Bacterial enteric organisms: the pathway in the body

This page shows the biochemical pathway behind the laboratory value Bacterial enteric organisms (Salmonella, Campylobacter, EHEC): which stations follow one another, which enzymes carry out each step and which cofactors they use. Every statement has a source. The page describes general textbook knowledge and says nothing about any individual person.

In brief

Salmonella, Shigella, Campylobacter, Yersinia and enterohaemorrhagic Escherichia coli are bacteria that fasten onto the gut lining. Some enter its cells; EHEC also makes Shiga toxins.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Uptake → Stomach acid · Magensäure The stomach holds an acidic milieu. It bears hard on many bacteria before they reach the gut. Some come through the passage because they buffer the acid for a while or are carried onwards quickly. Source 1, 2↓ depletes The acid lowers the number of bacteria that reach the small intestine alive. Where the stomach contents are less acidic, more of them arrive at the lining. observed in studies Source 1, 2
   ⚖ When the balance tips

   too much — Where the stomach contents are strongly acidic, a smaller share of the bacteria comes through the passage.

   too little — Where they are less acidic, for instance under acid-lowering medicines, more live bacteria arrive in the gut.

   observed in studies · Source 1, 2

2. Stomach acid → Mucus layer A layer of mucus lies over the gut cells. Campylobacter moves through it with flagella; other species let the gut contents carry them. Beneath lie the cells, joined as tightly as paving stones. Source 2, 14↕ both, depending on amount The mucus holds bacteria away from the cells and is food at the same time: its sugar chains are broken down by gut bacteria. Campylobacter uses it as a route to the cell surface. observed in studies Source 2, 14
   ⚖ When the balance tips

   too much — Where the mucus layer is thick, more bacteria are caught in it and carried off with the gut contents.

   too little — Where it is thin, the cells lie more exposed, and more bacteria reach their surface.

   observed in studies · Source 2, 14

3. Mucus layer → Attachment All of these species first bind to the surface of the gut cells. Enterohaemorrhagic Escherichia coli, EHEC for short and including type O157:H7, stay attached on the outside and remodel the cell surface beneath them. Source 6, 7↓ depletes Attachment holds the bacteria fast against the flow of the gut contents. Beneath attached EHEC the cell surface bulges into a pedestal, and the brush border is lost at that spot. observed in studies Source 6, 7
   ⚖ When the balance tips

   too much — Where many bacteria attach, more brush border is lost, and the surface for absorbing water and salts shrinks.

   too little — Where few attach, they are carried off with the gut contents.

   observed in studies · Source 6, 7

4. Attachment → Entry into the cells Salmonella and Yersinia enter the lining mainly in the lower small intestine, Yersinia going on into the lymphoid tissue of the gut wall. Shigella and enteroinvasive Escherichia coli multiply inside the cells of the colonic lining. Source 1, 3, 5↓ depletes Inside the cell antibodies do not reach the bacteria, and they draw on the building blocks of the cell. Shigella travels on with the cell actin scaffold and so passes into the neighbouring cell without touching the gut contents. observed in studies Source 1, 3, 5
   ⚖ When the balance tips

   too much — Where many bacteria enter, more cells perish, and the lining becomes permeable over a larger area.

   too little — Where few enter, the cell sheet stays largely closed, and the bacteria remain in the gut contents.

   observed in studies · Source 3, 4

   Field of research — Entry into the gut lining is studied in reviews on inflammation of the gut wall. Source 4

5. Entry into the cells → Organisms in stool The bacteria leave the body with the stool. In the laboratory their genetic material is sought in it by PCR, and for EHEC the Shiga toxins alongside. Shedding mostly lasts during and shortly after the illness, for Salmonella often longer. Source 1, 2↑ supplies With the stool the bacteria reach the surroundings and travel onto hands, surfaces and food. What arrives there also settles what the test finds. established physiology Source 1, 2
   ⚖ When the balance tips

   too much — Where many bacteria are shed, PCR finds more genetic material.

   too little — Where few are shed, for instance once symptoms have faded, detection may fail although an infection has run its course.

   established physiology · Source 1, 2

6. Shiga toxins → Protein building Inside the cell the second part of the toxin cuts a single building block out of the ribosome, the workbench at which the cell assembles its proteins. Source 7↓ depletes Without this building block the ribosome does not carry the chain further; protein building comes to a standstill. The cell then sets off its own orderly death. observed in studies Source 7
   ⚖ When the balance tips

   too much — Where much toxin reaches the cell interior, more cells stop building proteins and perish.

   too little — Where little reaches the interior, the cell goes on building proteins and is kept.

   observed in studies · Source 7

   Field of research — The action of Shiga toxins on cells is studied in reviews on changes in small blood vessels. Source 7

7. Protein building → Walls of small vessels If toxin passes from the gut into the circulation, it reaches the cells that form the inner wall of small vessels. The matching sugar chain sits particularly densely on the vessels of the kidneys. Source 7↓ depletes As these cells perish, the inner vessel wall turns rough. Platelets settle on it, small clots narrow the vessel, and red blood cells are torn apart as they pass. observed in studies Source 7
   ⚖ When the balance tips

   too much — Where much toxin reaches the circulation, more vessel walls are affected, and more platelets are used up.

   too little — Where the toxin stays in the gut, the vessel walls remain unchanged.

   observed in studies · Source 7

8. Signals of the gut cells → Immune cells Neutrophil granulocytes migrate between the gut cells all the way into the gut contents. They engulf bacteria and release substances that remodel the surrounding tissue; calprotectin from them can be measured in stool. Source 4, 8↕ both, depending on amount The granulocytes hold the bacteria in check and loosen the cell sheet themselves in doing so: where they pass through, gaps arise through which water and salts enter the gut lumen. observed in studies Source 4, 8
   ⚖ When the balance tips

   too much — Where many granulocytes pass through the sheet, more gaps arise, and more calprotectin appears in the stool.

   too little — Where few move in, the bacteria spread further in the lining.

   observed in studies · Source 4, 8

9. Immune cells → Water and salts The inflamed lining absorbs less sodium and releases more chloride. Water follows the salt into the gut lumen. At the same time cells of the gut wall signal through nerves that the contents are moved onwards faster. Source 8, 9↓ depletes Signalling molecules of inflammation slow sodium uptake and drive chloride release; water follows osmotically. Cells of the gut wall release serotonin in the process, which drives the movement of the gut. observed in studies Source 8, 9
   ⚖ When the balance tips

   too much — Where much chloride is released and the contents move onwards fast, the body loses more water and salts.

   too little — Where transport runs as usual, sodium and water are absorbed, and the stool stays formed.

   observed in studies · Source 8, 9

10. Signals of the gut cells → Antibodies and T cells Dendritic cells show fragments of the bacteria to the T cells in the lymphoid tissue of the gut wall. B cells then build IgA, which is released into the mucus and binds the surface of the bacteria. Source 4, 5↑ supplies IgA binds bacteria in the mucus before they attach and keeps them in the gut contents. T cells order the response and make phagocytes better at breaking down the bacteria they have engulfed. observed in studies Source 4, 5
    ⚖ When the balance tips

    too much — Where much IgA is in the mucus, fewer bacteria attach to the cells.

    too little — Where little IgA is built, more bacteria attach, and they stay longer in the gut.

    observed in studies · Source 4, 12

Further stations

• Uptake — Food, water, contact Salmonella, Shigella, Campylobacter, Yersinia and certain Escherichia coli strains reach the mouth through food, water or contact with people and animals. From there they travel through stomach and gut. Source 1, 2, 5↑ supplies Uptake begins the route; only in the gut is it settled whether the bacteria gain a hold. Each species has its own site for this: lower small intestine, large intestine, or the lymphoid tissue of the gut wall. established physiology Source 1, 2, 5
  ⚖ When the balance tips

  too much — Where many bacteria reach the gut, more of them arrive at the lining.

  too little — Where few arrive, stomach acid and gut flora settle whether they travel further.

  established physiology · Source 1, 14

• Shiga toxins — Made by attached EHEC Attached EHEC releases Shiga toxins into the gut. They consist of two parts: one binds a sugar chain on the surface of certain cells, the other passes into the cell interior. Source 6, 7↓ depletes The binding part settles which cells the toxin reaches: cells carrying the matching sugar chain absorb it, others do not. In the gut these are cells of the colonic lining and the walls of small vessels. observed in studies Source 7
  ⚖ When the balance tips

  too much — Where much toxin is made, more of it reaches cells with the matching sugar chain.

  too little — Where a strain makes no Shiga toxins, this route is absent, and the bacteria only attach to the lining.

  observed in studies · Source 6, 7

• Signals of the gut cells — Messengers from the wall Gut cells recognise building blocks of the bacterial surface and release signalling molecules. These draw immune cells out of the blood into the gut wall and make the vessels there more permeable. Source 1, 4↑ supplies The signalling molecules set the defence in motion: they call in granulocytes and prompt the cells of the wall to build antimicrobial peptides. observed in studies Source 1, 4
  ⚖ When the balance tips

  too much — Where many signalling molecules are released, many immune cells move in, and the gut wall swells.

  too little — Where few are released, the bacteria stay longer in the lining.

  observed in studies · Source 1, 4

Cofactors in this pathway

• Stomach acid (protons) — Acidic stomach contents lower the number of bacteria that reach the small intestine alive Source 1, 2
• Gut bacteria (microbiome) — Occupy the mucus layer and the nutrients; this holding of space is called colonisation resistance Source 14In the ORY catalogue as a laboratory value: Mikrobiom & Darmflora
• Sodium — Absorbed with water through transporters of the lining; signalling molecules of inflammation slow this route Source 8In the ORY catalogue as a laboratory value: Natrium (intrazellulär)
• Zinc — Building block of enzymes that form and renew the junctions between gut cells Source 10In the ORY catalogue as a laboratory value: Zink
• Glutamine — Fuel of the gut cells; from it they draw energy for cell junctions and renewal Source 11In the ORY catalogue as a laboratory value: Glutamin
• Vitamin A — Retinoic acid arises from it and switches B cells in the gut to the IgA build Source 12
• Vitamin D — Its active form has gut cells build junction proteins and antimicrobial peptides Source 13In the ORY catalogue as a laboratory value: Vitamin D

Sources

1. Ménard S et al. Cross-Talk Between the Intestinal Epithelium and Salmonella Typhimurium. Front Microbiol 2022 · PubMed 35733975
2. Kaakoush NO et al. Global Epidemiology of Campylobacter Infection. Clin Microbiol Rev 2015 · PubMed 26062576
3. Agaisse H. Molecular and Cellular Mechanisms of Shigella flexneri Dissemination. Front Cell Infect Microbiol 2016 · PubMed 27014639
4. Phalipon A et al. Shigellosis: innate mechanisms of inflammatory destruction of the intestinal epithelium, adaptive immune response, and vaccine development. Crit Rev Immunol 2003 · PubMed 15030306
5. Seabaugh JA et al. Pathogenicity and virulence of Yersinia. Virulence 2024 · PubMed 38389313
6. Kolodziejek AM et al. Escherichia coli 0157:H7 virulence factors and the ruminant reservoir. Curr Opin Infect Dis 2022 · PubMed 35665714
7. Seo US et al. Shiga toxin-centered pathophysiology defines the therapeutic limits of enterohemorrhagic Escherichia coli infection. Arch Microbiol 2026 · PubMed 42301365
8. Das S et al. The Role of Ion Transporters in the Pathophysiology of Infectious Diarrhea. Cell Mol Gastroenterol Hepatol 2018 · PubMed 29928670
9. Camilleri M et al. Enteroendocrine and neuronal mechanisms in pathophysiology of acute infectious diarrhea. Dig Dis Sci 2012 · PubMed 22001941
10. DiGuilio KM et al. Micronutrient Improvement of Epithelial Barrier Function in Various Disease States: A Case for Adjuvant Therapy. Int J Mol Sci 2022 · PubMed 35328419
11. Blachier F et al. Metabolism and functions of L-glutamate in the epithelial cells of the small and large intestines. Am J Clin Nutr 2009 · PubMed 19571215
12. Bos A et al. The role of retinoic acid in the production of immunoglobulin A. Mucosal Immunol 2022 · PubMed 35418672
13. Fakhoury HMA et al. Vitamin D and intestinal homeostasis: Barrier, microbiota, and immune modulation. J Steroid Biochem Mol Biol 2020 · PubMed 32194242
14. Woelfel S et al. Intestinal colonization resistance in the context of environmental, host, and microbial determinants. Cell Host Microbe 2024 · PubMed 38870899

Related pathways

• Clostridioides difficile — water and salts
• Intestinal parasites — attachment
• Viral enteric organisms — uptake
• Worms in the gut — uptake
• Microsporidia — Zink, Glutamin

As of 2026-10-05. Draft, written by Claude to schema v2; sources checked in PubMed; expert approval pending
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