Exotoxins and Endotoxins Flashcards
(Exotoxins/Endotoxins) are toxic molecules secreted by pathogenic bacteria or released during lysis; these are usually quite deadly
Exotoxins are toxic molecules secreted by pathogenic bacteria or released during lysis; these are usually quite deadly
* Exotoxins are normally proteins or polypeptides
* Ex: Clostridium botulinum/ tetani, corynebacterium diphtheriae
(Endotoxins/Exotoxins) are present in the LPS outer membranes of gram-negative bacteria
Endotoxins are present in the LPS outer membranes of gram-negative bacteria
* They are heat stable and get released during lysis
* They are generally polar heteropolysaccharide chains
* Ex: E. coli, Pseudomonas, Salmonella, V cholerae
* Lipid A portion usually determines toxicity
Human inflammatory response includes:
Inflammatory response:
* Increase temperature
* Greater blood flow to the infected area
* Increased blood vessel permeability
* Lymphocyte migration
May lead to accumulation of fluid/neutrophils in abscess or even cause septicemia
Programmed cell death is a [enzyme] dependent cell death process that can be triggered without toxins
Programmed cell death is a caspase I enzyme-dependent cell death process that can be triggered without toxins
_ is a process in which host cells destroy themselves in response to pathogens –> leads to inflammation
Pyroptosis is a process in which host cells destroy themselves in response to pathogens –> leads to inflammation
Type _ exotoxins bind to receptors on the host cell surface where they activate intracellular signaling pathways
Type I exotoxins bind to receptors on the host cell surface where they activate intracellular signaling pathways
* Include superantigens produced by staph aureus, strep pyogenes that can lead to toxic shock syndrome
Heat-stable exotoxins that can withstand over 100 degree temperatures are in type _ exotoxins
Heat-stable exotoxins that can withstand over 100 degree temperatures are in the type I exotoxin category
* Many produced by E.coli and cause diarrhea
Type _ exotoxins are membrane-damaging toxins
Type II exotoxins are membrane-damaging toxins
* They often lyse host cells or they alter the signal transduction in host cells
S pneumoniae can alter _ in the nuclei of host cells and impair the inflammatory response
S pneumoniae can alter histone production in the nuclei of host cells and impair the inflammatory response
The alpha toxin of Clostridium perfringens has _ activity that ruptures cell membranes and causes gas gangrene
The alpha toxin of Clostridium perfringens has phospholipase activity that ruptures cell membranes and causes gas gangrene
* Presents with large, black skin blisters and crepitus
Type _ exotoxins have intracellular action in host cells
Type III exotoxins have intracellular action in host cells
* These toxins must gain access to the interior of host cells to produce a pathogenic effect
* Some will inhibit protein synthesis by damaging ribosomes (Shiga toxin)
* Others interfere with protein elongation at elongation factor 2 (Diphtheria toxin)
* Cholera toxin increases cAMP –> massive diarrhea
The endotoxic structure of gram-negative bacteria is the LPS outer membrane, of which _ is a component that causes a toxic effect in host cells
The endotoxic structure of gram-negative bacteria is the LPS outer membrane, of which lipid A is a component that causes a toxic effect in host cells
Lipid A is made of two _ units and attached to _
Lipid A is made of two glucosamine units and attached to fatty acids
* Each carbohydrate has one phosphate group
LPS primarily binds to CD14, TLR4, and MD2 receptors on the host cells –> this triggers _ system
LPS primarily binds to CD14, TLR4, and MD2 receptors on the host cells –> this triggers complement system
* Triggers protease system to produce more proinflammatory cytokines
* Accompanied by fever and vasodilation
* Phagocytes are called to action
_ is septicemia in conjunction with hypotension
Endotoxic septic shock is septicemia in conjunction with hypotension
* LPS induces this
* LPS binds LPS-binding protein –> complex then attaches to CD14 receptors on immune cells –> proinflammatory response including cytokine production
The body will activate an anti-inflammatory response that includes _ antagonists and _ production
The body will activate an anti-inflammatory response that includes IL-10 antagonists and cortisol production
Endotoxic septic shock is often accompanied by _ : the LPS causes overproduction of clotting factors and excessive platelet migration
Endotoxic septic shock is often accompanied by disseminated intravascular coagulation (DIC) : the LPS causes overproduction of clotting factors and excessive platelet migration
* Presents with easy bleeding, purpura, and petechiae
Waterhouse-Friderichsen syndrome is caused by uncontrolled by bleeding into the _
Waterhouse-Friderichsen syndrome is caused by uncontrolled by bleeding into the adrenal glands –> leading to adrenal failure
* This is accompanied by DIC
* Can be caused by meningococcemia or Neisseria meningitidis
* Also Pseudomonas aeruginosa, S pneumoniae, S aureus, Haemophilus influenzae
* Presents with organ failure, adrenocortical insufficiency, sever hypotension, coma
Meningococcemia is when meningococcal infection gets into the _
Meningococcemia is when meningococcal infection gets into the bloodstream
* Can present with extremely high levels of TNF and IL-1
* Presents with petechiae and purpura
* Death caused by shock and cardiac failure
In some patients with meningococcal infections, the infection gets into the bloodstream and the meninges, where the meningococci shed _
In some patients with meningococcal infections, the infection gets into the bloodstream and the meninges, where the meningococci shed lipooligosaccharide –> leads to thrombocytopenia –> DIC, purpuric rash
The most common cause of waterhouse-friderichsen syndrome is _
The most common cause of waterhouse-friderichsen syndrome is Neisseria meningitidis
_ are type I endotoxins that activate a massive amount of T cells (up to 20% of the body’s total complement)
Superantigens (SAgs) are type I endotoxins that activate a massive amount of T cells (up to 20% of the body’s total complement)
* SAgs interact with receptors B7-2 and CD28
* Mass activation causes uncoordinated and nonspecific response
* Induces cytokine storm –> organ failure, shock
S pyogenes and S aureus release superantigens and are capable of causing _ syndrome
S pyogenes and S aureus release superantigens and are capable of causing toxic shock syndrome
* Permit nonspecific binding of T cell receptors and class II MHC –> cytokine storm
* Manifests as rash and skin peeling
* Large scale host cell death –> amputations sometimes needed
* Sx: high fever, fatigue, hypotension
