Damage To Host Cells And Tissues And Infection Outcome Flashcards
Direct damage from microbial activity
Metabolic
Cytolytic
EC enz
Metabolic direct damage
Microorg multiply within cell, competes for nutrients, microb products may dam host cell act
Eg viral, rickettsial and chlamydia infection
Cytolytic direct damage
Most dam caused when org lyses host CM
Contributes to most infections to some extent
EC enz direct damage
Proteases, lipases, glycosidases contrib locally to tissue dam as digest host cellular and EC components
Can provide convenient growth substrates for bact
Eg hyaluronidase of strep
Involved in local tissue invasion during infection bact metabolic activity also causes dam eg tooth decay by oral strep sugar fermentation
Immunopathology dam
Caused by inflam and imm resp during infection (indirect dam) due to release if inflam med from hist cells and microorg
Hypersensitivity reactions
Imm med danger can occur via autoAb dev
Toxins cause dam
Exotoxins Endotoxins Superantigens Aggressins Modulins
Exotoxin types
Mem damaging
Cellular modifying
Mem damaging exotox
Enzymatic or pore forming activities may cause haemolysis cytolysis leukolysis or other effects
Cellular modifying exotoxins
Mostly AB toxins
A subunit is active (toxic comp)
B subunit is binding (attachment and entry comp)
Differ in target pro/cells, action modes and effects.
Generally Toxin is internalised, A express activity within cytoplasm
E.coli LT exotoxin
Pore forming
Activate adenylate cyclase so incr cAMP and release of ions into gut - diarrhoea
C diptheria toxin (exotox)
A subunit act aa transfer, prev pro synth by ribosome and cause cell death
E.coli shiga-like tox (exotox)
Prod by EHEC
Bund cellular glycolipids and is internalised
A cleaves glycosidic bind of a euk rib subunit so prev pro synth
Cytotoxic for many cells, neurotoxic, alter vasc perm, induce enterocyte fluid loss
Neurotoxic clostridium (botulinum and tetani) spp toxins
Spec interact with neurons
Single pro activated by proteolysis
Bind via glycosides, internalised, toxins inact nurotransmitter release mech
Endotoxins
Integral microorg component
Key one: Lipid A of LPS, when released by lysis interact with many factors (CD14, TLR4) cause inflam med release
Can prod fever, shock, hypotension, hyperglycaemia, dissen intravasc coag
Can be fatal
Superantigens
Spec class of toxins Non-spec act lymphocytes Eg strep pyogenic ecotox Staph (TSS tox) Bind MHC class2 and induce excessive lymphokine prod
Modulins
Intrinsic and EC factors that activate and modulate responses
Fungal exotoxins
Prod by some fungi as 2o metabolites
Upon ingestion toxins are absorbed and can cause hepatotoxicity, mucosal haemorrhage, imm suppression, carcinogenesis
Usual outcome to non pathogenic challenge
Inact of infecting organism unless there is impairment or naivety in host D
Outcome of infect dep on
Microbial (virulence, dose, phenotype,etc) factors
Host (imm competence, genetics, prior exposure, stress) factors
Possible outcomes of infection
Acute
Chronic
Latency
Asymptomatic carrier
Acute outcome
Pathogen excretion followed by revovery or death, may be elim before spec imm resp generated
Chronic outcome
Pathogen excretion followed by recovery or death
Asympt carrier outcome
Show nonclinical signs but microorg persist for period after clinical recovery
Infection may be confined within tissues but can be triggered by predisposing factors
Can excrete pathogen
Latency
Exhibited by some pathogens eg viruses
Can enter a non-repl phase in host, no symptoms
Can reactivate under certain circumstances
Bacterial factors affecting outcome
Virulence factors
Global regulators of virulence, mutations in regulatory loci
Antibio res
Hist factors affecting infection outcome
Genetic susceptibility Existing factors Diet, gen health, other dis Stress Age
Enviro factors affecting outcome of infection
Weather Climate Crowding Hygiene Conditions (localised infection could become systemic under certain condition
End Outcome of infection
Complete recovery
Recover with persistent dam
Persistence and carrier
Death
