Exotoxins Cause Damage to the Host - Online Tutor, Practice Problems & Exam Prep

Exotoxins are categorized into three major groups: neurotoxins, enterotoxins, and cytotoxins, each targeting specific tissues. AB toxins consist of an active (A) subunit, responsible for toxicity, and a binding (B) subunit, which directs the toxin to specific cells. Membrane damaging toxins disrupt cytoplasmic membranes, leading to cell lysis, while superantigens cause excessive T cell activation, resulting in cytokine storms that can be life-threatening. Understanding these mechanisms is crucial for grasping pathogenesis and developing therapeutic strategies against infections.

Types of Exotoxins

In this video, we're going to talk more details about exotoxins and how they can cause damage to the host. Damage by exotoxins is actually highly specific. These exotoxins can be grouped based on the type of tissue they cause damage to. For example, neurotoxins are exotoxins that damage the tissues of the nervous system. Because they cause damage to the nervous system, these neurotoxins can potentially cause paralysis. Now, enterotoxins are exotoxins that cause damage to tissues of the intestinal tract. Because they cause damage to the intestinal tract, they can cause things such as diarrhea or vomiting. Lastly, cytotoxins are exotoxins that damage different cell types by interfering with the cellular mechanisms or by causing cell lysis. For example, cytotoxic T cells, which are actually part of our immune system, produce cytotoxins that kill infected host cells. But of course, there are some pathogens that can produce cytotoxins as well.

If we take a look at our image down below, notice the left-hand side here is an image focused on neurotoxins, which again are exotoxins that damage the nervous system. Notice here we have this pathogen, these blue microbes here that are producing these neurotoxins that damage the nervous system and could potentially cause paralysis. The middle image over here is focused on enterotoxins, which again are exotoxins that cause damage to the intestinal tract. Notice here we have these microbes in blue once again, and they are producing these enterotoxins, which are in yellow, those little yellow circles. Again, they can cause potentially diarrhea or vomiting. Lastly, over here on the far right, we're showing you an image of cytotoxins. Of course, our cytotoxic T cells are capable of releasing cytotoxins, these little purple circles that you see here, in order to induce cell lysis of infected host cells. Again, some pathogens are also able to use or release cytotoxins as well.

Also, recall from some of our previous lesson videos that exotoxins can also be categorized based on their different structures and functions. Moving forward in our course, we're going to be talking about these categorizations, which include AB toxins, membrane-damaging toxins, and superantigens. These are three different types or categories of exotoxins that we'll talk about moving forward. This here concludes our brief lesson on exotoxins and how they can cause damage to the host, and we'll get to learn more as we move forward. So I'll see you all in our next video.

The components which make up an exotoxin are:

• A. Proteins.
• B. Carbohydrates.
• C. Lipids.
• D. Lipopolysaccharides.
• E. Nucleic Acids.

Vibrio cholerae is the bacterium which causes the disease cholera. Vibrio cholerae is a toxigenic bacterium, meaning it creates toxins. The toxin created by Vibrio cholerae is and A-B toxin which disrupts the ionic balance of the host's intestinal cell membranes. This results in vomiting, diarrhea, and severe dehydration in infected individuals which could lead to death. The toxin created by Vibrio cholerae is an A-B toxin and a _________ toxin.

• A. Neurotoxin.
• B. Endotoxin.
• C. Cytotoxin.
• D. Enterotoxin.

Even though chemotherapy is used as a treatment for cancers it also causes cellular damage. Chemotherapy drugs possess toxins that attempt to target and destroy rapidly dividing cells, such as tumor cells. The toxins found in chemotherapy drugs are _________.

• A. Neurotoxins.
• B. Endotoxins.
• C. Cytotoxins.
• D. Enterotoxins.

1) A-B Toxins

In this video, we're going to discuss our first major group of exotoxins, which are the AB toxins. The AB toxins, once again, are exotoxins, and they actually consist of 2 parts as their name implies with A and B. The two parts of the AB toxin are the A subunit and the B subunit. Now the A in A subunit stands for the A in active, and so the A subunit is also known as the active subunit. It turns out that this A subunit is usually going to be an enzyme and it is going to be responsible for all of the toxic damaging activity of the AB toxin. Of this entire AB toxin, it's really the A or active subunit that is going to be responsible for the toxic damaging activity. Now the B subunit is going to also be known as the binding subunit. The B stands for the B in binding. And the B or binding subunit is not necessarily toxic. As its name implies, it's going to dictate the very specific type of cell that the AB toxin will bind to. The B subunit or the binding subunit is going to dictate the binding of the AB toxin. And because once again the B or binding subunit is not necessarily toxic, it's the A subunit that is toxic. What this means is that the B subunit can be isolated and separated from the A subunit and then the B subunit can be recombined with medicines so that those medicines can be delivered to very specific cell types. This is an area that is being researched and explored even today.

The AB toxins can actually infect host cells in a 3 step process that's being shown below in this image. If we take a look at this image down below, notice over here on the far left hand side, we're showing you the AB toxin right here at this location. Once again, the AB toxin has 2 subunits. It has the A subunit, or the active subunit, which is the portion that's responsible for the toxic damaging activity. And then it has the B subunit or the binding subunit, which is not necessarily toxic, but is important for binding to specific cell types, binding to specific receptors on specific host cells. What you can see here is in the first step, the B subunit binds specifically to a receptor on the host cell surface, and that's exactly what we see over here. The B subunit is binding to the cell receptor on the host cell. Now in the second step of AB toxin process, both the A and the B subunits are going to enter the cell via endocytosis. Here in this image, you can see that both the A and the B subunits of the AB toxin are going to be internalized into the host cell. Recall that when endocytosis occurs, these AB toxins are going to be brought into the cell in an endocytic vesicle. That's exactly what we see over here on the right hand side is the endocytic vesicle that results from endocytosis. Both the A and the B subunits are inside of this endocytic vesicle. However, the A subunit, which is again the active subunit, is able to leave the endocytic vesicle and enter into the cytoplasm of the cell. In the cytoplasm of the cell, the A subunit is going to be active and it can target cellular functions and inhibit cellular functions such as inhibiting translation here. Translation is being blocked and this mRNA cannot be translated into the protein and that is because of the catalytic activity of this A subunit of the AB toxin. Blocking translation could potentially be toxic and cause damage to that cell. This concludes our brief lesson on AB toxins, and we'll be able to get some practice applying these concepts as we move forward. So I'll see you all in our next video.

Anthrax is a serious illness caused by the Bacillus anthracis bacteria. The Bacillus anthracis bacteria create a dangerous toxin composed of three protein parts. Each individual part of the toxin does not cause symptoms of disease. However, when the three parts are combined, the toxin causes disease. Scientists know that one part of the toxin allows attachment to the host cells while the other two parts cause disease. The anthrax toxin is an example of a ____ toxin.  

• A. A-B toxin.
• B. LPS toxin.
• C. Endotoxin.
• D. Adhesin toxin.

Botox is a common, temporary cosmetic treatment. Botox injections use the botulinum toxin created by Clostridium botulinum bacteria to block certain nerves and paralyze muscles of the face to reduce the appearance of facial wrinkles. The botulinum toxin is an example of which type of toxin?

• A. Neurotoxin.
• B. Endotoxin.
• C. Cytotoxin.
• D. Enterotoxin.

2) Membrane-Damaging Toxins

In this video, we're going to begin our lesson on the 2nd major group of exotoxins, which are the membrane-damaging toxins. And so again, the membrane-damaging toxins are exotoxins. And as their name implies, these are toxins that are going to damage or disrupt cytoplasmic membranes. And by damaging or disrupting the cytoplasmic membranes, they can cause lysis of the host cells. Now really there are two main types of membrane-damaging toxins. There are the pore-forming toxins or the PFTs, and then there are the phospholipases. Now the pore-forming toxins or PFTs, as their name implies, are toxins that create pores, or in other words, holes in the phospholipid bilayer of the host cell, therefore causing cell lysis. Now, the phospholipases are going to be specific enzymes that are going to cleave or break down or hydrolyze phospholipids in the cytoplasmic membrane, again, causing cell lysis.

And so if we take a look at this image down below, we can get a better understanding of these membrane-damaging toxins. Notice on the left hand side we're showing you the pore-forming toxins or PFTs. And what you'll notice is that here we're showing you the PFT and it can bind to very specific cell receptors on the host cell, and that can lead to an accumulation of PFTs. And this accumulation of PFTs can ultimately end up generating a pore. And the pore is, like, once again, basically just a hole, and the hole can cause cell lysis and lead to the death of the host cell.

Now over here on the right-hand side, what we're showing you is an image of phospholipases. And again, phospholipases are enzymes that are going to break down or cleave phospholipids. And so the phospholipases are being represented as little tiny molecular scissors here, and what you'll notice is that here we have a phospholipid bilayer, and notice that these phospholipases are actually able to cleave and break down components of the phospholipid bilayer through hydrolysis, breaking them down and, that is going to disrupt the membrane and once again cause cell lysis and kill the host cell.

And so this here concludes our brief lesson on the membrane damaging toxins, and once again, we'll be able to get practice applying these concepts as we move forward. So I'll see you all in our next video.

Eisenia fetida is a species of earthworm which creates the lysenin toxin. The toxin defends the worm against infectious bacteria and fungi. The lysenin toxin forms pores in the membranes of pathogens which leads to apoptosis of the pathogens. The lysenin toxin is a _________.

• A. Pore-forming toxin.
• B. Exotoxin.
• C. Defense mechanism.
• D. All of the above.

Toxoid vaccines are vaccines for toxins made by pathogens. Toxoids are weakened versions of a toxin which do not cause disease but allows our immune system to recognize toxins in the future. Toxoid vaccines for toxic phospholipases C are being researched and tested. What would this vaccine protect patients from?

• A. Hydrolysis of phospholipids of host cell membranes leading to apoptosis.
• B. Pore formation in host cell membranes leading to apoptosis.
• C. Damage to nerve cells and muscle paralysis.
• D. Damage to digestive tract and intestinal epithelial cells.

3) Superantigens

In this video, we're going to begin discussing our 3rd major group of exotoxins, which are the superantigens. And so the superantigens are exotoxins that inappropriately stimulate helper T cells, ultimately leading to the overproduction of cytokines. And so recall that cytokines are a group of chemicals that are used for communication purposes and can help stimulate and generate immune responses. Now, these superantigens, the way that they work is that they bind to major histocompatibility complex 2 molecules or MHC 2 molecules on antigen presenting cells or APCs. And by doing that, they cause helper T cells to recognize and respond to antigens that they normally would not be responding to. And so it causes helper T cells to respond to harmless and potentially self antigens, which is not good. And so by doing this, it can lead to excessive proliferation and activation of the helper T cells, and it can also lead to a massive release of cytokines. And when there's a massive release of cytokines, this is referred to as a cytokine storm. And so a cytokine storm is really just a massive release of cytokines. And so cytokine storms can actually be life-threatening, and they can cause fevers, inflammation, and even shock.

If we take a look at our image down below, we can get a better understanding of these superantigens. And so what you'll notice is the image on the left-hand side is showing you the immune response in the absence of superantigens. And then the image on the right-hand side is showing you the immune response in the presence of superantigens. And so let's start on the left-hand side, the absence of superantigens. And so in the absence of superantigens, T cells, which have T Cell Receptors or TCRs, will only bind to and recognize antigens that are presented on MHC class twos on antigen presenting cells. And again, the T cells will only generate a response to the correct antigen or antigens that are dangerous and harmful, and therefore now, in the presence of superantigens, which are again a group of exotoxins, the superantigens will bind to the MHC class 2 molecule. And in doing so, even when the incorrect antigen is presented, such as perhaps a harmless self antigen, it will cause the helper T cell to recognize this incorrect antigen and generate a response to this incorrect antigen when it's not supposed to. That's what the superantigen does. It causes the helper T cells to generate a cytokine storm, a massive release of cytokines, which again can be life-threatening. And so, this here concludes our brief lesson on superantigens, and we'll be able to get some practice applying these concepts as we move forward. So I'll see you all in our next video.

Which is true about superantigens?

• A. They are exotoxins.
• B. They bind to MHC II antigens on APCs.
• C. They enhance antibody production.
• D. They enhance B cell production.
• E. A and B.
• F. C and D.

A superantigen:

• A. Is incredibly efficient at stimulating the production and response of T cells in the host.
• B. Is produced by APCs to increase their ability to bind and present antigens.
• C. Is an exceptionally large antigen molecule.
• D. A protein that activates B cells to release large amounts of antibodies in defense against a pathogen.

Some individuals infected with the SARS-CoV-2 virus have elevated cytokine levels that can lead to acute lung injury, respiratory distress, and even death. The excessive concentrations of cytokines created in response to the SARS-CoV-2 virus is likely:

• A. Caused by a portion of the virus being a superantigen.
• B. A life-threatening cytokine storm.
• C. Caused by the virus releasing AB toxins.
• D. A and B.
• E. B and C.

Here’s what students ask on this topic:

What are the different types of exotoxins and how do they affect the host?

Exotoxins are categorized into three major types: neurotoxins, enterotoxins, and cytotoxins. Neurotoxins target the nervous system and can cause paralysis by damaging nerve tissues. Enterotoxins affect the intestinal tract, leading to symptoms like diarrhea and vomiting. Cytotoxins damage various cell types by interfering with cellular mechanisms or causing cell lysis. Understanding these exotoxins is crucial for grasping how pathogens cause disease and for developing therapeutic strategies against infections.

How do AB toxins function in causing damage to host cells?

AB toxins consist of two subunits: the A (active) subunit and the B (binding) subunit. The B subunit binds to specific receptors on the host cell surface, facilitating the entry of the toxin. Once inside, the A subunit, which is usually an enzyme, becomes active and disrupts cellular functions. For example, it can inhibit protein synthesis by blocking translation, leading to cell damage or death. This mechanism is crucial for understanding the pathogenicity of certain bacteria and for developing targeted treatments.

What are membrane-damaging toxins and how do they cause cell lysis?

Membrane-damaging toxins are exotoxins that disrupt the cytoplasmic membrane of host cells, leading to cell lysis. There are two main types: pore-forming toxins (PFTs) and phospholipases. PFTs create pores in the phospholipid bilayer, causing the cell to burst. Phospholipases cleave phospholipids in the membrane, disrupting its integrity and leading to cell lysis. Understanding these toxins helps in comprehending how bacterial infections can lead to cell death and tissue damage.

What are superantigens and how do they lead to cytokine storms?

Superantigens are exotoxins that inappropriately stimulate helper T cells, causing an excessive release of cytokines, known as a cytokine storm. They bind to MHC class II molecules on antigen-presenting cells, causing T cells to respond to antigens they normally wouldn't. This leads to a massive proliferation of T cells and an overproduction of cytokines, which can result in severe inflammation, fever, and even shock. Understanding superantigens is crucial for managing conditions like toxic shock syndrome.

How do enterotoxins cause symptoms like diarrhea and vomiting?

Enterotoxins are exotoxins that specifically target the tissues of the intestinal tract. They disrupt the normal function of intestinal cells, leading to an imbalance in fluid and electrolyte secretion. This disruption causes symptoms like diarrhea and vomiting as the body attempts to expel the toxins. Understanding enterotoxins is essential for diagnosing and treating gastrointestinal infections caused by bacteria such as Escherichia coli and Vibrio cholerae.