Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (617 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Acute inflammation of the intestine associated with infectious diarrhea of various etiologies, generally acquired by eating contaminated food containing toxins, biological derived from bacteria or other microorganisms. Dysentery is characterized initially by watery feces then by bloody mucoid stools. It is often associated with abdominal pain; fever; and dehydration.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Infectious Diarrheal Disease; Diarrheal Disease, Infectious; Infectious Diarrheal Diseases.
Where it fits in the MeSH classification
- Broader topics
- Gastroenteritis; Intestinal Diseases
- Narrower topics
- Dysentery, Amebic; Dysentery, Bacillary
Related concepts
- Diarrhea
- Toxins
- Biological
- Bacteria
- Feces
- Abdominal Pain
- Fever
- Dehydration
Research landscape
PubMed indexes 14,960 records tagged with the MeSH heading “Dysentery” (counts retrieved 2026-11-04). 761 of them (5.1%) were published from 2020 onward, and the busiest period so far is through 1999 with 11,416 records.
Reviews account for 850 records (5.7%) and meta-analyses for 34. Randomized controlled trials number 168 (1.1%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 11,416 |
| 2000-2009 | 1,312 |
| 2010-2019 | 1,471 |
| 2020 onward | 761 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 850 | 5.7% |
| Meta-analyses | 34 | 0.2% |
| Randomized controlled trials | 168 | 1.1% |
Method: PubMed query "Dysentery"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in digestive system and liver
Gut and liver research ranges from laboratory studies of the microbiome to large trials of drugs and surgery. Symptoms such as pain, reflux or bowel change are reported by patients and overlap between conditions, and diet and microbiome studies are mostly observational. Check whether the study measured symptoms, tissue findings or long-term outcomes, how the diagnosis was made and how long people were followed. Nothing here replaces advice from a qualified clinician.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The Bacillus cereus Food Infection as Multifactorial Process | 2020 | Review article Design not recorded in structured metadata | 98 | cc by PMID 33167492 · DOI · PMC7694497 |
| NAIP-NLRC4-deficient mice are susceptible to shigellosis | 2020 | Research article Design not recorded in structured metadata | 94 | cc by PMID 33074100 · DOI · PMC7595732 |
| Dissecting the molecular evolution of fluoroquinolone-resistant Shigella sonnei | 2019 | Research article Design not recorded in structured metadata | 59 | cc by PMID 31645551 · DOI · PMC6811581 |
| Proximity biotinylation at the host-Shigella interface reveals UFMylation as an antibacterial pathway | 2026 | Research article Design not recorded in structured metadata | 0 | cc by PMID 42897205 · DOI · PMC13680623 |
The Bacillus cereus Food Infection as Multifactorial Process [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The ubiquitous soil bacterium Bacillus cereus presents major challenges to food safety.
- Closing excerpt
- cereus.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (160 words)
The ubiquitous soil bacterium Bacillus cereus presents major challenges to food safety. It is responsible for two types of food poisoning, the emetic form due to food intoxication and the diarrheal form emerging from food infections with enteropathogenic strains, also known as toxico-infections, which are the subject of this review. The diarrheal type of food poisoning emerges after production of enterotoxins by viable bacteria in the human intestine. Basically, the manifestation of the disease is, however, the result of a multifactorial process, including B. cereus prevalence and survival in different foods, survival of the stomach passage, spore germination, motility, adhesion, and finally enterotoxin production in the intestine. Moreover, all of these processes are influenced by the consumed foodstuffs as well as the intestinal microbiota which have, therefore, to be considered for a reliable prediction of the hazardous potential of contaminated foods. Current knowledge regarding these single aspects is summarized in this review aiming for risk-oriented diagnostics for enteropathogenic B. cereus.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33167492 · DOI · PMC7694497
NAIP-NLRC4-deficient mice are susceptible to shigellosis [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Bacteria of the genus Shigella cause shigellosis, a severe gastrointestinal disease that is a major cause of diarrhea-associated mortality in humans.
- Closing excerpt
- In addition to describing a new mouse model of shigellosis, our results suggest that the lack of an inflammasome response in IECs may help explain the susceptibility of humans to shigellosis.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (145 words)
Bacteria of the genus Shigella cause shigellosis, a severe gastrointestinal disease that is a major cause of diarrhea-associated mortality in humans. Mice are highly resistant to Shigella and the lack of a tractable physiological model of shigellosis has impeded our understanding of this important human disease. Here, we propose that the differential susceptibility of mice and humans to Shigella is due to mouse-specific activation of the NAIP-NLRC4 inflammasome. We find that NAIP-NLRC4-deficient mice are highly susceptible to oral Shigella infection and recapitulate the clinical features of human shigellosis. Although inflammasomes are generally thought to promote Shigella pathogenesis, we instead demonstrate that intestinal epithelial cell (IEC)-specific NAIP-NLRC4 activity is sufficient to protect mice from shigellosis. In addition to describing a new mouse model of shigellosis, our results suggest that the lack of an inflammasome response in IECs may help explain the susceptibility of humans to shigellosis.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33074100 · DOI · PMC7595732
Dissecting the molecular evolution of fluoroquinolone-resistant Shigella sonnei [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Shigella sonnei increasingly dominates the international epidemiological landscape of shigellosis.
- Closing excerpt
- sonnei develops further intolerance to the antimicrobial while the susceptible counterpart fails to attain complete resistance.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
Shigella sonnei increasingly dominates the international epidemiological landscape of shigellosis. Treatment options for S. sonnei are dwindling due to resistance to several key antimicrobials, including the fluoroquinolones. Here we analyse nearly 400 S. sonnei whole genome sequences from both endemic and non-endemic regions to delineate the evolutionary history of the recently emergent fluoroquinolone-resistant S. sonnei. We reaffirm that extant resistant organisms belong to a single clonal expansion event. Our results indicate that sequential accumulation of defining mutations (gyrA-S83L, parC-S80I, and gyrA-D87G) led to the emergence of the fluoroquinolone-resistant S. sonnei population around 2007 in South Asia. This clone was then transmitted globally, resulting in establishments in Southeast Asia and Europe. Mutation analysis suggests that the clone became dominant through enhanced adaptation to oxidative stress. Experimental evolution reveals that under fluoroquinolone exposure in vitro, resistant S. sonnei develops further intolerance to the antimicrobial while the susceptible counterpart fails to attain complete resistance.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31645551 · DOI · PMC6811581
Proximity biotinylation at the host-Shigella interface reveals UFMylation as an antibacterial pathway [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Host cells contest invasion by intracellular bacterial pathogens with multiple strategies that recognise and/or damage the bacterial surface.
- Closing excerpt
- Altogether, our proximity mapping of the host-bacterial interface identifies UFMylation as an ancient antibacterial pathway and holds great promise to reveal other cell-autonomous immunity mechanisms.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (161 words)
Host cells contest invasion by intracellular bacterial pathogens with multiple strategies that recognise and/or damage the bacterial surface. To identify host defence factors targeted to intracellular bacteria, we developed a proximity biotinylation approach coupled to quantitative mass spectrometry that maps the host-bacterial interface during infection. Using this method, we discovered that intracellular Shigella and Salmonella become targeted by UFM1-protein ligase 1 (UFL1), an E3 ligase that catalyses the covalent attachment of Ubiquitin-fold modifier 1 (UFM1) to target substrates in a process called UFMylation. Shigella antagonises UFMylation in a dual manner: first, using its lipopolysaccharide to shield from UFL1 recruitment; second, preventing UFM1 decoration by the bacterial effector IpaH9.8. Absence of UFMylation leads to an increase of bacterial burden in human cells and zebrafish larvae. Contrary to ubiquitylation, the protective role of UFMylation is independent of autophagy. Altogether, our proximity mapping of the host-bacterial interface identifies UFMylation as an ancient antibacterial pathway and holds great promise to reveal other cell-autonomous immunity mechanisms.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42897205 · DOI · PMC13680623
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Amoebiasis [5]
- Research article Shigellosis [6]
- Research article Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion [7]
- Research article Shigellosis [8]
- Research article Clinical trials of Shigella vaccines: two steps forward and one step back on a long, hard road [9]
- Research article Shiga toxin: biochemistry, genetics, mode of action, and role in pathogenesis [10]
References
- Jessberger N, Dietrich R, Granum PE, Märtlbauer E. The Bacillus cereus Food Infection as Multifactorial Process. . 2020. PMID 33167492 · DOI · PMC7694497
- Mitchell PS, Roncaioli JL, Turcotte EA, Goers L, Chavez RA, Lee AY, et al.. NAIP-NLRC4-deficient mice are susceptible to shigellosis. . 2020. PMID 33074100 · DOI · PMC7595732
- Chung The H, Boinett C, Pham Thanh D, Jenkins C, Weill FX, Howden BP, et al.. Dissecting the molecular evolution of fluoroquinolone-resistant Shigella sonnei. . 2019. PMID 31645551 · DOI · PMC6811581
- López-Jiménez AT, Théry F, Wright K, Painter H, Hoffmeister ST, Jarche L, et al.. Proximity biotinylation at the host-Shigella interface reveals UFMylation as an antibacterial pathway. . 2026. PMID 42897205 · DOI · PMC13680623
- Stanley SL. Amoebiasis. Lancet. 2003. PMID 12660071 · DOI
- Kotloff KL, Riddle MS, Platts-Mills JA, Pavlinac P, Zaidi AKM. Shigellosis. Lancet. 2018. PMID 29254859 · DOI
- Schroeder GN, Hilbi H. Molecular pathogenesis of Shigella spp.: controlling host cell signaling, invasion, and death by type III secretion. Clin Microbiol Rev. 2008. PMID 18202440 · DOI · PMC2223840
- Niyogi SK. Shigellosis. J Microbiol. 2005. PMID 15880088
- Levine MM, Kotloff KL, Barry EM, Pasetti MF, Sztein MB. Clinical trials of Shigella vaccines: two steps forward and one step back on a long, hard road. Nat Rev Microbiol. 2007. PMID 17558427 · DOI · PMC3771495
- O'Brien AD, Tesh VL, Donohue-Rolfe A, Jackson MP, Olsnes S, Sandvig K, et al.. Shiga toxin: biochemistry, genetics, mode of action, and role in pathogenesis. Curr Top Microbiol Immunol. 1992. PMID 1324134 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.