Related Experiment Video

Updated: May 14, 2026

Enrichment and Detection of Clostridium perfringens Toxinotypes in Retail Food Samples
08:00

Enrichment and Detection of Clostridium perfringens Toxinotypes in Retail Food Samples

Published on: October 18, 2019

Sudden death syndrome in adult cows associated with Clostridium perfringens type E

L M Redondo1, M Farber, A Venzano

  • 1Instituto de Patobiología, Centro Nacional de Investigaciones Agropecuarias, Instituto Nacional de Tecnología Agropecuaria, Calle Las Cabañas y Los Reseros s/n, Casilla de Correo 25 (1712), Castelar, Buenos Aires, Argentina.

Anaerobe
|January 29, 2013
PubMed

More Related Videos

A Ligated Intestinal Loop Model in Anesthetized Specific Pathogen Free Chickens to Study Clostridium Perfringens Virulence09:21

A Ligated Intestinal Loop Model in Anesthetized Specific Pathogen Free Chickens to Study Clostridium Perfringens Virulence

Published on: October 11, 2018

Myocardial Infarction by Percutaneous Embolization Coil Deployment in a Swine Model05:52

Myocardial Infarction by Percutaneous Embolization Coil Deployment in a Swine Model

Published on: November 4, 2021

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...
Stringent Response in E. coli01:23

Stringent Response in E. coli

Bacterial growth is closely tied to nutrient availability, with cells proliferating exponentially under favorable conditions and entering a stationary phase when resources become scarce. This transition is mediated by a regulatory mechanism known as the stringent response, which allows bacteria to adapt to nutrient deprivation by modulating gene expression and metabolic activity.During nutrient scarcity, intracellular amino acid levels decline. It results in the accumulation of uncharged tRNAs...
Bacterial Meningitis I: Introduction01:22

Bacterial Meningitis I: Introduction

Bacterial meningitis is a severe, life-threatening inflammation of the meninges, particularly the pia mater and arachnoid mater, affecting the subarachnoid space, ventricles, and cerebrospinal fluid (CSF). If untreated, it can lead to significant neurological complications or death.Causative AgentsCommon pathogens vary with age and immune status. In adults, major organisms include Streptococcus pneumoniae, Neisseria meningitidis, and Haemophilus influenzae. Streptococcus agalactiae (group B...
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...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...