Chapt 25 Lecture- Microbial Pathogenisis
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61 terms
Terms | Definitions |
|---|---|
Infection | entry of pathogen or parasite(doesnt always cause disease- most infections are removed by immune system) |
Primary pathogens | have ability to penetrate host defenses |
Opportunistic pathogens | cause disease only in compromised host (weakened immune system) (break in tissue allows organisms access to new site) (loss of other microflora allows organisms to bloom) |
Pathogenicity of organism | measure of ability to cause disease- determined by genetic makeup of organism |
Infectious dose | ID50number of organisms to colonize 50% of hosts |
Virulence | rate of lethal infectionsLethal dose = LD50 |
Lethal dose = LD50 | number of organisms to kill 50% of hosts |
Infection cycle | spread by:direct contact - body fluids indirect contact |
Spread by indirect contact | contact with fomite - inanimate objects or substances that can carry infectious microbes (eg. door knobs) |
Spread by indirect contact | Horizontal transmission via vectorseg. mosquitos - yellow fever, malaria, West Nile virus mosquito may not show symptoms of those diseases however |
Mode of entry of pathogen | mucosal surface, wounds, insect bites |
VIRULENCE FACTORS: virulence genes | Virulence genes encode factors that allow pathogen to iINVADE host |
Examples of virulence factors | toxinsattachment proteins capsules |
Pathogenicity islands | section of genome - contains multiple virulence genes that code for related function |
How are pathogenicity islands transferred? | As a block from one organism to another |
Virulence Factor definition | structure and characteristics of pathogens that allow them to cause disease |
Adhesion | ability to adhere to mucus membranes |
Virulence Factors affecting ADHESION | capsulefimbriae/pili adhesins |
Capsule | outer polysach layer- helps attachment- protects from phagocytosis |
fimbriae/pili | necessary for some orgs to attach.. Neiserria and E. coli |
Adhesins | surface proteins that bind host cells eg. S. pyogenes |
Invasion | pathogens must be able to penetrate epithelium of skinthey reach inner layer of skin cells through lesions or mucus membrane |
Colonization | Once it has invaded the host, it can establish itself and grow |
Virulence Factors affecting INVASION & GROWTH | O & Vi} salmonellaSiderophores Leukosidin |
O antigen - salmonella | O - (somatic antigen- part of LPS) cell surface polysaccharide- prevents phagocytosis |
Vi antigen- salmonella | Vi - (capsular antigen) prevents complement binding & antibody mediated killing |
Siderophores | compound that binds iron & make it available to the bacterial cell |
Leukosidin | Staph aureus produces LeukosidinLeukosidin lyses white blood cells, decreasing host resistance |
Localized infection | organisms grow locally at site of invasion |
Systemic infection | organisms spread through body using blood or lymphatic systems |
How do pathogens spread (disseminate) in the body? | they make virulence factors - many of these are enzyme which break down tissue |
Examples of virulence factors that break down tissue | Hyaluronidase Collagenase Streptokinase Hemolysins |
Hyaluronidase | destroys polysaccharides that glue animal cells together |
Collagenase | breaks down collagen - produced by clostridium |
Streptokinase | breaks down fibrin clots made by host to prevent spread - made by Strep pyogenes |
Hemolysins | disrupt cytoplasmic membrane of animal cells - lyse red blood cells |
3 MAJOR GROUPS OF TOXINS | Exotoxins (worst)Enterotoxins Endotoxins |
EXOTOXINS | protein secreted by bacteria that can damage tissues far away from infection site |
Examples of EXOTOXINS | Diphtheria toxinTetanus toxin Botulinum toxin |
Diphtheria toxin | inhibits protein synthesisWhen Corynebacterium diphtheriae is lysogenized by phase β, tox genes are formed that makes the toxin |
Tetanus toxin | Acts on motor neurons- causes continual contraction of muscles (lead to lock jaw)produced by Clostridium tetani- infects deep wounds |
Botulinum toxin | prevents muscle contraction - results in respiratory /cardiac failureproduced by Clostridium botulinum Botulism caused by ingesting toxin from canned foods |
ENTEROTOXINS | proteins that act on small intestine (cause diarrhea)produced by food poisoning organisms eg. Clostridium, E coli, Salmonella |
Example of ENTEROTOXIN | cholera toxinproduced by vibriocholera |
How does cholera toxin work? | Causes secretion of massive amounts of water in small intestine (diarrhea) - death by dehydration |
ENDOTOXINS | when gram negative bacteria lyselipid A portion of LPS is released |
Organisms that release toxic Lipid A from LPS | E coliSalmonella Shigella causes diarrhea, fever, vomiting |
Toxins that ****s up host function | AB toxinsADP Ribosylating toxins |
AB toxins | B subunit binds to host celldelivers A subunit to cell 5 B subunits form pore for lipid A entry 'A' subunit is toxic- releases ADP Ribosyltransferase |
ADP Ribosylating toxins | Cholera toxinsDiphtheria toxins |
Cholera toxins | ribosylates to overactivate adenylate cyclasecAMP activates ion transport, water follows} uncontrollable diarrhea |
Diphtheria toxins | ribosylates elongation factor 2 <-- cell that makes proteinsDiphtheria toxin blocks ribosome function - cell dies Diphtheria toxin forms pseudomembrane over trachea |
How do pathogens survive once they enter host cell | cells ingest pathogens in phagosome - fuses with lysosomebut some pathogens secrete proteins to prevent fusion (Salmonella, Chlamydia) some pathogens mature in acidic environment (Coxiella burnetti - Q fever) |
How do pathogens survive once they enter host cell | some pathogens use hemolysin to break out and leave (Shigella dysenteriae, Listeria monocytogenes) |
VIRUSES | influenza HIV |
Influenza virus antigenic DRIFT | RNA polymerase does not correct replication errors - mutations in haemagglutinin gene |
haemagglutinin gene | forms spikes on influenza virus- helps them attach to host |
Mutation in haemagglutinin gene | allows virus to avoid immune system - virus spreadsnew vaccine needed each year |
Influenza virus antigenic SHIFT | two strains infect host at the same time (chicken or swine)recombined virus have mix of chromosomes (alters several genes) cause of 1918/1919 influenza outbreak - largest loss of life in a single year |
HIV | avoids host immunity by infecting immune cellsbinds multiple receptors for entry (CD4 & CCR-5-chemokine receptors) |
Cells infected by HIV secrete | viral protein, which misregulates other immune system cells |
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