasmids that encode virulence factors.

2.1. EPEC

9Among the pathotypes of InPEC, EPEC is a major cause of infantile diarrhea in developing countries, varying from subclinical to fatal infections. The characteristic histopathological hallmark related to this group of E. coli is the production of lesions known as “Attaching and effacing (A/E)” lesions that are produced when bacteria intimately attach to intestinal epithelial cells and alter the cytoskeleton through the accumulation of polymerized actin beneath the adherent bacteria. EPEC is divided into typical EPEC (tEPEC) and atypical EPEC (aEPEC), based on the presence of EPEC adherence factor plasmid (pEAF). They have their own distinct adherence patterns. aEPEC strains exhibit diffuse adherence, localized adherence, and an aggregative adherence pattern, whereas tEPEC strains display a localized adherence pattern. The aEPEC can cause both acute diseases and persistent bloody diarrhea. The tEPEC strains are strongly associated with abundant secretory diarrhea with mucus and significant water and electrolyte losses. While aEPEC can be found in both humans and animals, the reservoir of tEPEC is human.

2.1.1. Molecular Pathogenesis

10EPEC pathogenesis involves three steps: (i) initial adherence to host cells, (ii) translocation of bacterial toxins using a type III secretion system, (iii) pedestal formation and intimate attachment (Figure 1). At first, EPEC strains adhere to the enterocytes in the small intestine and form microcolonies in localized or aggregative patterns. This adherence is fostered mostly by a plasmid-encoded, bundle-forming pilus (BFP). It has been shown that BFP mutant strains are less able to cause diarrhea in human volunteers. Initial adherence and microcolony formation are important for EPEC infections, and BFP is one of the key virulence factors in pathogenesis.

11The locus of enterocyte effacement (LEE), also found in EHEC, encodes a type III secretion system (TTSS), translocators (EspA, EspB and EspD), effectors (Tir, EspG, EspF, Map and EspH), chaperones (CesAB, CesD, CesD2, CesF, and CesT) and regulators (Ler, GrlA, and GrlR). TTSS generates a pore to translocate these proteins from bacterial cytoplasm to the outside environment. It has been shown that Esp translocators are necessary for A/E lesion formation. EspA mediates the translocation of EspB and EspD into host cytosol by making filamentous appendages surrounding the bacterium and forming a translocation tube that interacts with host cells. Rather than acting as translocated effectors, EspB and EspD primarily function to deliver virulence proteins to host cells.

12During the last stage of EPEC infection, pedestal formation, enterocyte effacement and intimate bacterial attachment to host cells take place. The model for EPEC pathogenesis suggests that EPEC initially adheres to epithelial cells by the interaction of intimin with the translocated intimin receptor (Tir) inserted in the membrane. Subsequent effacement of microvilli leads to loss of absorptive surface area, increased intestinal inflammation, and fluid accumulation in the intestinal lumen. In addition, some of the EPEC strains produce an enterotoxin, EspC which is a serine protease autotransporter. EspC has no role in the generation of EPEC A/E lesions but controls pore formation and cytotoxicity by cleaving EspA/EspD which are the translocator components of the Type III secretion system (T3SS). It is interesting to note that EspC could contribute to EPEC infection by degrading different biological substrates such as pepsin, glycoprotein, coagulation factor V, and spectrin) and by inducing apoptosis and necrosis in epithelial cells.

2.1.2. Vaccine Strategies against EPEC

13The aforementioned virulence factors which are important for the pathogenesis of EPEC are potential immunogens to stimulate intestinal immune responses and possible targets as vaccine candidates. One report has shown that recombinant Mycobacterium smegmatis (Smeg) and Mycobacterium bovis BCG strains expressing BfpA or intimin were able to trigger the immune response in mice. It is hypothesized that the binding of secretory IgA antibodies to BFP may interfere with bacterial binding or initial attachment of EPEC and may prevent the downstream signal transduction pathway to manifest diarrhea. Spleen cells grown in vitro from recombinant BfpA-immunized mice produced TNF-α and INF-γ. TNF- γ is produced by recombinant intimin. A successful immunization of cattle against an EHEC (E. coli O157) strain has been performed with a combination of recombinant EspA, intimin and Tir. In addition, humoral and cellular immune responses are triggered in mice immunized with Lactobacillus casei strains constructed to express intimin-β fragments (L. casei-Intcv) and immune dominant epitopes of Int280. These collectively signify virulence factors alone, or in combination with non-infectious immunogenic vectors, can work synergistically to protect against EPEC diarrhea. A list of vaccine projects in different stages against EPEC is listed in Table 1.

2.2. EHEC

14EHEC strains are Shiga-toxin encoding E. coli (STEC), also called verotoxin-producing E. coli (VTEC) that infect the alimentary tract and cause hemorrhagic diarrhea, hemorrhagic colitis and hemolytic-uremic syndrome (HUS) that can result in kidney failure and neurological complications in humans. Unlike EPEC which predominantly infects the small intestine, EHEC colonizes the large intestine. EHECs are mainly responsible for severe cases of foodborne infection out of >200 known serotypes of EHEC, whereas O157:H7 have been associated with most foodborne outbreaks. It was first isolated from undercooked minced meat after a multi-state outbreak in 1982 in the United States. Because of multiple outbreaks, easy transmission and complications for the use of antibiotics for EHEC treatment, this pathotype represents a major public health issue. EHEC naturally resides in the intestine of ruminant animals, and zoonotic transmission occurs after the consumption of contaminated animal products (mainly ground beef), contaminated water (cross-contaminated from beef), improperly cooked meats, and inefficiently washed fruits and vegetables. In the United States, an estimated 63,000 cases of hemorrhagic colitis caused by EHEC are reported annually. HUS is a leading cause of acute renal failure in children for the past two decades. While there is an increased burden of EHEC outbreaks mainly affecting developed countries, an EHEC-EAEC hybrid strain also caused a serious outbreak in Europe, with 3816 reported cases that included 54 deaths and 845 HUS cases.

2.2.1. Molecular Pathogenesis

15Stx toxins, also known as verotoxins (VT), are the key virulence factor of EHEC. The Shiga toxin family is composed of Stx1 which is nearly identical to the Shiga toxin of Shigella dysenteriae and differs only at a single amino acid whereas Stx2 shares less than 60% amino acid homology with Stx1. Stx consists of five identical B subunits that are soluble toxins. After bacteria release these powerful cytotoxins, they are translocated from the gut lumen to nearby tissues and the bloodstream. The holotoxin binds to the glycolipid globotriaosylceramide (Gb3) on the target cell surface, and the toxin is internalized where a single A subunit cleaves ribosomal RNA and halts host cell protein synthesis. Stx can also induce apoptosis in intestinal epithelial cells and can cause local damage in the colon resulting in hemorrhagic colitis, necrosis, and perforation of the intestine. EspP is a serine protease autotransporter, which contributes to biofilm formation by forming macroscopic rope-like polymers that are refractory to antibiotics and mediate adherence to host cells and cytopathic effects. EspP can also cleave host coagulation factor V and serpins which can result in prolonged hemorrhage and contribute to EHEC pathology.

2.2.2. Vaccine Strategies against EHEC

16In the past two decades, EHEC has been the most studied E. coli pathotype for vaccine development mainly due to the severity of infection with an increased number of HUS cases, and issues preventing the use of certain antibiotics to treat STEC. Unlike other pathotypes, the use of antibiotics exacerbates STEC disease as antibiotics can induce EHEC to increase the production of Shiga toxins and release more toxins during bacterial cell lysis. Since EHEC can colonize the intestine of animals, there have been successful experiments to assay the colonization ability of EHEC in different animal models ranging from neonatal calves, germ-free piglets (where they also show CNS symptoms such as severe infection in humans), ferrets (oral infection model) that develop HUS following O157 infection, to different murine models (intra-gastric inoculation model). The availability of a wide range of animals provides valuable models to investigate host immune responses following EHEC infection as well as for vaccine development.

17To date, different strategies such as Shiga toxin-based vaccination to neutralize the effect of toxin by using antibodies engineered against the A subunit of Stx2 and B subunit of Stx1, Stx toxoids, attenuated bacteria- where the LEE-encoded regulator (Ler) which regulates genes inside, and outside pathogenicity island region is deleted or disrupted making the bacteria non-pathogenic but immunogenic enough to impede the pathologic effects of the toxin. In addition, other methods such as bacterial ghosts where bacteria are engineered to have controlled expression of a lysis gene that lyses the bacteria and forms empty bacterial cell envelopes with the composition of the cell envelope of living cells which are non-infectious but induce the mucosal immune response. Other protein-based, peptide-based, plant-based, DNA-based, polysaccharide-based, or adjuvant-enhanced vaccines have been reported to induce the host immune response and decrease the lethality of EHEC in different animal models, and are summarized in Table 2.

18The attaching and effacing (A/E) family of gastrointestinal bacterial pathogens includes EPEC and EHEC. Both EPEC and EHEC have a high homology in their LEE and O islands. Virulence of these pathotypes depends on a T3SS and equivalent secreted proteins such as EspS and intimin. From epidemiological data, it has been observed that EHEC occurrence is significantly lower in the region where EPEC is endemic. This strategy has been exploited by researchers to utilize the attenuated EPEC O126:H6 where EspB and intimin antibodies from EPEC vaccination were cross-reactive with EspB and intimin from EHEC and showed reduced mortality in mice following an EHEC infection. These vaccines are summarized in Table 2.

2.3. ETEC

19The ETEC pathotype is one of the principal causes of acute “travelers’ diarrhea”, affecting tourists visiting low-income countries, and is predominant in areas with poor sanitation and inadequate clean water. ETEC infections are often characterized by diarrheal illness ranging from mild and self-limiting to cholera-like symptoms. They are defined by the production of heat-labile (LT) and heat-stable (ST) enterotoxins, which disrupt secretion mechanisms in the intestine, leading to watery diarrhea. Globally, there are millions of cases of ETEC infection and tens of thousands of deaths annually in developing countries among children less than 5 years old. ETEC infections are also a major cause of traveler`s diarrhea with more than one million annual cases worldwide. In the United States alone, there are 40,000 estimated cases of ETEC infection annually.

2.3.1. Molecular Pathogenesis

20ETEC strains adhere to the small intestinal mucosa with the help of one or more proteinaceous pili/fimbriae also called colonization factors (CFs). Following initial adhesion and colonization, ETECs cause diarrhea not by invading the mucosa but by producing plasmid-encoded heat-labile (LT) and/or heat-stable (ST) enterotoxin (Figure 1). LTs are closely related in structure and function to cholera enterotoxin produced by Vibrio cholerae. LTs increase host intracellular cAMP through the activation of a cAMP-dependent kinase and activate the main chloride channel of epithelial cells, resulting in increased chloride secretion from crypt cells. This ion imbalance causes an alteration in electrolyte homeostasis, resulting in loss of fluids from tissue and subsequent diarrhea. ETEC is also an important veterinary pathogen associated with post-weaning diarrhea in both pigs and cattle, and STb toxin is involved in diarrhea. ETECs also secrete plasmid-encoded virulence factors EatA and EtpBAC. EatA is a serine protease autotransporter of Enterobacteriaceae (SPATE) which can cleave substrates identified for cathepsin G and EtpBAC is an extracellular adhesin which is a 2-partner secretion system responsible for the export of EatA. The yghJ gene present in the chromosome upstream of genes encoding the type II secretion system of multiple ETEC isolates encodes another antigen YghJ (SslE). EatA and YghJ both degrade MUC2 mucin secreted by goblet cells of small intestinal epithelia and facilitate bacteria to overcome the mucin barrier and release ETEC enterotoxins upon host enterocytes (Figure 1).

2.3.2. Vaccine Strategies against ETEC

21Because of the substantial morbidity and mortality in the pediatric population and the long-term consequences of enteric infections on child growth and development, vaccination could be a promising means of ETEC prevention. In the past two decades, different strategies were developed and employed for ETEC vaccine development either to prevent attachment of ETEC to the proximal small intestinal mucosa or to protect via immunity, through IgA antibodies directed against LT. Among these strategies, ETVAX is the most advanced candidate which is currently in Phase 2b clinical trials. This strategy utilizes inactivated whole cell (one E. coli K-12 and three O78 positive E. coli) vaccine strains that overexpress CFA/I, CS3, CS5 and CS6 antigens combined with hybrid LT/CTB (B subunit BS of cholera toxin) with and without dmLT adjuvant. ETEC strains are heterogenous, exhibiting different O:H serotypes and to provide broad spectrum protection, various fimbrial antigens present in the most prevalent ETEC pathotypes have been used in this strategy. This vaccine demonstrated excellent safety in an age-descending trial in Bangladesh, and the inclusion of the dmLT adjuvant increased the magnitude and kinetics of mucosal antibody responses in both Bangladeshi infants and Swedish adults. Theoretically, a multivalent ETEC vaccine which can express CFA/I, CFA/II and CFA/IV antigens can protect against the majority of ETEC strains worldwide.

22Another vaccine that is further along in the development is live attenuated E. coli expressing ETEC fimbriae. E. coli strain E1392-75-2A is a prototype demonstrated in clinical trials that expresses CS1 and CS3 fimbriae but lacks genes that encode LT and ST. This strain was derived in the Central Public Health Laboratory, London, U.K., wherein the genes encoding LT and ST were spontaneously deleted from the CFA/II plasmid. All volunteers who received 1010 CFU doses of strain E1392-75-2A developed significant rises in intestinal fluid SIgA antibody to CS1 and CS3 and the vaccinees were significantly protective (p < 0.005, 75% vaccine efficacy) against ETEC challenge strain E24377A (O139:H28). However, around 15% of the subjects had mild diarrhea after taking this live oral vaccine. On the same lines, live attenuated vectors such as Shigella and Salmonella have been used to express ETEC fimbrial antigens and LT antigens. An attenuated Shigella strain expressing ETEC CFA/I and CS3 fimbriae elicited SIgA mucosal antibody responses to those antigens in a guinea pig model. A multivalent live oral vaccine against both Shigella and ETEC is being developed and is in Phase 1 clinical trial known as a ShigETEC toxin hybrid which is an LPS-free cell expressing conserved ETEC and Shigella antigens. Likewise, a Shigella hybrid (1208S-122) is also in the Phase 1 trial which is an attenuated Shigella vaccine strain engineered to express ETEC CF and LT. If this attenuated Shigella expresses ETEC fimbrial colonization factors and genetically detoxified LT, protection is undeniable. Further, a fimbrial tip adhesin-based vaccine, a multiple epitope fusion antigen (MEFA) based vaccine and protein-based vaccines against ETEC virulence factors are also in various preclinical phases of testing. These different ETEC vaccine candidates are listed in Table 3.

2.4. EIEC

23EIEC strains show similar genetic, biochemical and pathogenic characteristics to Shigella, for example, the ability to invade the mucosa of the colon. Unlike other pathotypes such as EPEC, EHEC, and ETEC that replicate and infect extracellularly; EIEC strains penetrate the mucosa after invading epithelial cells, and can replicate and migrate within epithelial cells and macrophages as well. A large (>200 kb) virulence plasmid (pINV) found in EIEC and all Shigella species encodes genes required for pathogenesis. This pathogenesis is known to be the result of multiple effects of the plasmid-borne type III secretion system encoded by the mxi-spa locus that secretes invasin proteins including IpaA, IpaB, IpaC and IpgD for signaling events and other actions. Although EIEC infections are reported in countries with poor sanitation, hygiene and socioeconomic status, there have been EIEC outbreaks in the USA, Japan, Israel and recently in Italy in 2012 and Nottingham, U.K. in 2014. Most of these outbreaks are sporadic and travel related. These outbreaks signify the ability of EIEC to induce gastrointestinal disease outbreaks across the world.

2.4.1. Molecular Pathogenesis

24During infection, EIEC strains initially penetrate and enter into epithelial cells, lyse the endocytic vacuole, multiply inside the cells and migrate to adjacent cells through the cytoplasm (Figure 2). During initial penetration, T3SS inserts a pore containing IpaB and IpaC into host cell membranes. IpaC induces actin polymerization and activates GTPases Cdc42 and Rac which leads to the formation of cell extensions. Actin polymerization and lamellipodial extensions of host cells are induced by IpaC. In the same line, IpaAs alter cell extensions induced by IpaC by binding to vinculin and inducing actin depolymerization, leading to a structure that mediates bacterial cell entry. IpgD helps the internalization by inducing host cell membrane blebbing. Multiple factors including T3SS effectors such as IpaB and IpaC, which are used for phagosomal escape by bacteria; host factors such as Rab5 and Rab11; and other cytosolic access factors utilized by intracellular bacterial pathogens are involved in rupturing the endocytic vacuole in less than 10 min following cell entry. After this, bacteria multiply inside cells and invade and damage surrounding epithelial cells that results in Shigellosis-like symptoms such as watery diarrhea with mucus, with leukocytes and blood in the stool, abdominal pain with cramps and tenesmus, fever, and systemic toxicity as well.

2.4.2. Relationship with Shigella

25In the past, enteroinvasive strains that cause shigellosis were divided into EIEC and Shigella species (with four subgroups: S. dysenteriae, S. flexneri, S. boydii and S. sonnei). Genetically, all these groups are so closely related they could be considered as the same genus or even species comprising other pathogenic and commensal E. coli. Like Shigella, EIEC strains are usually nonmotile, lysine decarboxylase negative, and commonly lactose negative. The biochemical similarity between EIEC and Shigella is characterized by their ability to utilize serine, xylose or sodium acetate and ferment mucate. It has been reported that non-motile serotypes of EIEC produce unusually large flagellin assembled into functional flagellum filaments. EIEC/Shigella utilizes similar modes of action to manipulate host innate and adaptive immunity for penetration, multiplication and replication in host epithelial cells. Two main features of EIEC and Shigella are evolution, requiring both the gain of virulence genes and the loss of function or deletion of other genes. In S. flexneri, approximately 200 genes were acquired, and 900 genes have been lost during the divergence from commensal E. coli. Some of the examples include loss of outer membrane protease (OmpT) that interferes with the localization of the actin nucleator IcsA, which is necessary for the invasion phenotype; loss of lysine decarboxylase that catalyzes cadaverine production, which inhibits enterotoxins of Shigella; and the absence of functional flagella and fimbriae that are active activators of the host innate immune response, and might interfere with the initial colonization process(other genomic regions “black holes” lost by EIEC and Shigella are reviewed in detail in). Due to the similarities shared between EIEC and Shigella, virulence factors responsible for EIEC or Shigella infections and various subtypes of attenuated Shigella strains can be exploited to devise a potential vaccine against these enteroinvasive pathotypes.

2.4.3. Vaccine Strategies against EIEC/Shigella

26EIEC/Shigella does not have any animal reservoir. They are usually transmitted among the human population through poor hygiene and sanitation. Licensed vaccines are currently not available against EIEC/Shigella and basic hygiene and proper sanitation remain the best way of preventing infection. However, these approaches are not feasible in many low-income countries. Therefore, there is an increased demand for vaccine development, and strategies include the utilization of a live-attenuated strain, glycoconjugate-based candidates, novel antigen candidates such as Shigella outer membrane vesicles (OMV) encapsulated in nanoparticles, and protein subunit candidates. There are several animal and human studies that have described the potential for vaccination using invasion plasmid antigens (IPAs), virG or Shigella O antibodies that cross-react with EIEC O antigens. Table 4 summarizes vaccine approaches against EIEC/Shigella.

2.5. EAEC and DAEC

27EAEC is the cause of several diarrheal outbreaks worldwide and is mostly associated with mildly inflammatory diarrhea in young (< 2 years old) and malnourished children; persistent diarrhea in HIV-infected adults and children and acute diarrhea in travelers in both developing and industrialized countries. It was first described in 1987 based on an auto-aggregative “stacked-brick” adherence pattern to Hep-2 cells in culture. This phenotype is mediated by the aggregative adherence fimbriae (AAF) and aggregative adherence regulator.

2.5.1. Molecular Pathogenesis

28EAEC infection involves the colonization of bacterial cells in dense clusters to the intestinal mucosa followed by the secretion of EAEC heat-stable enterotoxin (EAST1) and ShET1 (Shigella enterotoxin 1) which causes a loss of fluid (Figure 1). EAEC also produces a plasmid-encoded SPATE autotransporter enterotoxin called Pet. Pet has enterotoxic activity and induces cytoskeletal changes and epithelial cell rounding due to the breakdown of fodrin/spectrin in host cells. In addition, EAEC produces another SPATE with mucinase activity called Pic, which contributes to intestinal colonization. Pic was also shown to reduce complement activation by cleaving complement cascade factors C3, C4 and C2, which also induces polymorphonuclear leucocyte/neutrophil (PMN) activation and programmed T-cell death. In this context, Pic activity can contribute to immune evasion and promote EAEC virulence.

29Like EAEC, the DAEC pathotype is defined by its diffused adherence pattern on epithelial cells such as HeLa or Hep-2 cells in culture. More than 70% of DAEC strains produce fimbrial adhesins from the Afa (AfaE-I, AfaE-II, AfaE-III and AfaE) or Dr (F185) family that mediate the diffused adherence phenotype and pathogenesis. These fimbriae recognize DAF (Delay accelerating factor), a cell-surface glycosyl phosphatidylinositol-anchored protein, as the receptor and cause dismantling of the actin network in intestinal cells, resulting in long cellular extensions and elongation and malfunction of microvilli which wrap around the bacteria (Figure 2). Reports have suggested the presence of virulence factors other than Afa/Dr family adhesins and they can be pro-inflammatory, suggesting a potential significance in the initiation of inflammatory bowel disease. In addition to causing diarrhea in children, adults and the elderly, DAECs are also known to be associated with urinary tract infections (UTIs), pregnancy complication and asymptomatic intestinal infections in both children and adults.

2.5.2. Vaccine Strategies against EAEC and DAEC

30For DAEC and EAEC pathotypes, there is currently limited vaccine development. Nevertheless, bacterial adhesins are considered the best candidates, and AAF/I and AAF/II could be the possible target for EAEC. When Balb/c mice were immunized with three different modes of vaccination, namely, DNA/DNA, DNA/Protein, or Protein/Protein of AAF/I or AAF/II of EAEC, respectively, (only the DNA/Protein immunization and Protein/Protein doses of AAF/I significantly induced total IgG).

31Likewise, afimbrial adhesins (AFA), Dr hemagglutinin, and F1845 fimbriae are the important adhesins of DAEC and could be target antigens for vaccine development. Vaccination of C3H/HeJ mice with Escherichia coli Dr fimbrial antigen reduced urinary tract infection due to a homologous strain bearing Dr adhesin. Immune sera with high titers of anti-Dr antibody inhibited bacterial binding to bladders and kidneys. Although Dr adhesin was shown to be immunogenic in this urinary tract model, its role as an antigen in vaccination against the intestinal disease is yet to be explored.

2.6. AIEC

32In contrast to enteroinvasive E. coli, Adherent-invasive E. coli (AIEC) is the pathotype with both abilities to adhere to and invade intestinal epithelial cells. AIEC can also survive and replicate within macrophages. AIEC is associated with inflammatory bowel disease (IBD), Crohn`s disease (CD) and ulcerative colitis (UC). AIEC infections are usually characterized by diarrhea, abdominal pain, rectal bleeding, fatigue, and life-threatening complications in severe cases of AIEC and IBD. Reports of bacteriological analysis from Europe and North America showed 30–50% of Invasive E. coli strains are present in the ileal mucosa of Crohn’s disease patients. However, it is still not clear whether AIEC induces intestinal inflammation resulting in IBD or whether they act as an intensifying factor by colonizing the mucosa of patients with pre-existing IBD. AIEC possesses a wide range of virulence factors.

2.6.1. Molecular Pathogenesis

33AIEC invades host cells in a similar fashion to other pathogens such as EIEC and Shigella. These strains penetrate epithelial cells by either directly invading the epithelial layer or by entering via microfold (M) cells in the epithelium of the small intestine. Following the invasion, AIEC reduces epithelial barrier function and integrity. Since CD and AIEC are interrelated, most of the studies of AIEC pathogenesis were carried out in epithelial cells from CD patients. During initial adherence, it has been shown that type 1 fimbriae can bind to GP2 protein located on the apical plasma membrane of M cells. Reports also suggest that AIEC strains expressing long polar fimbriae (LPF) adhere to M cells and mediate transcytosis of bacteria. Host glycoprotein CEACAM6 (Carcinoembryonic Cell Adhesion Molecule 6) expressed in ileal mucosa has been shown to recognize the FimH type 1 fimbrial adhesin and facilitate internalization of AIEC. Outer membrane vesicles (OMVs) have a role in AIEC invasion. It has been demonstrated that outer membrane proteins (OmpA and OmpC) promote the fusion of OMVs with the Gp96 receptor expressed on the surface of epithelial cells and mediate invasion. In addition, VAT-AIEC a protease secreted by AIEC has been reported to mediate the colonization of bacteria in a murine intestinal infection model. Following the invasion, AIEC strains can replicate in host cells, including macrophages.

2.6.2. Relation of AIEC and Crohn’s Disease

34Crohn’s disease (CD) is a chronic inflammatory condition of the GI tract and AIEC strains have been isolated from the guts of CD and UC patients. AIEC strains are pathobionts, which means they can reside in the guts of healthy individuals without causing any diseases. However, the host intestinal environment under certain conditions that affect the innate immune response could promote AIEC-induced inflammatory bowel diseases. Following AIEC infection, autophagy, which is a cytosolic process, is induced in host cells to curb the activity of bacteria. During autophagy, bacteria are recognized by NOC proteins such as CD-associated nucleotide-binding oligomerization domain-containing-2 (NOD2) and form autophagosomes which further fuse with lysosomes. After fusion, the bacteria are degraded in auto-phagolysosomes. In addition to NOC proteins, other proteins such as ATG16L1, IGRM, and LC3 are also known to mediate autophagy. It has been reported that these mediators of autophagy are defective in CD and UC patients and may favor the intra-macrophagic replication of AIEC. Genetics models have reported that the knock-down of NOC proteins shows a loss of function against AIEC infections. Knock-down of ATG16L1 and IRGM genes results in defective clearances of CD-associated AIEC.

2.6.3. Insights for Vaccine Development

35In recent years, many studies have elucidated AIEC virulence and its role in CD. Various therapeutic strategies other than vaccination to prevent AIEC infection and concurrent CD and UC have been tested. Among these, the most popular strategies are (i) the use of prebiotics/probiotics and postbiotics and chemical compounds to inhibition or exclude AIEC; (ii) the elimination of AIEC using antibiotics, bacteriocins/colicins, phototherapy and bacterial predation; (iii) activation of autophagy; (iv) nutritional interventions; and (v) fecal transplantation and combinational therapy. One vaccine-based approach involves the use of flagellar antigens. A Summary of approaches for AIEC and IBD prevention is listed in Table 5.

3. Extraintestinal Pathogenic E. coli

36Extraintestinal Pathogenic E. coli (ExPEC) are responsible for most urinary tract infections (UTIs) and are a common cause of bloodstream infections and neonatal meningitis in humans and respiratory tract and other systemic infections in poultry. This group of pathogens has a broad range of virulence factors and exhibits genomic plasticity. Depending on the type of infectious disease, ExPEC has been classed into uropathogenic E. coli (UPEC), neonatal meningitis-associated E. coli (NMEC), and sepsis-causing E. coli (SEPEC) in humans and avian pathogenic E. coli (APEC) in poultry. Some ExPECs that cause infections in humans share a close phylogenetic relationship and virulence genes with certain APEC strains. Studies have shown that poultry and poultry products can be a reservoir of potential ExPEC strains and could pose a health risk to humans. Both animal and human ExPEC strains were shown to be able to cause UTI or meningitis in rodent models, and human ExPECs were shown to be virulent in poultry infections as well. As such, some ExPEC strains have clearly been shown to infect multiple host species.

3.1. Uropathogenic E. coli (UPEC)

37Urinary tract infection is a very common bacterial infection, particularly in women, and UPEC strains account for up to 90% of community-acquired urinary tract infections (UTIs), 50% of hospital-acquired UTIs, and around 80% of uncomplicated. UPEC isolates exhibit a high degree of genetic diversity due to the presence of mobile DNA segments which are scattered around the chromosome known as pathogenicity islands. The key virulence factors harbored by UPEC strains are type 1 fimbriae, P fimbriae, mannose-resistant adhesins, hemolysin, serum resistance, siderophores and K1 capsule. Normally, UTI infection is initiated when uropathogenic E. coli originating from the bowel, is transferred to the urogenital region and ascends towards the periurethral area. Colonization is facilitated by adhesins such as Pap (P), type 1 and other fimbriae such as S, M, and F1C that mediate adherence to uroepithelial cells, which is an important initial step in the development of UTI. It has been shown that by virtue of type 1 fimbriae, E. coli can attach to mannose moieties that coat transitional epithelial cells. Further, several toxins including hemolysin, a serine-protease autotransporters called Vat, Sat, and Pic and the cytotoxic necrotizing factor (CNF-1) can contribute to urinary tract colonization. However, these virulence factors are not always present among different subgroups of UPEC, suggesting that there can be multiple mechanisms of UPEC pathogenesis.

3.1.1. Urinary Tract Infection (UTI)

38The urinary tract can be affected by a variety of diseases including microbial colonization of the urine and infection of the urinary tract tissues (kidney, renal pelvis, ureters, bladder, and urethra). Clinically, urinary tract infections (UTIs) have been categorized as uncomplicated or complicated. Uncomplicated UTIs occur in the normal urinary tract of immunocompetent individuals who are otherwise healthy. UTI is characterized by the presence of bacteria and neutrophils in the urine which is known as bacteriuria (presence of uropathogens in urine with more than 105 CFU/mL). Bacteriuria can be asymptomatic in the host and have adverse outcomes for pregnant women and people undergoing traumatic genitourinary procedures. UTI can manifest itself into cystitis (inflammation of the bladder) and acute pyelonephritis (kidney infection) (Figure 3). Cystitis is typically characterized by symptoms including frequency, burning sensation, urgency, pyuria (leukocytes in urine), dysuria, suprapubic pain and/or lower abdominal discomfort with cloudy urine. If left untreated, these infections can result in pyelonephritis which is distinguished clinically from cystitis by the presence of flank pain, fever and nausea. Antibiotics are given for the treatment of symptomatic UTI but up to 25% will suffer a recurrence of infection within 6 months following treatment of the initial UTI. Mounting evidence is showing that two-thirds of these recurrences are attributable to the identical initial strain recovered from a given patient suffering from uncomplicated UTIs.

3.1.2. Molecular Pathogenesis of UPEC

39The pathogenesis of UTI is complex and influenced by multiple host and microbial factors. Years of research and the use of different animal and cellular models have elucidated some of the pathogenic mechanisms. The mechanisms of UPEC infection include adherence to host cells, motility, acquisition of essential metals and other micronutrients, toxin production and evasion of the host immune response (Figure 3).

40Bacterial adherence to host cells plays a key initial step in colonization and subsequent disease progression. Uropathogens must adhere to or penetrate the mucosal barrier to persist. A UTI typically initiates by contamination of the periurethra by a uropathogen from intestinal sources, followed by bacterial colonization of the urethra and bladder through filamentous adhesins known as fimbriae (pili). For example, UPEC strain CFT073, a well-characterized reference strain, encodes 12 distinct fimbrial gene clusters which code for type 1, P, F1C, Dr, Auf fimbriae as well as their chaperone and usher proteins. Type 1 fimbriae have been found essential for the colonization, invasion, and persistence of UPEC in the mouse bladder. The FimH adhesin of type 1 fimbriae binds to mannosylated receptors and bladder cell surfaces known as molecules such as uroplakins, α 3 β 1 integrins and the pattern recognition receptor TLR4. The expression of type 1 fimbriae is a phase variable and is controlled by the orientation of an invertible element in the promoter region.

41E. coli expresses another fimbria known as P fimbriae which have been associated with acute pyelonephritis in humans and showed a subtle role in pathogenesis in the murine model. P fimbrial adherence conferred by the PapG adhesin protein binds specifically to glycosphingolipids containing digalactoside moieties found in renal epithelium and the P blood group antigen which is on the surface of some host erythrocytes. So, human individuals lacking the receptor for P-fimbriae may be less susceptible to P-fimbriae-mediated adherence during UTIs caused by UPEC.

42Type 1 fimbriae bind to epithelial cells and trigger a signal transduction cascade that activates the Rho family of GTP-binding proteins, resulting in cytoskeleton rearrangements in host cells and internalization of UPEC by a zippering mechanism in which the plasma membrane engulfs the bacterium. This invasion benefits bacteria since the intracellular location shelters UPEC from host defenses, may reduce access to antibiotics, and prevent clearance from micturition. Although intracellular UPEC can evade host defenses, the expulsion of UPEC in urothelial cells does occur by innate immune defense through lipopolysaccharide (LPS) mediated activation of TLR4. However, a minority of internalized UPEC can escape into the epithelial cell cytoplasm and subvert expulsion and rapidly replicate exponentially in coccoid form, forming an amorphous biofilm-like intracellular bacterial community (IBC) which can cause superficial cells to protrude. Later, the maturation of IBCs can lead to bacterial dispersion and the cycle of invasion of other urothelial cells. Alternatively, UPEC can establish quiescent intracellular reservoirs (QIRs) in the underlying bladder cells which can later serve as seeds for UPEC release back into the bladder lumen. Due to this phenomenon, the source of recurrent infections can be due to several sources including recurrent intestinal source contamination, vaginal colonization, or reinfection by latent bacteria within the urinary tract.

43Other virulence determinants of some UPEC include hemolysin, cytotoxic necrotizing factor 1 (CNF1) and autotransporter proteins. Hemolysin (HlyA), encoded by the hlyCABD operon, oligomerizes and inserts into the host cell membrane in a Ca+2-dependent manner. Hemolysin is implicated in pore formation in bladder cells and promotes their lysis and facilitates iron and nutrient acquisition. Further, it can trigger cell exfoliation, apoptosis, and cytokine production and induce an inflammatory response. CNF1 secreted by some UPEC strains alters actin remodeling and membrane ruffling, which leads to the internalization of UPEC in the host cell through the activation of Rho GTP-binding proteins: Rac1, RhoA and CDC42 and may also play a role in bladder cell exfoliation. In addition, activation of Rac1 and GTP induces the anti-apoptotic pathway, preventing apoptosis of the colonized uroepithelium and prolonging UPEC survival. Another family of toxins that are members of the serine protease autotransporters of Enterobacteriaceae (SPATEs) including Sat, Pic and Vat has been characterized in UPEC. Sat (secreted autotransporter protein) can cause cytotoxic effects on bladder and kidney cells in vitro; elongation of kidney cells with apparent impairment of cellular junctions; degradation of fodrin and human coagulation factor V; and induction of autophagic cell detachment. Pic SPATE acts as a mucinase and Vat SPATE can also contribute to UTIs.

44To survive and compete in different host niches, UPEC also evolved multiple means of obtaining essential metals, such as iron. The most diverse and broadly distributed iron uptake mechanisms used by microorganisms are siderophore acquisition systems. Siderophores are small chelating compounds with a very high affinity for iron. The direct capture of host iron is either from free heme or heme-containing proteins, such as hemoglobin. The presence of heme uptake systems in UPEC also provides a direct iron source in vivo, heme. Iron binding receptors Hma and ChuA bind to heme and transport it to the periplasm; ChuT mediates further transfer to the cytoplasm through an ATP-binding cassette (ABC) transporter. In addition, UPEC can sequester host iron through high-affinity siderophores including salmochelins, C-glycosylated derivatives of enterobactin, and other siderophores, such as aerobactin, and yersiniabactin. Salmochelins are encoded by the iroBCDEN gene cluster. This siderophore contributes to the virulence of ExPEC strains by escaping the action of host lipocalin-2 (siderocalin). The aerobactin siderophore is highly expressed and stable and displays a higher affinity than enterobactin at low pH. Interestingly, yersiniabactin which is a confirmed siderophore also contributes to UPEC resistance to copper toxicity in urine. Like iron, zinc is also an essential element for bacterial growth. The high-affinity zinc transport system ZnuACB has been expressed during UTI to acquire zinc in the host.

45Polysaccharidic capsules and serum resistance are also important traits associated with UPEC strains, especially those which can infect the kidney and develop into systemic infections. Antiphagocytic capsules can reduce the uptake of bacteria by host phagocytes and promote dissemination in blood and extra-intestinal tissues.

3.1.3. Vaccine Strategies against UPEC

46Generally, antibiotics are used to treat UTIs. However, increased antibiotic resistance has become an obstacle to UTI treatment. Recently World Health Organization (WHO) revealed that UPEC strains causing UTI are 54.4% resistant to first-line antibiotics co-trimoxazole and 43.1% resistant to broad-spectrum ciprofloxacin. Fluoroquinolone-resistant E. coli are widespread in the world and there are countries where Fluoroquinolone treatment is completely ineffective in more than 50% of patients. To address such issues, vaccination against UTI strains might provide an important alternative to antibiotics for UTI prevention, particularly in individuals more susceptible to recurring infections.

47An effective vaccine against UPEC might help reduce the current spread of infection and morbidity rate of patients as well as address the challenge of treatment of some UTIs. Effective UPEC vaccine strategies should consider the following aspects: (i) the heterogeneity of UPEC strains, (ii) the potential side effects on the commensal microbiota of the intestine and (iii) the production of multiple virulence factors by UPEC strains. Since UPEC infections involve multiple steps (Figure 3), an effective vaccine should be able to provide a protective immune response against key virulence factors required at specific stages of UTI pathogenesis, such as colonization, invasion, and the formation of IBC reservoirs. Currently, vaccines against UPEC are being developed using either cell-based or live-attenuated vaccines, killed bacteria, or antigen-based subunit vaccines against antigens such as toxins and polysaccharide-based conjugate vaccines.

48Solco-Urovac is a whole bacterial cell-lysate-based vaccine that is multivalent and comprises cells for 10 distinct bacterial strains (6 UPEC strains, 1 strain of each Proteus mirabilis, Klebsiella pneumoniae, Morganella morganii and Enterococcus faecalis). This vaccine is known to protect against recurrent UTIs, and multiple doses reduce the prevalence of cases caused by UPEC. However, this vaccine caused major side effects such as fever, burning, bleeding, vaginal itching and nausea. Such deleterious side effects dismiss the use of Urovac as a vaccine against UTIs. Uro-vaxom is an oral vaccine against UTIs, which was commercialized in Switzerland in 1994, and later in other countries. This vaccine comprises membrane proteins of 18 UPEC strains and is known to prevent recurrent UTIs in women. Uro-vaxom has significantly fewer side effects than Urovac; however, repeated doses taken every three months are required, which has raised issues concerning the practicality of using this vaccine in some populations of patients. Other vaccines against UTIs include Urvakol and Urostim that each contain a mixture of killed bacterial pathogens including E. coli, P. mirabilis, E. faecalis, and K. pneumoniae (Urostim) and an additional Pseudomonas aeruginosa strain (Uravakol). These two vaccines promote immunogenicity in animals and humans, but clinical trials for Uravakol and Urostim have not been completed. ExPEC9V is a newer vaccine which is currently in phase 3 trials (NCT04899336) and targets Invasive Extraintestinal Pathogenic Escherichia coli Disease (IED) in individuals aged 60 years and older with a history of UTIs. In addition to this, several attempts were also made to design live-attenuated vaccines by mutating capsular or somatic O antigens of UPEC strains. For example, attenuated strains such as CP923 and NU14 Δwaal have been shown to produce significant humoral immune responses in mice. However, protection from UTI has not been demonstrated yet and optimization and continued testing of such vaccine candidates are ongoing.

49In other strategies, antigen-based vaccines such as capsular- or LPS-based vaccines, fimbrial and non-fimbrial adhesin vaccines, iron scavenger receptor-based, and toxin-based vaccines have been investigated as protective targets. Currently, in a phase 2 clinical trial, ExPEC4V (NCT03500679), is a polysaccharide-based vaccine which contains O-antigens specific to serogroup O1A, O2, O6A and O25B. Two doses of this vaccine can prevent UTI even with higher bacterial doses and decrease bacteremia in women aged 18 years or older. UPEC colonization to the bladder epithelium is promoted by adhesins which also trigger host immune responses. This principle can be utilized to develop anti-adhesin-based vaccines against UPEC. The FimH adhesin from type 1 fimbriae plays an important role in UPEC pathogenesis. It has been shown that a vaccine composed of truncated FimH or a complex of FimH with chaperone FimC (FimCH) was able to prevent the colonization of different UPEC strains in a murine model. In addition, the FimCH vaccine with Freund’s adjuvant and the FimH vaccine with Alum and MF59 adjuvants promoted an immune response against UPEC and prevented colonization in murine and primate models, respectively. The FimH vaccine was tested in a phase II clinical trial; however, it was later rejected due to ineffectiveness in humans. Because of the variation of expression of type 1 fimbriae, UPEC strains are not consistently recognized by the immune system. In addition, antigens developed against the fimbriae do not target its mannose-binding region, and differences in the expression of virulence genes in animal and human models are some of the reasons for the failure of the FimH-based vaccine. An effective UTI vaccine will potentially require multiple tests using a variety of target antigens in urinary tract models in animals. Other vaccine candidates using FimH adhesin are currently being tested, including a TLR ligand-based vaccine where the fusion of FimH adhesin to flagellin of UPEC as a TLR5 ligand was able to induce an immune response and protected mice against UTI. Moreover, a PapG fimbrial adhesin-based vaccine and Dr fimbriae with Freund’s adjuvant were also shown to generate immune responses and reduce UPEC colonization in a mouse model.

50E. coli iron acquisition systems also have the same potential as UPEC vaccine candidates. It has been reported that the salmochelin receptor IroN or IroN with Freund’s adjuvant can provide protection against UTI in a murine model. The aerobactin receptor IutA conjugated with cholera toxin and the yersiniabactin receptor FyuA with Alum as an adjuvant also generated strong immune responses and protection against UPEC infection in murine models. In another study, the efficacy of a multi-epitope vaccine composed of siderophore receptors had been evaluated using an attenuated Salmonella vaccine delivery system, where IroN, IutA, IreA and FyuA improved protection in the urinary tract of mice. In the same line, a toxin-based vaccine containing antigens such as hemolysin HlyA, recombinant hemolysin, or mutated CNF1 and HlyA toxins, has reduced UTI symptoms in murine experimental infection models. Auto-transporter toxins such as Vat from UPEC strains have also been investigated as vaccine targets. In the sepsis model study, Vat improved protection by 32% and 78% after active and passive immunization, respectively, compared to unvaccinated controls.

3.2. MNEC, SEPEC

51This ExPEC pathotype is associated with cases of meningitis particularly in neonates. Approximately 80% of isolates from neonatal meningitis harbor antiphagocytic K1 capsular polysaccharide and most belong to serogroups such as O18, O7, O16, O1, and O45. Inflammation of the meninges by MNEC comprises various stages of infection. Firstly, the translocation of bacteria into the circulatory system and upon reaching at least 103 CFU/mL in the blood, MNEC can breach the blood-brain barrier (BBB). The meninges which form a structural and functional blood-brain barrier are composed of endothelial cells called brain microvascular endothelial cells (BMECs). Most MNEC produce S fimbrial adhesins involved in BMEC binding to the NeuAc α-2,3-galactose receptor, type 1 fimbriae and OmpA, which contribute to adherence and invasion of brain endothelial cells. Furthermore, an outer membrane protein, NlpI, can also mediate the binding/invasion of MNEC to brain endothelial cells. The CNF1 toxin through activation of the RhoA pathway may also contribute to MNEC invasion of BMECs and penetration into the brain. IbeA has also been associated with the invasion of BMEC. In addition to the role of IbeA in the invasion and crossing of BBB, it has been linked to the regulation of expression of type 1 fimbriae which can mediate endothelial cell adherence and invasion. Further, IbeA may contribute to oxidative stress resistance and the protection of bacteria against H2O2 stress. The K1 polysaccharide capsule can contribute to serum resistance, antiphagocytic properties and intracellular survival and, as such, it is an important virulence factor of most MNEC strains.

Vaccine Strategies against MNEC

52Despite many efforts, no vaccine has yet been developed to help prevent neonatal meningitis caused by E. coli. The vaccine development is impeded by technical difficulties. There are well-established animal models of MNEC-induced meningitis in neonatal mice and rats to investigate MNEC pathogenesis, but vaccine assessment is not favorable because it takes 2–3 weeks for active immunization. Since this is a devastating disease among newborns and premature infants, alternative prophylactic therapies such as passive protection antibodies can be beneficial for the control of MNEC infection. There has been research on capsular polysaccharides (CPs) as a good candidate for vaccine development, but O-acetylated colominic acid produced by E. coli K1 was poorly immunogenic due to its similarity to polysaccharides found on the surface of human tissues. Preventative approaches against MNEC may benefit by using virulence proteins as vaccine targets or for the generation of protective antibodies for passive immunotherapy of neonates against MNEC.

4. Pathogenic E. coli of Importance to Animal Health

53The first section of this review is focused on E. coli pathotypes associated with human infections and vaccination strategies to potentially prevent pathogenic E. coli from causing disease in humans. Importantly, E. coli is also an important pathogen of livestock and poultry and can cause both enteric and systemic infections. As such, it is important to consider the pathotypes of E. coli associated with infections of importance to animal health and potential approaches to prevent such infections through vaccination strategies.

4.1. Avian Pathogenic Escherichia coli (APEC)

54Avian colibacillosis is a common disease in the poultry industry worldwide. As such, APEC is a major cause of morbidity and mortality in chickens due to localized or systemic infections, resulting in heavy economic losses to the poultry industry. APEC also infects other avian species including turkeys and ducks. A variety of disease types have been observed: including yolk sac infection, omphalitis, swollen head syndrome, respiratory tract infection, septicemia, enteritis, and cellulitis. Colibacillosis in chickens results in death by septicemia in acute infection, whereas subacute infections can result in pericarditis, airsacculitis and perihepatitis. APEC strains commonly belong to three serogroups, O1, O2, and O78 although many different serogroups have been identified in APEC and O1, O2, and O78 are not always predominant in certain studies. Several virulence factors have been associated with APEC strains. These include fimbrial adhesins (type 1 fimbriae, P fimbriae, and Stg fimbriae, curli, Yqi; outer membrane proteins and other surface molecules contributing to serum resistance or antiphagocytic properties (Increased serum survival (Iss)), two-component signal transduction systems (RstA/RstB, PhoB/PhoR, BarA/UvrY), O78 lipopolysaccharide, and K1 capsule; iron and metal acquisition systems (aerobactin, salmochelin, yersiniabactin), heme utilization/transport protein ChuA and the Sit metal transport system; autotransporters (Tsh, Vat, Sha, TagB, TagC, AatA, phosphate transport and the Pho regulon (the Pst system); sugar metabolism; and nitrite transporter NirC. Specific virulence genes including iss, iroN, ompT, iutA and hlyF are commonly present in APEC and are frequently encoded on large plasmids such as Colicin V (ColV) plasmids. In addition, other factors such as IbeA, and the type VI secretion system, which are known to affect the expression of type I fimbriae, are involved in the colonization of the respiratory tract. However, no single common virulence factor has been identified in all strains.

4.1.1. APEC Pathogenesis

55E. coli is an intestinal commensal of poultry, but some of these fecal isolates when inhaled by poultry can colonize the respiratory tract and then cause colibacillosis which can include respiratory infection as well as a systemic fatal disease. Colonization in the trachea and the air sacs is considered the first step of systemic infection for APEC (Figure 4). Airsacculitis is a common type of infection in poultry of all ages. In addition to the respiratory route, various other infection routes have been described: neonatal infections, infections through dermal lesions and infections of the reproductive organs. Once in the blood, APEC can then disseminate to the liver and pericardium, and the infection may also lead to bacteremia and septicemia. A laying hen having E. coli-induced salpingitis can have an infected egg before shell formation. This can lead to infection and a high mortality rate among young chicks during the first few days or weeks after hatching through yolk sac infection.

56Adhesins such as fimbriae, Stg, Tsh and Yqi can contribute to APEC colonization of the respiratory tract: the trachea and the lungs. Carbohydrate metabolism may also contribute to the colonization of the lung or air sacs. To disseminate in the bloodstream, bacteria need to translocate through the lungs and air sac interstitium. K1 capsule was shown to facilitate the translocation of APEC into the vascular system. When APEC disseminate in the blood, they are confronted by innate immune defenses and nutrient limitation. In this context, siderophores such as aerobactin and salmochelins, the ChuA heme uptake and Sit metal transporter sequester iron and other metals from the host environment. In addition, protectins which help to evade the host immune system such as K1 capsules, Iss, Type III secretion system, and specific O antigens can contribute to survival and virulence through resistance to the avian immune cells and the serum complement system.

4.1.2. Vaccines and Vaccination Strategies against APEC

57After registration in the EU in 2013, O78 (Poulvac® E. coli, Zoetis) is commercially used as a vaccine, which is a live-attenuated aroA-mutant of an Escherichia coli serogroup O78 strain. The vaccine is available as a freeze-dried powder (lyophilisate) and is given as a single-dose vaccine either by spray application with chicks from one day of age or by adding to the drinking water of chicks from five days of age. One important limitation of this vaccine that has been reported is limited protection against the diversity of APEC belonging to a multitude of different serotypes. There is, therefore, a need to develop a vaccine against APEC that would provide broader spectrum protection against multiple serotypes. Another vaccination strategy is the use of autogenous killed bacterial isolates as vaccines, which can provide an important means of reducing recurring APEC infections in poultry rearing and production facilities. Autogenous vaccines have a long tradition, and the use of killed pathogenic strains as vaccines isolated from the farm of origin can provide a decrease in recurring outbreaks. Both risks and benefits are associated with this technique, with the major risk being the potential transmission of viral, bacterial, and/or fungal contaminants. On the positive side, autogenous vaccination can provide an important protective advantage when there is a sudden outbreak, and other commercially available vaccines could not adequately protect due to the heterogeneity of the APEC outbreak strains. Other techniques include the use of inactivated or killed vaccines prepared from the whole bacterial preparation combined with adjuvant and subunit vaccines prepared from outer membrane proteins, whole-cell proteins, flagellin, pilus proteins, or LPS (Figure 5). It is important to note that although vaccination may provide some level of potential protection against colibacillosis, proper management and biosecurity in the poultry farm are paramount for maintaining good poultry health. Some of the ongoing research regarding vaccines and vaccine development against APEC is presented in Table 6.

4.2. Porcine Colibacillosis

58Porcine colibacillosis are enteric infectious diseases caused by pathogenic E. coli which accounts for one of the major diseases affecting the swine industry. Colibacillosis in swine includes mainly neonatal diarrhea and post-weaning diarrhea, resulting in illness and death occurring worldwide in neonatal and recently weaned pigs. Neonatal swine diarrhea is observed in piglets aged 1–4 days after farrowing, pre-weaning diarrhea within 1–2 weeks post-farrowing to weaning, post-weaning diarrhea occurs 2–3 weeks after weaning with a peak rise of diarrhea from 6 to 8 weeks and even at 12 weeks after weaning. In addition, Edema disease is usually observed after weaning and other E. coli infections such as mastitis, UTIs (cystitis) and septicemia are also observed. Although EHEC, EAEC and EIEC are also known to cause pathogenesis in pigs; ETEC and EPEC are major pathovars that cause serious health problems and even death in piglets around the world. Enterotoxigenic E. coli (ETEC) is the most important pathotype and is commonly associated with post-weaning diarrhea (PWD) and neonatal diarrhea. Cases of PWD have also been associated with EPEC. Neonatal diarrhea and PWD are the most prevalent porcine diseases, accounting for substantial economic losses worldwide. Common serotypes of ETEC causing neonatal and post-weaning diarrhea include O8: K88, O149: K88 and O157: K88. In addition, many other serotypes are associated with ETEC infections in piglets. Apart from ETEC and EPEC, Verotoxigenic E. coli is also known to be associated with PWD, edema disease and other related infections in swine. Among verotoxigenic E. coli isolates of weaned pigs with enteric diseases, common serotypes include O157: K17, O149:K91 and O groups 138, 139 and 141.

59Adhesins and enterotoxins are major virulence factors of E. coli causing diarrheal disease in pigs. Adhesins contribute to the colonization, proliferation and development of infection, and enterotoxins also play a role in the colonization and development of disease. ETEC strains can produce a number of different fimbrial adhesins. Fimbriae in ETEC are divided into four main types: F4 (K88), F5 (K99), F6 (987P), and F41. The ETEC strains also produce LT and ST (STa and STb) enterotoxins. It has been reported that ETEC strains producing F4 fimbrial adhesins and producing LT and ST enterotoxins are responsible for causing diarrhea in neonatal, pre- and post-weaning pigs. In addition, EPEC strains with F41 and F18 fimbriae and producing STb enterotoxin STb are known to cause swine diarrhea. Moreover, VTEC strains with F4 (K91) fimbriae and LT and ST enterotoxins are also reported to cause infections in pigs.

4.2.1. Resistance to Multiple Antibiotics in E. coli Causing Diarrhea in Swine

60Swine production is one of the major sources of animal meat production. Over the years the presence of bacterial diseases has resulted in increased use of antibiotics to prevent such infections and reduce economic losses and improve animal health. The wide use of antibiotics has consequences, and there is a global concern in increasing antibiotic resistance. It has been reported that there is a high level of antibiotic resistance in porcine E. coli isolates from China. Antibiotic resistance in E. coli is also prevalent on pork farms across Europe, including Spain, and other pork exporting countries such as Denmark, France, Italy, and Sweden are also found to be multi-drug resistant to antibiotics such as ampicillin, streptomycin, sulphonamide, tetracycline, and trimethoprim.

4.2.2. Need of Vaccines and Vaccine Strategies against Porcine Pathogenic E. coli

61The pork industry is one of the most important meat industries in terms of numbers and biomass. The UN Food and Agriculture Organization has predicted that the pork meat industry will experience strong growth among all meat industries with an expected increase of 8.6% by 2030 and 12.7% by 2050. It is therefore crucial to understand and structure sustainable growth of the pork production industry in terms of animal health, antibiotic resistance, and alternative routes to the antibiotic through the development and implementation of vaccines and other approaches to improve porcine health and provide a high-quality consumer product globally.

62Since adhesins and enterotoxins are vital for ETEC pathogenesis and virulence, various approaches have been developed to inhibit the initial stages of ETEC pathogenesis by developing anti-adhesin and anti-toxin-based vaccines. Over the past decade, multiple vaccination strategies have been developed. For example, a live-attenuated S. typhimurium Δlon ΔcpxR Δasd strain has been used to deliver ETEC fimbriae in order to promote an anti-adhesin-based vaccine immune response in swine. This vaccine showed no clinical signs of diarrhea in the vaccinated and challenged group and generated increased levels of IgG and IgA in both serum and colostrum. Some porcine ETEC strains produce enterotoxins but use fewer common types of fimbriae, so it is important to design a vaccine that can provide a large spectrum of protection against multiple types of porcine pathogenic E. coli. One such example is a live-attenuated E. coli strain expressing an adhesin-toxoid fusion antigen that has been shown to elicit a good systemic and mucosal antibody response and protect piglets from ETEC-associated diarrhea. Another group designed a multivalent vaccine candidate comprising STa-LTB-STb (SLS) toxin-based antigens, and two fimbrial proteins, which showed significant protection against an ETEC strain. Likewise, a peptide-based vaccine constructed by genetically fusing nucleotides encoding peptides for fimbria and toxins to obtain tripartite adhesion-adhesin-toxoid chimeric antigens were given to piglets and they provided protection against a challenge using a fimbrial/LT/STb producing ETEC strain. This study demonstrated that multiple adhesin antigens and multiple toxin antigens could be expressed simultaneously within a single recombinant fusion protein. In the future, non-pathogenic E. coli isolates from a farm that expresses a tripartite antigen could also be used to develop a live attenuated vaccine against porcine ETEC. Along with these, other strategies such as an oral fimbrial subunit vaccine, live oral vaccine, encapsulated subunit, and other live vaccine candidates are described in detail in the following reviews.

63Another interesting strategy that is being considered is a parenteral vaccine which is based on the presence of lactogenic maternal antibodies via parenteral immunization. The entero-mammary route allows oral maternal immunization to elicit a mucosal and systemic immune response to reach the gut of the suckling piglet with humoral and cellular components with effector activity. This will provide protection against infection by either maternal antibodies and leukocytes present in the suckling infants or by acquiring specific piglet immunity through the sow. Research has suggested that suckling piglets born from immunized sows with Sta toxoid fusion antigens were protected from a challenge with an STa-positive ETEC strain. Another vaccine candidate containing a Sta toxoid fusion and chemical conjugates was used to immunize sows, and the suckling piglets passively acquired anti-STa IgG and IgA antibodies and were better protected from challenges with an STa positive ETEC strain. Some popular commercially available vaccines are manufactured by Elanco and Vencofarma and are composed of inactivated ETEC bacterins which are administered to pregnant pigs two weeks before farrowing.

64Overall, some approaches to vaccination against porcine E. coli have shown promise against some common types of strains causing swine diarrhea. However, due to the diversity of pathogenic E. coli, certain strains are still a problem to the industry. Importantly, a global and integrative approach is needed to regulate and monitor multiple aspects from sanitation, feed regimen, antibiotic usage, and vaccine strategies to maintain and improve the production of sustainable pork production industry worldwide.

4.3. Bovine Colibacillosis

65Bovine colibacillosis is an infection caused by ETEC strains. Although EPEC, EHEC and VTEC strains are commonly present in the bovine intestinal tract, they are generally considered non-pathogenic to cattle. Enteric colibacillosis is usually observed in young calves that are from 2 to 10 days old. Stress can also lead to ETEC-associated diarrhea in older calves. During the infection, calves suffer from profuse and watery diarrhea, become dehydrated, depressed, anorexic, do not suckle and may die rapidly. Depending on the severity of symptoms, calves frequently die in 3 to 5 days. Colibacillosis outbreaks in cattle have been associated with multi-resistant strains under poor sanitation conditions and with susceptible calves in the herd population. It has been shown that calves of first-calf heifers are more susceptible to infection, mainly due to the presence of lower levels of immunoglobulin in colostrum and the production of less colostrum itself. Calves are also known to develop septicemic colibacillosis due to invasive serotypes of ETEC that can enter the bloodstream and cause systemic infection and rapid death due to septicemia. Generally, ETEC strains adhere to the ileum of calves and release toxins to induce severe diarrhea. Septicemic E. coli strains can cause systemic infection and, in some cases, EHEC and VTEC strains produce Shiga-toxins that destroy gut microvilli and can cause hemorrhagic diarrhea in 15-to-30-day-old calves.

66Bovine ETEC isolates from diseased calves commonly produce K99 (F5) adhesin and heat stable (STa or STb) or heat liable (LT1 or LT2) enterotoxins. It has been reported that out of 173 isolates of ETEC 49% of strains produced toxins where 53 isolates harbored Sta toxin and 9 contained both STa and LT toxin encoding sequences. Interestingly, nine isolates harbored Shiga-toxin genes. There is also a high incidence of multiple drug resistance in bovine ETEC isolates throughout the world. With an increased concern due to multiple antibiotic resistance, there is a greater interest in vaccines and other preventative measures to reduce the incidence of colibacillosis in calves (See Table 6 which lists such vaccine strategies).

4.4. Mastitis in Cattle and Swine

67Mastitis is a disease characterized by intramammary infections caused mainly by microorganisms and, in some cases, worsened by physical trauma that results in persistent inflammation of the udder and mammary tissue. Microorganisms such as viruses, fungi, mycoplasma, and numerous bacterial species can cause mastitis. E. coli are a common cause of mastitis. Mastitis in swine is one of the causes of maternal and pre-weaning piglet mortality. E. coli is known to be one of the leading causes of inflammatory infection of mammary glands in sows, resulting in abnormal and decreased milk production and even death in severe cases. Among different pathotypes of E. coli, a novel MPEC (Mammary pathogenic E. coli) is one of the most common causative agents of coliform mastitis. MPEC strains have evolved by acquiring virulence factors that promote colonization and invasion of the mammary glands and increase survival in milk.

68Due to excessive use of antibiotics to treat bovine mastitis, there has been an increased concern about the presence of antibiotic-resistant bacteria on dairy farms and in milk and dairy products. Therefore, to overcome this challenge, different vaccination approaches to prevent coliform mastitis have also been tested. Commercially, mutant strains of E. coli O111:B4 (J5) and Salmonella Typhimurium Re-17 are being used to immunize cows against coliform mastitis. In addition, recombinant OmpA (outer membrane protein A) is also being studied as a potential vaccine candidate to prevent infection against mastitis-associated E. coli. Other vaccination strategies against mastitis caused by organisms other than E. coli are also described in Table 7.

5. Conclusions

69The diversity of pathogenic E. coli which collectively includes distinct pathotypes of importance for both human and animal health has been and remains an important challenge for the development of effective vaccines. Identifying protective and conserved antigens to prevent specific types of E. coli disease is complicated by the different types of diseases as well as the heterogeneity of gene content contributing to the pathogenic potential among, and even within, pathotypes associated with distinct disease syndromes in either humans or other animals. Thus far, for vaccine candidates to prevent human infections, almost all the studies have been in animals and the few human studies conducted to date have either been failures, generated inconclusive data, or have not been further pursued. Based on the aforementioned diverse nature of E. coli virulence factors, one can predict that an “ideal” vaccine that can prevent multiple types of Escherichia coli infection and disease is unlikely. However, the development of different vaccine types and innovative immunization strategies appears promising. A major hurdle in overcoming E. coli pathotypes in some cases is the presence of multiple serotypes that are responsible for either human or animal infections. Surface-exposed components are often attractive and effective candidates or vaccine development, but in the case of E. coli vaccines, particularly in humans, the selection of targets more specific to pathogenic strains may be a more favorable approach, than targeting highly conserved antigens, considering that E. coli strains are also common members of the intestinal microbiota. As such, the generation of an immune response to highly conserved antigens in most E. coli and other enterobacteria may be protective against some types of infection but may also affect the host intestinal mucosal immune response and colonization of commensal E. coli in the intestinal tract. Such aspects of the effects of selection of highly conserved vs. more patho-specific antigens need to be more fully investigated in both animal models and humans in future studies. In addition to the vaccine development strategies presented herein, it will be of interest as well to investigate how other novel vaccine approaches such as mRNA vaccination may provide protection against certain pathotypes of E. coli. However, the use of such vaccines may be limited due to cost or issues with vaccine stability and the requirement of a cold chain particularly for vaccination of populations in outlying regions and in developing countries where endemic infections such as diarrhea caused by intestinal pathogenic E. coli and other pathogens remain a global health challenge. Apart from vaccination campaigns, different preventive strategies such as improved sanitation and hygiene, access to safe drinking water, exclusive breastfeeding, optimal nutrition, and vaccines against other pathogens (rotavirus and measles) are equally important. In any case, continued development of new strategies for E. coli vaccine discovery is warranted in the context of its antibiotic resistance. Hopefully such strategies will lead to the development of more effective means to reduce the incidence of the spectrum of infectious diseases that E. coli can cause in both humans and animals of agricultural importance which remain a globally important economic and public health burden.

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Ventola C.L. Cancer immunotherapy, part 1: Current strategies and agents. Pharm. Ther. 2017;42:375.
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69.
Dadonaite B., Ritchie H., Roser M. Diarrheal Diseases. Our World Data. 2018.
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70.
Roser M., Ritchie H. Burden of Disease. Our World Data. 2021.
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Rojas-Lopez M., Monterio R., Pizza M., Desvaux M., Rosini R. Intestinal pathogenic Escherichia coli: Insights for vaccine development. Front. Microbiol. 2018;9:440.
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Kliegman R.M., Stanton B.M., Geme J.S. Nelson’s textbook of pediatrics (20th edn.), by R. Kliegman, B. Stanton, J. St. Geme, N. Schor (eds). Pediatr. Radiol. 2017;47:1364-1365.
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Donnenberg M.S., Kaper J. Enteropathogenic Escherichia coli. Infect. Immun. 1992;60:3953-3961.
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Deborah Chen H., Frankel G. Enteropathogenic Escherichia coli: Unravelling pathogenesis. FEMS Microbiol. Rev. 2005;29:83-98.
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Hernandes R.T., Elias W.P., Vieira M.A., Gomes T.A. An overview of atypical enteropathogenic Escherichia coli. FEMS Microbiol. Lett. 2009;297:137-149.
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76.
Typical and Atypical Enteropathogenic Escherichia coli · 2002
No notice
77.
Govindarajan D.K., Viswalingam N., Meganathan Y., Kandaswamy K. Adherence patterns of Escherichia coli in the intestine and its role in pathogenesis. Med. Microecol. 2020;5:100025.
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Donnenberg M.S., Kaper J.B., Finlay B.B. Interactions between enteropathogenic Escherichia coli and host epithelial cells. Trends Microbiol. 1997;5:109-114.
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Bieber D., Ramer S.W., Wu C.-Y., Murray W.J., Tobe T., Fernandez R., Schoolnik G.K. Type IV pili, transient bacterial aggregates, and virulence of enteropathogenic Escherichia coli. Science. 1998;280:2114-2118.
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Zahavi E.E., Lieberman J.A., Donnenberg M.S., Nitzan M., Baruch K., Rosenshine I., Turner J.R., Melamed-Book N., Feinstein N., Zlotkin-Rivkin E. Bundle-forming pilus retraction enhances enteropathogenic Escherichia coli infectivity. Mol. Biol. Cell. 2011;22:2436-2447.
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Girón J.A., Donnenberg M.S., Martin W.C., Jarvis K.G., Kaper J.B. Distribution of the bundle-forming pilus structural gene (bfpA) among enteropathogenic Escherichia coli. J. Infect. Dis. 1993;168:1037-1041.
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Giron J.A., Ho A.S.Y., Schoolnik G.K. An inducible bundle-forming pilus of enteropathogenic Escherichia coli. Science. 1991;254:710-713.
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83.
Vasconcellos H.L.F., da Silva W.D., Nascimento I.P., Kipnis A. Vaccine Against Entheropathogenic E. coli: A Systematic Review. Int. J. Vaccine Res. 2017;2:1-8.
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Vallance B., Finlay B. Exploitation of host cells by enteropathogenic Escherichia coli. Proc. Natl. Acad. Sci. USA. 2000;97:8799-8806.
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Ide T., Laarmann S., Greune L., Schillers H., Oberleithner H., Schmidt M.A. Characterization of translocation pores inserted into plasma membranes by type III-secreted Esp proteins of enteropathogenic Escherichia coli. Cell. Microbiol. 2001;3:669-679.
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86.
Gruenheid S., DeVinney R., Bladt F., Goosney D., Gelkop S., Gish G.D., Pawson T., Finlay B.B. Enteropathogenic E. coli Tir binds Nck to initiate actin pedestal formation in host cells. Nat. Cell Biol. 2001;3:856-859.
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Goosney D.L., Gruenheid S., Finlay B.B. Gut feelings: Enteropathogenic E. coli (EPEC) interactions with the host. Annu. Rev. Cell Dev. Biol. 2000;16:173-189.
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Goosney D.L., de Grado M., Finlay B.B. Putting E. coli on a pedestal: A unique system to study signal transduction and the actin cytoskeleton. Trends Cell Biol. 1999;9:11-14.
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Guignot J., Segura A., Tran Van Nhieu G. The serine protease EspC from enteropathogenic Escherichia coli regulates pore formation and cytotoxicity mediated by the type III secretion system. PLoS Pathog. 2015;11:e1005013.
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Serapio-Palacios A., Navarro-Garcia F. EspC, an autotransporter protein secreted by enteropathogenic Escherichia coli, causes apoptosis and necrosis through caspase and calpain activation, including direct procaspase-3 cleavage. MBio. 2016;7:e00479-16.
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Vasconcellos H.L.F., Scaramuzzi K., Nascimento I.P., Ferreira J.M.D.C., Abe C.M., Piazza R.M., Kipnis A., da Silva W.D. Generation of recombinant bacillus Calmette–Guérin and Mycobacterium smegmatis expressing BfpA and intimin as vaccine vectors against enteropathogenic Escherichia coli. Vaccine. 2012;30:5999-6005.
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92.
Mare A.D., Ciurea C.N., Man A., Tudor B., Moldovan V., Decean L., Toma F. Enteropathogenic Escherichia coli—A summary of the literature. Gastroenterol. Insights. 2021;12:28-40.
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Loureiro I., Frankel G., Adu-Bobie J., Dougan G., Trabulsi L.R., Carneiro-Sampaio M.M. Human Colostrum Contains IgA Antibodies Reactive to EnteropathogenicEscherichia coli Virulence-Associated Proteins: Intimin, BfpA, EspA, and EspB. J. Pediatr. Gastroenterol. Nutr. 1998;27:166-171.
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94.
Ellis R.W., Brodeur B.R. New Bacterial Vaccines. 2003;40-63.
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95.
Flores V.M.Q., de Souza Fernandes R.C.C., de Macedo Z.S., Medina-Acosta E. Expression and purification of the recombinant enteropathogenic Escherichia coli vaccine candidates BfpA and EspB. Protein Expr. Purif. 2002;25:16-22.
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McNeilly T.N., Mitchell M.C., Corbishley A., Nath M., Simmonds H., McAteer S.P., Mahajan A., Low J.C., Smith D.G., Huntley J.F. Optimizing the protection of cattle against Escherichia coli O157: H7 colonization through immunization with different combinations of H7 flagellin, Tir, intimin-531 or EspA. PLoS ONE. 2015;10:e0128391.
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McNeilly T.N., Mitchell M.C., Rosser T., McAteer S., Low J.C., Smith D.G., Huntley J.F., Mahajan A., Gally D.L. Immunization of cattle with a combination of purified intimin-531, EspA and Tir significantly reduces shedding of Escherichia coli O157: H7 following oral challenge. Vaccine. 2010;28:1422-1428.
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Ferreira P.C., Campos I.B., Abe C.M., Trabulsi L.R., Elias W.P., Ho P.L., Oliveira M.L.S. Immunization of mice with Lactobacillus casei expressing intimin fragments produces antibodies able to inhibit the adhesion of enteropathogenic Escherichia coli to cultivated epithelial cells. FEMS Immunol. Med. Microbiol. 2008;54:245-254.
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99.
da Silva J.V., Garcia A.B., Flores V.M.Q., de Macedo Z.S., Medina-Acosta E. Phytosecretion of enteropathogenic Escherichia coli pilin subunit A in transgenic tobacco and its suitability for early life vaccinology. Vaccine. 2002;20:2091-2101.
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100.
Wang S., Xia X., Liu Y., Wan F. Oral Administration with Live Attenuated Citrobacter rodentium Protects Immunocompromised Mice from Lethal Infection. Infect. Immun. 2022;90:e00198-22.
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Gohar A., Abdeltawab N.F., Fahmy A., Amin M.A. Development of safe, effective and immunogenic vaccine candidate for diarrheagenic Escherichia coli main pathotypes in a mouse model. BMC Res. Notes. 2016;9:80.
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Welinder-Olsson C., Kaijser B. Enterohemorrhagic Escherichia coli (EHEC). Scand. J. Infect. Dis. 2005;37:405-416.
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Karpman D., Ståhl A.l. Enterohemorrhagic Escherichia coli pathogenesis and the host response. Enterohemorrhagic Escherichia coli and Other Shiga Toxin-Producing E. coli. 2015;381-402.
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104.
Treatment and outcome of Shiga-toxin-associated hemolytic uremic syndrome (HUS) · 2008
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105.
Frankel G., Phillips A.D., Rosenshine I., Dougan G., Kaper J.B., Knutton S. Enteropathogenic and enterohaemorrhagic Escherichia coli: More subversive elements. Mol. Microbiol. 1998;30:911-921.
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Bavaro M.F.E. E. coli O157: H7 and other toxigenic strains: The curse of global food distribution. Curr. Gastroenterol. Rep. 2012;14:317-323.
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EA G.G. Animal health and foodborne pathogens: Enterohaemorrhagic O157: H7 strains and other pathogenic Escherichia coli virotypes (EPEC, ETEC, EIEC, EHEC). Pol. J. Vet. Sci. 2002;5:103-115.
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Meng J., LeJeune J.T., Zhao T., Doyle M.P. Enterohemorrhagic Escherichia coli. Food Microbiol. Fundam. Front. 2012;287-309.
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Smith K.E., Wilker P.R., Reiter P.L., Hedican E.B., Bender J.B., Hedberg C.W. Antibiotic treatment of Escherichia coli O157 infection and the risk of hemolytic uremic syndrome, Minnesota. Pediatr. Infect. Dis. J. 2012;31:37-41.
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Tarr P.I., Gordon C.A., Chandler W.L. Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome. Lancet. 2005;365:1073-1086.
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Manitz J., Kneib T., Schlather M., Helbing D., Brockmann D. Origin detection during food-borne disease outbreaks—A case study of the 2011 EHEC/HUS outbreak in Germany. PLoS Curr. 2014;2014:6.
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112.
Braeye T., Denayer S., De Rauw K., Forier A., Verluyten J., Fourie L., Dierick K., Botteldoorn N., Quoilin S., Cosse P. Lessons learned from a textbook outbreak: EHEC-O157: H7 infections associated with the consumption of raw meat products, June 2012, Limburg, Belgium. Arch. Public Health. 2014;72:1-7.
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113.
Gaspar R., Gorjão S., Seibt B., Lima L., Barnett J., Moss A., Wills J. Tweeting during food crises: A psychosocial analysis of threat coping expressions in Spain, during the 2011 European EHEC outbreak. Int. J. Hum.-Comput. Stud. 2014;72:239-254.
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Kanayama A., Yahata Y., Arima Y., Takahashi T., Saitoh T., Kanou K., Kawabata K., Sunagawa T., Matsui T., Oishi K. Enterohemorrhagic Escherichia coli outbreaks related to childcare facilities in Japan, 2010–2013. BMC Infect. Dis. 2015;15:539.
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Meagher K.D. Policy responses to foodborne disease outbreaks in the United States and Germany. Agric. Hum. Values. 2022;39:233-248.
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Scharff R.L. Economic burden from health losses due to foodborne illness in the United States. J. Food Prot. 2012;75:123-131.
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117.
Williams D.M., Sreedhar S.S., Mickell J.J., Chan J.C. Acute kidney failure: A pediatric experience over 20 years. Arch. Pediatr. Adolesc. Med. 2002;156:893-900.
Not in our library10.1001/archpedi.156.9.893
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Trachtman H. HUS and TTP in children. Pediatr. Clin. 2013;60:1513-1526.
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119.
Prager R., Lang C., Aurass P., Fruth A., Tietze E., Flieger A. Two novel EHEC/EAEC hybrid strains isolated from human infections. PLoS ONE. 2014;9:e95379.
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120.
Diversity of Hybrid- and Hetero-Pathogenic Escherichia coli and Their Potential Implication in More Severe Diseases · 2020
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121.
Enterohemorrhagic E. coli (EHEC) pathogenesis · 2012
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122.
Tesh V., O’brien A. The pathogenic mechanisms of Shiga toxin and the Shiga-like toxins. Mol. Microbiol. 1991;5:1817-1822.
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Karch H. The role of virulence factors in enterohemorrhagic Escherichia coli (EHEC)-associated hemolytic-uremic syndrome. Semin. Thromb. Hemost. 2001;27:207-214.
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Xicohtencatl-Cortes J., Saldaña Z., Deng W., Castañeda E., Freer E., Tarr P.I., Finlay B.B., Puente J.L., Girón J.A. Bacterial macroscopic rope-like fibers with cytopathic and adhesive properties. J. Biol. Chem. 2010;285:32336-32342.
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Dutta P.R., Cappello R., Navarro-García F., Nataro J.P. Functional comparison of serine protease autotransporters of Enterobacteriaceae. Infect. Immun. 2002;70:7105-7113.
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126.
Tse C.M., In J.G., Yin J., Donowitz M., Doucet M., Foulke-Abel J., Ruiz-Perez F., Nataro J.P., Zachos N.C., Kaper J.B. Enterohemorrhagic E. coli (EHEC)—Secreted serine protease EspP stimulates electrogenic ion transport in human colonoid monolayers. Toxins. 2018;10:351.
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Weiss A., Brockmeyer J. Prevalence, biogenesis, and functionality of the serine protease autotransporter EspP. Toxins. 2012;5:25-48.
Not in our library10.3390/toxins5010025
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An H., Fairbrother J.M., Désautels C., Mabrouk T., Dugourd D., Dezfulian H., Harel J. Presence of the LEE (locus of enterocyte effacement) in pig attaching and effacing Escherichia coli and characterization of eae, espA, espB and espD genes of PEPEC (pig EPEC) strain 1390. Microb. Pathog. 2000;28:291-300.
Not in our library10.1006/mpat.1999.0346
129.
Dean-Nystrom E.A., Bosworth B.T., Cray W.C., Moon H.W. Pathogenicity of Escherichia coli O157: H7 in the intestines of neonatal calves. Infect. Immun. 1997;65:1842-1848.
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Tzipori S., Gunzer F., Donnenberg M.S., de Montigny L., Kaper J.B., Donohue-Rolfe A. The role of the eaeA gene in diarrhea and neurological complications in a gnotobiotic piglet model of enterohemorrhagic Escherichia coli infection. Infect. Immun. 1995;63:3621-3627.
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Dean-Nystrom E.A., Pohlenz J.F., Moon H.W., O’Brien A.D. Escherichia coli O157: H7 causes more-severe systemic disease in suckling piglets than in colostrum-deprived neonatal piglets. Infect. Immun. 2000;68:2356-2358.
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Karpman D., Connell H., Svensson M., Scheutz F., Aim P., Svanborg C. The role of lipopolysaccharide and Shiga-like toxin in a mouse model of Escherichia coli O157: H7 infection. J. Infect. Dis. 1997;175:611-620.
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Taguchi H., Takahashi M., Yamaguchi H., Osaki T., Komatsu A., Fujioka Y., Kamiya S. Experimental infection of germ-free mice with hyper-toxigenic enterohaemorrhagic Escherichia coli O157: H7, strain 6. J. Med. Microbiol. 2002;51:336-343.
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134.
Conlan J.W., Perry M.B. Susceptibility of three strains of conventional adult mice to intestinal colonization by an isolate of Escherichia coli O157: H7. Can. J. Microbiol. 1998;44:800-805.
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Woods J.B., Schmitt C.K., Darnell S.C., Meysick K.C., O’Brien A.D. Ferrets as a model system for renal disease secondary to intestinal infection with Escherichia coli O157: H7 and other Shiga toxin-producing E. coli. J. Infect. Dis. 2002;185:550-554.
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Bitzan M., Poole R., Mehran M., Sicard E., Brockus C., Thuning-Roberson C., Rivière M. Safety and pharmacokinetics of chimeric anti-Shiga toxin 1 and anti-Shiga toxin 2 monoclonal antibodies in healthy volunteers. Antimicrob. Agents Chemother. 2009;53:3081-3087.
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137.
Mejías M.P., Hiriart Y., Lauché C., Fernández-Brando R.J., Pardo R., Bruballa A., Ramos M.V., Goldbaum F.A., Palermo M.S., Zylberman V. Development of camelid single chain antibodies against Shiga toxin type 2 (Stx2) with therapeutic potential against Hemolytic Uremic Syndrome (HUS). Sci. Rep. 2016;6:24913.
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Liu J., Sun Y., Feng S., Zhu L., Guo X., Qi C. Towards an attenuated enterohemorrhagic Escherichia coli O157: H7 vaccine characterized by a deleted ler gene and containing apathogenic Shiga toxins. Vaccine. 2009;27:5929-5935.
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139.
Schmidt M.A. LEEways: Tales of EPEC, ATEC and EHEC. Cell Microbiol. 2010;12:1544-1552.
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140.
Calderon Toledo C., Arvidsson I., Karpman D. Cross-reactive protection against enterohemorrhagic Escherichia coli infection by enteropathogenic E. coli in a mouse model. Infect. Immun. 2011;79:2224-2233.
Not in our library10.1128/iai.01024-10
141.
Garrine M., Matambisso G., Nobela N., Vubil D., Massora S., Acácio S., Nhampossa T., Alonso P., Mandomando I. Low frequency of enterohemorrhagic, enteroinvasive and diffusely adherent Escherichia coli in children under 5 years in rural Mozambique: A case-control study. BMC Infect. Dis. 2020;20:659.
Not in our library10.1186/s12879-020-05380-1
142.
Gu J., Ning Y., Wang H., Xiao D., Tang B., Luo P., Cheng Y., Jiang M., Li N., Zou Q. Vaccination of attenuated EIS-producing Salmonella induces protective immunity against enterohemorrhagic Escherichia coli in mice. Vaccine. 2011;29:7395-7403.
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143.
Cepeda Molero M.E. Generation of Enteropathogenic E. coli Strains Lacking the Repertoire of Effectors Translocated by the Type III Protein Secretion System and Their Characterization in the Infection of Cultured Cell Lines and Human Intestinal Biopsies. 2016.
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144.
Fujii J., Naito M., Yutsudo T., Matsumoto S., Heatherly D.P., Yamada T., Kobayashi H., Yoshida S.-i., Obrig T. Protection by a recombinant Mycobacterium bovis Bacillus Calmette-Guerin vaccine expressing Shiga toxin 2 B subunit against Shiga toxin-producing Escherichia coli in mice. Clin. Vaccine Immunol. 2012;19:1932-1937.
Not in our library10.1128/cvi.00473-12
145.
Cai K., Tu W., Liu Y., Li T., Wang H. Novel fusion antigen displayed-bacterial ghosts vaccine candidate against infection of Escherichia coli O157: H7. Sci. Rep. 2015;5:17479.
Not in our library10.1038/srep17479
146.
Mayr U.B., Kudela P., Atrasheuskaya A., Bukin E., Ignatyev G., Lubitz W. Rectal single dose immunization of mice with Escherichia coli O157: H7 bacterial ghosts induces efficient humoral and cellular immune responses and protects against the lethal heterologous challenge. Microb. Biotechnol. 2012;5:283-294.
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147.
Zhang X.-h., He K.-w., Zhang S.-x., Lu W.-c., Zhao P.-d., Luan X.-t., Ye Q., Wen L.-b., Li B., Guo R.-l. Subcutaneous and intranasal immunization with Stx2B–Tir–Stx1B–Zot reduces colonization and shedding of Escherichia coli O157: H7 in mice. Vaccine. 2011;29:3923-3929.
Not in our library10.1016/j.vaccine.2011.02.007
148.
Wan C.s., Zhou Y., Yu Y., Peng L.J., Zhao W., Zheng X.L. B-cell epitope KT-12 of enterohemorrhagic Escherichia coli O157: H7: A novel peptide vaccine candidate. Microbiol. Immunol. 2011;55:247-253.
Not in our library10.1111/j.1348-0421.2011.00316.x
149.
Cheng Y., Feng Y., Luo P., Gu J., Yu S., Zhang W.-J., Liu Y.-Q., Wang Q.-X., Zou Q.-M., Mao X.-H. Fusion expression and immunogenicity of EHEC EspA-Stx2Al protein: Implications for the vaccine development. J. Microbiol. 2009;47:498-505.
Not in our library10.1007/s12275-009-0116-8
150.
Rosales-Mendoza S., Nieto-Gómez R. Green therapeutic biocapsules: Using plant cells to orally deliver biopharmaceuticals. Trends Biotechnol. 2018;36:1054-1067.
Not in our library10.1016/j.tibtech.2018.05.010
151.
Garcia-Angulo V.A., Kalita A., Torres A.G. Advances in the development of enterohemorrhagic Escherichia coli vaccines using murine models of infection. Vaccine. 2013;31:3229-3235.
Not in our library10.1016/j.vaccine.2013.05.013
152.
Khanifar J., Salmanian A.H., Haji Hosseini R., Amani J., Kazemi R. Chitosan nano-structure loaded with recombinant E. coli O157: H7 antigens as a vaccine candidate can effectively increase immunization capacity. Artif. Cells Nanomed. Biotechnol. 2019;47:2593-2604.
Not in our library10.1080/21691401.2019.1629947
153.
Szu S.C., Ahmed A. Clinical studies of Escherichia coli O157: H7 conjugate vaccines in adults and young children. Microbiol. Spectr. 2014;2:2-6.
Not in our library10.1128/microbiolspec.ehec-0016-2013
154.
Tapia D., Ross B.N., Kalita A., Kalita M., Hatcher C.L., Muruato L.A., Torres A.G. From in silico protein epitope density prediction to testing Escherichia coli O157: H7 vaccine candidates in a murine model of colonization. Front. Cell Infect. Microbiol. 2016;6:94.
Not in our library10.3389/fcimb.2016.00094
155.
García-Angulo V.A., Kalita A., Kalita M., Lozano L., Torres A.G. Comparative genomics and immunoinformatics approach for the identification of vaccine candidates for enterohemorrhagic Escherichia coli O157: H7. Infect. Immun. 2014;82:2016-2026.
Not in our library10.1128/iai.01437-13
156.
Riquelme-Neira R., Rivera A., Sáez D., Fernández P., Osorio G., del Canto F., Salazar J.C., Vidal R.M., Oñate A. Vaccination with DNA encoding truncated enterohemorrhagic Escherichia coli (EHEC) factor for adherence-1 gene (efa-1′) confers protective immunity to mice infected with E. coli O157: H7. Front. Cell Infect. Microbiol. 2016;5:104.
Not in our library10.3389/fcimb.2015.00104
157.
Qadri F., Svennerholm A.-M., Faruque A., Sack R.B. Enterotoxigenic Escherichia coli in developing countries: Epidemiology, microbiology, clinical features, treatment, and prevention. Clin. Microbiol. Rev. 2005;18:465-483.
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158.
Okoh A.I., Osode A.Ν. Enterotoxigenic Escherichia coli (ETEC): A recurring decimal in infants’ and travelers’ diarrhea. Rev. Environ. Health. 2008;23:135-148.
Not in our library10.1515/reveh.2008.23.2.135
159.
Vicente A.C., Teixeira L.F., Iniguez-Rojas L., Luna M.d.G., Silva L., Andrade J.R.d.C., Guth B.E.C. Outbreaks of cholera-like diarrhoea caused by enterotoxigenic Escherichia coli in the Brazilian Amazon Rainforest. Trans. R. Soc. Trop. Med. Hyg. 2005;99:669-674.
Not in our library10.1016/j.trstmh.2005.03.007
160.
Fleckenstein J.M., Hardwidge P.R., Munson G.P., Rasko D.A., Sommerfelt H., Steinsland H. Molecular mechanisms of enterotoxigenic Escherichia coli infection. Microbes Infect. 2010;12:89-98.
Not in our library10.1016/j.micinf.2009.10.002
161.
Fleckenstein J.M., Kuhlmann F.M. Enterotoxigenic Escherichia coli infections. Curr. Infect. Dis. Rep. 2019;21:9.
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162.
Khalil I., Walker R., Porter C.K., Muhib F., Chilengi R., Cravioto A., Guerrant R., Svennerholm A.-M., Qadri F., Baqar S. Enterotoxigenic Escherichia coli (ETEC) vaccines: Priority activities to enable product development, licensure, and global access. Vaccine. 2021;39:4266-4277.
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Hosangadi D., Smith P.G., Kaslow D.C., Giersing B.K. WHO consultation on ETEC and Shigella burden of disease, Geneva, 6–7th April 2017: Meeting report. Vaccine. 2019;37:7381-7390.
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McGregor A.C., Wright S.G. Gastrointestinal symptoms in travellers. Clin. Med. 2015;15:93.
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Steffen R. Epidemiology of traveler’s diarrhea. Clin. Infect. Dis. 2005;41:S536-S540.
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Travelers’ diarrhea: update on the incidence, etiology and risk in military and similar populations – 1990-2005 versus 2005–2015, does a decade make a difference? · 2019
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167.
Girón J.A., Levine M.M., Kaper J.B. Longus: A long pilus ultrastructure produced by human enterotoxigenic Escherichia coli. Mol. Microbiol. 1994;12:71-82.
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Spangler B.D. Structure and function of cholera toxin and the related Escherichia coli heat-labile enterotoxin. Microbiol. Rev. 1992;56:622-647.
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Nataro J.P., Kaper J.B. Diarrheagenic Escherichia coli. Clin. Microbiol. Rev. 1998;11:142-201.
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170.
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Patel S.K., Dotson J., Allen K.P., Fleckenstein J.M. Identification and molecular characterization of EatA, an autotransporter protein of enterotoxigenic Escherichia coli. Infect. Immun. 2004;72:1786-1794.
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Qadri F., Akhtar M., Bhuiyan T.R., Chowdhury M.I., Ahmed T., Rafique T.A., Khan A., Rahman S.I., Khanam F., Lundgren A. Safety and immunogenicity of the oral, inactivated, enterotoxigenic Escherichia coli vaccine ETVAX in Bangladeshi children and infants: A double-blind, randomised, placebo-controlled phase 1/2 trial. Lancet Infect. Dis. 2020;20:208-219.
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Norton E.B., Lawson L.B., Freytag L.C., Clements J.D. Characterization of a mutant Escherichia coli heat-labile toxin, LT (R192G/L211A), as a safe and effective oral adjuvant. Clin. Vaccine Immunol. 2011;18:546-551.
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The Mucosal Vaccine Adjuvant LT(R192G/L211A) or dmLT · 2018
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175.
Leach S., Lundgren A., Carlin N., Löfstrand M., Svennerholm A.-M. Cross-reactivity and avidity of antibody responses induced in humans by the oral inactivated multivalent enterotoxigenic Escherichia coli (ETEC) vaccine ETVAX. Vaccine. 2017;35:3966-3973.
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Barry E.M., Levine M.M. A tale of two bacterial enteropathogens and one multivalent vaccine. Cell Microbiol. 2019;21:e13067.
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Lundgren A., Bourgeois L., Carlin N., Clements J., Gustafsson B., Hartford M., Holmgren J., Petzold M., Walker R., Svennerholm A.-M. Safety and immunogenicity of an improved oral inactivated multivalent enterotoxigenic Escherichia coli (ETEC) vaccine administered alone and together with dmLT adjuvant in a double-blind, randomized, placebo-controlled Phase I study. Vaccine. 2014;32:7077-7084.
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Turner A.K., Stephens J.C., Beavis J.C., Greenwood J., Gewert C., Randall R., Freeman D., Darsley M.J. Generation and characterization of a live attenuated enterotoxigenic Escherichia coli combination vaccine expressing six colonization factors and heat-labile toxin subunit B. Clin. Vaccine Immunol. 2011;18:2128-2135.
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Turner A.K., Terry T.D., Sack D.A., Londoño-Arcila P., Darsley M.J. Construction and characterization of genetically defined aro omp mutants of enterotoxigenic Escherichia coli and preliminary studies of safety and immunogenicity in humans. Infect. Immun. 2001;69:4969-4979.
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Levine M.M., Girón J.A., Noriega F.R. Fimbrial vaccines. Fimbriae. 2020;255-270.
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181.
Barry E.M., Levine M.M. Multivalent Shigella Enterotoxigenic Escherichia coli Vaccine. New Generation Vaccines. 2016;751-755.
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182.
Barry E., Cassels F., Riddle M., Walker R., Wierzba T. Vaccines against Shigella and Enterotoxigenic Escherichia coli: A summary of the 2018 VASE Conference. Vaccine. 2019;37:4768-4774.
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Koprowski H., Levine M.M., Anderson R.J., Losonsky G., Pizza M., Barry E.M. Attenuated Shigella flexneri 2a vaccine strain CVD 1204 expressing colonization factor antigen I and mutant heat-labile enterotoxin of enterotoxigenic Escherichia coli. Infect. Immun. 2000;68:4884-4892.
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184.
Svennerholm A.-M., Glenn G. Vaccines against enterotoxigenic Escherichia coli. New Generation Vaccines. 2016;742-750.
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Akhtar M., Chowdhury M.I., Bhuiyan T.R., Kaim J., Ahmed T., Rafique T.A., Khan A., Rahman S.I., Khanam F., Begum Y.A. Evaluation of the safety and immunogenicity of the oral inactivated multivalent enterotoxigenic Escherichia coli vaccine ETVAX in Bangladeshi adults in a double-blind, randomized, placebo-controlled Phase I trial using electrochemiluminescence and ELISA assays for immunogenicity analyses. Vaccine. 2019;37:5645-5656.
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Seo H., Zhang W. Development of effective vaccines for enterotoxigenic Escherichia coli. Lancet Infect. Dis. 2020;20:150-152.
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Harro C., Sack D., Bourgeois A.L., Walker R., DeNearing B., Feller A., Chakraborty S., Buchwaldt C., Darsley M.J. A combination vaccine consisting of three live attenuated enterotoxigenic Escherichia coli strains expressing a range of colonization factors and heat-labile toxin subunit B is well tolerated and immunogenic in a placebo-controlled double-blind phase I trial in healthy adults. Clin. Vaccine Immunol. 2011;18:2118-2127.
Not in our library10.1128/cvi.05342-11
189.
Tobias J., Lebens M., Bölin I., Wiklund G., Svennerholm A.-M. Construction of non-toxic Escherichia coli and Vibrio cholerae strains expressing high and immunogenic levels of enterotoxigenic E. coli colonization factor I fimbriae. Vaccine. 2008;26:743-752.
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Chakraborty S., Randall A., Vickers T.J., Molina D., Harro C.D., DeNearing B., Brubaker J., Sack D.A., Bourgeois A.L., Felgner P.L. Interrogation of a live-attenuated enterotoxigenic Escherichia coli vaccine highlights features unique to wild-type infection. NPJ Vaccines. 2019;4:1-9.
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Tobias J., Holmgren J., Hellman M., Nygren E., Lebens M., Svennerholm A.-M. Over-expression of major colonization factors of enterotoxigenic Escherichia coli, alone or together, on non-toxigenic E. coli bacteria. Vaccine. 2010;28:6977-6984.
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Roy K., Bartels S., Qadri F., Fleckenstein J.M. Enterotoxigenic Escherichia coli elicits immune responses to multiple surface proteins. Infect. Immun. 2010;78:3027-3035.
Not in our library10.1128/iai.00264-10
193.
Roy K., Hamilton D., Ostmann M.M., Fleckenstein J.M. Vaccination with EtpA glycoprotein or flagellin protects against colonization with enterotoxigenic Escherichia coli in a murine model. Vaccine. 2009;27:4601-4608.
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Roy K., Hamilton D.J., Munson G.P., Fleckenstein J.M. Outer membrane vesicles induce immune responses to virulence proteins and protect against colonization by enterotoxigenic Escherichia coli. Clin. Vaccine Immunol. 2011;18:1803-1808.
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Zhang C., Iqbal J., Gómez-Duarte O.G. Murine immunization with CS21 pili or LngA major subunit of enterotoxigenic Escherichia coli (ETEC) elicits systemic and mucosal immune responses and inhibits ETEC gut colonization. Vet. Microbiol. 2017;202:90-100.
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196.
A combined vaccine approach against Vibrio cholerae and ETEC based on outer membrane vesicles · 2015
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197.
Harris J.A., Roy K., Woo-Rasberry V., Hamilton D.J., Kansal R., Qadri F., Fleckenstein J.M. Directed evaluation of enterotoxigenic Escherichia coli autotransporter proteins as putative vaccine candidates. PLoS Negl. Trop. Dis. 2011;5:e1428.
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Behrens R.H., Cramer J.P., Jelinek T., Shaw H., von Sonnenburg F., Wilbraham D., Weinke T., Bell D.J., Asturias E., Pauwells H.L.E. Efficacy and safety of a patch vaccine containing heat-labile toxin from Escherichia coli against travellers’ diarrhoea: A phase 3, randomised, double-blind, placebo-controlled field trial in travellers from Europe to Mexico and Guatemala. Lancet Infect. Dis. 2014;14:197-204.
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Rahjerdi A.K., Jafari M., Motamedi M.J., Amani J., Salmanian A.H. Immunogenic Evaluation of Bivalent Vaccine Candidate against Enterohemorrhagic and Enterotoxigenic Escherichia coli. Iran. J. Immunol. 2019;16:200-211.
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Pasqua M., Michelacci V., Di Martino M.L., Tozzoli R., Grossi M., Colonna B., Morabito S., Prosseda G. The intriguing evolutionary journey of enteroinvasive E. coli (EIEC) toward pathogenicity. Front. Microbiol. 2017;8:2390.
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201.
Ud-Din A., Wahid S. Relationship among Shigella spp. and enteroinvasive Escherichia coli (EIEC) and their differentiation. Braz. J. Microbiol. 2014;45:1131-1138.
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Lan R., Alles M.C., Donohoe K., Martinez M.B., Reeves P.R. Molecular evolutionary relationships of enteroinvasive Escherichia coli and Shigella spp. Infect. Immun. 2004;72:5080-5088.
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Lagerqvist N., Löf E., Enkirch T., Nilsson P., Roth A., Jernberg C. Outbreak of gastroenteritis highlighting the diagnostic and epidemiological challenges of enteroinvasive Escherichia coli, County of Halland, Sweden, November 2017. Eurosurveillance. 2020;25:1900466.
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Dhakal R., Wang Q., Howard P., Sintchenko V. Genome Sequences of Enteroinvasive Escherichia coli Sequence Type 6, 99, and 311 Strains Acquired in Asia Pacific. Microbiol. Resour. Announc. 2019;8:e00944-19.
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Kotloff K.L., Riddle M.S., Platts-Mills J.A., Pavlinac P., Zaidi A.K. Shigellosis. Lancet. 2018;391:801-812.
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Ramos H.C., Rumbo M., Sirard J.-C. Bacterial flagellins: Mediators of pathogenicity and host immune responses in mucosa. Trends Microbiol. 2004;12:509-517.
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MacLennan C.A., Grow S., Ma L.-F., Steele A.D. The Shigella vaccines pipeline. Vaccines. 2022;10:1376.
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Tian H., Li B., Xu T., Yu H., Chen J., Yu H., Li S., Zeng L., Huang X., Liu Q. Outer Membrane Vesicles Derived from Salmonella enterica Serotype Typhimurium Can Deliver Shigella flexneri 2a O-Polysaccharide Antigen To Prevent Shigella flexneri 2a Infection in Mice. Appl. Environ. Microbiol. 2021;87:e00968-0021.
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Camacho A.I., Irache J.M., Gamazo C. Recent progress towards development of a Shigella vaccine. Expert Rev. Vaccines. 2013;12:43-55.
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Camacho A., Irache J., De Souza J., Sánchez-Gómez S., Gamazo C. Nanoparticle-based vaccine for mucosal protection against Shigella flexneri in mice. Vaccine. 2013;31:3288-3294.
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Barel L.-A., Mulard L.A. Classical and novel strategies to develop a Shigella glycoconjugate vaccine: From concept to efficacy in human. Hum. Vaccines Immunother. 2019;15:1338-1356.
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Levine M.M., Kotloff K.L., Barry E.M., Pasetti M.F., Sztein M.B. Clinical trials of Shigella vaccines: Two steps forward and one step back on a long, hard road. Nat. Rev. Microbiol. 2007;5:540-553.
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Alexander W.A., Hartman A.B., Oaks E.V., Venkatesan M.M. Construction and characterization of virG (icsA)-deleted Escherichia coli K12-Shigella flexneri hybrid vaccine strains. Vaccine. 1996;14:1053-1061.
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232.
Harutyunyan S., Neuhauser I., Mayer A., Aichinger M., Szijártó V., Nagy G., Nagy E., Girardi P., Malinoski F.J., Henics T. Characterization of shigetec, a novel live attenuated combined vaccine against shigellae and etec. Vaccines. 2020;8:689.
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Venkatesan M.M., Ballou C., Barnoy S., McNeal M., El-Khorazaty J., Frenck R., Baqar S. Antibody in Lymphocyte Supernatant (ALS) responses after oral vaccination with live Shigella sonnei vaccine candidates WRSs2 and WRSs3 and correlation with serum antibodies, ASCs, fecal IgA and shedding. PLoS ONE. 2021;16:e0259361.
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Kim M.J., Moon Y.-h., Kim H., Rho S., Shin Y.K., Song M., Walker R., Czerkinsky C., Kim D.W., Kim J.-O. Cross-protective Shigella whole-cell vaccine with a truncated O-polysaccharide chain. Front. Microbiol. 2018;9:2609.
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Martin P., Alaimo C. The Ongoing Journey of a Shigella Bioconjugate Vaccine. Vaccines. 2022;10:212.
Not in our library10.3390/vaccines10020212
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Phalipon A., Mulard L.A. Toward a Multivalent Synthetic Oligosaccharide-Based Conjugate Vaccine against Shigella: State-of-the-Art for a Monovalent Prototype and Challenges. Vaccines. 2022;10:403.
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Mo Y., Fang W., Li H., Chen J., Hu X., Wang B., Feng Z., Shi H., He Y., Huang D. Safety and Immunogenicity of a Shigella Bivalent Conjugate Vaccine (ZF0901) in 3-Month-to 5-Year-Old Children in China. Vaccines. 2021;10:33.
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Harrington S.M., Dudley E.G., Nataro J.P. Pathogenesis of enteroaggregative Escherichia coli infection. FEMS Microbiol. Lett. 2006;254:12-18.
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Czeczulin J.R., Balepur S., Hicks S., Phillips A., Hall R., Kothary M.H., Navarro-Garcia F., Nataro J.P. Aggregative adherence fimbria II, a second fimbrial antigen mediating aggregative adherence in enteroaggregative Escherichia coli. Infect. Immun. 1997;65:4135-4145.
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Savarino S.J., McVeigh A., Watson J., Cravioto A., Molina J., Echeverria P., Bhan M.K., Levine M.M., Fasano A. Enteroaggregative Escherichia coli heat-stable enterotoxin is not restricted to enteroaggregative E. coli. J. Infect. Dis. 1996;173:1019-1022.
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Eslava C., Navarro-García F., Czeczulin J.R., Henderson I.R., Cravioto A., Nataro J.P. Pet, an autotransporter enterotoxin from enteroaggregative Escherichia coli. Infect. Immun. 1998;66:3155-3163.
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Villaseca J.M., Navarro-García F., Mendoza-Hernández G., Nataro J.P., Cravioto A., Eslava C. Pet toxin from enteroaggregative Escherichia coli produces cellular damage associated with fodrin disruption. Infect. Immun. 2000;68:5920-5927.
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Harrington S.M., Sheikh J., Henderson I.R., Ruiz-Perez F., Cohen P.S., Nataro J.P. The Pic protease of enteroaggregative Escherichia coli promotes intestinal colonization and growth in the presence of mucin. Infect. Immun. 2009;77:2465-2473.
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Abreu A.G., Fraga T.R., Granados Martínez A.P., Kondo M.Y., Juliano M.A., Juliano L., Navarro-Garcia F., Isaac L., Barbosa A.S., Elias W.P. The serine protease Pic from enteroaggregative Escherichia coli mediates immune evasion by the direct cleavage of complement proteins. J. Infect. Dis. 2015;212:106-115.
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Ruiz-Perez F., Wahid R., Faherty C.S., Kolappaswamy K., Rodriguez L., Santiago A., Murphy E., Cross A., Sztein M.B., Nataro J.P. Serine protease autotransporters from Shigella flexneri and pathogenic Escherichia coli target a broad range of leukocyte glycoproteins. Proc. Natl. Acad. Sci. USA. 2011;108:12881-12886.
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249.
Servin A.L. Pathogenesis of human diffusely adhering Escherichia coli expressing Afa/Dr adhesins (Afa/Dr DAEC): Current insights and future challenges. Clin. Microbiol. Rev. 2014;27:823-869.
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Le Bouguénec C., Servin A.L. Diffusely adherent Escherichia coli strains expressing Afa/Dr adhesins (Afa/Dr DAEC): Hitherto unrecognized pathogens. FEMS Microbiol. Lett. 2006;256:185-194.
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251.
Servin A.L. Pathogenesis of Afa/Dr diffusely adhering Escherichia coli. Clin. Microbiol. Rev. 2005;18:264-292.
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252.
New Insights Into DAEC and EAEC Pathogenesis and Phylogeny · 2020
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253.
Mirsepasi-Lauridsen H.C., Vallance B.A., Krogfelt K.A., Petersen A.M. Escherichia coli pathobionts associated with inflammatory bowel disease. Clin. Microbiol. Rev. 2019;32:e00060-18.
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255.
Canizalez-Roman A., Flores-Villaseñor H.M., Gonzalez-Nuñez E., Velazquez-Roman J., Vidal J.E., Muro-Amador S., Alapizco-Castro G., Díaz-Quiñonez J.A., León-Sicairos N. Surveillance of diarrheagenic Escherichia coli strains isolated from diarrhea cases from children, adults and elderly at Northwest of Mexico. Front. Microbiol. 2016;7:1924.
Not in our library10.3389/fmicb.2016.01924
256.
Mohamed Ali M. Evaluation of antimicrobial susceptibility &rapid urine screening tests in asymptomatic urinary tract infection in pregnant women in Karbala. Karbala J. Pharm. Sci. 2011;2:22-34.
Not in our library
257.
Bouzari S., Dashti A., Jafari A., Oloomi M. Immune response against adhesins of enteroaggregative Escherichia coli immunized by three different vaccination strategies (DNA/DNA, Protein/Protein, and DNA/Protein) in mice. Comp. Immunol. Microbiol. Infect. Dis. 2010;33:215-225.
Not in our library10.1016/j.cimid.2008.10.002
258.
Saeedi P., Yazdanparast M., Behzadi E., Salmanian A.H., Mousavi S.L., Nazarian S., Amani J. A review on strategies for decreasing E. coli O157: H7 risk in animals. Microb. Pathog. 2017;103:186-195.
Not in our library10.1016/j.micpath.2017.01.001
259.
Goluszko P., Goluszko E., Nowicki B., Nowicki S., Popov V., Wang H.-Q. Vaccination with purified Dr Fimbriae reduces mortality associated with chronic urinary tract infection due to Escherichia coli bearing Dr adhesin. Infect. Immun. 2005;73:627-631.
Not in our library10.1128/iai.73.1.627-631.2005
260.
Smith E.J., Thompson A.P., O’Driscoll A., Clarke D.J. Pathogenesis of adherent–invasive Escherichia coli. Future Microbiol. 2013;8:1289-1300.
Not in our library10.2217/fmb.13.94
261.
Palmela C., Chevarin C., Xu Z., Torres J., Sevrin G., Hirten R., Barnich N., Ng S.C., Colombel J.-F. Adherent-invasive Escherichia coli in inflammatory bowel disease. Gut. 2018;67:574-587.
Not in our library10.1136/gutjnl-2017-314903
262.
Chervy M., Barnich N., Denizot J. Adherent-Invasive E. coli: Update on the Lifestyle of a Troublemaker in Crohn’s Disease. Int. J. Mol. Sci. 2020;21:3734.
Not in our library10.3390/ijms21103734
263.
Martinez-Medina M., Aldeguer X., Lopez-Siles M., González-Huix F., López-Oliu C., Dahbi G., Blanco J.E., Blanco J., Garcia-Gil J.L., Darfeuille-Michaud A. Molecular diversity of Escherichia coli in the human gut: New ecological evidence supporting the role of adherent-invasive E. coli (AIEC) in Crohn’s disease. Inflamm. Bowel Dis. 2009;15:872-882.
Not in our library10.1002/ibd.20860
264.
Conte M.P., Longhi C., Marazzato M., Conte A.L., Aleandri M., Lepanto M.S., Zagaglia C., Nicoletti M., Aloi M., Totino V. Adherent-invasive Escherichia coli (AIEC) in pediatric Crohn’s disease patients: Phenotypic and genetic pathogenic features. BMC Res. Notes. 2014;7:748.
Not in our library10.1186/1756-0500-7-748
265.
Kamali Dolatabadi R., Feizi A., Halaji M., Fazeli H., Adibi P. The prevalence of adherent-invasive Escherichia coli and its association with inflammatory bowel diseases: A systematic review and meta-analysis. Front. Med. 2021;8:730243.
Not in our library10.3389/fmed.2021.730243
266.
Darfeuille-Michaud A., Boudeau J., Bulois P., Neut C., Glasser A.-L., Barnich N., Bringer M.-A., Swidsinski A., Beaugerie L., Colombel J.-F. High prevalence of adherent-invasive Escherichia coli associated with ileal mucosa in Crohn’s disease. Gastroenterology. 2004;127:412-421.
Not in our library10.1053/j.gastro.2004.04.061
267.
Leccese G., Bibi A., Mazza S., Facciotti F., Caprioli F., Landini P., Paroni M. Probiotic Lactobacillus and Bifidobacterium strains counteract adherent-invasive Escherichia coli (AIEC) virulence and hamper IL-23/Th17 axis in ulcerative colitis, but not in crohn’s disease. Cells. 2020;9:1824.
Not in our library10.3390/cells9081824
268.
Denizot J., Sivignon A., Barreau F., Darcha C., Chan C.H., Stanners C.P., Hofman P., Darfeuille-Michaud A., Barnich N. Adherent-invasive Escherichia coli induce claudin-2 expression and barrier defect in CEABAC10 mice and Crohn’s disease patients. Inflamm. Bowel Dis. 2012;18:294-304.
Not in our library10.1002/ibd.21787
269.
Bringer M.-A., Darfeuille-Michaud A. Bacterial Adhesion to Intestinal Mucosa. Mucosal Immunology. 2015;949-953.
Not in our library
270.
Barnich N., Carvalho F.A., Glasser A.-L., Darcha C., Jantscheff P., Allez M., Peeters H., Bommelaer G., Desreumaux P., Colombel J.-F. CEACAM6 acts as a receptor for adherent-invasive E. coli, supporting ileal mucosa colonization in Crohn disease. J. Clin. Investig. 2007;117:1566-1574.
Not in our library10.1172/jci30504
271.
Rolhion N., Hofman P., Darfeuille-Michaud A. The endoplasmic reticulum stress response chaperone Gp96, a host receptor for Crohn disease-associated adherent-invasive Escherichia coli. Gut Microbes. 2011;2:115-119.
Not in our library10.4161/gmic.2.2.15725
272.
Rolhion N., Barnich N., Bringer M.-A., Glasser A.-L., Ranc J., Hébuterne X., Hofman P., Darfeuille-Michaud A. Abnormally expressed ER stress response chaperone Gp96 in CD favours adherent-invasive Escherichia coli invasion. Gut. 2010;59:1355-1362.
Not in our library10.1136/gut.2010.207456
273.
Gibold L., Garenaux E., Dalmasso G., Gallucci C., Cia D., Mottet-Auselo B., Faïs T., Darfeuille-Michaud A., Nguyen H.T.T., Barnich N. The Vat-AIEC protease promotes crossing of the intestinal mucus layer by Crohn’s disease-associated Escherichia coli. Cell Microbiol. 2016;18:617-631.
Not in our library10.1111/cmi.12539
274.
Prudent V., Demarre G., Vazeille E., Wery M., Quenech’Du N., Ravet A., Dauverd-Girault J., Van Dijk E., Bringer M.-A., Descrimes M. The Crohn’s disease-related bacterial strain LF82 assembles biofilm-like communities to protect itself from phagolysosomal attack. Commun. Biol. 2021;4:627.
Not in our library10.1038/s42003-021-02161-7
275.
Chassaing B., Koren O., Carvalho F.A., Ley R.E., Gewirtz A.T. AIEC pathobiont instigates chronic colitis in susceptible hosts by altering microbiota composition. Gut. 2014;63:1069-1080.
Not in our library10.1136/gutjnl-2013-304909
276.
Nadalian B., Yadegar A., Houri H., Olfatifar M., Shahrokh S., Asadzadeh Aghdaei H., Suzuki H., Zali M.R. Prevalence of the pathobiont adherent-invasive Escherichia coli and inflammatory bowel disease: A systematic review and meta-analysis. J. Gastroenterol. Hepatol. 2021;36:852-863.
Not in our library10.1111/jgh.15260
277.
Negroni A., Colantoni E., Vitali R., Palone F., Pierdomenico M., Costanzo M., Cesi V., Cucchiara S., Stronati L. NOD2 induces autophagy to control AIEC bacteria infectiveness in intestinal epithelial cells. Inflamm. Res. 2016;65:803-813.
Not in our library10.1007/s00011-016-0964-8
278.
Homer C.R., Richmond A.L., Rebert N.A., Achkar J.P., McDonald C. ATG16L1 and NOD2 interact in an autophagy-dependent antibacterial pathway implicated in Crohn’s disease pathogenesis. Gastroenterology. 2010;139:1630-1641.e2.
Not in our library10.1053/j.gastro.2010.07.006
279.
Alvarez Dorta D., Sivignon A., Chalopin T., Dumych T.I., Roos G., Bilyy R.O., Deniaud D., Krammer E.M., De Ruyck J., Lensink M.F. The antiadhesive strategy in Crohn′ s disease: Orally active mannosides to decolonize pathogenic Escherichia coli from the gut. ChemBioChem. 2016;17:936-952.
Not in our library10.1002/cbic.201600018
280.
Sivignon A., Yan X., Alvarez Dorta D., Bonnet R., Bouckaert J., Fleury E., Bernard J., Gouin S.G., Darfeuille-Michaud A., Barnich N. Development of heptylmannoside-based glycoconjugate antiadhesive compounds against adherent-invasive Escherichia coli bacteria associated with crohn’s disease. MBio. 2015;6:e01298-15.
Not in our library10.1128/mbio.01298-15
281.
Chalopin T., Dorta D.A., Sivignon A., Caudan M., Dumych T., Bilyy R., Deniaud D., Barnich N., Bouckaert J., Gouin S. Second generation of thiazolylmannosides, FimH antagonists for E. coli-induced Crohn’s disease. Org. Biomol. Chem. 2016;14:3913-3925.
Not in our library10.1039/c6ob00424e
282.
Yan X., Sivignon A., Yamakawa N., Crepet A., Travelet C., Borsali R., Dumych T., Li Z., Bilyy R., Deniaud D. Glycopolymers as antiadhesives of E. coli strains inducing inflammatory bowel diseases. Biomacromolecules. 2015;16:1827-1836.
Not in our library10.1021/acs.biomac.5b00413
283.
Boudeau J., Glasser A.L., Julien S., Colombel J.F., Darfeuille-Michaud A. Inhibitory effect of probiotic Escherichia coli strain Nissle 1917 on adhesion to and invasion of intestinal epithelial cells by adherent–invasive E. coli strains isolated from patients with Crohn’s disease. Aliment. Pharmacol. Ther. 2003;18:45-56.
Not in our library10.1046/j.1365-2036.2003.01638.x
284.
Van den Abbeele P., Marzorati M., Derde M., De Weirdt R., Joan V., Possemiers S., Van de Wiele T. Arabinoxylans, inulin and Lactobacillus reuteri 1063 repress the adherent-invasive Escherichia coli from mucus in a mucosa-comprising gut model. NPJ Biofilms Microbiomes. 2016;2:16016.
Not in our library10.1038/npjbiofilms.2016.16
285.
Hossain S. Targeting Siderophores to Reduce Adherent-Invasive E. coli Colonization: A Potential Therapy for Inflammatory Bowel Disease. 2021.
Not in our library
286.
Gerner R.R., Hossain S., Sargun A., Siada K., Norton G.J., Zheng T., Neumann W., Nuccio S.-P., Nolan E.M., Raffatellu M. Siderophore Immunization Restricted Colonization of Adherent-Invasive Escherichia coli and Ameliorated Experimental Colitis. Mbio. 2022;13:e02184-22.
Not in our library10.1128/mbio.02184-22
287.
Roussel C., Sivignon A., De Vallee A., Garrait G., Denis S., Tsilia V., Ballet N., Vandekerckove P., Van de Wiele T., Barnich N. Anti-infectious properties of the probiotic Saccharomyces cerevisiae CNCM I-3856 on enterotoxigenic E. coli (ETEC) strain H10407. Appl. Microbiol. Biotechnol. 2018;102:6175-6189.
Not in our library10.1007/s00253-018-9053-y
288.
Mantegazza C., Molinari P., D’Auria E., Sonnino M., Morelli L., Zuccotti G.V. Probiotics and antibiotic-associated diarrhea in children: A review and new evidence on Lactobacillus rhamnosus GG during and after antibiotic treatment. Pharmacol. Res. 2018;128:63-72.
Not in our library10.1016/j.phrs.2017.08.001
289.
Gut microbiota modulation with long-chain corn bran arabinoxylan in adults with overweight and obesity is linked to an individualized temporal increase in fecal propionate · 2020
No notice
290.
Canfora E.E., van der Beek C.M., Hermes G.D., Goossens G.H., Jocken J.W., Holst J.J., van Eijk H.M., Venema K., Smidt H., Zoetendal E.G. Supplementation of diet with galacto-oligosaccharides increases bifidobacteria, but not insulin sensitivity, in obese prediabetic individuals. Gastroenterology. 2017;153:87-97.e3.
Not in our library10.1053/j.gastro.2017.03.051
291.
Kittana H.H.B. Deciphering Interactions Between the Gut Microbiota and Host Immune System During Intestinal Inflammation. 2018.
Not in our library
292.
Pickard J.M., Zeng M.Y., Caruso R., Núñez G. Gut microbiota: Role in pathogen colonization, immune responses, and inflammatory disease. Immunol. Rev. 2017;279:70-89.
Not in our library10.1111/imr.12567
293.
Zhang Y., Rowehl L., Krumsiek J.M., Orner E.P., Shaikh N., Tarr P.I., Sodergren E., Weinstock G.M., Boedeker E.C., Xiong X. Identification of candidate adherent-invasive E. coli signature transcripts by genomic/transcriptomic analysis. PLoS ONE. 2015;10:e0130902.
Not in our library10.1371/journal.pone.0130902
294.
Kotsiliti E. Phage therapy suppresses gut inflammation in IBD. Nat. Biotechnol. 2022;40:1327.
Not in our library10.1038/s41587-022-01477-x
295.
Skyberg J.A., Johnson T.J., Johnson J.R., Clabots C., Logue C.M., Nolan L.K. Acquisition of avian pathogenic Escherichia coli plasmids by a commensal E. coli isolate enhances its abilities to kill chicken embryos, grow in human urine, and colonize the murine kidney. Infect. Immun. 2006;74:6287-6292.
Not in our library10.1128/iai.00363-06
296.
Bauchart P., Germon P., Brée A., Oswald E., Hacker J., Dobrindt U. Pathogenomic comparison of human extraintestinal and avian pathogenic Escherichia coli–search for factors involved in host specificity or zoonotic potential. Microb. Pathog. 2010;49:105-115.
Not in our library10.1016/j.micpath.2010.05.004
297.
Moulin-Schouleur M., Répérant M., Laurent S., Brée A., Mignon-Grasteau S., Germon P., Rasschaert D., Schouler C. Extraintestinal pathogenic Escherichia coli strains of avian and human origin: Link between phylogenetic relationships and common virulence patterns. J. Clin. Microbiol. 2007;45:3366-3376.
Not in our library10.1128/jcm.00037-07
298.
Three new serine-protease autotransporters of Enterobacteriaceae (SPATEs) from extra-intestinal pathogenic Escherichia coli and combined role of SPATEs for cytotoxicity and colonization of the mouse kidney · 2019
Not checked
299.
Tabasi M., Karam M.R.A., Habibi M., Mostafavi E., Bouzari S. Genotypic characterization of virulence factors in Escherichia coli isolated from patients with acute cystitis, pyelonephritis and asymptomatic bacteriuria. J. Clin. Diagn. Res. JCDR. 2016;10:DC01.
Not in our library10.7860/jcdr/2016/21379.9009
300.
Foxman B. The epidemiology of urinary tract infection. Nat. Rev. Urol. 2010;7:653-660.
Not in our library10.1038/nrurol.2010.190
301.
Lloyd A.L., Rasko D.A., Mobley H.L. Defining genomic islands and uropathogen-specific genes in uropathogenic Escherichia coli. J. Bacteriol. 2007;189:3532-3546.
Not in our library10.1128/jb.01744-06
302.
Navarro-Garcia F., Gutierrez-Jimenez J., Garcia-Tovar C., Castro L.A., Salazar-Gonzalez H., Cordova V. Pic, an autotransporter protein secreted by different pathogens in the Enterobacteriaceae family, is a potent mucus secretagogue. Infect. Immun. 2010;78:4101-4109.
Not in our library10.1128/iai.00523-10
303.
Dhakal B.K., Mulvey M.A. The UPEC pore-forming toxin α-hemolysin triggers proteolysis of host proteins to disrupt cell adhesion, inflammatory, and survival pathways. Cell Host Microbe. 2012;11:58-69.
Not in our library10.1016/j.chom.2011.12.003
304.
Zhao L., Gao S., Huan H., Xu X., Zhu X., Yang W., Gao Q., Liu X. Comparison of virulence factors and expression of specific genes between uropathogenic Escherichia coli and avian pathogenic E. coli in a murine urinary tract infection model and a chicken challenge model. Microbiology. 2009;155:1634-1644.
Not in our library10.1099/mic.0.024869-0
305.
UroPathogenic Escherichia coli (UPEC) Infections: Virulence Factors, Bladder Responses, Antibiotic, and Non-antibiotic Antimicrobial Strategies · 2017
No notice
306.
Schmiemann G., Kniehl E., Gebhardt K., Matejczyk M.M., Hummers-Pradier E. The diagnosis of urinary tract infection: A systematic review. Dtsch. Ärzteblatt Int. 2010;107:361.
Not in our library10.3238/arztebl.2010.0361
307.
Ranjan A., Sridhar S.T.K., Matta N., Chokkakula S., Ansari R.K. Prevalence of UTI among pregnant women and its complications in newborns. Indian J. Pharm. Pract. 2017;10:45-49.
Not in our library10.5530/ijopp.10.1.10
308.
Wagenlehner F.M., Umeh O., Steenbergen J., Yuan G., Darouiche R.O. Ceftolozane-tazobactam compared with levofloxacin in the treatment of complicated urinary-tract infections, including pyelonephritis: A randomised, double-blind, phase 3 trial (ASPECT-cUTI). Lancet. 2015;385:1949-1956.
Not in our library10.1016/s0140-6736(14)62220-0
309.
Foxman B. Urinary tract infection syndromes: Occurrence, recurrence, bacteriology, risk factors, and disease burden. Infect. Dis. Clin. 2014;28:1-13.
Not in our library10.1016/j.idc.2013.09.003
310.
Nielsen K.L., Stegger M., Kiil K., Lilje B., Ejrnæs K., Leihof R.F., Skjøt-Rasmussen L., Godfrey P., Monsen T., Ferry S. Escherichia coli causing recurrent urinary tract infections: Comparison to non-recurrent isolates and genomic adaptation in recurrent infections. Microorganisms. 2021;9:1416.
Not in our library10.3390/microorganisms9071416
311.
Ejrnæs K. Bacterial characteristics of importance for recurrent urinary tract infections caused by Escherichia coli. Dan Med. Bull. 2011;58:B4187.
Not in our library
312.
Ikähelmo R., Siitonen A., Heiskanen T., Kärkkäinen U., Kuosmanen P., Lipponen P., Mäkelä P.H. Recurrence of urinary tract infection in a primary care setting: Analysis of a I-year follow-up of 179 women. Clin. Infect. Dis. 1996;22:91-99.
Not in our library10.1093/clinids/22.1.91
313.
O’Connell Motherway M., Houston A., O’Callaghan G., Reunanen J., O’Brien F., O’Driscoll T., Casey P.G., de Vos W.M., van Sinderen D., Shanahan F. A Bifidobacterial pilus-associated protein promotes colonic epithelial proliferation. Mol. Microbiol. 2019;111:287-301.
Not in our library10.1111/mmi.14155
314.
Welch R.A., Burland V., Plunkett G., Redford P., Roesch P., Rasko D., Buckles E., Liou S.-R., Boutin A., Hackett J. Extensive mosaic structure revealed by the complete genome sequence of uropathogenic Escherichia coli. Proc. Natl. Acad. Sci. USA. 2002;99:17020-17024.
Not in our library10.1073/pnas.252529799
315.
Zhou G., Mo W.-J., Sebbel P., Min G., Neubert T.A., Glockshuber R., Wu X.-R., Sun T.-T., Kong X.-P. Uroplakin Ia is the urothelial receptor for uropathogenic Escherichia coli: Evidence from in vitro FimH binding. J. Cell Sci. 2001;114:4095-4103.
Not in our library10.1242/jcs.114.22.4095
316.
Kisiela D.I., Avagyan H., Friend D., Jalan A., Gupta S., Interlandi G., Liu Y., Tchesnokova V., Rodriguez V.B., Sumida J.P. Inhibition and reversal of microbial attachment by an antibody with parasteric activity against the FimH adhesin of uropathogenic E. coli. PLoS Pathog. 2015;11:e1004857.
Not in our library10.1371/journal.ppat.1004857
317.
Ashkar A.A., Mossman K.L., Coombes B.K., Gyles C.L., Mackenzie R. FimH adhesin of type 1 fimbriae is a potent inducer of innate antimicrobial responses which requires TLR4 and type 1 interferon signalling. PLoS Pathog. 2008;4:e1000233.
Not in our library10.1371/journal.ppat.1000233
318.
Bjarke Olsen P., Klemm P. Localization of promoters in the fim gene cluster and the effect of H-NS on the transcription of fimB and fimE. FEMS Microbiol. Lett. 1994;116:95-100.
Not in our library10.1111/j.1574-6968.1994.tb06681.x
319.
Abraham J.M., Freitag C.S., Clements J.R., Eisenstein B.I. An invertible element of DNA controls phase variation of type 1 fimbriae of Escherichia coli. Proc. Natl. Acad. Sci. USA. 1985;82:5724-5727.
Not in our library10.1073/pnas.82.17.5724
320.
Wullt B., Bergsten G., Connell H., Röllano P., Gebretsadik N., Hull R., Svanborg C. P fimbriae enhance the early establishment of Escherichia coli in the human urinary tract. Mol. Microbiol. 2000;38:456-464.
Not in our library10.1046/j.1365-2958.2000.02165.x
321.
Lane M., Mobley H. Role of P-fimbrial-mediated adherence in pyelonephritis and persistence of uropathogenic Escherichia coli (UPEC) in the mammalian kidney. Kidney Int. 2007;72:19-25.
Not in our library10.1038/sj.ki.5002230
322.
Lund B., Lindberg F., Marklund B.-I., Normark S. The PapG protein is the alpha-D-galactopyranosyl-(1----4)-beta-D-galactopyranose-binding adhesin of uropathogenic Escherichia coli. Proc. Natl. Acad. Sci. USA. 1987;84:5898-5902.
Not in our library10.1073/pnas.84.16.5898
323.
Martinez J.J., Mulvey M.A., Schilling J.D., Pinkner J.S., Hultgren S.J. Type 1 pilus-mediated bacterial invasion of bladder epithelial cells. EMBO J. 2000;19:2803-2812.
Not in our library10.1093/emboj/19.12.2803
324.
Song J., Bishop B.L., Li G., Grady R., Stapleton A., Abraham S.N. TLR4-mediated expulsion of bacteria from infected bladder epithelial cells. Proc. Natl. Acad. Sci. USA. 2009;106:14966-14971.
Not in our library10.1073/pnas.0900527106
325.
Justice S.S., Hung C., Theriot J.A., Fletcher D.A., Anderson G.G., Footer M.J., Hultgren S.J. Differentiation and developmental pathways of uropathogenic Escherichia coli in urinary tract pathogenesis. Proc. Natl. Acad. Sci. USA. 2004;101:1333-1338.
Not in our library10.1073/pnas.0308125100
326.
Mysorekar I.U., Hultgren S.J. Mechanisms of uropathogenic Escherichia coli persistence and eradication from the urinary tract. Proc. Natl. Acad. Sci. USA. 2006;103:14170-14175.
Not in our library10.1073/pnas.0602136103
327.
Schilling J.D., Mulvey M.A., Vincent C.D., Lorenz R.G., Hultgren S.J. Bacterial invasion augments epithelial cytokine responses to Escherichia coli through a lipopolysaccharide-dependent mechanism. J. Immunol. 2001;166:1148-1155.
Not in our library10.4049/jimmunol.166.2.1148
328.
Wiles T.J., Kulesus R.R., Mulvey M.A. Origins and virulence mechanisms of uropathogenic Escherichia coli. Exp. Mol. Pathol. 2008;85:11-19.
Not in our library10.1016/j.yexmp.2008.03.007
329.
Role of Uropathogenic Escherichia coli Virulence Factors in Development of Urinary Tract Infection and Kidney Damage · 2012
No notice
330.
Visvikis O., Boyer L., Torrino S., Doye A., Lemonnier M., Lorès P., Rolando M., Flatau G., Mettouchi A., Bouvard D. Escherichia coli producing CNF1 toxin hijacks Tollip to trigger Rac1-dependent cell invasion. Traffic. 2011;12:579-590.
Not in our library10.1111/j.1600-0854.2011.01174.x
331.
Mills M., Meysick K.C., O’Brien A.D. Cytotoxic necrotizing factor type 1 of uropathogenic Escherichia coli kills cultured human uroepithelial 5637 cells by an apoptotic mechanism. Infect. Immun. 2000;68:5869-5880.
Not in our library10.1128/iai.68.10.5869-5880.2000
332.
Miraglia A.G., Travaglione S., Meschini S., Falzano L., Matarrese P., Quaranta M.G., Viora M., Fiorentini C., Fabbri A. Cytotoxic necrotizing factor 1 prevents apoptosis via the Akt/IκB kinase pathway: Role of nuclear factor-κB and Bcl-2. Mol. Biol. Cell. 2007;18:2735-2744.
Not in our library10.1091/mbc.e06-10-0910
333.
Guyer D.M., Henderson I.R., Nataro J.P., Mobley H.L. Identification of sat, an autotransporter toxin produced by uropathogenic Escherichia coli. Mol. Microbiol. 2000;38:53-66.
Not in our library10.1046/j.1365-2958.2000.02110.x
334.
Guyer D.M., Radulovic S., Jones F.-E., Mobley H.L. Sat, the secreted autotransporter toxin of uropathogenic Escherichia coli, is a vacuolating cytotoxin for bladder and kidney epithelial cells. Infect. Immun. 2002;70:4539-4546.
Not in our library10.1128/iai.70.8.4539-4546.2002
335.
Liévin-Le Moal V., Comenge Y., Ruby V., Amsellem R., Nicolas V., Servin A.L. Secreted autotransporter toxin (Sat) triggers autophagy in epithelial cells that relies on cell detachment. Cell Microbiol. 2011;13:992-1013.
Not in our library10.1111/j.1462-5822.2011.01595.x
336.
Henderson I.R., Czeczulin J., Eslava C., Noriega F., Nataro J.P. Characterization of Pic, a secreted protease of Shigella flexneri and enteroaggregative Escherichia coli. Infect. Immun. 1999;67:5587-5596.
Not in our library10.1128/iai.67.11.5587-5596.1999
337.
Nichols K.B., Totsika M., Moriel D.G., Lo A.W., Yang J., Wurpel D.J., Rossiter A.E., Strugnell R.A., Henderson I.R., Ulett G.C. Molecular characterization of the vacuolating autotransporter toxin in uropathogenic Escherichia coli. J. Bacteriol. 2016;198:1487-1498.
Not in our library10.1128/jb.00791-15
338.
The Vacuolating Autotransporter Toxin (Vat) of Escherichia coli Causes Cell Cytoskeleton Changes and Produces Non-lysosomal Vacuole Formation in Bladder Epithelial Cells · 2020
Not checked
339.
Jones R.L., Peterson C.M., Grady R.W., Cerami A. Low molecular weight iron-binding factor from mammalian tissue that potentiates bacterial growth. J. Exp. Med. 1980;151:418-428.
Not in our library10.1084/jem.151.2.418
340.
Stojiljkovic I., Perkins-Balding D. Processing of heme and heme-containing proteins by bacteria. DNA Cell Biol. 2002;21:281-295.
Not in our library10.1089/104454902753759708
341.
Hagan E.C., Mobley H.L. Haem acquisition is facilitated by a novel receptor Hma and required by uropathogenic Escherichia coli for kidney infection. Mol. Microbiol. 2009;71:79-91.
Not in our library10.1111/j.1365-2958.2008.06509.x
342.
Quantitative Metabolomics Reveals an Epigenetic Blueprint for Iron Acquisition in Uropathogenic Escherichia coli · 2009
No notice
343.
Raffatellu M., George M.D., Akiyama Y., Hornsby M.J., Nuccio S.-P., Paixao T.A., Butler B.P., Chu H., Santos R.L., Berger T. Lipocalin-2 resistance confers an advantage to Salmonella enterica serotype Typhimurium for growth and survival in the inflamed intestine. Cell Host Microbe. 2009;5:476-486.
Not in our library10.1016/j.chom.2009.03.011
344.
Valdebenito M., Crumbliss A.L., Winkelmann G., Hantke K. Environmental factors influence the production of enterobactin, salmochelin, aerobactin, and yersiniabactin in Escherichia coli strain Nissle 1917. Int. J. Med. Microbiol. 2006;296:513-520.
Not in our library10.1016/j.ijmm.2006.06.003
345.
Chaturvedi K.S., Hung C.S., Crowley J.R., Stapleton A.E., Henderson J.P. The siderophore yersiniabactin binds copper to protect pathogens during infection. Nat. Chem. Biol. 2012;8:731-736.
Not in our library10.1038/nchembio.1020
346.
Sabri M., Houle S., Dozois C.M. Roles of the extraintestinal pathogenic Escherichia coli ZnuACB and ZupT zinc transporters during urinary tract infection. Infect. Immun. 2009;77:1155-1164.
Not in our library10.1128/iai.01082-08
347.
Cross A.S., Kim K.S., Wright D.C., Sadoff J.C., Gemski P. Role of lipopolysaccharide and capsule in the serum resistance of bacteremic strains of Escherichia coli. J. Infect. Dis. 1986;154:497-503.
Not in our library10.1093/infdis/154.3.497
348.
O’brien V.P., Hannan T.J., Nielsen H.V., Hultgren S.J. Drug and vaccine development for the treatment and prevention of urinary tract infections. Urin. Tract Infect. Mol. Pathog. Clin. Manag. 2017;4:589-646.
Not in our library10.1128/microbiolspec.uti-0013-2012
349.
Mortazavi-Tabatabaei S.A.R., Ghaderkhani J., Nazari A., Sayehmiri K., Sayehmiri F., Pakzad I. Pattern of antibacterial resistance in urinary tract infections: A systematic review and meta-analysis. Int. J. Prev. Med. 2019;10:169.
Not in our library10.4103/ijpvm.ijpvm_419_17
350.
Antibiotic Resistance Among Uropathogenic Escherichia coli · 2019
Not checked
351.
World Health Organization. Target Product Profiles for Oral Therapy of Urinary Tract Infections. 2020.
Not in our library
352.
Aarestrup F.M., Wiuff C., Mølbak K.r., Threlfall E.J. Is it time to change fluoroquinolone breakpoints for Salmonella spp.? Antimicrob. Agents Chemother. 2003;47:827-829.
Not in our library10.1128/aac.47.2.827-829.2003
353.
Karam M.R.A., Habibi M., Bouzari S. Urinary tract infection: Pathogenicity, antibiotic resistance and development of effective vaccines against Uropathogenic Escherichia coli. Mol. Immunol. 2019;108:56-67.
Not in our library10.1016/j.molimm.2019.02.007
354.
Hickling D.R., Nitti V.W. Management of recurrent urinary tract infections in healthy adult women. Rev. Urol. 2013;15:41.
Not in our library
355.
Prát V., Matousovic K., Horcicková M., Hatala M., Milotová Z. Prevention of recurrent urinary infections using Solco Urovac, a polymicrobial vaccine. Cas. Lek. Ceskych. 1989;128:1106-1109.
Not in our library
356.
Kochiashvili D., Khuskivadze A., Kochiashvili G., Koberidze G., Kvakhajelidze V. Role of the bacterial vaccine Solco-Urovac® in treatment and prevention of recurrent urinary tract infections of bacterial origin. Georgian Med. News. 2014;231:11-16.
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357.
Hopkins W.J., Elkahwaji J., Beierle L.M., Leverson G.E., Uehling D.T. Vaginal mucosal vaccine for recurrent urinary tract infections in women: Results of a phase 2 clinical trial. J. Urol. 2007;177:1349-1353.
Not in our library10.1016/j.juro.2006.11.093
358.
Wade D., Cooper J., Derry F., Taylor J. Uro-Vaxom® versus placebo for the prevention of recurrent symptomatic urinary tract infections in participants with chronic neurogenic bladder dysfunction: A randomised controlled feasibility study. Trials. 2019;20:223.
Not in our library10.1186/s13063-019-3275-x
359.
Trial M.D.-B. Uro-Vaxom@ and the Management of Recurrent Urinary Tract Infection in Adults: A Randomized Multicenter Double-Blind Trial. Eur. Urol. 1994;26:137-140.
Not in our library10.1159/000475363
360.
Cruz F., Dambros M., Naber K.G., Bauer H.W., Cozma G. Recurrent urinary tract infections: Uro-Vaxom®, a new alternative. Eur. Urol. Suppl. 2009;8:762-768.
Not in our library10.1016/j.eursup.2009.07.002
361.
Kim K.S., Kim J.-Y., Jeong I.G., Paick J.-S., Son H., Lim D.J., Shim H.B., Park W.H., Jung H.C., Choo M.-S. A prospective multi-center trial of Escherichia coli extract for the prophylactic treatment of patients with chronically recurrent cystitis. J. Korean Med. Sci. 2010;25:435-439.
Not in our library10.3346/jkms.2010.25.3.435
362.
Magistro G., Stief C.G. Vaccine development for urinary tract infections: Where do we stand? Eur. Urol. Focus. 2019;5:39-41.
Not in our library10.1016/j.euf.2018.07.034
363.
Marinova S., Nenkov P., Markova R., Nikolaeva S., Kostadinova R., Mitov I., Vretenarska M. Cellular and humoral systemic and mucosal immune responses stimulated by an oral polybacterial immunomodulator in patients with chronic urinary tract infections. Int. J. Immunopathol. Pharmacol. 2005;18:457-473.
Not in our library10.1177/039463200501800306
364.
Del Bino L., Østerlid K.E., Wu D.-Y., Nonne F., Romano M.R., Codée J., Adamo R. Synthetic Glycans to Improve Current Glycoconjugate Vaccines and Fight Antimicrobial Resistance. Chem. Rev. 2022;122:15672-15716.
Not in our library10.1021/acs.chemrev.2c00021
365.
Billips B.K., Yaggie R.E., Cashy J.P., Schaeffer A.J., Klumpp D.J. A live-attenuated vaccine for the treatment of urinary tract infection by uropathogenic Escherichia coli. J. Infect. Dis. 2009;200:263-272.
Not in our library10.1086/599839
366.
Russo T.A., Beanan J.M., Olson R., Genagon S.A., MacDonald U., Cope J.J., Davidson B.A., Johnston B., Johnson J.R. A killed, genetically engineered derivative of a wild-type extraintestinal pathogenic E. coli strain is a vaccine candidate. Vaccine. 2007;25:3859-3870.
Not in our library10.1016/j.vaccine.2007.01.100
367.
Van den Dobbelsteen G.P., Faé K.C., Serroyen J., van den Nieuwenhof I.M., Braun M., Haeuptle M.A., Sirena D., Schneider J., Alaimo C., Lipowsky G. Immunogenicity and safety of a tetravalent E. coli O-antigen bioconjugate vaccine in animal models. Vaccine. 2016;34:4152-4160.
Not in our library10.1016/j.vaccine.2016.06.067
368.
Forsyth V.S., Himpsl S.D., Smith S.N., Sarkissian C.A., Mike L.A., Stocki J.A., Sintsova A., Alteri C.J., Mobley H.L. Optimization of an experimental vaccine to prevent Escherichia coli urinary tract infection. MBio. 2020;11:e00555-20.
Not in our library10.1128/mbio.00555-20
369.
Huttner A., Hatz C., van den Dobbelsteen G., Abbanat D., Hornacek A., Frölich R., Dreyer A.M., Martin P., Davies T., Fae K. Safety, immunogenicity, and preliminary clinical efficacy of a vaccine against extraintestinal pathogenic Escherichia coli in women with a history of recurrent urinary tract infection: A randomised, single-blind, placebo-controlled phase 1b trial. Lancet Infect. Dis. 2017;17:528-537.
Not in our library10.1016/s1473-3099(17)30108-1
370.
Smith W.B., Abbanat D., Spiessens B., Go O., Haazen W., Rosa T.d., Fae K., Poolman J., Thoelen S., Palacios P.I.d. 2712. Safety and Immunogenicity of two Doses of ExPEC4V Vaccine Against Extraintestinal Pathogenic Escherichia coli Disease in Healthy Adult Participants. Open Forum Infect. Dis. 2019;6:S954.
Not in our library10.1093/ofid/ofz360.2389
371.
Frenck R.W., Ervin J., Chu L., Abbanat D., Spiessens B., Go O., Haazen W., van den Dobbelsteen G., Poolman J., Thoelen S. Safety and immunogenicity of a vaccine for extra-intestinal pathogenic Escherichia coli (ESTELLA): A phase 2 randomised controlled trial. Lancet Infect. Dis. 2019;19:631-640.
Not in our library10.1016/s1473-3099(18)30803-x
372.
Hasanzadeh S., Habibi M., Shokrgozar M.A., Ahangari Cohan R., Ahmadi K., Asadi Karam M.R., Bouzari S. In silico analysis and in vivo assessment of a novel epitope-based vaccine candidate against uropathogenic Escherichia coli. Sci. Rep. 2020;10:16258.
Not in our library10.1038/s41598-020-73179-w
373.
Karam M.R.A., Oloomi M., Mahdavi M., Habibi M., Bouzari S. Assessment of immune responses of the flagellin (FliC) fused to FimH adhesin of uropathogenic Escherichia coli. Mol. Immunol. 2013;54:32-39.
Not in our library10.1016/j.molimm.2012.11.002
374.
Karam M.R.A., Oloomi M., Mahdavi M., Habibi M., Bouzari S. Vaccination with recombinant FimH fused with flagellin enhances cellular and humoral immunity against urinary tract infection in mice. Vaccine. 2013;31:1210-1216.
Not in our library10.1016/j.vaccine.2012.12.059
375.
Savar N.S., Jahanian-Najafabadi A., Mahdavi M., Shokrgozar M.A., Jafari A., Bouzari S. In silico and in vivo studies of truncated forms of flagellin (FliC) of enteroaggregative Escherichia coli fused to FimH from uropathogenic Escherichia coli as a vaccine candidate against urinary tract infections. J. Biotechnol. 2014;175:31-37.
Not in our library10.1016/j.jbiotec.2014.01.037
376.
Karam M.R.A., Habibi M., Bouzari S. Use of flagellin and cholera toxin as adjuvants in intranasal vaccination of mice to enhance protective immune responses against uropathogenic Escherichia coli antigens. Biologicals. 2016;44:378-386.
Not in our library10.1016/j.biologicals.2016.06.006
377.
Spaulding C.N., Hultgren S.J. Adhesive pili in UTI pathogenesis and drug development. Pathogens. 2016;5:30.
Not in our library10.3390/pathogens5010030
378.
Russo T.A., McFadden C.D., Carlino-MacDonald U.B., Beanan J.M., Olson R., Wilding G.E. TheSiderophore Receptor IroN of Extraintestinal Pathogenic Escherichia coli Is a Potential VaccineCandidate. Infect. Immun. 2003;71:7164-7169.
Not in our library10.1128/iai.71.12.7164-7169.2003
379.
Habibi M., Karam M.R.A., Bouzari S. Evaluation of prevalence, immunogenicity and efficacy of FyuA iron receptor in uropathogenic Escherichia coli isolates as a vaccine target against urinary tract infection. Microb. Pathog. 2017;110:477-483.
Not in our library10.1016/j.micpath.2017.07.037
380.
Brumbaugh A.R., Smith S.N., Mobley H.L. Immunization with the yersiniabactin receptor, FyuA, protects against pyelonephritis in a murine model of urinary tract infection. Infect. Immun. 2013;81:3309-3316.
Not in our library10.1128/iai.00470-13
381.
Wieser A., Romann E., Magistro G., Hoffmann C., Nörenberg D., Weinert K., Schubert S.r. A multiepitope subunit vaccine conveys protection against extraintestinal pathogenic Escherichia coli in mice. Infect. Immun. 2010;78:3432-3442.
Not in our library10.1128/iai.00174-10
382.
Wieser A., Magistro G., Nörenberg D., Hoffmann C., Schubert S. First multi-epitope subunit vaccine against extraintestinal pathogenic Escherichia coli delivered by a bacterial type-3 secretion system (T3SS). Int. J. Med. Microbiol. 2012;302:10-18.
Not in our library10.1016/j.ijmm.2011.09.012
383.
Durant L., Metais A., Soulama-Mouze C., Genevard J.-M., Nassif X., Escaich S. Identification of candidates for a subunit vaccine against extraintestinal pathogenic Escherichia coli. Infect. Immun. 2007;75:1916-1925.
Not in our library10.1128/iai.01269-06
384.
Dietzman D.E., Fischer G.W., Schoenknecht F.D. Neonatal Escherichia coli septicemia—Bacterial counts in blood. J. Pediatr. 1974;85:128-130.
Not in our library10.1016/s0022-3476(74)80308-2
385.
Kim K.S., Itabashi H., Gemski P., Sadoff J., Warren R.L., Cross A.S. The K1 capsule is the critical determinant in the development of Escherichia coli meningitis in the rat. J. Clin. Investig. 1992;90:897-905.
Not in our library10.1172/jci115965
386.
Robbins J.B., McCracken G.H., Gotschlich E.C., Ørskov F., Ørskov I., Hanson L.A. Escherichia coli K1 capsular polysaccharide associated with neonatal meningitis. N. Engl. J. Med. 1974;290:1216-1220.
Not in our library10.1056/nejm197405302902202
387.
Bonacorsi S., Clermont O., Houdouin V., Cordevant C., Brahimi N., Marecat A., Tinsley C., Nassif X., Lange M., Bingen E. Molecular analysis and experimental virulence of French and North American Escherichia coli neonatal meningitis isolates: Identification of a new virulent clone. J. Infect. Dis. 2003;187:1895-1906.
Not in our library10.1086/375347
388.
Prasadarao N.V., Wass C.A., Weiser J.N., Stins M.F., Huang S.-H., Kim K.S. Outer membrane protein A of Escherichia coli contributes to invasion of brain microvascular endothelial cells. Infect. Immun. 1996;64:146-153.
Not in our library10.1128/iai.64.1.146-153.1996
389.
Teng C.-H., Cai M., Shin S., Xie Y., Kim K.-J., Khan N.A., Di Cello F., Kim K.S. Escherichia coli K1 RS218 interacts with human brain microvascular endothelial cells via type 1 fimbria bacteria in the fimbriated state. Infect. Immun. 2005;73:2923-2931.
Not in our library10.1128/iai.73.5.2923-2931.2005
390.
Teng C.-H., Tseng Y.-T., Maruvada R., Pearce D., Xie Y., Paul-Satyaseela M., Kim K.S. NlpI contributes to Escherichia coli K1 strain RS218 interaction with human brain microvascular endothelial cells. Infect. Immun. 2010;78:3090-3096.
Not in our library10.1128/iai.00034-10
391.
Khan N.A., Wang Y., Kim K.J., Chung J.W., Wass C.A., Kim K.S. Cytotoxic necrotizing factor-1 contributes to Escherichia coli K1 invasion of the central nervous system. J. Biol. Chem. 2002;277:15607-15612.
Not in our library10.1074/jbc.m112224200
392.
Huang S.H., Jong A.Y. Cellular mechanisms of microbial proteins contributing to invasion of the blood–brain barrier: MicroReview. Cell Microbiol. 2001;3:277-287.
Not in our library10.1046/j.1462-5822.2001.00116.x
393.
Cortes M.A., Gibon J., Chanteloup N.K., Moulin-Schouleur M., Gilot P., Germon P. Inactivation of ibeA and ibeT results in decreased expression of type 1 fimbriae in extraintestinal pathogenic Escherichia coli strain BEN2908. Infect. Immun. 2008;76:4129-4136.
Not in our library10.1128/iai.00334-08
394.
Fléchard M., Cortes M.A., Répérant M., Germon P. New role for the ibeA gene in H2O2 stress resistance of Escherichia coli. J. Bacteriol. 2012;194:4550-4560.
Not in our library10.1128/jb.00089-12
395.
Wang P., Zhang J., Chen Y., Zhong H., Wang H., Li J., Zhu G., Xia P., Cui L., Li J. ClbG in Avian Pathogenic Escherichia coli Contributes to Meningitis Development in a Mouse Model. Toxins. 2021;13:546.
Not in our library10.3390/toxins13080546
396.
Zhu N., Liu W., Prakash A., Zhang C., Kim K.S. Targeting E. coli invasion of the blood–brain barrier for investigating the pathogenesis and therapeutic development of E. coli meningitis. Cell Microbiol. 2020;22:e13231.
Not in our library10.1111/cmi.13231
397.
Kim K.S. Current concepts on the pathogenesis of Escherichia coli meningitis: Implications for therapy and prevention. Curr. Opin. Infect. Dis. 2012;25:273-278.
Not in our library10.1097/qco.0b013e3283521eb0
398.
Nguyen D.N., Jiang P., Frøkiær H., Heegaard P.M., Thymann T., Sangild P.T. Delayed development of systemic immunity in preterm pigs as a model for preterm infants. Sci. Rep. 2016;6:1-13.
Not in our library10.1038/srep36816
399.
Kim K., Cross A., Zollinger W., Sadoff J. Prevention and therapy of experimental Escherichia coli infection with monoclonal antibody. Infect. Immun. 1985;50:734-737.
Not in our library10.1128/iai.50.3.734-737.1985
400.
Finne J., Leinonen M., Mäkelä P.H. Antigenic similarities between brain components and bacteria causing meningitis: Implications for vaccine development and pathogenesis. Lancet. 1983;322:355-357.
Not in our library10.1016/s0140-6736(83)90340-9
401.
A world without bacterial meningitis: how genomic epidemiology can inform vaccination strategy [version 1; referees: 2 approved] · 2018
Not checked
402.
Saif Y. Diseases of Poultry. 2009.
Not in our library
403.
Wei S., Morrison M., Yu Z. Bacterial census of poultry intestinal microbiome. Poult. Sci. 2013;92:671-683.
Not in our library10.3382/ps.2012-02822
404.
Olsen R.H., Chadfield M., Christensen J.P., Scheutz F., Christensen H., Bisgaard M. Clonality and virulence traits of Escherichia coli associated with haemorrhagic septicaemia in turkeys. Avian Pathol. 2011;40:587-595.
Not in our library10.1080/03079457.2011.618942
405.
Emery D., Nagaraja K.V., Shaw D., Newman J., White D. Virulence factors of Escherichia coli associated with colisepticemia in chickens and turkeys. Avian Dis. 1992;36:504-511.
Not in our library10.2307/1591741
406.
Norton R., Macklin K., McMurtrey B. The association of various isolates of Escherichia coli from the United States with induced cellulitis and colibacillosis in young broiler chickens. Avian Pathol. 2000;29:571-574.
Not in our library10.1080/03079450020016814
407.
Ewers C., Janßen T., Kießling S., Philipp H.-C., Wieler L.H. Molecular epidemiology of avian pathogenic Escherichia coli (APEC) isolated from colisepticemia in poultry. Vet. Microbiol. 2004;104:91-101.
Not in our library10.1016/j.vetmic.2004.09.008
408.
Feng A., Akter S., Leigh S.A., Wang H., Pharr G.T., Evans J., Branton S.L., Landinez M.P., Pace L., Wan X.-F. Genomic diversity, pathogenicity and antimicrobial resistance of Escherichia coli isolated from poultry in the southern United States. BMC Microbiol. 2023;23:15.
Not in our library10.1186/s12866-022-02721-9
409.
La Ragione R., Sayers A., Woodward M. The role of fimbriae and flagella in the colonization, invasion and persistence of Escherichia coli O78 [ratio] K80 in the day-old-chick model. Epidemiol. Infect. 2000;124:351-363.
Not in our library10.1017/s0950268899004045
410.
Johnson T.J., Nolan L.K. Pathogenomics of the virulence plasmids of Escherichia coli. Microbiol. Mol. Biol. Rev. 2009;73:750-774.
Not in our library10.1128/mmbr.00015-09
411.
Lymberopoulos M.H., Houle S., Daigle F., Léveillé S., Brée A., Moulin-Schouleur M., Johnson J.R., Dozois C.M. Characterization of Stg fimbriae from an avian pathogenic Escherichia coli O78: K80 strain and assessment of their contribution to colonization of the chicken respiratory tract. J. Bacteriol. 2006;188:6449-6459.
Not in our library10.1128/jb.00453-06
412.
Aleksandrowicz A., Khan M.M., Sidorczuk K., Noszka M., Kolenda R. Whatever makes them stick–Adhesins of avian pathogenic Escherichia coli. Vet. Microbiol. 2021;257:109095.
Not in our library10.1016/j.vetmic.2021.109095
413.
Nolan M.F., Malleret G., Lee K.H., Gibbs E., Dudman J.T., Santoro B., Yin D., Thompson R.F., Siegelbaum S.A., Kandel E.R. The hyperpolarization-activated HCN1 channel is important for motor learning and neuronal integration by cerebellar Purkinje cells. Cell. 2003;115:551-564.
Not in our library10.1016/s0092-8674(03)00884-5
414.
Foley S.L., Horne S.M., Giddings C.W., Robinson M., Nolan L.K. Iss from a virulent avian Escherichia coli. Avian Dis. 2000;44:185-191.
Not in our library10.2307/1592523
415.
Gao Q., Ye Z., Wang X., Mu X., Gao S., Liu X. RstA is required for the virulence of an avian pathogenic Escherichia coli O2 strain E058. Infect. Genet. Evol. 2015;29:180-188.
Not in our library10.1016/j.meegid.2014.11.022
416.
Chakraborty S., Sivaraman J., Leung K.Y., Mok Y.-K. Two-component PhoB-PhoR regulatory system and ferric uptake regulator sense phosphate and iron to control virulence genes in type III and VI secretion systems of Edwardsiella tarda. J. Biol. Chem. 2011;286:39417-39430.
Not in our library10.1074/jbc.m111.295188
417.
Herren C.D., Mitra A., Palaniyandi S.K., Coleman A., Elankumaran S., Mukhopadhyay S. The BarA-UvrY two-component system regulates virulence in avian pathogenic Escherichia coli O78: K80: H9. Infect. Immun. 2006;74:4900-4909.
Not in our library10.1128/iai.00412-06
418.
Mellata M., Dho-Moulin M., Dozois C.M., Curtiss R., Brown P.K., Arné P., Brée A., Desautels C., Fairbrother J.M. Role of virulence factors in resistance of avian pathogenic Escherichia coli to serum and in pathogenicity. Infect. Immun. 2003;71:536-540.
Not in our library10.1128/iai.71.1.536-540.2003
419.
Mellata M., Ameiss K., Mo H., Curtiss R. Characterization of the contribution to virulence of three large plasmids of avian pathogenic Escherichia coli χ7122 (O78: K80: H9). Infect. Immun. 2010;78:1528-1541.
Not in our library10.1128/iai.00981-09
420.
Gao Q., Jia X., Wang X., Xiong L., Gao S., Liu X. The avian pathogenic Escherichia coli O2 strain E058 carrying the defined aerobactin-defective iucD or iucDiutA mutation is less virulent in the chicken. Infect. Genet. Evol. 2015;30:267-277.
Not in our library10.1016/j.meegid.2014.12.038
421.
Caza M., Lépine F., Milot S., Dozois C.M. Specific roles of the iroBCDEN genes in virulence of an avian pathogenic Escherichia coli O78 strain and in production of salmochelins. Infect. Immun. 2008;76:3539-3549.
Not in our library10.1128/iai.00455-08
422.
Perry R.D., Fetherston J.D. Yersiniabactin iron uptake: Mechanisms and role in Yersinia pestis pathogenesis. Microbes Infect. 2011;13:808-817.
Not in our library10.1016/j.micinf.2011.04.008
423.
Roles of iron acquisition systems in virulence of extraintestinal pathogenic Escherichia coli: salmochelin and aerobactin contribute more to virulence than heme in a chicken infection model · 2012
No notice
424.
Sabri M., Caza M., Proulx J., Lymberopoulos M.H., Brée A., Moulin-Schouleur M., Curtiss R., Dozois C.M. Contribution of the SitABCD, MntH, and FeoB metal transporters to the virulence of avian pathogenic Escherichia coli O78 strain χ7122. Infect. Immun. 2008;76:601-611.
Not in our library10.1128/iai.00789-07
425.
Li G., Feng Y., Kariyawasam S., Tivendale K.A., Wannemuehler Y., Zhou F., Logue C.M., Miller C.L., Nolan L.K. AatA is a novel autotransporter and virulence factor of avian pathogenic Escherichia coli. Infect. Immun. 2010;78:898-906.
Not in our library10.1128/iai.00513-09
426.
Pokharel P., Díaz J.M., Bessaiah H., Houle S., Guerrero-Barrera A.L., Dozois C.M. The serine protease autotransporters tagb, tagc, and sha from extraintestinal pathogenic Escherichia coli are internalized by human bladder epithelial cells and cause actin cytoskeletal disruption. Int. J. Mol. Sci. 2020;21:3047.
Not in our library10.3390/ijms21093047
427.
Dozois C.M., Dho-Moulin M., Brée A., Fairbrother J.M., Desautels C., Curtiss R. Relationship between the Tsh autotransporter and pathogenicity of avian Escherichia coli and localization and analysis of the Tsh genetic region. Infect. Immun. 2000;68:4145-4154.
Not in our library10.1128/iai.68.7.4145-4154.2000
428.
Parreira V., Gyles C. A novel pathogenicity island integrated adjacent to the thrW tRNA gene of avian pathogenic Escherichia coli encodes a vacuolating autotransporter toxin. Infect. Immun. 2003;71:5087-5096.
Not in our library10.1128/iai.71.9.5087-5096.2003
429.
Lamarche M.G., Dozois C.M., Daigle F., Caza M., Curtiss R., Dubreuil J.D., Harel J. Inactivation of the pst system reduces the virulence of an avian pathogenic Escherichia coli O78 strain. Infect. Immun. 2005;73:4138-4145.
Not in our library10.1128/iai.73.7.4138-4145.2005
430.
Chouikha I., Germon P., Brée A., Gilot P., Moulin-Schouleur M., Schouler C. A selC-associated genomic island of the extraintestinal avian pathogenic Escherichia coli strain BEN2908 is involved in carbohydrate uptake and virulence. J. Bacteriol. 2006;188:977-987.
Not in our library10.1128/jb.188.3.977-987.2006
431.
de Paiva J.B., Leite J.L., da Silva L.P.M., Rojas T.C.G., de Pace F., Conceição R.A., Sperandio V., da Silveira W.D. Influence of the major nitrite transporter NirC on the virulence of a Swollen Head Syndrome avian pathogenic E. coli (APEC) strain. Vet. Microbiol. 2015;175:123-131.
Not in our library10.1016/j.vetmic.2014.11.015
432.
Johnson T.J., Siek K.E., Johnson S.J., Nolan L.K. DNA sequence of a ColV plasmid and prevalence of selected plasmid-encoded virulence genes among avian Escherichia coli strains. J. Bacteriol. 2006;188:745-758.
Not in our library10.1128/jb.188.2.745-758.2006
433.
Germon P., Chen Y.-H., He L., Blanco J.E., Bree A., Schouler C., Huang S.-H., Moulin-Schouleur M. ibeA, a virulence factor of avian pathogenic Escherichia coli. Microbiology. 2005;151:1179-1186.
Not in our library10.1099/mic.0.27809-0
434.
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515.
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Fingermann M., Avila L., De Marco M.B., Vázquez L., Di Biase D.N., Müller A.V., Lescano M., Dokmetjian J.C., Fernández Castillo S., Pérez Quiñoy J.L. OMV-based vaccine formulations against Shiga toxin producing Escherichia coli strains are both protective in mice and immunogenic in calves. Hum. Vaccines Immunother. 2018;14:2208-2213.
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Ingelheim B. J-VAC® by Merial—Protects Dairy Cows from Coliform Mastitis.
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Ingelheim B. Bovine E. coli Vaccine Products of the Company Against Mastitis.
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Quiroga J., Vidal S., Siel D., Caruffo M., Valdés A., Cabrera G., Lapierre L., Sáenz L. Novel Proteoliposome-Based Vaccine against E. coli: A Potential New Tool for the Control of Bovine Mastitis. Animals. 2022;12:2533.
Not in our library10.3390/ani12192533

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Urinary Tract Infections Caused by Uropathogenic Escherichia coli: Mechanisms of Infection and Treatment Options · 2023
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