Virulence in Bacteria Flashcards
free living bacteria
no importance for animals and disease
symbionts
living together
obligate symbionts: need host
facultative symbionts
mutualism symbionts
both are necessary
positive for both
commensalism symbionts
good for one, no problem for the other
ex. intestinal flora
parasitism symbionts
one takes advantage of the other
harms the host
pathogenic bacteria
facultative and obligate
facultative pathogenic
endogenic infection
exogenic infection
endogenic infection
from inside
bacteria is inside and due to certain circumstances (stress) you get disease
exogenic infection
disease comes from outside
balanced pathogenicity
damage with recovery
unbalanced pathogenicity
high damage/death
infection
invasion and multiplication of micro-organism
eventually with disease
disease
structural and functional damage clinical/subclinical opportunistic septicaemiae/bacteraemia hyperacute/acte/subacute/chronic
clinical disease
we see it and make diagnosis
subclinical disease
cant really see it
Ex. mastitis cow produces less milk but still looks happy and healthy
Cause disease
must adhere to something inside body
invasion- cause damage
toxin release- produced by bacteria and makes you sick
Flagella
not in all bacteria motility H-antigens mainly in gram neg bacteria composed of flagellin
E. coli O157:H7
food borne pathogen
hemorrhagic
can have toxins and cause kidney damage
Pili, fimbria & fibrillae
all the same
main role is adhesion
F-antigens
special pili
sex pili bacteria conjugation (plasmid transfer)
Extracellular invasion
thromboses, local use of oxygen/nutrients (parasitic)
immunological reaction: oxygen radicals/enzymes by macrophages and neutrophils
Facultative intracellular invasion
cell lysis
obligate intracellular invasion
cell lysis
virulence factors involved in invasion
capsule
proteins that circumvent innate immunity
iron uptake
production of extracellular enzymes
extracellular enzymes
hyaluronidases collagenases fibrinolysins coagulases hemolysins leucocidins
capsule
not in all bacteria polysaccharides-proteins virulence factor enviromental protection capsular antigens (k-antigens)
virulence factor
colonization
invasion
adhesion
protection against: phagocytosis, complement
Exotoxins
2 methods of injection
1- exports the toxin, not delivered directly into cell
2- injects toxin into cell, contact with cell
Type 1 Exotoxins
bind receptor
disturbance of cell metabolism
ex. sta of ETEC, Clostridium perfringens, Staphylococci and Streptococci
Type 2 exotoxins
cell wall damage
Staphylococcus aureus: alfa-toxin (hemolysis)
Actinobacillus pleuropneumoniae: Apx Toxins (pore forming)
Type 3 exotoxins
intracellular toxins
A component: goes IC
B (binding) component: binds membrane
ex. heat labile toxin (LT) of ETEC, shiga toxin (ST) of VTEC, EHEC, Botulism toxin, tetanospasmin
Gram negative Endotoxins
cell wall components lots of damage immune reaction limited lipopolysaccharide (LPS) heat stable causes: fever, general sickness, tissue damage, cardiovascular shock, death
Function of LPS
protection against: toxic products, complement
Acts as endotoxin: infection with a gram negative bacterium
could be around cell wall to create barrier that toxin cant pass
Gram positive toxins cell wall
lipoteichoic acid (LTA) lipoarabinomannan (Mycobacteria) (LAM) pepitdoglycan less toxic, less frequent causes: general sickness, fever, tissue damage, cardiovascular shock, death
Secretion systems
Type 1-7
membrane vesicles
porin
injection system (needle like)
Membrane vesicles
tries to get products out of cell not only for toxins but also metabolites lipid membrane- part of outer membrane outer membrane will bubble and leave contain: enzymes, exotoxins, DNA (transformation), signal molecules
Membrane vesicles role
pathogenesis signaling (quorum sensing) excretion of toxic products killing of competitors immunomodulation excretion of bacterial toxic products transformation
Biofilms
very dormant, metabolically not active
composed of polysaccharides, proteins, nucleic acids (DNA)
bacterial persistence (endocarditis)-protection
reduction of host immunity
local damage
reduced susceptibility to antibiotics
on different surfaces: catheters, pipelines, dog bowls
cant treat the bacteria in the biofilm
Lipoproteins-porins
role:
pathogenesis- adhesions, iron uptake
physiological role
Iron uptake
by cell wall protiens first line of defense no free iron in body intracellular: epithelial cells: ferritin erythrocytes: hemoglobin muscular cells: myoglobin serum: transferrin mucosae: lactoferrin infection: neutrophils-lactoferrin
intracellular- epithelial cells
ferritin
intracellular- erythrocytes
hemoglobin
intracellular- muscular cells
myoglobin
serum
transferrin
mucosae
lactoferrin
infection
neutrophils
Circumvent Iron restriction
alternative for iron:
manganese in Borrelia burgdorferi
expression of iron uptake system under iron restrictive conditions
siderophore receptor (neonatal E. Coli septicaemiae)
Transferrine/lactoferrine receptor
Hemoglobine receptor
no complement activation
sialic acid (e. coli) on the surface enzymes that degrade the complement system
no lysis of bacterium
LPs
capsule
membrane vesicles
inhibition of the complement mediated inflammation
expel complement factors
intracellular multiplication
bacteria are hiding in intracellular niche
Mechanism of innate immunity
phagocytes: macrophages, neutrophils
NK cells
Factors against phagocytes
extracellular bacteria: capsule, metabolites-exotoxins
biofil
faculatative intracellular
