Pathogens Flashcards
do all strains of a species have the same ability to cause disease?
no
pathogen usually identified by the set of ________ that it carries and expresses
virulence genes
virulence
ability to cause damage to the host
-depends on virulence factors
mutually exclusive
when two outcomes can’t happen or be true at the same time
ex) coin toss
invasivness definition and what different virulence factors does the pathogen use?
the ability of the microorganism to become established in the host
uses different virulences factors:
- adhesions capsules
-enzymes
-invasions
-type 3 secretion system and type 4 (T3SS and T$SS)
toxigenicity definition
the capacity of the microogrganism to produce substances known as toxins that damage specific tissues of the host
two basic features of virulence (that are NOT mutually exclusive)
toxigenity and invasivness
what are Adhesins?
prompt specific attachment to the host cell surfaces
what adhesions mediate close attachment?
fibril adhesins (glycolic/lipo proteins )
what adhesion mediate loose attachment?
Fimbriae/Pili
Capsule
produced by some bacterial pathogens
- prevent the pathogen from being destroyed by the host immune cells (phagocytes)
- also mediates attachment to the host cells
- essential virulent factor for some bacterial species
- NOT only a virulent factor( non-pathogenic bacteria produce it too sometimes)
which 2 exotoxin enzymes have an effect on the ECM? which 1 on the host cell membrane
Hyaluronidase
Collagenase
host cell membrane - lecithinase
Hyaluronidase
Hya-lur-on-i-dase
degrades hyaluronic acid, a sticky polysaccharide that holds host cells together. Staphylococci and streptococci and clostridia
Collagenase
degaraades collagen present in connective tissue. Clostridia
Lecithinase
degrades lecithin in cell membrane and casques the lysis of red blood cells and destroys tissue cells
Gas gangrene
Clostridium perfringens (strict anaerobe) infection in deep wounds
- uses lecithinase to lyse host cells, collagenase and hyaluronidase to destroy ECM
- gross stitches picture on slide
Hyaluronidase producer (such as streptococcus progenies) attaches to _____.
epithelia
Hemolysins
- cause lysis of RBC and other cell types
- some are enzymes (lecithinase and phospholipase)
- some are cytolysis (pore-forming).
- produces by a great variety of bacteria
Leucocidin
causes lysis of leucocytes- WBC
- produced by staphylococci, streptococci and few other gram- neg
Coagulase
produced by virulent staphylococci, causes insoluble fibrin to be deposited on bacterial cells and protects/blocks bacteria from the immune system
- invisible cloak
Invasins
invasive surface proteins or injected proteins that allow microgansims (pathogens) to enter the cells (invade host)
Which bacteria use invasin proteins
mycobacterium, salmonella, listeria, chlamydia
Ways to modify the properties of the host cells
- block phagosome maturation (block digestion)
- increase size of the vacuole
- acquire nutrients
- block detection of intracellular infection and response (block host response)
type 3 secretion systems (T3SS)
- also called injectisome
large number of gram neg use these systems - T3SS forms a channel through the bacterial cytoplasmic membrane, the periplasm, the outer membrane and the host cell membrane so that bacterial proteins can be injected into the host cell cytosol
T4SS
similar to T3SS but absence of needle like structure
timeline for pathogenicity
exposure–> adherence–> invasion through epithelium–> multiplication–> toxicity and invasiveness (further growth and into distant sites)–> tissue or systemic damage
Toxigenicity
micro org to produce toxins that cause damage o specific tissues
are extracellular enzymes toxins?
yes, anything that cause damage to the host cell
toxins not always associated with high virulence. other factors that can damage host include
large number of pathogens
damage by hosts own immune system
2 types of bacterial pathogens
infectious disease- result from pathogens own growth and multiplying
intoxications- result from pathogens toxins produced (food poisoning)
2 types of toxins
exotoxins- excreted int the environment
endotoxins- part of the bacterial pathogen (internal)
Exotoxins
soluble, secreted or release when the organism is lysed, usually proteins and heat liable (destroyed by heat)
- highly immunogenic (antibody response inactivates exotoxins)
-extremely potent
categorized by their target (neurotoxins, enterotoxins eat.)
AB toxins- what are the 2 subunits
A= enzymatic subunit B= binding/cell entry
Subunit A’s job
modifies a target inside the host cell leading to damage to the host “ the actual toxic part”
subunit B
binds to cell receptors providing tissue/cell type specificity “ the binding part” B for binding
Clostridium botulinum
is an AB toxin/neuro toxin that blocks acetylcholine release in neuromuscular junction
- leads to flaccid paralysis
- effects human cattle horses and ducks
- BOTOX
- reduces wrinkle
AB toxin (Botulinum toxin) normal state vs with botulism
normal- acetylcholine induces contraction of muscle fibers (think contracted is like wrinkles)
with botulism –> blocks release of Acetylcholine, inhibits contraction (flaccid)
AB toxin: Tetanus toxin
found in soil
infects deep puncture wounds and produces toxin TeNT which causes spastic paralysis; bowed spine, locked jaw (weird picture on slide )
Tetanus toxin normal vs with toxin
normal–> Glycine release from inhibitory interneurons stop acetylcholine release and allowing relaxation of muscles
with tetanus toxin–> prevents the release of glycine and therefore acetylcholine is released and muscles contract
AB5 Toxin: Cholera toxin
B binds to intestinal cells
A activates adenylate cyclase, produces cAMP
- blocks Na+ uptake, neg ions travel in to balance and water moves with the ions
explain how cholera toxin produces excess water in intestine
normally Na+ moves from intestine into blood stream
with toxin–> A subunit binds to adenylyl cyclase and this creates lots of cAMP which blocks Na+ uptake. because of surplus in + charge in intestine, CL- and HCO2- move out and with the ion movement water also moves out
Endotoxins
Are apart of the toxin, as opposed to exotoxin which gets released from within the pathogen
lipid A of LPS (example)
- released during lysis
-heat stable, cannot be activated
- weakly immunogenic- (no antibodies are produced)
-BUT very effective activator of the immune system - produce general systemic effects- fever– septic shock
key points of endotoxins
Main point is that they are HEAT STABLE and very effective activators of immune systems- fever and general systemic effects, BUT weakly immunogenic (no antibodies produced)
- can’t make vaccines bc can’t inactivated with heat (they are heat stable)
Vaccines against toxins
exotoxins are highly antigenic meaning that they stimulate the host defese to produce antibodies that can neutralize them
so vaccines can imitate these BUT endotoxins cannot be inactivated by heat and so no vaccine!
-toxins are first inactivated by heat or formaldehyde–> toxoids (no longer toxic but still antigenic)
toxoids
no longer toxic but still antigenic, can be used in a vaccine
Acetylcholin causes
contracted muscles and winkles
so with botulism–> inhibits the release of acteltycholine–> flaccid
with tetanus–> prevents the release of glycine, which allows more acetylcholing–> stiff
Diphtheria
AB, inhibits protein synthesis