Related Experiment Video

Updated: Jul 9, 2026

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
08:27

Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat

Published on: October 29, 2014

Staphylococcal enterotoxins G and I, a cause of severe but reversible neonatal enteropathy

Sandhia Naik1, Fabienne Smith, John Ho

  • 1Department of Paediatric Gastroenterology, Barts and the London NHS Trust, London, United Kingdom. Sandhia.naik@bartsandthelondon.nhs.uk

Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association
|December 8, 2007
PubMed

Insights

Staphylococcal enterotoxin G and I cause severe neonatal diarrhea and enteropathy. Prompt treatment with flucloxacillin and parenteral nutrition can reverse intestinal damage, allowing infants to thrive.

Area of Science:

  • Gastroenterology
  • Neonatal Medicine
  • Microbiology

Background:

  • Staphylococcus aureus produces various toxins linked to food poisoning and toxic shock syndrome.
  • Staphylococcal enterotoxin G (SE G) and staphylococcal enterotoxin I (SE I) are associated with scarlet fever and toxic shock.
  • SE G and SE I are implicated in severe neonatal intractable diarrhea and enteropathy.

Observation:

  • Two infants presented with intractable diarrhea, severe malnutrition, and failure to thrive from early infancy.
  • Staphylococcus aureus producing SE G and SE I was isolated from stool samples in both infants.
  • Both infants required total parenteral nutrition due to intolerance to elemental feeds.

Findings:

  • Histological examination revealed subtotal villous atrophy and abnormal brush borders.
  • Electron microscopy demonstrated severe microvilli destruction, mitochondrial dilation, and lysosomal debris.
  • Clinical improvement and histological normalization occurred following treatment with intravenous flucloxacillin and parenteral nutrition.

Implications:

  • Staphylococcal enterotoxin G- and I-induced enteropathy is a critical condition with potentially reversible enterocyte damage.
  • Early diagnosis and supportive care, including antibiotics and parenteral nutrition, are crucial for recovery.
  • This condition should be considered in the differential diagnosis of neonatal intractable diarrhea.
Abstract

More Related Videos

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis08:46

A Neonatal Imaging Model of Gram-Negative Bacterial Sepsis

Published on: August 12, 2020

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis05:39

A Neonatal BALB/c Mouse Model of Necrotizing Enterocolitis

Published on: November 30, 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...
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...
Staphylococcal Skin Infections01:29

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
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...
Diphtheria01:28

Diphtheria

Diphtheria is an acute, toxin-mediated infectious disease that primarily affects the upper respiratory tract. It is caused by Corynebacterium diphtheriae, a Gram-positive, pleomorphic rod that lacks spore-forming capability and exhibits a characteristic club-shaped morphology under microscopic examination. While C. diphtheriae can asymptomatically colonize mucosal surfaces, clinical disease manifests only when the bacterial strain is lysogenized by a specific β-corynephage. This phage...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...