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Micro - Pathogenesis of bacterial infection (ii) (Host factors (disease…
Micro - Pathogenesis of bacterial infection (ii)
How bacteria evade immune responses
motility (flagellae)
interrupting phagocytosis
capsule
M TB v good @ this
survival in phagocytes
M protein
antiphagocytic virulence factor
aids attachment
produced by beta-haemolytic strep
over 80 types
1,3,12,28 associated with shock + organ failure
producing extracellular substances that promote invasion (invasins, enzymes)
leukocidins
WBC-killing cytotoxins
prevent phagocytosis
cause lysosome release (hydrolytic enzymes inside cause tissue damage)
e.g. Panton-Valentin leukocidin in S aureus (NB in CA-MRSA)
Bacterial enzymes
damage cells + play a role in immune evasion
toxins + superantigens
hyaluronidase
breaks down hyaluronic acid in host connective tissue (causes cellulitis)
lipase breaks down fat
coagulase
causes blood to clot
helps evade immune responses
most important virulence factor of S aureus (also an identifying feature)
kinases
dissolve clots - help bacterial spread
streptokinase
sometimes used in the management of MI, PE, arterial thromboembolism
staphylokinsae
collagenase
produced by clostridium perfringens (gas gangrene)
urease
produced by H pylori
peptic ulcer disease
50% of world pop carry this
Haemolysins
lyse RBCs
produced by strep
alpha - incomplete
beta - complete
endotoxins
released after bacterial death
due to lysis by host defence of bactericidal antibiotics (e.g. beta-lactams)
host response = severe inflamm
fever
complement
thrombocytopenia
septic shock (skin/digit loss)
lipid A of LPS in gram -ve
LOS in N meningitides (severe invasive meningococcal disease
exotoxins
polypeptides produced by living (mostly gram +ve) bacteria
different types/classes, with specific target tissues...
cytotoxins kills cells (e.g. Shigella)
neurotoxins interfere with N function (e.g. C botulinum + tetani)
enterotoxins affect GIT cells (e.g. E coli, salmonella)
superantigens cause non-specific T cell activation + CK release
secreted normally or after death
effects
local tissue necrosis (e.g. C perfringens - gas gangrene)
can act @ distal sites (e.g. C tetani)
invasion @ colonisation site (e.g. corynebacterium diphtheriae toxin)
some diseases are only toxin-related + can occur in the absence of bacteria (e.g. food botulism, staph food poisoning)
pathogen tranmission
resp (coughing/sneezing)
GI (diarrhoea + inadequate hand hygiene)
sexual (genital discharge/ulcer)
vertically/perinatally)
direct contact (skin carriage)
Host factors
extremes of age
DM
disease-induced immunosuppression
cancer
hyposplenism
HIV
renal/hepatic failure
medication-induced immunosuppression
chemo
steroids
breach in skin/mucosa (surgery)
antibiotics
prosthetics
IV lines
catheters
ventilation
joints
anatomical abnormality/malfunction