Escherichia albertii is an emerging enteropathogen of humans and many avian species. This bacterium is a close relative of Escherichia coli and has been frequently misidentified as enteropathogenic ...or enterohemorrhagic E. coli due to their similarity in phenotypic and genetic features, such as various biochemical properties and the possession of a type III secretion system encoded by the locus of enterocyte effacement. This pathogen causes outbreaks of gastroenteritis, and some strains produce Shiga toxin. Although many genetic and phenotypic studies have been published and the genome sequences of more than 200 E. albertii strains are now available, the clinical significance of this species is not yet fully understood. The apparent zoonotic nature of the disease requires a deeper understanding of the transmission routes and mechanisms of E. albertii to develop effective measures to control its transmission and infection. Here, we review the current knowledge of the phylogenic relationship of E. albertii with other Escherichia species and the biochemical and genetic properties of E. albertii, with particular emphasis on the repertoire of virulence factors and the mechanisms of pathogenicity, and we hope this provides a basis for future studies of this important emerging enteropathogen.
Escherichia albertii is an emerging enteropathogen of humans and many avian species. This bacterium is a close relative of Escherichia coli and has been frequently misidentified as enteropathogenic ...or enterohemorrhagic E. coli due to their similarity in phenotypic and genetic features, such as various biochemical properties and the possession of a type III secretion system encoded by the locus of enterocyte effacement. This pathogen causes outbreaks of gastroenteritis, and some strains produce Shiga toxin. Although many genetic and phenotypic studies have been published and the genome sequences of more than 200 E. albertii strains are now available, the clinical significance of this species is not yet fully understood. The apparent zoonotic nature of the disease requires a deeper understanding of the transmission routes and mechanisms of E. albertii to develop effective measures to control its transmission and infection. Here, we review the current knowledge of the phylogenic relationship of E. albertii with other Escherichia species and the biochemical and genetic properties of E. albertii, with particular emphasis on the repertoire of virulence factors and the mechanisms of pathogenicity, and we hope this provides a basis for future studies of this important emerging enteropathogen.
Milk is an excellent nutrient medium in which most saprophytic bacteria and pathogenic microbes grow well under certain conditions. Contamination of milk substrates by microbial pathogens is the ...cause of the spread of infectious diseases not only from the group of intestinal infections, but also infections with multiple mechanisms of pathogen transmission. Widespread consumption of milk determines the ubiquitination of infectious diseases, in which this product can serve as a factor of pathogen transmission. About 4% of infectious diseases worldwide are associated with milk consumption. The sources of infection are, as a rule, dairy animals, which are the reservoir of pathogens; the factors contributing to the contamination of milk with pathogenic and opportunistic pathogens are technological and sanitary-hygienic violations in the production, storage and sale of dairy products. Despite the fact that the route of transmission of infections with milk is widespread, it is the most underestimated among other intestinal infections. To date, there are no simple and rapid tests to detect the presence of pathogens such as Brucella spp., Coxiella burnetii, Salmonella typhimurium, Campylobacter spp. in milk, the invention of which could significantly reduce the burden of milkborne diseases. This review discusses the epidemiologic importance of milk and milk products in the spread of infectious diseases and possible areas of prevention.
The intestinal mucosa is constantly exposed to commensal microbes, opportunistic pathogens, toxins, luminal components and other environmental stimuli. The intestinal mucosa consists of multiple ...differentiated cellular and extracellular components that form a critical barrier, but is also equipped for efficient absorption of nutrients. Combination of genetic susceptibility and environmental factors are known as critical components involved in the pathogenesis of intestinal diseases. The innate immune system plays a critical role in the recognition and elimination of potential threats by detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). This host defense is facilitated by pattern recognition receptors (PRRs), in which the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) pathway has gained attention due to its role in sensing host and foreign double-stranded DNA (dsDNA) as well as cyclic dinucleotides (CDNs) produced by bacteria. Upon binding with dsDNA, cGAS converts ATP and GTP to cyclic GMP-AMP (cGAMP), which binds to STING and activates TANK binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF3), inducing type I interferon (IFN) and nuclear factor kappa B (NF-κB)-mediated pro-inflammatory cytokines, which have diverse effects on innate and adaptive immune cells and intestinal epithelial cells (IECs). However, opposite perspectives exist regarding the role of the cGAS-STING pathway in different intestinal diseases. Activation of cGAS-STING signaling is associated with worse clinical outcomes in inflammation-associated diseases, while it also plays a critical role in protection against tumorigenesis and certain infections. Therefore, understanding the context-dependent mechanisms of the cGAS-STING pathway in the physiopathology of the intestinal mucosa is crucial for developing therapeutic strategies targeting the cGAS-STING pathway. This review aims to provide insight into recent findings of the protective and detrimental roles of the cGAS-STING pathway in intestinal diseases.
To estimate, overall and by organism, the incidence of infectious intestinal disease (IID) in the community, presenting to general practice (GP) and reported to national surveillance.
Prospective, ...community cohort study and prospective study of GP presentation conducted between April 2008 and August 2009.
Eighty-eight GPs across the UK recruited from the Medical Research Council General Practice Research Framework and the Primary Care Research Networks.
6836 participants registered with the 88 participating practices in the community study; 991 patients with UK-acquired IID presenting to one of 37 practices taking part in the GP presentation study.
IID rates in the community, presenting to GP and reported to national surveillance, overall and by organism; annual IID cases and GP consultations by organism.
The overall rate of IID in the community was 274 cases per 1000 person-years (95% CI 254 to 296); the rate of GP consultations was 17.7 per 1000 person-years (95% CI 14.4 to 21.8). There were 147 community cases and 10 GP consultations for every case reported to national surveillance. Norovirus was the most common organism, with incidence rates of 47 community cases per 1000 person-years and 2.1 GP consultations per 1000 person-years. Campylobacter was the most common bacterial pathogen, with a rate of 9.3 cases per 1000 person-years in the community, and 1.3 GP consultations per 1000 person-years. We estimate that there are up to 17 million sporadic, community cases of IID and 1 million GP consultations annually in the UK. Of these, norovirus accounts for 3 million cases and 130,000 GP consultations, and Campylobacter is responsible for 500,000 cases and 80,000 GP consultations.
IID poses a substantial community and healthcare burden in the UK. Control efforts must focus particularly on reducing the burden due to Campylobacter and enteric viruses.
Primary Sjögren's syndrome (pSS) is an autoimmune disease with increased risk of infections. Here, we assessed whether pSS patients were at higher risk of hospitalization for community and ...opportunistic infections.
We selected newly hospitalized pSS patients between 2011 and 2018, through a nationwide population-based retrospective study using the French Health insurance database. We compared the incidence of hospitalization for several types of infections (according to International Classification for Disease codes, ICD-10) between pSS patients and an age- and sex-matched (1:10) hospitalized control group. We calculated adjusted Hazard Ratios (aHR, 95% CI) adjusted on socio-economic status, past cardiovascular or lung diseases and blood malignancies factors.
We compared 25 661 pSS patients with 252 543 matched patients. The incidence of hospitalizations for a first community infection was increased in pSS patients aHR of 1.29 (1.22-1.31), p < .001. The incidence of hospitalization for bronchopulmonary infections was increased in pSS patients aHR of 1.50 (1.34-1.69), p < .001, for pneumonia. Hospitalizations for pyelonephritis and intestinal infections were increased aHR of 1.55 (1.29-1.87), p < .001 and 1.18 (1.08-1.29), p < .001, respectively. Among opportunistic infections, only zoster, and mycobacteria infections (tuberculosis and non-tuberculous) were at increased risk of hospitalization aHR of 3.32 (1.78-6.18), p < .001; 4.35 (1.41-13.5), p = .011 and 2.54 (1.27-5.06), p = .008, respectively.
pSS patients are at higher risk of hospitalization for infections. The increased risk of hospitalization for mycobacterial infections illustrates the potential bilateral relationship between the two conditions. Vaccination against respiratory pathogens and herpes zoster virus may help prevent some hospitalizations in pSS patients.
KEY MESSAGES
Primary Sjögren's syndrome (pSS) increases hospitalization risk for community infections: bronchopulmonary, skin, dental, ear-nose-throat, intestinal infections and pyelonephritis.
Hospitalizations for zoster and mycobacterial infections are also increased in this population.
Dedicated preventive measures and vaccination campaigns could decrease the burden of infections in pSS patients.
Individuals in the developing world live in conditions of intense exposure to enteric pathogens due to suboptimal water and sanitation. These environmental conditions lead to alterations in ...intestinal structure, function, and local and systemic immune activation that are collectively referred to as environmental enteropathy (EE). This condition, although poorly defined, is likely to be exacerbated by undernutrition as well as being responsible for permanent growth deficits acquired in early childhood, vaccine failure, and loss of human potential. This article addresses the underlying theoretical and analytical frameworks informing the methodology proposed by the Etiology, Risk Factors and Interactions of Enteric Infections and Malnutrition and the Consequences for Child Health and Development (MAL-ED) cohort study to define and quantify the burden of disease caused by EE within a multisite cohort. Additionally, we will discuss efforts to improve, standardize, and harmonize laboratory practices within the MAL-ED Network. These efforts will address current limitations in the understanding of EE and its burden on children in the developing world.
The mucus layer coating the gastrointestinal tract is the front line of innate host defense, largely because of the secretory products of intestinal goblet cells. Goblet cells synthesize secretory ...mucin glycoproteins (
MUC2
) and bioactive molecules such as epithelial membrane-bound mucins (
MUC1, MUC3, MUC17
), trefoil factor peptides (TFF), resistin-like molecule β (RELMβ), and Fc-γ binding protein (Fcgbp). The
MUC2
mucin protein forms trimers by disulfide bonding in cysteine-rich amino terminal von Willebrand factor (vWF) domains, coupled with crosslinking provided by TFF and Fcgbp proteins with
MUC2
vWF domains, resulting in a highly viscous extracellular layer. Colonization by commensal intestinal microbiota is limited to an outer “loose” mucus layer, and interacts with the diverse oligosaccharides of mucin glycoproteins, whereas an “inner” adherent mucus layer is largely devoid of bacteria. Defective mucus layers resulting from lack of
MUC2
mucin, mutated
Muc2
mucin vWF domains, or from deletion of core mucin glycosyltransferase enzymes in mice result in increased bacterial adhesion to the surface epithelium, increased intestinal permeability, and enhanced susceptibility to colitis caused by dextran sodium sulfate. Changes in mucin gene expression and mucin glycan structures occur in cancers of the intestine, contributing to diverse biologic properties involved in the development and progression of cancer. Further research is needed on identification and functional significance of various components of mucus layers and the complex interactions among mucus layers, microbiota, epithelial cells, and the underlying innate and adaptive immunity. Further elucidation of the regulatory mechanisms involved in mucin changes in cancer and inflammation may lead to the development of novel therapeutic approaches.
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