Shigella flexneri
Shigella
Dysentery, Bacillary
Shigella dysenteriae
Shigella boydii
Shigella Vaccines
O Antigens
Virulence
Congo Red
Plasmids
Escherichia coli
Virulence Factors
Serotyping
HeLa Cells
Bacterial Vaccines
Gene Expression Regulation, Bacterial
Molecular Sequence Data
Bacterial Outer Membrane Proteins
Rhamnose
Diarrhea
Feces
Dysentery
Plesiomonas
Lipopolysaccharides
Succinic Anhydrides
Salmonella
The virulence plasmid-encoded impCAB operon enhances survival and induced mutagenesis in Shigella flexneri after exposure to UV radiation. (1/922)
Upon exposure to UV radiation, Shigella flexneri SA100 displayed survival and mutation frequencies comparable to those of Escherichia coli AB1157, which contains a functional UmuDC error-prone DNA repair system. Survival of SA100 after UV irradiation was associated with the presence of the 220-kb virulence plasmid, pVP. This plasmid encodes homologues of ImpA and ImpB, which comprise an error-prone DNA repair system encoded on plasmid TP110 that was initially identified in Salmonella typhimurium, and ImpC, encoded upstream of ImpA and ImpB. Although the impB gene was present in representatives of all four species of Shigella, not all isolates tested contained the gene. Shigella isolates that lacked impB were more sensitive to UV radiation than isolates that contained impB. The nucleotide sequence of a 2.4-kb DNA fragment containing the imp operon from S. flexneri SA100 pVP was 96% identical to the imp operon from the plasmid TP110. An SA100 derivative with a mutation in the impB gene had reduced survival following UV irradiation and less UV-induced mutagenesis relative to the parental strain. We also found that S. flexneri contained a chromosomally encoded umuDC operon; however, the umuDC promoter was not induced by exposure to UV radiation. This suggests that the imp operon but not the umuDC operon contributes to survival and induced mutagenesis in S. flexneri following exposure to UV radiation. (+info)Interleukin-8 controls bacterial transepithelial translocation at the cost of epithelial destruction in experimental shigellosis. (2/922)
In shigellosis, the network of cellular interactions mediated by a balance of pro- and anti-inflammatory cytokines or chemokines is clearly tipped toward acute destructive inflammation of intestinal tissues by the bacterial invader. This work has addressed the role played by interleukin-8 (IL-8) in a rabbit model of intestinal invasion by Shigella flexneri. IL-8, which is largely produced by the epithelial cells themselves, appears to be a major mediator of the recruitment of polymorphonuclear leukocytes (PMNs) to the subepithelial area and transmigration of these cells through the epithelial lining. Neutralization of IL-8 function by monoclonal antibody WS-4 caused a decrease in the amount of PMNs streaming through the lamina propria and the epithelium, thus significantly attenuating the severity of epithelial lesions in areas of bacterial invasion. These findings are in agreement with our previous work (31). In contrast to the PMNs, the bacteria displayed increased transepithelial translocation, as well as overgrowth in the lamina propria and increased passage into the mesenteric blood. By mediating eradication of bacteria at their epithelial entry site, although at the cost of severe epithelial destruction, IL-8 therefore appears to be a key chemokine in the control of bacterial translocation. (+info)The mxi-Spa type III secretory pathway of Shigella flexneri requires an outer membrane lipoprotein, MxiM, for invasin translocation. (3/922)
Invasion of epithelial cells by Shigella flexneri is mediated by a set of translocated bacterial invasins, the Ipa proteins, and its dedicated type III secretion system, called Mxi-Spa. We show here that mxiM, part of the mxi-spa locus in the S. flexneri virulence plasmid, encodes an indispensable type III secretion apparatus component, required for both Ipa translocation and tissue culture cell invasion. We demonstrated that mature MxiM, first identified as a putative lipoprotein, is lipidated in vivo. Consistent with features of known lipoproteins, MxiM (i) can be labeled with [3H]palmitate and [2-3H]glycerol, (ii) is associated with the cell envelope, (iii) is secreted independently of the type III pathway, and (iv) requires an intact lipoprotein modification and processing site for full activity. The lipidated form of MxiM was detected primarily in the outer membrane, where it establishes a peripheral association with the inner leaflet. Through analysis of subcellular Ipa distribution in a mxiM null mutant background, MxiM was found to be required for the assembly and/or function of outer, but not inner, membrane regions of Mxi-Spa. This function probably requires interactions with other Mxi-Spa subunits within the periplasmic space. We discuss implications of these findings with respect to the function of MxiM and the structure of Mxi-Spa as a whole. (+info)Adaptive immune response to Shigella flexneri 2a cydC in immunocompetent mice and mice lacking immunoglobulin A. (4/922)
Shigella flexneri cydC, which is deficient in cytochrome bd, was rapidly cleared from the lungs of intranasally inoculated mice and was Sereny negative, yet it induced 93% protection against challenge with wild-type S. flexneri. Mice that lack immunoglobulin A (IgA) were fully protected, suggesting that IgA may not be required for adaptive immunity in this model system. (+info)Rupture of the intestinal epithelial barrier and mucosal invasion by Shigella flexneri. (5/922)
Invasion of the intestinal barrier by Shigella flexneri involves complex interactions with epithelial and phagocytic cells. Major perturbation of the signals that maintain epithelial integrity permits mucosal invasion, leading to tissue destruction. Expression of this invasive phenotype depends on the secretion of Ipa proteins (invasins), which can trigger entry of the pathogen into epithelial cells by causing massive rearrangement of the host cell cytoskeleton and cause macrophage apoptotic death by direct interaction of IpaB with interleukin-1beta (IL-1beta)-converting enzyme. This results in the killing of defense cells and in the release of IL-1beta. In vivo, bacteria translocate through the epithelial barrier, essentially via M cells of the follicle-associated epithelium in the colonic and rectal mucosa. Apoptotic death of macrophages in subepithelial tissues allows bacterial survival and triggers inflammation, which destabilizes epithelial structures and facilitates further bacterial entry. Once they are intracellular, bacteria multiply within the cytoplasm and move from cell to cell by an actin-dependent process. (+info)Enteropathogenic E. coli, Salmonella, and Shigella: masters of host cell cytoskeletal exploitation. (6/922)
Bacterial pathogens have evolved numerous strategies to exploit their host's cellular processes so that they can survive and persist. Often, a bacterium must adhere very tightly to the cells and mediate its effects extracellularly, or it must find a way to invade the host's cells and survive intracellularly. In either case, the pathogen hijacks the host's cytoskeleton. The cytoskeleton provides a flexible framework for the cell and is involved in mediating numerous cellular functions, from cell shape and structure to programmed cell death. Altering the host cytoskeleton is crucial for mediating pathogen adherence, invasion, and intracellular locomotion. We highlight recent advances in the pathogenesis of enteropathogenic Escherichia coli, Salmonella Typhimurium, and Shigella flexneri. Each illustrates how bacterial pathogens can exert dramatic effects on the host cytoskeleton. (+info)Safety and immunogenicity of Shigella sonnei and Shigella flexneri 2a O-specific polysaccharide conjugates in children. (7/922)
O-specific polysaccharide conjugates of shigellae were safe and immunogenic in young adults, and a Shigella sonnei conjugate conferred protection [1-3]. Shigellosis is primarily a disease of children; therefore, the safety and immunogenicity of S. sonnei and Shigella flexneri 2a conjugates were studied in 4- to 7-year-old children. Local and systemic reactions were minimal. The first injection of both conjugates elicited significant rises in geometric mean levels of serum IgG only to the homologous lipopolysaccharide (LPS) (S. sonnei, 0.32-8.25 ELISA units [EU]; S. flexneri 2a, 1.15-20.5 EU; P<.0001). Revaccination at 6 weeks induced a booster response to S. flexneri 2a LPS (20.5-30.5 EU, P=.003). Six months later, the geometric mean levels of IgG anti-LPS for both groups were higher than the prevaccination levels (P<.0001). Similar, but lesser, rises were observed for IgM and IgA anti-LPS. The investigational Shigella conjugates were safe and immunogenic in children and merit evaluation of their efficacy. (+info)A comparative study of the actin-based motilities of the pathogenic bacteria Listeria monocytogenes, Shigella flexneri and Rickettsia conorii. (8/922)
Listeria monocytogenes, Shigella flexneri, and Rickettsia conorii are three bacterial pathogens that are able to polymerize actin into 'comet tail' structures and move within the cytosol of infected cells. The actin-based motilities of L. monocytogenes and S. flexneri are known to require the bacterial proteins ActA and IcsA, respectively, and several mammalian cytoskeleton proteins including the Arp2/3 complex and VASP (vasodilator-stimulated phosphoprotein) for L. monocytogenes and vinculin and N-WASP (the neural Wiskott-Aldrich syndrome protein) for S. flexneri. In contrast, little is known about the motility of R. conorii. In the present study, we have analysed the actin-based motility of this bacterium in comparison to that of L. monocytogenes and S. flexneri. Rickettsia moved at least three times more slowly than Listeria and Shigella in both infected cells and Xenopus laevis egg extracts. Decoration of actin with the S1 subfragment of myosin in infected cells showed that the comet tails of Rickettsia have a structure strikingly different from those of L. monocytogenes or S. flexneri. In Listeria and Shigella tails, actin filaments form a branching network while Rickettsia tails display longer and not cross-linked actin filaments. Immunofluorescence studies revealed that the two host proteins, VASP and (&agr;)-actinin colocalized with actin in the tails of Rickettsia but neither the Arp2/3 complex which we detected in the Shigella actin tails, nor N-WASP, were detected in Rickettsia actin tails. Taken together, these results suggest that R. conorii may use a different mechanism of actin polymerization. (+info)The diagnosis of bacillary dysentery is based on a combination of clinical findings and laboratory tests, such as fecal cultures or polymerase chain reaction (PCR) assays. Treatment typically involves antibiotics, which can shorten the duration of diarrhea and reduce the risk of complications. In severe cases, hospitalization may be necessary to manage dehydration and other complications.
Prevention measures include maintaining good hygiene practices, such as washing hands after using the bathroom or before handling food, and avoiding contaminated water or food. Vaccines are also available for some types of Shigella infections.
Symptoms of keratoconjunctivitis may include redness and discharge in both eyes, itching or burning sensations in the eyes, blurred vision, and sensitivity to light. Treatment options for keratoconjunctivitis depend on the underlying cause, but may include antibiotic eye drops, anti-inflammatory medication, or topical creams or ointments.
In severe cases, keratoconjunctivitis can lead to complications such as corneal ulcers, glaucoma, or vision loss if left untreated. Therefore, it is important to seek medical attention if you experience any symptoms of keratoconjunctivitis.
There are several types of diarrhea, including:
1. Acute diarrhea: This type of diarrhea is short-term and usually resolves on its own within a few days. It can be caused by a viral or bacterial infection, food poisoning, or medication side effects.
2. Chronic diarrhea: This type of diarrhea persists for more than 4 weeks and can be caused by a variety of conditions, such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), or celiac disease.
3. Diarrhea-predominant IBS: This type of diarrhea is characterized by frequent, loose stools and abdominal pain or discomfort. It can be caused by a variety of factors, including stress, hormonal changes, and certain foods.
4. Infectious diarrhea: This type of diarrhea is caused by a bacterial, viral, or parasitic infection and can be spread through contaminated food and water, close contact with an infected person, or by consuming contaminated food.
Symptoms of diarrhea may include:
* Frequent, loose, and watery stools
* Abdominal cramps and pain
* Bloating and gas
* Nausea and vomiting
* Fever and chills
* Headache
* Fatigue and weakness
Diagnosis of diarrhea is typically made through a physical examination, medical history, and laboratory tests to rule out other potential causes of the symptoms. Treatment for diarrhea depends on the underlying cause and may include antibiotics, anti-diarrheal medications, fluid replacement, and dietary changes. In severe cases, hospitalization may be necessary to monitor and treat any complications.
Prevention of diarrhea includes:
* Practicing good hygiene, such as washing hands frequently and thoroughly, especially after using the bathroom or before preparing food
* Avoiding close contact with people who are sick
* Properly storing and cooking food to prevent contamination
* Drinking safe water and avoiding contaminated water sources
* Avoiding raw or undercooked meat, poultry, and seafood
* Getting vaccinated against infections that can cause diarrhea
Complications of diarrhea can include:
* Dehydration: Diarrhea can lead to a loss of fluids and electrolytes, which can cause dehydration. Severe dehydration can be life-threatening and requires immediate medical attention.
* Electrolyte imbalance: Diarrhea can also cause an imbalance of electrolytes in the body, which can lead to serious complications.
* Inflammation of the intestines: Prolonged diarrhea can cause inflammation of the intestines, which can lead to abdominal pain and other complications.
* Infections: Diarrhea can be a symptom of an infection, such as a bacterial or viral infection. If left untreated, these infections can lead to serious complications.
* Malnutrition: Prolonged diarrhea can lead to malnutrition and weight loss, which can have long-term effects on health and development.
Treatment of diarrhea will depend on the underlying cause, but may include:
* Fluid replacement: Drinking plenty of fluids to prevent dehydration and replace lost electrolytes.
* Anti-diarrheal medications: Over-the-counter or prescription medications to slow down bowel movements and reduce diarrhea.
* Antibiotics: If the diarrhea is caused by a bacterial infection, antibiotics may be prescribed to treat the infection.
* Rest: Getting plenty of rest to allow the body to recover from the illness.
* Dietary changes: Avoiding certain foods or making dietary changes to help manage symptoms and prevent future episodes of diarrhea.
It is important to seek medical attention if you experience any of the following:
* Severe diarrhea that lasts for more than 3 days
* Diarrhea that is accompanied by fever, blood in the stool, or abdominal pain
* Diarrhea that is severe enough to cause dehydration or electrolyte imbalances
* Diarrhea that is not responding to treatment
Prevention of diarrhea includes:
* Good hand hygiene: Washing your hands frequently, especially after using the bathroom or before preparing food.
* Safe food handling: Cooking and storing food properly to prevent contamination.
* Avoiding close contact with people who are sick.
* Getting vaccinated against infections that can cause diarrhea, such as rotavirus.
Overall, while diarrhea can be uncomfortable and disruptive, it is usually a minor illness that can be treated at home with over-the-counter medications and plenty of fluids. However, if you experience severe or persistent diarrhea, it is important to seek medical attention to rule out any underlying conditions that may require more formal treatment.
1. Bacterial dysentery: This type of dysentery is caused by bacteria such as Shigella or Salmonella and is typically spread through contaminated food or water. Symptoms include diarrhea, fever, abdominal cramps, and blood in the stool.
2. Amebic dysentery: This type of dysentery is caused by a parasite called Entamoeba histolytica and is typically spread through contaminated food or water. Symptoms include diarrhea, fever, abdominal pain, and blood in the stool.
Dysentery can be diagnosed through a physical examination, medical history, and laboratory tests such as stool samples or blood tests. Treatment typically involves antibiotics for bacterial dysentery and antiparasitic medication for amebic dysentery. In severe cases, hospitalization may be necessary to manage symptoms and prevent complications such as dehydration and electrolyte imbalances.
Prevention measures for dysentery include:
* Practicing good hygiene, such as washing hands frequently and avoiding close contact with people who are sick
* Avoiding contaminated food and water
* Properly storing and preparing food to prevent bacterial growth
* Avoiding risky behaviors such as anal sex, which can increase the risk of contracting amebic dysentery.
The prognosis for dysentery is generally good if treated promptly and effectively. However, if left untreated, it can lead to serious complications such as dehydration, electrolyte imbalances, and potentially life-threatening infections.
Shigella flexneri
Simon Flexner
Arturo Zychlinsky
Interspecies quorum sensing
Type three secretion system
Phosphopolyprenol glucosyltransferase
Bacterial effector protein
RyhB
Chris Higgins (academic)
Shigella sonnei
Profilin 1
VIPR1
Shigella
WASL (gene)
Bacillary dysentery
List of sequenced bacterial genomes
Glutamate decarboxylase
RnaG
RANBP9
Pathogenomics
Microfilament
RydB RNA
Felix Armin Randow
Haemolysin E
IS128 RNA
Aspartate racemase
Protein-secreting ATPase
Actin
Paracytophagy
IS102 RNA
Congo red
Microfold cell
Inferring horizontal gene transfer
C0719 RNA
Katrina Ray
Rong Li
GlmY RNA
Serum amyloid A1
Inflammasome
Othello Washington
Nucleomodulin
Omptin
Shigella flexneri Serotype 3 Infections Among Men Who Have Sex with Men --- Chicago, Illinois, 2003--2004
Multidrug resistance protein MdtK (Shigella flexneri) | Protein Target - PubChem
IpaB mediates macrophage apoptosis induced by Shigella flexneri - PubMed
RCSB PDB - 3C8H: Crystal structure of the enterobactin esterase FES from Shigella flexneri in the presence of 2,3-Di-hydroxy-N...
CARD4/Nod1 mediates NF-kappaB and JNK activation by invasive Shigella flexneri - Research - Institut Pasteur
2023 ICD-10-CM Diagnosis Code A03.1: Shigellosis due to Shigella flexneri
Extensively Drug-Resistant Shigella flexneri 2a, California, USA, 2022. | Emerg Infect Dis;29(7): 1473-1475, 2023 07. |...
Shigella flexneri (EW-10) | The Antimicrobial Index Knowledgebase - TOKU-E
Atomic structure of bacteriophage Sf6 tail needle knob
DailyMed - CIPROFLOXACIN HYDROCHLORIDE tablet, coated
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Structures of the Shigella flexneri type 3 secretion system protein MxiC reveal conformational variability amongst homologues. ...
Transcytosis subversion by M cell-to-enterocyte spread promotes Shigella flexneri and Listeria monocytogenes intracellular...
Exit from dormancy in microbial organisms | Nature Reviews Microbiology
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Shigellosis Biology and Genetics | NIH: National Institute of Allergy and Infectious Diseases
Sonnei7
- The majority of Shigella infections in the United States are caused by S. sonnei and affect young children and their caretakers. (cdc.gov)
- since the 1970s, outbreaks of shigellosis attributable to S . flexneri and more recently S . sonnei have been reported among MSM in major cities in North America ( 3-- 5 ) , Europe ( 6 ), and Australia ( 7 ). (cdc.gov)
- Characterization of virulence plasmids and plasmid-associated outer membrane proteins in Shigella flexneri, Shigella sonnei, and Escherichia coli. (nih.gov)
- There are four known Shigella species, and the vast majority of infections in the US are caused by Shigella sonnei and flexneri . (cdc.gov)
- Shigella sonnei , also called "group D" Shigella, is responsible for most cases of shigellosis in the United States. (medlineplus.gov)
- The purpose of this Funding Opportunity Announcement (FOA) is to solicit research applications focused on advancing development of vaccine candidates against Enterotoxigenic Escherichia coli (ETEC), Salmonella enterica serotype Paratyphi A, and two Shigella species, Shigella flexneri and Shigella sonnei . (nih.gov)
- This FOA reflects priorities for further development of vaccines against select NIAID high priority Category B enteric bacteria responsible for a high burden of diarrheal disease globally, specifically - ETEC, Salmonella enterica serotype Paratyphi A, Shigella flexneri and Shigella sonnei . (nih.gov)
Serotype4
- Atypical va- from S. flexneri serotype X variant (SFxv), which was rieties were prevalent mainly in developed regions, and 1 recently reported in China ( 8 ), because it reacted with variant has become the dominant Shigella spp. (cdc.gov)
- During 2003--2004, the Chicago Department of Public Health (CDPH) investigated an increase in reported Shigella flexneri serotype 3 infections among adult males. (cdc.gov)
- 18 years, with accompanying isolation of S. flexneri serotype 3 from stool culture. (cdc.gov)
- All invasive S. flexneri strains, irrespective of serotype, were found to harbor a large plasmid of approximately 140 megadaltons in size, although some strains carried additional plasmid species. (nih.gov)
Proteins2
- 3. Lactoferrin-binding proteins in Shigella flexneri. (nih.gov)
- The HLA-B27 antigen shares some amino acid homology with proteins from several gram-negative bacteria, including Yersinia enterocolitica , Shigella flexneri , and Chlamydia trachomatis , as well as from gram-negative bacteria found in the GI tract. (medscape.com)
Escherichia2
Salmonella7
- ABSTRACT In this study, the serogroup and susceptibility patterns of Shigella and Salmonella spp. (who.int)
- Antibiograms of Shigella and Salmonella spp. (who.int)
- Shigella were susceptible to gentamicin (100%) and nalidixic acid (97.3%) and Shigella and Salmonella were 100.0% susceptible to norfloxacin. (who.int)
- Dans cette étude, le sérogroupe et le profil de sensibilité de bactéries Shigella et de Salmonella spp. (who.int)
- Les antibiogrammes réalisés sur les espèces Shigella et Salmonella ont montré une résistance de 100 % à l'érythromycine et des taux de résistance élevés (≥ 75 %) à l'ampicilline, à la céfalotine, au chloramphénicol et à la tétracycline. (who.int)
- Shigella était sensible à la gentamicine (100 %) et à l'acide nalidixique (97,3 %) et Shigella et Salmonella étaient sensibles à 100 % à la norfloxacine. (who.int)
- Further, Salmonella and Shigella are listed at the Serious threat level in the Centers for Disease Control and Prevention's (CDC) 2013 and 2019 reports on Antibiotic Resistance Threats in the United States , which cite urgent need to combat multi drug resistant (MDR) strains. (nih.gov)
Strains2
- Representative Shigella flexneri strains were studied to determine whether plasmids are involved in their virulence. (nih.gov)
- Shigella flexneri sensitive and resistant strains were used for checking antimicrobial activity of Asiatic acid by gentamicin protection assay. (bvsalud.org)
Intracellular4
- Asiatic acid inhibits intracellular Shigella flexneri growth by inducing antimicrobial peptide gene expression. (bvsalud.org)
- The aim of this study is to show how Asiatic acid , a plant-derived compound , inhibits the intracellular growth of Shigella flexneri . (bvsalud.org)
- Overall, Asiatic acid up-regulates antimicrobial peptide gene expression and inhibits intracellular S. flexneri growth . (bvsalud.org)
- We focused on the intracellular pathogen Shigella flexneri, classically reported to transcytose through M cells to initiate bacillary dysentery in humans, while eliciting poorly protective immune responses. (archives-ouvertes.fr)
Bacterial2
- Shigella is the third most common cause of bacterial gastroenteritis in the United States ( 1 ). (cdc.gov)
- Invasive bacterial pathogens such as Shigella flexneri force their uptake into non-phagocytic host cells. (pasteur.fr)
Isolates4
- Health-care providers were asked to report all Shigella infections among Chicago residents to CDPH and to send Shigella isolates to the state public health laboratory for speciation. (cdc.gov)
- the remaining two isolates were S. flexneri subtype 3b. (cdc.gov)
- Seven closely related PFGE patterns were identified among the 11 S. flexneri subtype 3a isolates subtyped by PFGE. (cdc.gov)
- Among the 76 Shigella isolates serogroup B (Sh. (who.int)
Bacteria4
- Recently, scientists have determined the complete genome sequences (genetic blueprint) for Shigella flexneri , as well as other major enteric bacteria. (nih.gov)
- It is caused by a group of bacteria called Shigella. (medlineplus.gov)
- Getting just a little bit of the Shigella bacteria into your mouth is enough to cause infection. (medlineplus.gov)
- Bacteria que es uno de los agentes que producen DISENTERÍA BACILAR y en ocasiones gastroenteritis infantil. (bvsalud.org)
Infections5
- S. flexneri causes approximately 18% of U.S. Shigella infections ( 1 ). (cdc.gov)
- The national incidence of S. flexneri infections decreased 64% from 1989 to 2002 ( 1 ). (cdc.gov)
- Some grantees will look into issues unique to their regions, countries and communities: sickle cell disease in infants, the role of genetics in craniofacial and dental anomalies, treatment for Guillain-Barré syndrome, and causes of Shigella flexneri infections. (nih.gov)
- First, we'll share some background on Shigella infections, including transmission and populations at greatest risk. (cdc.gov)
- Next, we'll provide an overview of the national surveillance systems used to detect XDR Shigella infections. (cdc.gov)
Vaccine1
- The World Health Organization (WHO) published the ETEC vaccine Preferred Product Characteristics (PPC) in August 2021, and the Shigella vaccine PPC in November 2021. (nih.gov)
Clinical2
Organisms1
- The low inoculum required for Shigella infection (as few as 10--200 organisms) facilitates person-to-person transmission. (cdc.gov)
Resistance1
- A rapid rise in resistance to conventional antibiotics for Shigella spp. (bvsalud.org)
Navigation1
- fr]En cliquant sur « Accepter tous les cookies », vous acceptez le stockage de cookies sur votre appareil pour améliorer la navigation sur le site, analyser son utilisation et contribuer à nos efforts de marketing pour soutenir la recherche. (pasteur.fr)
Group2
- Samples were screened for the presence of Shigella agglutinate with monovalent anti-II type antisera and mon- ovalent anti-3,4 and anti-7,8 group antisera. (cdc.gov)
- Shigella dysenteriae, or "group A" Shigella is rare in the United States. (medlineplus.gov)
Data1
- These data directly demonstrate that this large S. flexneri plasmid encodes or regulates some function(s) required for epithelial cell penetration. (nih.gov)
Children1
- About 1 in 10 children (under age 15) with severe Shigella enteritis develop nervous system problems. (medlineplus.gov)
Public Health1
- and review what CDC is doing to learn more about extensively drug-resistant Shigella in the United States and how clinicians and public health officials can help through testing and reporting. (cdc.gov)
Year1
- An estimated 450,000 persons each year in the US are infected with Shigella , resulting in over 6,000 hospitalizations and over 3 million dollars in direct healthcare costs annually. (cdc.gov)
Cells1
- Our workflow was critical to reveal that S. flexneri develops a bimodal lifestyle within M cells leading to rapid transcytosis or delayed vacuolar rupture, followed by direct actin motility-based propagation to neighboring enterocytes. (archives-ouvertes.fr)
Susceptibility3
- S. flexneri 2a was isolated from all three patients and tested for antimicrobial susceptibility using semi-automated broth microdilution panels. (medscape.com)
- Azithromycin inhibited the isolates at a minimum concentration of 2 or 4 µ g/mL, which is similar to the azithromycin minimum inhibitory concentrations among Shigellae in the United States during 2005-2007 (no breakpoint for Shigella susceptibility to azithromycin has been established). (medscape.com)
- ABSTRACT In this study, the serogroup and susceptibility patterns of Shigella and Salmonella spp. (who.int)
Infections3
- Some grantees will look into issues unique to their regions, countries and communities: sickle cell disease in infants, the role of genetics in craniofacial and dental anomalies, treatment for Guillain-Barré syndrome, and causes of Shigella flexneri infections. (nih.gov)
- First, we'll share some background on Shigella infections, including transmission and populations at greatest risk. (cdc.gov)
- Next, we'll provide an overview of the national surveillance systems used to detect XDR Shigella infections. (cdc.gov)
Organism1
- Shigella flexneri is a facultative intracellular organism that causes bacillary dysentery. (nih.gov)
ETEC1
- The World Health Organization (WHO) published the ETEC vaccine Preferred Product Characteristics (PPC) in August 2021, and the Shigella vaccine PPC in November 2021. (nih.gov)
Diarrheal2
- On October 20, 2010, the South Carolina Department of Health and Environmental Control and CDC began investigating a cluster of three diarrheal illnesses caused by multidrug-resistant Shigella flexneri 2a. (medscape.com)
- 5 years of sionally designated S. flexneri X variant (-:7,8, E1037), age die from diarrheal diseases ( 1 ), which is of par- indole-negative variety. (cdc.gov)
Invasion2
Severe1
- About 1 in 10 children (under age 15) with severe Shigella enteritis develop nervous system problems. (medlineplus.gov)
Clinical1
- Prolonged laboratory observations on clinical cases and carriers of Shigella flexneri III following an epidemic. (nih.gov)
Persons1
- An estimated 450,000 persons each year in the US are infected with Shigella , resulting in over 6,000 hospitalizations and over 3 million dollars in direct healthcare costs annually. (cdc.gov)
Study1
- Therefore, the objective of this study was to determine if Shigella has the ability to inhibit apoptosis in epithelial cells. (nih.gov)
Result1
- Investigators are further defining the ways by which the toxins produced by Shigella result in the kidney damage leading to hemolytic uremic syndrome (HUS), a life-threatening condition. (nih.gov)
Human1
- Scientists have identified genes that permit Shigella to obtain iron, an essential nutrient, from the human body. (nih.gov)