Damage To Host Cells And Tissues And Infection Outcome Flashcards

1
Q

Direct damage from microbial activity

A

Metabolic
Cytolytic
EC enz

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2
Q

Metabolic direct damage

A

Microorg multiply within cell, competes for nutrients, microb products may dam host cell act
Eg viral, rickettsial and chlamydia infection

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3
Q

Cytolytic direct damage

A

Most dam caused when org lyses host CM

Contributes to most infections to some extent

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4
Q

EC enz direct damage

A

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

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5
Q

Immunopathology dam

A

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

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6
Q

Toxins cause dam

A
Exotoxins
Endotoxins
Superantigens
Aggressins
Modulins
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7
Q

Exotoxin types

A

Mem damaging

Cellular modifying

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8
Q

Mem damaging exotox

A

Enzymatic or pore forming activities may cause haemolysis cytolysis leukolysis or other effects

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9
Q

Cellular modifying exotoxins

Mostly AB toxins

A

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

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10
Q

E.coli LT exotoxin

A

Pore forming

Activate adenylate cyclase so incr cAMP and release of ions into gut - diarrhoea

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11
Q

C diptheria toxin (exotox)

A

A subunit act aa transfer, prev pro synth by ribosome and cause cell death

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12
Q

E.coli shiga-like tox (exotox)

A

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

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13
Q

Neurotoxic clostridium (botulinum and tetani) spp toxins

A

Spec interact with neurons
Single pro activated by proteolysis
Bind via glycosides, internalised, toxins inact nurotransmitter release mech

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14
Q

Endotoxins

A

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

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15
Q

Superantigens

A
Spec class of toxins
Non-spec act lymphocytes
Eg strep pyogenic ecotox
Staph (TSS tox)
Bind MHC class2 and induce excessive lymphokine prod
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16
Q

Modulins

A

Intrinsic and EC factors that activate and modulate responses

17
Q

Fungal exotoxins

A

Prod by some fungi as 2o metabolites

Upon ingestion toxins are absorbed and can cause hepatotoxicity, mucosal haemorrhage, imm suppression, carcinogenesis

18
Q

Usual outcome to non pathogenic challenge

A

Inact of infecting organism unless there is impairment or naivety in host D

19
Q

Outcome of infect dep on

A

Microbial (virulence, dose, phenotype,etc) factors

Host (imm competence, genetics, prior exposure, stress) factors

20
Q

Possible outcomes of infection

A

Acute
Chronic
Latency
Asymptomatic carrier

21
Q

Acute outcome

A

Pathogen excretion followed by revovery or death, may be elim before spec imm resp generated

22
Q

Chronic outcome

A

Pathogen excretion followed by recovery or death

23
Q

Asympt carrier outcome

A

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

24
Q

Latency

A

Exhibited by some pathogens eg viruses
Can enter a non-repl phase in host, no symptoms
Can reactivate under certain circumstances

25
Q

Bacterial factors affecting outcome

A

Virulence factors
Global regulators of virulence, mutations in regulatory loci
Antibio res

26
Q

Hist factors affecting infection outcome

A
Genetic susceptibility
Existing factors
Diet, gen health, other dis
Stress
Age
27
Q

Enviro factors affecting outcome of infection

A
Weather
Climate
Crowding
Hygiene
Conditions (localised infection could become systemic under certain condition
28
Q

End Outcome of infection

A

Complete recovery
Recover with persistent dam
Persistence and carrier
Death