ch 34 Flashcards
Infectivtiy
ability to create a discrete point fo infection
invasiveness
ability to spread to adjacent tissues
Active Penetration
- occurs thru production of lytic substances that alter host tissue
- attack extracellular matrix and basement memebranse of integuments and intestinal linings
- degrade carbo-protein complexes b/w cells
- disrupt host-cell surface
Passive Penetration
- not related to the pathogen itself
Bacteremia
presence of viable bacteria in the blood
Specticemia
bacterial or fungal toxins in the blood
Clostridium Tetani (tetanus)
noninvasive bc it does not spread from one tissue to another, but toxins become blood borne
Bacillus Anthracis (anthrax)
Yersinia pestis (plague)
produce toxins and are highly invasive
Streptococcus
span the spectrum of virulence factors and invasiveness
Bacterial Pathogens within the cell (listeria, shigella, and rickettsia) form Actin Tail to spread bw cells
- actin tail propels bacteria to host cell surface where it forms a protrusion
- protrusion is engulfed by adjacent cell
- evades immune response
Pathogens way of success
- produce type IV secretion system
- find shelter to avoid detection
- survive and replicate within host
- squeeze bw host cells
make capsules to avoid phagocytosis - burrow under mucus
- secrete exopolysacchrides to form shelter within biofilms
- produce enzymes that inactivate innate resistance
- excrete specialized proteins to selectively kill host cells
How do strep and staphly interfere with immune response?
- complement evasion factor (CEF), prevents C3b from opsonizing, interacts with complement proteins C1r, C1s, C3, and C5
-C5a peptidase inactivates C5a - Protein A (staph) or Protein M (strep) bind to Fc regions of IgG or IgA
-Enzymes cut IgG
Pathogenicity Islands (PAI)
what: large segments of DNA
function: encode for virulence (disease-causing ability) in bacteria
how come: Horizontal gene transfer (diff G/C ratio, short repeated DNA sequences that border PAIs which suggest a transfer mechanism, may contain genes for transposases or integrases (enzymes involved in gene transfer)
why care: helps distinguish nonpathogenic and pathogenic bacteria
Cholera PAI
- ctxA and ctxB are encoded in prophage (toxins that cause disease)
Toxin
substance that disrupts the normal metabolism of host cells
Toxigenicity
pathogens ability to produce toxin
Intoxications
diseases that result from entry of a specific performed toxin into host (toxin is alr produced before entering host dont need live bacteria to make it)
Exotoxins
- soluble, heat-liabel proteins
- travel from infection to other body tissues or target cells
- encoded by genes on plasmids or prophages within bacteria
- lethal substance
Types of Exotoxins
AB Toxin
- A catalyzes reaction causes toxicity
- B binds to host-cell receptor
- target specific hosts
destabilize membrane
- superantigens overwhelme immune system by non-specific binding to T-cells and MHC 2 cells can lead to Toxic shock synd
Superantigens
- stimulate 20% of host T cells
- T cells end up overexpressing cytokine release genes
- causes for the failure of multiple host organs allowing time for the microbe to disseminate
LPS (lipopolysacchride)
- in gram neg is toxic to mammals
- endotoxin bc its bound to bacterium and released when microoragnism lyses
- lipid A is toxic
Endotoxins
- heat stable
- toxic
0 cause fever, shock, damage to lining of blood vessels, weakness, diarrhea, inflammation, etc.
