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Cloned from: Microbiology

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Where is diptheria toxin encoded?
phage encoded, gene \"tox\" resides on a lysogenic phage (B phage)
What diseases does diptheria toxin cause?
infects throat, occasionally skin wounds
When does Corynebacterium diptheriae release diptheria toxin?
under pressure of iron restriction
How does diptheria toxin work?
synthesized as single AA chain (must be cleaved to work), A is active chain, B mediates entry; toxin catalyses ADP ribosylation of EF2, knocking out host protein synthesis
How does diptheria toxin present clinically?
necrosis of posterior pharynx; if absorbed systematically, produces heart toxicity that presents as heart failrue
Where is exotoxin A (P. aeruginosa) encoded?
chromosomally encoded, under control of las R
When is exotoxin A produced?
in response to iron restriction
What is the mechanism of action of exotoxin A?
catalyzes ADP ribosylation of EF2, knocking out host protein synthesis; not the only virulence factor and must unfod for activity
exotoxin A has convergent evolution with what other toxin?
Where is the Tetanus toxin of Clostridium tetani encoded?
plasmid; same found in all strains
What is the mechanism of action of tetanus toxin?
terminal spores inoculated into injury, as redox potential drops S. tetani can gow; toxin is also a metalloprotease, causes disinhibition of motor neurons and overstimulation causes spastic paralysis
Why is an individual who has had a tetanus infection not immune in the future?
not enxough toxin
What organism makes botulism toxin?
Clostridium botulinum
What is the mechanism of action of botulinum toxin (BoNT)?
metalloprotease, binds to presynaptic receptors and is taken up, blocks ACh release irreversibly, death occurs from respiratory failure
Will an individual make an antibody response to botulism toxin?
What causes floppy baby syndrome?
children under 1 year old consume honey but Clostridium botulinum spores are there); as low levels of toxin are produced, child develops progressive muscular weakness and poor motor development
What is wound botulism?
when tissue is colonized by C. botulinum with absorption of toxin from the wound site; infection is usually inapparent
What is wound botulism most commonly associated with in the US?
drug abuse
What does Bacillus anthracis look like?
Gram+ rod that produces spores, nonmotile and grows well on blood aga
What are the three major anthrax syndromes?
cutaneous (most common), inhaled (most lethal) and gastrointestinal
Where are anthrax virulence factors encoded?
two plasmids: one for antiphagocytic capsuel and the other carrying the toxin genes
What are the three B. anthracis exotoxins that cause disease?
edema factor (EF)- calmodulin-dpependent adenyly cyclase; lethal factor (LF)- metalloprotease that cleaves MAPK 1 and 2; protective antigen (PA) is in protective anthrax vaccines, couples with edema factor and lethal factor to promote their entry into cells
What is anthrax vaccine abdsorbed (AVA)?
the only licensed human anthrax vaccine int he US-- contains crude preparation of protective antiben;
Lecture 17
Molecular Mimicry
What are classic autoimmune diseases resulting from molecular mimicry?
acute rheumatic fever (ARF) and Guillain-Barre syndrome (GBS)
What is the necessary preceeding infection to acute rheumatic fever?
pharyngeal infection with GAS
What are major risk factors for developing ARF?
high Ab titer to GAS, family history, previous episode of ARF, certain MHC II aleles (HLA-DR4 and HLA-DR2)
What is the primary suspect for molecular mimicry in GAS?
M protein, ±-helical structure matches myosin, collagen, tropomyosin
Why is it possible that a vaccine against M protein (GAS) may never be made?
it has a high likelihood of generating cross-reacting human antibodies
What are the diagnostic criteria for ARF?
Jones criteria: 2 major (carditis, polyarthritis, Sydenham\'s Chorea, Erythema marginatum, Subcutaneous nodules) or 1 major and 2 minor (fever, arthralgia, previous ARF or rheumatic disease, acute phase reactions, prolonged P-R interval); all must be supported by evidence of GAS infection
What are ways of assessing for a previous strep infection?
increased antistreptolysin (ASO) titer or other antibody titers, Hx of recent scarlet fever, positive throat culture for GAS, anti-DNAse B, antihyaluronidase, streptokinase
How does ARF-caused carditis look?
most severe manifestation, wide range, valves affected=mitral>aortic>tricuspid; valve damage leads to insufficiency or stenosis and heart failure
When do most people develop rheumatic heart disease?
only after multiple episodes of ARF
What is characteristic of the arthritis induced by ARF?
migratory joint pain and swelling, two or more are affected (usually large joints of the extremities), pain responds to aspirin and NSAIDs, heals with no permanent disability
What is Syndenham\'s Chorea (St. Vitus dance)?
gradual onset with long latent period, characterized by sudden, aimless, irregular movements accompanied by muscular weakness/emotional instability; disappears during sleep
What is erythema marginatum?
evanescent pink rash with clear center, pathognomic for ARF; has round or serpiginous margins and never appears on the face; monly on trunk or proximal extremities, and only occurs in children
What are the subcutaneous nodes and Aschoff bodies?
nodules are small, pea-sized, painless swellings over bony prominences (only seen with severe carditis), nodules consist of spindle shaped interstitial aggregate for large mononuclear cells surrounding the fibrosis, Aschoff bodies are found throughout the body (typically in heart) and are pathognomonic for RHD
What factors indicate an acute phase reaction?
change in erythrocyte sed rate, presence of C-reactive protein
What is the treatment of ARF?
PCN is mainstay, erythromycin can be given to those with PCN allergies; in patients with acute carditis corticosteroids are often prescribed to shut down inflammation injury
What is a good way to prevent ARF?
prophylaxis: treat GAS pharyngitis with PCN for 10 days; since recurrences are common prophylactic antibiotics need to be given
What is Guillain-Barre (GBS)?
acute polyneuropathy that can lead to motor and sensory deficits
What are some Sx of GBS?
rapid onset symmetrical limb weakness, loss of deep tendon reflexes, variable sensory loss and ascending neuropathy
What organisms cause GBS?
viruses: (cytomegalvirus, epstein barr, varicella zoster); vaccines e.g. rabies vaccine; bacteria (Mycoplasma pneumoniae and Campylobacter jejuni
What is the most common antecent infection for GBS?
Campylobacter jejnui
What serotype of GAS is associated with higher likelihood of developing GBS
What disease is more likely to be isolated from patients wtih serotype O19 GBS?
Miller-Fischer variant (Sx include ophthalmoplegia, ataxia and areflexia
What is a potential molecule causing molecular mimicry in E. cole?
O19 and others contain neuraminic acid (AKA sialic acid) in the O side chain of LPS; antibodies raised against them are thought to cross react with peripheral nerves; many serotypes also have gropus mimicking the polar head group of gangliosides; biopsies of GBS patients show C3 or Ab-C3 bound to Schwann cells
What important clinical problem may be linked to Chlamydia infection?
atherosclerotic plaques
What are the ≤-lactam antibiotics?
antibiotics that share a ≤-lactam ring; include penicillins, cephalosporins, monobactams, carbapenems
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