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Related Concept Videos

Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid receptor...
Bacterial Toxins01:12

Bacterial Toxins

Bacterial toxins are sophisticated virulence factors that enable pathogenic bacteria to interact with, invade, and damage host tissues. These toxins fall broadly into two types: protein exotoxins, which are secreted into the environment and target specific host receptors, and lipopolysaccharide endotoxins, which are structural components of the bacterial outer membrane released primarily during bacterial lysis or membrane shedding. Exotoxins generally act more selectively, binding to cell...
Botulism01:22

Botulism

Botulism is a life-threatening neuroparalytic condition caused by botulinum neurotoxin, which is produced by the bacterium Clostridium botulinum, a Gram-positive, spore-forming, obligate anaerobe.In adults, the toxin enters the body in different ways: in foodborne botulism, the preformed toxin is absorbed in the intestine. In wound botulism, spores grow in injured tissue and release the toxin into the blood. Infant botulism differs mechanistically from adult forms. In infants, botulism commonly...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Intestinal Obstruction II: Pathophysiology01:07

Intestinal Obstruction II: Pathophysiology

Intestinal obstruction triggers a series of physiological responses, starting with gas and fluid accumulation in the bowel segment proximal to the obstruction, leading to distension. This distended intestine compresses the diaphragm, hindering lung expansion and potentially leading to reduced respiratory effort, atelectasis, and pneumonia.To overcome the blockage, the gut intensifies contractions, causing colicky abdominal pain, nausea, and vomiting, which reduces fluid and food intake and...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...

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Related Experiment Video

Updated: Jun 13, 2026

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome
06:51

Microfluidic Model of Necrotizing Enterocolitis Incorporating Human Neonatal Intestinal Enteroids and a Dysbiotic Microbiome

Published on: July 28, 2023

Clostridium perfringens and necrotizing enterocolitis

Luregn J Schlapbach, Olaf Ahrens, Peter Klimek

    The Journal of Pediatrics
    |May 4, 2010
    PubMed
    Summary

    No abstract available in PubMed .

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