Ch.15 Microbial Pathogenesis Flashcards
Virulence
allows the pathogen to cause disease
Virulence genes
chromosomal
plasmid
phage-based
what are virulence factors?
adherence
cell invasion
immune response inhibitors
colonization
toxins
how does a disease develop?
by virulence and virulence factor
PATHOGEN -> HOST
The pathogen process of infection and causing disease
- Enter Host
-adhesion number of infecting microbes - penetrate /evade host defenses
-capsule enzymes fimbriae/pili - damage host
-toxins intracellular pathogen - exit host
Mucous Membrane portals of entry
respiratory tact
gastrointestinal tract
genitourinary tract
skin portals of entry
hair follicles
sweat glands
conjunctiva
parental route portals of entry
deposition of microbes directly under the skin or mucous membrane
A measure of virulence:
ID50
infectious dose needed to cause disease symptoms in 50 experiential hosts
A Measure of potency :
LD50 (lethal dose 50%)
dose of pathogen required to kill 50% of an experimental group of animal hosts
Example of Measure of Virulence:
Bacillus Anthracis
portal of entry / ID50
skin: 10-50 endospores
inhalation: 10,000-20,000 endospores
ingestion: 250,000 - 10^6 endospores
Example of Measure of potency:
toxin/ LD50
Botulinum: 0.03 ng/kg
Shiga Toxin:i250 ng/kg
Staphylococcal enterotoxin: 1350 ng/kg
attachment of pathogens at the portal of entry:
bind via adhesins/ligands on the pathogen to host cell receptors
EXAMPLES of attachment of pathogens at the portal of entry:
glycocalyx
fimbriae
M protein of Streptococcus pyogenes
biofilm formation:
microbial community contained in exopolysaccharide matrix
adhere to surface
very resistant
EXAMPLES of Biofilm :
dental plaque
catheters
IV’s
Heart valves
factors that allow for bacterial invasion:
capsule
cell wall
what does the capsule do?
impairs phagocytosis by host cells
what are the cell wall components?
cell wall mycolic acids of Mycobacterium Tuberculosis
M protein: streptococcus pneumonia
-attachment, anti-phagocytic properties, inactivate complement
Opa Protein of Neisseria Gonorrhea and others
extracellular enzymes:
COAGULASES
clot blood
isolate bacteria from the host (staphylococci)
fibrinogen—Coagulase—-> Fibrin
extracellular enzymes:
KINASES
destroy blood clots
ex: streptokinase
extracellular enzymes:
HYALURONIDASE
hydrolyzes hyaluronic acids
polysaccharide bridging cells of connective tissue-> allow the microbe to spread
ex: streptococcus
extracellular enzymes:
COLLAGENASE
digest collagen
in the connective tissue of muscle, organs, and tissue
extracellular enzymes:
PROTEIN A
STAPHYLOCOCCUS
extracellular enzymes:
PROTEASES
destroy host proteins
IgA protease
antigenic variation
alteration of pathogen surface proteins
posses alternate genes
invasins
pathogen surface proteins that rearrange actin filaments
induces membrane ruffling
pathogen engulfed into the cell
penetration into the host cell cytoskeleton:
some pathogens enter cells of the host using filaments of the cystolention
what is an example of a common means of entry?
actin filaments
pathogen damage to host cells by:
host nutrients
using host nutrients
pathogen acquire host iron via siderophores
Iron (Fe) Chelator
pathogen damage to host cells by:
damage in the area of infection
causing direct damage in the vicinity of infection
intracellular pathogens
ex: viral infection
pathogen damage to host cells by:
production of toxins
production of toxins; transported by blood, lymph
inhibit protein s ytehsis
Disruption of membrane
pathogen damage to host cells by:
induction of hypersensitive reactions
Induction of hypersensitivity reactions
overproduction of cytokines
exotoxins are secreted to what?
to the surrounding environment
what is the action of exotoxins:
destroy specific host cell structures or inhibit metabolic functions
can be very lethal
types of exotoxins:
A-B toxins
Membrane-disrupting Toxins
Superantigens
describe the components of exotoxins
water-soluble proteins (many are enzymes
most are plasmid-based or inpageges (lysogenic conversion)
what do toxoid forms of antitoxins do?
provide immunity
A-B toxins consist of what?
A: an active enzyme component
B: cell binding component
A-B Toxin:
DIPHTHERIA TOXIN
Corynebacterium diphtheriae
inhibits protein synthesis
phage carries tox gene
A-B Toxin:
Botulism Toxin
Clostridium botulinum neurotoxin;
prevents nerve impulses to muscles;
causes flaccid paralysis.
A-B Toxin:
Tetanus Toxin
Clostridium tetani neurotoxin tetanospasmin;
blocks inhibitory nerve impulses to
muscles;
causes spasmodic contractions.
A-B Toxin:
Vibrio Enterotoxin
Vibrio cholerae cholera toxin; causes cellular
secretion of fluids & electrolytes ->
severe diarrhea & dehydration
membrane-disrupting toxin:
cause lysis of host cells by disrupting the plasma membrane
how does membrane-disrupting toxin cause lysis of host cells by disrupting the plasma membrane?
forming protein channels in the membrane or by disrupting phospholipids
Leukocidins
kill phagocytic white blood cells
hemolysins:
kill red blood cells
super antigens stimulate
intense immune response of T cells
T cells stimulated to produce:
cytokines
regulate immune response
what happens due to excessive cytokine levels?
enter the bloodstream and induce symptoms
can lead to shock & death
Erythrogenic toxins (Streptococcus pyogenes):
damage blood capillaries under the skin
Cause: rash; scarlet fever.
Staphylococcal enterotoxin
superantigen
(S. aureus)
what are endotoxins?
are the lipid portion (lipid A) of the
LPS (lipopolysaccharide) layer of Gram-negative
bacteria
when are endotoxins released?
Released when cells die & lyse
how do endotoxins exert effect?
by stimulating macrophages to
release toxic levels of cytokines
what do endotoxins activate?
blood clotting proteins and induce fever.
endotoxic shock:
drastic drop in blood pressure
cytopathic effect is
visible effects of viral infection
what does the cytocidal effect result in?
cell death
what do cytocidal viruses do?
stop host cell biosynthesis &
induce cell’s lysosomes to release content
what is found in some infected cells?
inclusion bodies/granules
Are usually viral parts (nucleic acids, proteins) to be assembled;
can be diagnostic
infected cells may fuse to form?
multinucleate syncytium
some virus-infected cells form what?
interferons
protect bib-infected cells
syncytium formation:
- virus entry via membrane fusion
- viral capsid enters, replication practices
(viral envelope w/protiens) - cells fuse w/non-infected cells
- multinucleate cell: fusion with more cells gets bigger forming syncytium
portals of exit:
secretion, exertions, discharges tissue that is shed
portal of exit is related to the?
part of the body that was infected
most common portal of exit:
respiratory tract and GI tract
