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Kaplan1b - General Microbiology; Toxins

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What is the difference between endotoxins and exotoxins?
-Endotoxins are *LPSs, not proteins, and are secreted until death of the bacteria
-Exotoxins are actively secreted *proteins

-The proteins tend to be directly toxic while LPS's toxicity lies in its ability to overstimulate the immune system
In what cells do we see endotoxins? What is the actual toxic portion? Can we make it into a toxoid for vaccination? What makes it toxic?
-Endotoxin is basically another name for LPS, which we see in gram- bacteria only
-The toxic portion is lipid A which is not released until death (except in the case of N. meningitidis
-LPS is heat stable (how we convert it) and strongly immunogenic, so we cannot make it into a toxoid

-It is toxic because it over-activates **macrophages leading to secretion of many cytokines and stimulating bradykinin(-->vasodilation & shock) and Hageman factor(-->DIC) over-activation

-Reminder; Hageman factor (AKA F12) is at the top of the endogenous pathway of the coagulation cascade
What is Teichoic acid?
-It is another structural protein (like LPS) that acts as a toxin
-Similar, but less severe, than LPS, but from gram+ cells
-However, not considered an endotoxin!
What cells secrete exotoxins? Can we make them into toxoids? Give the two examples of exotoxins?
-Gram+ bac (and some gram-) produce these proteins
-We can make them into toxoids for vaccination

A-B component toxins;
-B component Binds allowing internalization
-A component is Active (toxic)
-Can be enterotoxins, neurotoxins, or cytotoxins

Cytolysins; lyse cells
-C. perfringens alpha toxin & Staphlococcus aureus alpha toxin are both examples
What are four examples of protein synthesis inhibiting exotoxins? Give organism, toxin, and mode of action?
-There are two main mechanisms employed

ADP Ribosylation of EF-2 (elongation factor 2);
-Diphtheria toxin from Corynebacterium diphtheriae (+)
-Exotoxin A from Pseudomonas aeruginosa (-)

Interference with 60S ribosomal subunit;
-Shiga toxin from Shigella dysenteriae (-) (causes bloody diarrhea)
-Verotoxin from Enterohemorrhagic E. coli (-) (same)
Give the two neurotoxin examples of exotoxins? What kind of paralysis do they present with? Mode of action?
-Tetanus toxin from Clostridium tetani (+) causes a spastic type of paralysis (arched back etc.)
-Works by blocking inhibitory transmitters glycine and GABA

-Botulinum toxin from Clostridium botulinum (+) causes flaccid type paralysis
-Works by blocking release of acetylcholine at cholinergic synapses
-This is the active ingredient in BOTOX

-Notice that both are from the same genus (I think lol)
Give the two super-antigen examples of exotoxins? When do they result in?
-TSST-1 from Staphylococcus aureus (+)
-Exotoxin A from Streptococcus pyogenes (+) (note; diff than one from pseudomonas)

-Both have their effect by overstimulating the immune system and causing toxic shock (toxic shock synd. toxin)
Go through the cAMP inducing exotoxins (4) and mode of action?
1. Heat labile toxin (LT) from Enterotoxigenic e. Coli (-)
-ADP ribosylation and *stimulation of Gs protein

2. Cholera toxin from Bibrio cholerae (-)
-Same as E. coli LT (both causing profuse diarrhea)

3. Anthrax toxin from Bacillus anthracis (+)
-Actually a mix of three proteins, two of which are toxins
-EF (edema factor) and LF (lethal factor) are the toxins (causing edema and cell death, respectively)
-PA (protective antigen) is the B component (binding) for both of the toxins above

4. Pertussis toxin from Bordetella pertussis (-)
-ADP ribosylation and *inhibition of Gi protein
What are the two cytolysin exotoxins?
-Both are Alpha toxins
-One is from Clostridium perfringens (+) and the other from Staph. aureus
-Note, however, that staph aureus also has TSST-1 which is much more important to its virulence

Both form puncture membrane;
-CP's alpha toxin is a *lecithinase (a phospholipase)
-SA's intercalates to form a pore

-Neither are really that potent of exotoxins
As a review, what antibiotics act on the ribosome?
-Chloramphenicol (blocks pep bond)
-Erythromyosin (blocks translocation)
-Tetracycline (blocks incoming AAs)
-Aminoglycosides (e.g. kanamysin and stroptomysin) (blocks fMet and causes misreading)

-The protein inhibiting exotoxins do the same sort of things, but to eukaryotic cells
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