MICR223_L14_toxins

What is Toxic Shock Syndrome Toxin (TSST)?

What is Toxic Shock Syndrome Toxin (TSST)?

A superantigen produced by Staphylococcus aureus that causes Toxic Shock Syndrome.

How does TSST cause disease?

By stimulating T cells, causing uncontrolled cytokine release, leading to septic shock.

What is the primary effect of the Cytokine release due to TSST?

It causes blood vessels to leak, reducing blood flow to key organs, leading to decreased tissue perfusion.

What type of bacteria produces Diphtheria toxin?

Cornyebacterium diptheriae.

What disease does Diphtheria toxin cause?

Diphtheria, an upper respiratory tract infection.

How does Diphtheria toxin block protein synthesis?

By ADP ribosylating elongation factor 2 (EF2), inhibiting protein synthesis.

What is the main vaccination strategy for Diphtheria?

Use of a toxoid, an inactivated toxin, in a trivalent vaccine (DTaP).

What does Cholera toxin cause in humans?

Severe diarrhea and dehydration.

What is the mechanism of action of Cholera toxin?

ADP ribosylates the Gsa host GTPase, increasing cAMP levels, leading to secretion of ions and water into the intestinal lumen.

What is the role of TCP in Vibrio cholerae?

TCP, or Toxin Co-regulated Pilus, is an adhesin necessary for the bacteria to adhere to host cells and acquire the cholera toxin gene.

Which bacterial toxins are classified as A/B toxins?

Cholera toxin, Diphtheria toxin, and Botulinum neurotoxins.

What type of toxin is TSST classified as?

A superantigen.

How does Diphtheria toxin enter the host cell?

Via endocytosis, through interaction with its receptor HB-EGF.

What is the fatal complication of Diphtheria caused by the pseudo membrane?

Suffocation due to blockage of air passages.

Why are superantigens like TSST beneficial for S. aureus?

They prevent the development of protective antibodies, enhancing survival and transmission.

How does Cholera toxin affect electrolyte balance?

It promotes secretion of chloride and bicarbonate ions, leading to hypertonic conditions in the intestinal lumen and diarrhea.

What cellular change does Cholera toxin induce regarding sodium?

It inhibits sodium import into intestinal cells.

What historical impact did Diphtheria toxin have before the development of vaccines?

It caused many deaths, especially in children, until effective vaccines were developed.

Describe the internalization process of Cholera toxin into host cells.

Cholera toxin binds to a receptor and is internalized through endocytosis, then trafficked through Golgi to the ER.

What is a key characteristic of the cholera toxin structure?

It comprises one A subunit and five B subunits.

What does ADP ribosylation mean?

It is a process where an ADP ribose group is transferred to a target protein, altering its function.

What is the significance of diphthamide in Diphtheria toxin’s mechanism?

Diphthamide is a modified histidine in EF2, which is the specific target for ADP ribosylation by the toxin.

How is cholera toxin spread among bacteria?

Through lysogenic bacteriophages that transfer toxin genes during infection.

What common feature do many bacterial toxins share?

They are often encoded by lysogenic bacteriophages.

What effect does Cholera toxin have on cAMP levels?

It locks Gsa in an active state, leading to continuous activation of adenylyl cyclase and increased cAMP.

What contributes to the virulence of Vibrio cholerae?

The presence of TCP, which allows adherence to host cells and acquisition of the cholera toxin gene.

What complication arises from the Hypertonic environment caused by Cholera toxin?

Severe dehydration due to water moving out of host cells into the intestinal lumen.

How does TSST affect T cell activation?

It forces the activation of a large proportion of T cells (up to 20%) instead of the normal small proportion.

What are the potential advantages of bacterial toxins beyond affecting humans?

They may target other organisms, aiding in the bacteria's survival and spreading.

What is the ultimate result of the action of Botulinum toxin?

It causes paralysis by blocking the release of neurotransmitters.