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Related Concept Videos

Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

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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...
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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...
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Bacterial Toxins01:12

Bacterial Toxins

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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...
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Cholera01:25

Cholera

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Cholera is an acute gastrointestinal disease caused by the Gram-negative bacterium Vibrio cholerae. It is transmitted primarily via the fecal-oral route through the ingestion of contaminated water or food.Vibrio cholerae is a motile, Gram-negative bacterium of the family Vibrionaceae, primarily associated with waterborne outbreaks in areas with inadequate sanitation. Although over 200 serogroups of V. cholerae exist, only O1 and O139 are responsible for epidemic cholera. The O1 serogroup,...
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Lysogenic Cycle of Bacteriophages00:43

Lysogenic Cycle of Bacteriophages

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In contrast to the lytic cycle, phages infecting bacteria via the lysogenic cycle do not immediately kill their host cell. Instead, they combine their genome with the host genome, allowing the bacteria to replicate the phage DNA along with the bacterial genome. The incorporated copy of the phage genome is called the prophage. Some prophages can re-activate and enter the lytic cycle. This often occurs in response to a perturbation, such as DNA damage, but can also transpire in the absence of...
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Receptor-mediated Endocytosis01:20

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Receptor-mediated endocytosis is when bulk amounts of specific molecules are imported into a cell after binding to cell surface receptors. The molecules bound to these receptors are taken into the cell through inward folding of the cell surface membrane, which is eventually pinched off into a vesicle within the cell. Structural proteins, such as clathrin, coat the budding vesicle.
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Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
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Typhoid toxin: reframing enteric fever.

Jorge E Galán1

  • 1Department of Microbial Pathogenesis, Yale School of Medicine, New Haven, Connecticut, USA.

Microbiology and Molecular Biology Reviews : MMBR
|April 27, 2026
PubMed
Summary
This summary is machine-generated.

Typhoid toxin, produced by Salmonella, causes enteric fever by disrupting the gut and brain. Understanding this toxin reveals new therapeutic targets for this global disease.

Keywords:
AB5 toxinsSalmonella Paratyphi ASalmonella Typhibacterial pathogenesisblood-brain barrier (BBB)enteric fevergut vascular barrierinfectious diseasesintestinal perforationleukopeniasialoglycans (Neu5-Ac)type 10 secretiontyphoid fever

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Area of Science:

  • Microbiology
  • Toxicology
  • Immunology

Background:

  • Enteric fevers caused by Salmonella Typhi and Paratyphi A are significant global health burdens.
  • Distinctive clinical features of typhoid fever lacked a clear mechanistic explanation.
  • Recent research focuses on the role of typhoid toxin in disease pathogenesis.

Purpose of the Study:

  • To elucidate the structure and mechanism of typhoid toxin.
  • To understand how typhoid toxin causes specific clinical manifestations.
  • To identify potential therapeutic targets for enteric fever.

Main Methods:

  • Characterization of the chimeric A2B5 exotoxin structure and components (PltA, CdtB, PltB/PltC).
  • Investigation of toxin assembly, secretion (type 10 secretion system), and host cell entry (CI-M6PR/COPIV, retrograde transport to ER).
  • Linking toxin activity to observed disease symptoms like leukopenia, encephalopathy, and intestinal perforation.

Main Results:

  • Typhoid toxin is an intracellularly assembled exotoxin recognizing human sialoglycans.
  • The toxin mediates leukopenia, blood-brain barrier disruption, encephalopathy, intestinal perforation, and hepatobiliary injury.
  • Discovery of an alternate B-subunit (PltC) demonstrates modularity in receptor binding and function.

Conclusions:

  • Typhoid fever is redefined as a toxin-driven immunovascular disease.
  • The toxin's mechanism involves specific host cell interactions and trafficking pathways.
  • Identified targets include neutralizing antibodies and barrier-protective therapies for enteric fever.