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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...
Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
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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,...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...

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Related Experiment Video

Updated: Jun 3, 2026

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis
05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 2021

Necrotic enteritis in young calves.

Winston E Morris1, Agustín J Venzano, Ana Elizondo

  • 1Instituto de Patobiología, CICVyA-INTA Castelar, De los reseros y las Cabañas, CC 25, 1712 Castelar, Buenos Aires, Argentina. wmorris@cnia.inta.gov.ar

Journal of Veterinary Diagnostic Investigation : Official Publication of the American Association of Veterinary Laboratory Diagnosticians, Inc
|March 15, 2011
PubMed
Summary

Non-enterotoxin producing Clostridium perfringens type A, without beta2 toxin, caused calf enteritis. Pathogenic E. coli may enhance these effects, indicating a complex etiology for calf intestinal disease.

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Area of Science:

  • Veterinary Pathology
  • Microbiology
  • Animal Science

Background:

  • Clostridium perfringens type A, specifically non-enterotoxin producing strains, is suspected in calf enteritis.
  • The role of the beta2 toxin (CPB2) in this pathogenesis remains unclear, with limited supporting evidence.

Observation:

  • Two calves with apathy, anorexia, and limb paresis were necropsied, revealing acute enteritis, rumenitis, meningitis, and pneumonia.
  • Clostridium perfringens type A (non-CPE, non-CPB2) and pathogenic Escherichia coli (ONTH8 with cdtBIII and f17 genes) were isolated from multiple tissues.

Findings:

  • Experimental inoculation of the C. perfringens strain into bovine intestinal loops induced significant pathological changes, including cell detachment, erosion, and hemorrhage.
  • These lesions were most pronounced in the small intestine, supporting the bacterium's role in intestinal damage.

Implications:

  • Non-CPE, non-CPB2 Clostridium perfringens type A can independently cause intestinal pathology in calves.
  • Co-infection with other pathogens, such as specific E. coli strains, may exacerbate the severity and presentation of calf enteritis.