Bacteria toxins, Anaerobes

Question 1

Which bacteria produce exotoxins? General features of exotoxins?

Answer 1

Made by both Gram + and Gram -
Heat labile proteins
Converted to toxoid to generate vaccine by formalin
Toxic at microgram amounts

Question 2

Exotoxins produce a fever response by host. True or false?

Answer 2

False; mode of action does NOT include fever response by host

Question 3

What are the four classes of bacterial toxins?

Answer 3

Surface acting
Pore-forming
A/B toxins
Type 3 and 4 secretion systems

Question 4

Bacteria secrete toxins in active form. True of false?

Answer 4

False; secreted as protoxin that is stable in environment but not active until modified by proteolysis, disulfide bond reduction, etc

Question 5

How does diphtheria work to cause it pathology?

Answer 5

Cornyebacterium diphtheriae colonize upper respiratory tract to produce a localized infection

Produces diphtheria toxin, forms pseudomembrane, active part of toxin gets into cytoplasm and ADP-ribosylates EF2 using NAD. Pathology within heart, liver, lung, and nervous system.

DEATH DUE TO CARDIAC FAILURE

Question 6

What are the vaccines for diphtheria, etc? Who should get which?

Answer 6

DTap, DT, Tdap, Td
DTaP:
Five doses for children at 2, 4, 6, 15-18 months and 4-6 years
DT:
If children can’t tolerate pertussis vaccine
Tdap:
Single does for adolescents 11-18 and adults 19+
Women for each of their pregnancies in 3rd trimester (27-36th week)
7-10 year olds not fully immunized against pertussis
*can be given no matter when Td was last received
Td:
Tetanus-diphtheria booster for adolescents and adults every 10 years OR after an exposure to tetanus

Question 7

Different between DT/TT vaccine vs conjugate vaccine?

Answer 7

DT/TT: formalin inactivated diphtheria/tetanus toxins

Conjugate vaccines: Hib polysaccharides conjugated to diphtheria toxoid to make a T-dell dependent response (IgM -> IgG)

Question 8

How does C. perfringens work? Treatment?

Answer 8

Invasive, causes majority of clostridial mediated myonecrosis
Deep wound to muscle predisposes infection
Reduction of tissue redox potential (host cell death) pyruvate->lactate, lowers pH
Host Proteases: releases nutrients for clostridia to grow
Alpha toxin release (phospholipase), degrades cells -> gas gangrene

Treatment: antibiotics, often amputation