Dd - Bacterial Toxins

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o Microbial toxins:

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macromolecular products of microbes that harm the host by altering cellular structure or function

very potent.

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o Lipopolysaccharides:

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called "endotoxins" since they're an intrinsic part of the outer membrane of Gram-negative bacteria. Can interact with a large number of components of the body to cause pathogenesis (principal cause of Gram-negative septic shock).

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o Bacterial protein toxins

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: heat-labile, immunogenic; called "exotoxins" since they're released from the bacterial cells

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cytolysins

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damage cell membranes
insert into membranes and form pores

considered a exotoxin (bacterial protein toxin)

*hemolysins

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superantigens

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toxins that induce production of excessive cytokines

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superantigens.

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Binds antigen-presenting cells artificially to T cells, causing massive overactivation of T cells, which triggers a cytokine storm. The inflammation is what causes the disease pathology.

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molecular version of kochs postulate

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1) show that phenotype / property (toxin production) is associated with a pathogenic species or with pathogenic strains of a species

2) show taht inactivation of a specific gene that determine teh putative virulence trait causes a measurable decrease in pathogenicity or virulence

3) show that reversion or replacement of the mutated gene by the while type allele restores pathogenicity to the wild type level

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bacterial protein toxins

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-heat labile
-immunogenic
-neutralized by antibodies

-called exotoxins (found outside bacterial cells)

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LPS

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of gram negative bacteria

-called endotoxins

PAMP

recognized by innate immune system

elicits hot responses by LPS binding protein, CD14, TLR4 and other signal transduction molecules

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low dose of LPS causes

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-activates macrophages
-B-cells
-alternative complement pathway to cause fever
-productoin of acute phase reactants
-polyclonal antibody synthesis and inflammatoin

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high dose of LPS causes

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-shock and disseminited intravascular coagulation

mediated by cytokines

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toxins that facilitate spread of microbes

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hyaluronidase
collagenase
elastase
deoxyribonuclease
streptokinase

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toxin taht damage cellular membranes

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hemolysins

cytolysins

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toxins that stimulate cytokine production

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pyrogenic exotoxins
-erythrogenic (scarlatinal) toxins of streptococcus pyogenes

-enterotoxins and TSST-1 of staph aureus.

scarlet fever
food poisoning
TSS.

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pyrogenic exotoxins

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superantigens

most potent t cell activators
act by binding both MHCII on APC and Vbeta chians on tcells atdifferent site than Ag binding site.
activate larger numbers of t-cells than typical Ag.

XS production of cytokines

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how do diphtheria toxin and pseudomonas aeruginosa inhibit protein synthesis

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produe toxins that inactivate elongation factor 2 (EF-2) which is used for peptide chian elongatoin.

ADP ribosytransferases taht transfer ADP-ribose from NAD to diphthamide on EF-2. this inactivates EF-2

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how do shiga toxins of shigella dysenteriae and e coli inhibit protein synthesis

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toxins are RNA-N-glycosidases that remove certain adenine residue from 28S RNA of 60S ribosomal subunit. this inactivates ribosomes.

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toxins that modify intracellular signaling pathways

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-heat labile enterotoxins of vibrio cholerae and e coli
-pertussis toxin
-heat stable enterotoxin I (ST-I) of E coli
-anthrax edema factor (EF)
-anthrax lethal factor (LF)
-clostridium difficile toxins A and B

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• Pertussis toxin acts on

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respiratory epithelial cells- also increases cAMP production, but by inhibiting the Gi pathway

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• Cholera toxin / heat-labile enterotoxin of E. coli- cause

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massive, watery diarrhea and dehydration. They do this by increasing cAMP production in the small intestine epithelia (cAMP opens chloride channels, water efflux follows) by continuously activating the Gs pathway.

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• Heat-stable enterotoxin of E. coli activates

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cGMP production instead of cAMP to cause diarrhea.

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Anthrax lethal factor

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acts as a peptidase that cleaves MAP kinase kinase proteins and leads to cell death.

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Toxins that inhibit the release of neurotransmitters:

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 Botulinum toxin: flaccid muscle paralysis (including muscles of respiration) by inhibiting ACh release at neuromuscular junctions.

 Tetanus: sustained, involuntary muscular contractions by inhibiting NT release from inhibiting interneurons in spinal cord.
• Both botulinum and tetanus toxin work by inactivating SNARE membrane fusion proteins that allow stored neurotransmitters to be released into the synapse.

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Antitoxin:

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antibodies against a toxin (prevent toxic action before it binds to target cells).

you can make use of the "A" (active) part of the toxin by coupling it to an antibody that's specific to a type of cell that you want to destroy (tumors, etc). Then you have a little tame toxin that can go kill specific cells for you

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toxoid

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o Many toxins can be converted to toxoids: toxins that no longer have toxic effect but can be recognized by the immune system so as to make antibodies against the active form.

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clostridium difficile toxins A and B

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glucosyl transferases that alter actin cytoskeleton of target cells by transferring glucose from UDP-glucose to Rho family GTP binding proteins. this inactivates Rho Rac and Cdc42

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botulinum toxin

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flaccid paralysis
inhibits release of Ach

used therpeutically for dystonias and involuntary mvmt disorders (strabismus and blepharospasm)

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tetanus toxin

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tetan

inhibits release of NT from inhibitory interneurons in the SC

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zinc dependent endopeptidases

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tetanus toxin and botulinum toxins

inactivate SNARE proteins required for neuroexocytosis
(VAMPs and SNAREs)
each toxin cleaves a protein

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innate humoral defense factors

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lysozyme
lactoerrin, transferrin
chemotactic factors
properdin
defensins

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lysozyme
(function & source)

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hydrolysis of peptidoglycan

body fluids, lysosomes

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lactoferrin, transferrin

(function & source)

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chelates iron

phagocytes
mucosal secretions

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chemotactic factors

(function & source)

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initiate inflammtory response

bacterial products
chemokines, complement

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properdin

(function & source)

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activates alternative complement pathway

plasma

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innate humoral defense factors

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lysozyme
lactoerrin, transferrin
chemotactic factors
properdin
defensins

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lysozyme
(function & source)

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hydrolysis of peptidoglycan

body fluids, lysosomes

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lactoferrin, transferrin

(function & source)

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chelates iron

phagocytes
mucosal secretions

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chemotactic factors

(function & source)

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initiate inflammtory response

bacterial products
chemokines, complement

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properdin

(function & source)

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activates alternative complement pathway

plasma

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defensins

(function & source)

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bacterial killing

neutrophils
epithelial surfaces

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complement system

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innate immunity
differentiate self and non self

activated by antibodies

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alternative pathway

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activated by pathogen specific sugars (mannose) or absence of galactose nd sialic acid residues that normally decorate mammalian glycoproteins

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lectin pathway

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initiated by mannnan binding lectin

binds sugars present onsurface of microorganisms

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late complement deficiencies can cause what

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recurrent memingococcal infections

at risk - C6C8alpha-gamma deficiency common in blacks

at risk - C7-C8beta common in caucasians

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what are Nods

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cytosolic proteins that recognize PAMPs that reach the cytosom


intracellular pathogens like shigella, listeria, rickettsia


mutations in Nod2 --> Crohns disease

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Crohns disease

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mutation in Nod2 (Nods are proteins that recognize intracellular PAMPs)

inflammatory disorder or GI

defective sensing of bacterial contributes to abnormal t-cell mediated immune response

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signals transduced by PRRs

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-inflammatory response (IL1-IL6, TNFalpha)

-costimulators of T cell activation (B7.1 and B7.2)

-promote lymphocytes differentiation (IL12 induces Th1 differentiation IFNgamma)

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chronic granulomatous disease

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hereditary
lack respiratory burst

prone to infections