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Questions and Answers
Why are mucous membranes considered a more sensitive route of entry for pathogens compared to the skin?
Why are mucous membranes considered a more sensitive route of entry for pathogens compared to the skin?
- The pH of mucous membranes is more acidic, destroying pathogens.
- Mucous membranes have thinner layers and are designed for absorption. (correct)
- Mucous membranes lack a distinct function that allows absorption into the body.
- Mucous membranes have thicker layers of dead cells that pathogens must penetrate.
How do bacteria utilize quorum sensing to enhance their ability to cause disease?
How do bacteria utilize quorum sensing to enhance their ability to cause disease?
- By altering their genetic code to produce antibiotic resistance.
- By producing a protective capsule that shields them from the host's immune response.
- By coordinating the expression of virulence factors when the population reaches a critical density. (correct)
- By entering a dormant state, which reduces their vulnerability to the host's defenses.
Why is determining the LD50 (lethal dose 50) significant in the study of bacterial pathogenesis?
Why is determining the LD50 (lethal dose 50) significant in the study of bacterial pathogenesis?
- It indicates the concentration of toxin required to cause disease symptoms in 50% of the population.
- It identifies the specific genes a pathogen uses to cause infection.
- It measures the toxin concentration needed to kill 50% of a test population, indicating the toxin's potency. (correct)
- It shows the number of bacteria needed to initiate an immune response in a host.
How do bacterial capsules contribute to immune evasion?
How do bacterial capsules contribute to immune evasion?
What is the MOST direct consequence of hyaluronidase production by bacteria like Staphylococcus aureus during an infection?
What is the MOST direct consequence of hyaluronidase production by bacteria like Staphylococcus aureus during an infection?
How does antigenic variation in bacteria, such as Neisseria gonorrhoeae, complicate the host's immune response?
How does antigenic variation in bacteria, such as Neisseria gonorrhoeae, complicate the host's immune response?
What role do invasins play in bacterial pathogenesis?
What role do invasins play in bacterial pathogenesis?
What is the PRIMARY importance of the exopolysaccharide matrix in a bacterial biofilm?
What is the PRIMARY importance of the exopolysaccharide matrix in a bacterial biofilm?
In the context of bacterial pathogenesis, what is the significance of siderophores?
In the context of bacterial pathogenesis, what is the significance of siderophores?
How do exotoxins differ fundamentally from endotoxins in their mechanism of action?
How do exotoxins differ fundamentally from endotoxins in their mechanism of action?
Why might an antitoxin, rather than an antibiotic, be the preferred treatment for a Clostridium tetani infection?
Why might an antitoxin, rather than an antibiotic, be the preferred treatment for a Clostridium tetani infection?
What is the MECHANISM by which AB toxins, such as the Shiga toxin, disrupt cellular function?
What is the MECHANISM by which AB toxins, such as the Shiga toxin, disrupt cellular function?
How do membrane-disrupting toxins, such as those produced by Clostridium perfringens, cause damage to host cells?
How do membrane-disrupting toxins, such as those produced by Clostridium perfringens, cause damage to host cells?
What is the MAIN effect of superantigens on the host immune system?
What is the MAIN effect of superantigens on the host immune system?
Why are LPS (lipopolysaccharides) considered endotoxins?
Why are LPS (lipopolysaccharides) considered endotoxins?
How does the hydrophobicity of the insoluble portion in bacterial tetramers that disrupt host cell membrane contribute to their function?
How does the hydrophobicity of the insoluble portion in bacterial tetramers that disrupt host cell membrane contribute to their function?
For H. pylori, which infects the stomach and express genotoxins, what are the consequences for a cell when a genotoxin randomly cuts DNA?
For H. pylori, which infects the stomach and express genotoxins, what are the consequences for a cell when a genotoxin randomly cuts DNA?
How does Staph aureus infiltrate tissues, causing skin infections, and why would blackening of nerve tissue occur?
How does Staph aureus infiltrate tissues, causing skin infections, and why would blackening of nerve tissue occur?
What role does secretion of EXO polysaccharide play in biofilm formation?
What role does secretion of EXO polysaccharide play in biofilm formation?
What benefit do the bacteria in biofilms get by building towers instead of a single continuous thick substance?
What benefit do the bacteria in biofilms get by building towers instead of a single continuous thick substance?
The ID50 (infectious dose 50) for cutaneous bacillus anthracis is 10-50 spores, but the ID50 through the GI tract is 2,000,000 spores. What accounts for this discrepancy?
The ID50 (infectious dose 50) for cutaneous bacillus anthracis is 10-50 spores, but the ID50 through the GI tract is 2,000,000 spores. What accounts for this discrepancy?
If a new strain of Staphylococcus gains the ability to produce coagulase, what advantage would it have over a strain that cannot?
If a new strain of Staphylococcus gains the ability to produce coagulase, what advantage would it have over a strain that cannot?
What is a PRIMARY reason for bacteria performing antigenic variation to get around host defenses.
What is a PRIMARY reason for bacteria performing antigenic variation to get around host defenses.
Why must bacteria undergo a coordinated effort, called quorum sensing, to make a bacterial infection effective?
Why must bacteria undergo a coordinated effort, called quorum sensing, to make a bacterial infection effective?
How does the process of membrane ruffling, induced by bacterial invasins, facilitate bacterial entry into host cells?
How does the process of membrane ruffling, induced by bacterial invasins, facilitate bacterial entry into host cells?
Why have antibiotic treatments improved, but face an uphill battle, for CF (cystic fibrosis) patients?
Why have antibiotic treatments improved, but face an uphill battle, for CF (cystic fibrosis) patients?
What is the MOST COMMON mechanism of tissue damage caused by bacterial growth?
What is the MOST COMMON mechanism of tissue damage caused by bacterial growth?
An AB toxin has a binding domain and an active domain. After the binding domain binds to a cell surface receptor, what occurs?
An AB toxin has a binding domain and an active domain. After the binding domain binds to a cell surface receptor, what occurs?
Consider a scenario where a newly identified bacterial pathogen is found to secrete a toxin that forms pores in the host cell membranes. What would be the MOST likely downstream effect of this toxin on the host cells?
Consider a scenario where a newly identified bacterial pathogen is found to secrete a toxin that forms pores in the host cell membranes. What would be the MOST likely downstream effect of this toxin on the host cells?
How would a bacterium's ability to produce siderophores contribute to its survival and virulence within a host?
How would a bacterium's ability to produce siderophores contribute to its survival and virulence within a host?
In the context of bacterial infections, what is the PRIMARY significance of understanding the mechanisms by which bacteria evade host defenses?
In the context of bacterial infections, what is the PRIMARY significance of understanding the mechanisms by which bacteria evade host defenses?
A researcher is studying a bacterium that produces a toxin causing uncontrolled activation of T cells, leading to a cytokine storm. Which type of toxin is MOST likely responsible for these effects?
A researcher is studying a bacterium that produces a toxin causing uncontrolled activation of T cells, leading to a cytokine storm. Which type of toxin is MOST likely responsible for these effects?
How does the activation of the alternative complement pathway by LPS contribute to the pathophysiology of Gram-negative bacterial infections?
How does the activation of the alternative complement pathway by LPS contribute to the pathophysiology of Gram-negative bacterial infections?
How do bacterial kinases counteract the effects of coagulases during infection?
How do bacterial kinases counteract the effects of coagulases during infection?
What is the MOST significant implication of antigenic variation for vaccine development?
What is the MOST significant implication of antigenic variation for vaccine development?
What is the PRIMARY reason that biofilm-associated infections often require higher doses of antibiotics compared to infections caused by planktonic bacteria?
What is the PRIMARY reason that biofilm-associated infections often require higher doses of antibiotics compared to infections caused by planktonic bacteria?
What is a CRITICAL difference in the host's immune response to exotoxins compared to endotoxins?
What is a CRITICAL difference in the host's immune response to exotoxins compared to endotoxins?
How do intracellular bacterial pathogens exploit the host cell cytoskeleton to enhance their survival and spread within the host?
How do intracellular bacterial pathogens exploit the host cell cytoskeleton to enhance their survival and spread within the host?
If a bacterium loses its ability to produce capsules, what is the MOST likely direct consequence regarding its interaction with a host's immune system?
If a bacterium loses its ability to produce capsules, what is the MOST likely direct consequence regarding its interaction with a host's immune system?
How does the activity of bacterial kinases counteract the effects of coagulases during an infection?
How does the activity of bacterial kinases counteract the effects of coagulases during an infection?
If a bacterium হঠাৎ acquires the ability to produce hyaluronidase, what advantage would it gain in establishing an infection?
If a bacterium হঠাৎ acquires the ability to produce hyaluronidase, what advantage would it gain in establishing an infection?
What is the MOST direct consequence of a bacterium's ability to undergo antigenic variation on its surface?
What is the MOST direct consequence of a bacterium's ability to undergo antigenic variation on its surface?
How do bacterial invasins facilitate the entry of pathogens into host cells?
How do bacterial invasins facilitate the entry of pathogens into host cells?
What is the PRIMARY benefit for bacteria within a biofilm to form tower-like structures instead of a uniform layer?
What is the PRIMARY benefit for bacteria within a biofilm to form tower-like structures instead of a uniform layer?
Why are biofilm-associated infections difficult to treat with antibiotics?
Why are biofilm-associated infections difficult to treat with antibiotics?
What is the MOST likely outcome of a bacterial infection in a cystic fibrosis (CF) patient's lungs?
What is the MOST likely outcome of a bacterial infection in a cystic fibrosis (CF) patient's lungs?
How do bacteria exploit siderophores to enhance their survival and virulence within a host?
How do bacteria exploit siderophores to enhance their survival and virulence within a host?
How do bacterial exotoxins differ from endotoxins in their mechanism of action?
How do bacterial exotoxins differ from endotoxins in their mechanism of action?
If a patient is infected with Clostridium tetani, why might an antitoxin be preferred over an antibiotic for treatment?
If a patient is infected with Clostridium tetani, why might an antitoxin be preferred over an antibiotic for treatment?
How do AB toxins disrupt cellular function?
How do AB toxins disrupt cellular function?
What is the MOST likely downstream effect of a toxin that forms pores in the host cell membranes?
What is the MOST likely downstream effect of a toxin that forms pores in the host cell membranes?
A newly identified bacterial pathogen secretes a toxin that causes uncontrolled activation of T cells, leading to a cytokine storm. Which type of toxin is MOST likely responsible for these effects?
A newly identified bacterial pathogen secretes a toxin that causes uncontrolled activation of T cells, leading to a cytokine storm. Which type of toxin is MOST likely responsible for these effects?
A bacterial species expresses a surface protein that inhibits the complement cascade. What is the MOST likely advantage this bacterium gains during infection?
A bacterial species expresses a surface protein that inhibits the complement cascade. What is the MOST likely advantage this bacterium gains during infection?
Which of the following is the MOST significant implication of antigenic variation for vaccine development?
Which of the following is the MOST significant implication of antigenic variation for vaccine development?
What is the MOST plausible mechanism by which the exopolysaccharide (EPS) matrix in biofilms contributes to antibiotic resistance?
What is the MOST plausible mechanism by which the exopolysaccharide (EPS) matrix in biofilms contributes to antibiotic resistance?
How does understanding the mechanisms by which bacteria evade host defenses impact the development of antimicrobial therapies?
How does understanding the mechanisms by which bacteria evade host defenses impact the development of antimicrobial therapies?
What is a CRITICAL difference in the host's immune response to exotoxins compared to endotoxins regarding antibody production?
What is a CRITICAL difference in the host's immune response to exotoxins compared to endotoxins regarding antibody production?
If Helicobacter pylori expresses a genotoxin, and the toxin randomly cuts DNA, what are the consequences for a cell?
If Helicobacter pylori expresses a genotoxin, and the toxin randomly cuts DNA, what are the consequences for a cell?
What is the role of kinases for bacteria that produce coagulase?
What is the role of kinases for bacteria that produce coagulase?
If a patient has a heart valve transplant, and that valve gets infected and forms a biofilm, what outcomes are most likely?
If a patient has a heart valve transplant, and that valve gets infected and forms a biofilm, what outcomes are most likely?
Why is it important for bacteria to be able to cause a coordinated effort, called quorum sensing, to make bacterial infection effective?
Why is it important for bacteria to be able to cause a coordinated effort, called quorum sensing, to make bacterial infection effective?
Why is mucous membrane a more sensitive entry point than normal skin?
Why is mucous membrane a more sensitive entry point than normal skin?
Why do bacteria form towers instead of a thick substance?
Why do bacteria form towers instead of a thick substance?
What is the importance of secreting EXO polysaccharide?
What is the importance of secreting EXO polysaccharide?
What is the result of a bacterial infection that causes cutaneous infections?
What is the result of a bacterial infection that causes cutaneous infections?
How does bacteria perform antigenic variation to get around host defenses?
How does bacteria perform antigenic variation to get around host defenses?
Why are there different ID 50 levels between cutaneous and GI tract spores?
Why are there different ID 50 levels between cutaneous and GI tract spores?
What is the MAIN reason for bacteria performing antigenic variation to get around host defenses?
What is the MAIN reason for bacteria performing antigenic variation to get around host defenses?
Why do intracellular pathogens evade the host?
Why do intracellular pathogens evade the host?
What is the effect of super antigens on the host's immune system cells?
What is the effect of super antigens on the host's immune system cells?
If a patient has a Clostridium tetani infection, and antibiotics aren't working, what approach is best?
If a patient has a Clostridium tetani infection, and antibiotics aren't working, what approach is best?
When the host's cells are affected by AB toxins, what will happen?
When the host's cells are affected by AB toxins, what will happen?
What is LPS?
What is LPS?
Why are proteins the best form of fighting against exotoxins?
Why are proteins the best form of fighting against exotoxins?
What is the PRIMARY significance of the exopolysaccharide matrix in a bacterial biofilm?
What is the PRIMARY significance of the exopolysaccharide matrix in a bacterial biofilm?
Why might bacteria that produce kinases, like Streptococcus pyogenes, have an advantage in spreading through tissues?
Why might bacteria that produce kinases, like Streptococcus pyogenes, have an advantage in spreading through tissues?
How does the random switching of expressed genes during antigenic variation impact the host's ability to develop immunity?
How does the random switching of expressed genes during antigenic variation impact the host's ability to develop immunity?
If a new bacterial strain secreted a modified EXO polysaccharide that repelled water, making it hydrophobic, how might this affect biofilm formation and function?
If a new bacterial strain secreted a modified EXO polysaccharide that repelled water, making it hydrophobic, how might this affect biofilm formation and function?
Under what conditions would LPS from a Gram-negative bacterium MOST likely trigger a systemic inflammatory response leading to septic shock?
Under what conditions would LPS from a Gram-negative bacterium MOST likely trigger a systemic inflammatory response leading to septic shock?
How does the activity of bacterial coagulases contribute to the establishment of an infection?
How does the activity of bacterial coagulases contribute to the establishment of an infection?
A bacterium has a mutation that disables its quorum sensing system. What is the MOST likely consequence of this mutation on its virulence?
A bacterium has a mutation that disables its quorum sensing system. What is the MOST likely consequence of this mutation on its virulence?
Why is the difference in the infectious dose 50 (ID50) between cutaneous and gastrointestinal Bacillus anthracis significant for understanding anthrax pathogenesis?
Why is the difference in the infectious dose 50 (ID50) between cutaneous and gastrointestinal Bacillus anthracis significant for understanding anthrax pathogenesis?
How might the ability of pathogenic E. coli to induce membrane ruffling in host cells contribute to its virulence?
How might the ability of pathogenic E. coli to induce membrane ruffling in host cells contribute to its virulence?
What is the MOST likely reason why antitoxin therapy is preferred over antibiotics for treating Clostridium tetani infections?
What is the MOST likely reason why antitoxin therapy is preferred over antibiotics for treating Clostridium tetani infections?
How does the hydrophobic portion of bacterial tetramers, which disrupt host cell membranes by forming pores, contribute to their function?
How does the hydrophobic portion of bacterial tetramers, which disrupt host cell membranes by forming pores, contribute to their function?
Flashcards
Pathogen Evasion
Pathogen Evasion
Pathogens must evade the immune system and overcome barriers to entry (mucous membranes, skin) to instigate disease within a host.
Mucous Membrane Sensitivity
Mucous Membrane Sensitivity
Mucous membranes are generally more sensitive routes of entry for pathogens due to their thinner layers and absorptive functions.
Quorum Sensing
Quorum Sensing
Many bacteria coordinate their activity to cause disease when they reach high numbers, a process called quorum sensing.
ID50
ID50
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LD50
LD50
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Adherence
Adherence
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Capsules
Capsules
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Intracellular Pathogens
Intracellular Pathogens
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Coagulases
Coagulases
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Kinases
Kinases
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Hyaluronidase
Hyaluronidase
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Antigenic Variation
Antigenic Variation
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Invasions
Invasions
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Biofilms
Biofilms
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Siderophores
Siderophores
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Exotoxins
Exotoxins
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Antitoxins
Antitoxins
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AB Toxins
AB Toxins
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Membrane-Disrupting Toxins
Membrane-Disrupting Toxins
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Superantigens
Superantigens
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Endotoxins
Endotoxins
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Study Notes
Pathogen Evasion Overview
- Pathogens must evade the immune system and overcome entry barriers to cause disease.
- Entry routes include mucous membranes (respiratory, GI, genitourinary) and skin.
- Mucous membranes are generally more sensitive due to their thinner layers and absorptive functions.
- Most bacteria have a preferred entry route based on receptors and immune evasion strategies.
- Streptococcus pneumoniae prefers lung entry, differing from ingestion.
- Mycobacterium tuberculosis also favors lung entry.
Importance of Bacterial Numbers
- The number of bacteria matters for causing disease.
- A higher number increases the likelihood of survival through acidic conditions, such as in the stomach.
- Bacteria coordinate activity via quorum sensing, where small signals prompt gene expression at high population densities.
- This coordinated activity often involves secreting virulence factors.
- Coordinated bacterial activity is common, involving the secretion of virulence factors.
- Low populations do not secrete virulence factors until a certain threshold is reached.
Infectious Dose (ID50) and Lethal Dose (LD50)
- ID50 is the infectious dose required to cause disease symptoms in 50% of the population.
- LD50 is the lethal dose required to kill 50% of the population, typically determined using animal models.
- Bacillus anthracis (anthrax) has varying ID50 levels based on entry route: cutaneous (10-50 spores), inhalation (8,000-10,000 spores), and GI tract (250,000-2 million spores).
- Botulinum toxin has a very low LD50 in mice (0.03 nanograms per kilogram), equating to approximately 1.5-2 nanograms for humans.
Bacterial Adherence
- Adherence is essential for bacteria to interact with host tissues or cells, similar to viruses.
- Pathogens use adhesions or ligands (surface proteins, glycoproteins, or glycolipids) to bind to specific host cell receptors.
- This binding can facilitate entry or modify the host cell.
- Host cell receptors are not evolved to recognize pathogens.
- Bacteria exploit existing proteins and their functions on human cells.
Host Defense Evasion
- Capsule production protects bacteria from the immune system, unless there are antibodies against the capsule.
- Streptococcus pneumoniae uses capsules for immune protection.
- Mycobacterium tuberculosis uses waxy surface lipids for protection against macrophages.
- Intracellular pathogens evade the immune system by living inside white blood cells.
- Secreting EXO enzymes and factors helps bacteria evade host defenses.
EXO Enzymes
- Coagulases clot fibrinogen to form fibrin, walling off bacteria from host defenses.
- Staphylococcus aureus produces coagulase.
- Kinases (e.g., streptokinase from Streptococcus pyogenes) break down fibrin, preventing isolation by the body.
- Hyaluronidase hydrolyzes hyaluronic acid, breaking down tight junctions between cells and facilitating tissue infiltration.
- Staphylococcus aureus uses hyaluronidase to cause skin infections.
- Hyaluronidase contributes to tissue blackening.
Antigenic Variation
- This involves changing surface proteins over time to evade the immune system.
- Neisseria gonorrhoeae uses pili for attachment, but randomly changes the genes used to make the pili.
- The immune system recognizes the altered pili as new, making previous antibodies ineffective.
- Clinical Significance
- Antigenic variation complicates vaccine and treatment development due to the changing nature of surface antigens.
Invasions
- Invasions are proteins that cause cell surface ruffling to facilitate entry.
- Salmonella typhimurium produces invasion, leading to membrane ruffles that trap bacteria.
- Pathogenic E. coli also uses this mechanism.
- Bacteria use the host cell's cytoskeleton to move around inside the cell, even moving between adjacent cells.
Biofilms
- Biofilms are structured communities of bacteria encased in an EXO polysaccharide matrix.
- Free-swimming bacteria attach to a surface and secrete EXO polysaccharide, forming a sticky substance.
- Quorum sensing activates the production of EXO polysaccharide, leading to the building of towers of cells.
- Bacteria in mature towers may differentiate and be released to colonize new areas.
- Tower Structure
- Towers provide more surface area for nutrient exchange.
- Polysaccharide is hydrophilic and absorbs water.
- Small molecules diffuse more quickly than proteins.
- Significance
- Antibiotics and antibodies penetrate slowly, protecting bacteria from the immune system and antibiotics.
- They can form in catheters, lungs, and heart valves, which are difficult to remove.
Biofilms in Cystic Fibrosis (CF)
- CF patients cannot clear their lungs effectively, leading to bacterial growth and biofilm formation.
- Early infection shows some biofilm formation.
- Late stage infection can show extensive Exo polysaccharide production, obscuring lung tissues and bacterial cells.
- Implications
- Treatment is difficult due to poor antibiotic penetration.
- Breathing exercises help break up the material.
- Biofilms are a major factor in early deaths of CF patients.
Mechanisms of Bacterial Damage
- Bacteria damage their host by competing for nutrients.
- Siderophores are molecules that trap metal ions (e.g., iron) for bacterial uptake.
- Direct Damage
- Direct damage occurs from bacterial growth, whether intracellular or extracellular.
- Tissue damage, cell death, and waste products result from bacterial multiplication.
- Staphylococcus skin infections cause damage through growth and specific factors.
- Toxins are specific factors produced by bacteria to cause disease.
Exotoxins vs. Endotoxins
- Exotoxins are secreted toxins.
- Clostridium botulinum produces a potent exotoxin.
- Exotoxins are typically proteins, soluble, and effective at low concentrations.
- Grouping Exotoxins
- Neurotoxins: affect the nervous system.
- Hepatotoxins: affect the liver.
- Cardiotoxins: affect the heart.
- Cytotoxins: cause general cytotoxic effects, inhibiting protein or DNA synthesis.
Antitoxins
- Antitoxins are antibodies produced in response to exotoxins.
- Antitoxins are used to treat infections.
- In Clostridium tetani infection, antitoxins target the toxin, and are used in treatment.
Types of Exotoxins
- AB type toxins.
- Toxins that disrupt membranes.
- Super antigen toxins.
AB Toxins
- These have an active (A) domain and a binding (B) domain.
- Clostridium toxins (botulinum and tetanus) bind to nerve cells via the B domain, with the A domain cleaving proteins required for acetylcholine release.
- A genotoxin (example)
- The binding domain attaches to the cell surface receptor
- The signal for the A domain is cleaved for it to be released
- The A domain is a new lease, and acts as a nuclease
- DNA is cut, and the cell is not able produce proteins and gene
- Cell division stops and the cell eventually dies and releases nutrients
Membrane-Disrupting Toxins
- These toxins disrupt cell membranes.
- Bacteria make channel-forming proteins that insert into the host cell membrane, creating openings.
- The openings cause leakage, disrupting cell function and causing lysis.
- These can significantly affect white blood cells.
Super Antigens
- Super antigens provoke a strong immune response by stimulating T cell proliferation.
- This leads to a cytokine storm, with excessive production of immune signaling molecules.
- Cytokine storm symptoms include fever, nausea, vomiting, diarrhea, shock, and death.
- Staphylococcus toxins can cause food poisoning symptoms due to cytokine responses.
Endotoxins
- Endotoxins are part of the bacterial cell and released upon cell death.
- LPS (lipopolysaccharide) is a component of the outer membrane of gram-negative bacteria.
- LPS components are toxic and stimulate white blood cells, resulting in excessive cytokine release and potential cytokine storm.
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