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Related Concept Videos

Colonisation of Pathogens01:25

Colonisation of Pathogens

Pathogen colonization of host tissues is a critical step in the development of infectious diseases. Various pathogenic microorganisms, including bacteria, fungi, viruses, and protozoa, have evolved complex strategies to attach to, invade, and persist within host environments. These mechanisms enable pathogens to establish infections, evade immune responses, and resist antimicrobial treatments.Attachment to Host CellsIn bacteria, colonization typically begins with adherence to host epithelial...
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Microbiota Modulation by Antibiotics

Antibiotics have revolutionized modern medicine by saving countless lives from bacterial infections. However, their widespread use has inadvertently harmed the delicate balance of the human gut microbiota. The gut microbiota, a complex community of bacteria, archaea, viruses, and fungi, plays a vital role in regulating metabolism, immune responses, and maintaining intestinal health. Antibiotics, especially broad-spectrum types, disrupt this ecosystem by eradicating both harmful and beneficial...
Microbiota of the Stomach and Small Intestine01:27

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The human gastrointestinal (GI) tract is characterized by distinct physicochemical conditions that shape its microbial communities. Among these, the stomach presents a particularly challenging environment for microbial colonization due to its highly acidic pH, ranging from 1 to 3. This extreme acidity effectively limits microbial density. However, certain acid-tolerant microorganisms are capable of surviving in this niche. Notably, Helicobacter pylori can colonize the gastric mucosa,...
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Microbiota of the Large Intestine

The large intestine hosts the most densely populated microbial ecosystem in the human body. This complex community primarily consists of anaerobic bacteria, with Bacillota (formerly Firmicutes) and Bacteroidota (formerly Bacteroidetes) as the predominant groups. The distribution of these microbes varies along different sections of the large intestine, influenced by local environmental factors such as oxygen availability and nutrient composition.The cecum, located at the beginning of the large...

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Related Experiment Video

Updated: Jun 21, 2026

Colon Ascendens Stent Peritonitis (CASP) - a Standardized Model for Polymicrobial Abdominal Sepsis
06:45

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Published on: December 18, 2010

Intestinal Enterococcus faecium colonization improves host defense during polymicrobial peritonitis.

Masja Leendertse1, Rob J L Willems, G Anneke Oei

  • 1Center for Infection and Immunity Amsterdam (CINIMA), Academic Medical Center, Amsterdam, The Netherlands. m.leendertse@amc.uva.nl

The Journal of Infectious Diseases
|July 17, 2009
PubMed
Summary
This summary is machine-generated.

Vancomycin-resistant Enterococcus faecium colonization did not worsen sepsis outcomes in mice. Instead, it aided bacterial clearance and reduced inflammation, suggesting a protective role in polymicrobial infections.

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Published on: September 22, 2019

Area of Science:

  • Microbiology
  • Infectious Diseases
  • Immunology

Background:

  • Vancomycin-resistant Enterococcus faecium (VRE) colonization is increasing in hospitalized patients.
  • Enterococci are common in intestinal polymicrobial infections.
  • The interaction between VRE and polymicrobial infections is not well understood.

Purpose of the Study:

  • To investigate the impact of vancomycin-resistant Enterococcus faecium colonization on polymicrobial peritonitis and sepsis.
  • To determine if VRE colonization affects the outcome of infections originating from the intestinal tract.

Main Methods:

  • Mice were colonized with VRE during vancomycin treatment.
  • Cecal ligation and puncture (CLP) was performed to induce polymicrobial peritonitis.
  • Systemic infection, bacterial loads, and inflammatory markers were assessed.

Main Results:

  • VRE colonization did not lead to systemic VRE spread before CLP.
  • CLP induced systemic VRE infection in colonized mice.
  • VRE-infected mice showed lower bacterial loads and reduced inflammation post-CLP.
  • Organ damage (liver, kidney) from CLP recovered faster in VRE-colonized mice.

Conclusions:

  • Intestinal VRE infection does not exacerbate CLP-induced polymicrobial peritonitis and sepsis.
  • VRE colonization facilitates bacterial clearance and attenuates host inflammatory responses.
  • VRE may play a beneficial role in polymicrobial infections originating from the gut.