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Microbiology 101 Week 9 Lecture Notes

by: Isabel Markowski

Microbiology 101 Week 9 Lecture Notes 101.0

Marketplace > University of Wisconsin - Madison > Microbiology > 101.0 > Microbiology 101 Week 9 Lecture Notes
Isabel Markowski
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Here are the compiled notes for week 9 Microbiology lectures! Topics include human and microbe associations, pathogens, and specific pathogen examples.
General Microbiology
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This 8 page Class Notes was uploaded by Isabel Markowski on Friday November 13, 2015. The Class Notes belongs to 101.0 at University of Wisconsin - Madison taught by a professor in Fall 2015. Since its upload, it has received 40 views. For similar materials see General Microbiology in Microbiology at University of Wisconsin - Madison.


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Date Created: 11/13/15
Microbiology101Week9 LectureNotes  Termites o Use microbesforfooddegradation o Feedonwood,freshplants,fungi,orsoil o Complexhindgutmicrobialcommunityforcellulosedegradation o SomemicrobesalsofixNforhosts o Cellulyticmicrobesmaybebacteriaorprotists  Large populationofacetogens:useCO2ase-acceptorand Has e- donor(like methanogens),butreduceittoAcetate(shortchainfattyacid =food/nutrients foranimal)  Cellulose-degradingprotozoa(protist)withintermite  Containbacterialandarchaealsymbiontswithinprotist  IntracellularbacteriafixNforhosts  N-fixingbacteriahelptermites Microbes and Humans Human-MicrobeAssociations  “Commensals” o Commensals=Thenormalhuman microbiota o Calledcommensals,butnowmaybemutualists(discoveringbenefits) o Somemay causedisease(commensalpathogens)  Pathogens:cause disease o PrimaryPathogens:causedisease–healthypeople o OpportunisticPathogens:causedisease–peoplewithcompromisedhealth o May colonizeasymptomatically  Outcomedeterminedbymicrobialgenetics,humandiversity,andenvironmentalfactors Normal Microbiota  Humans= colonizedbymicrobesforlife  1885: TheodorEscherichisolated“BacillusColi”frominfantfeces(initiallylabeledasnormal “flora”)  The Human MicrobiomeProject o Establishedtostudymicrobiota o Try to answerquestions(whatmicrobes=commoninhealthpeople,howdoesitvary overlifetime/people,etc.) What Microbes Where on us?  Bacteria(mostly)  Majorsites: o Only4-6of 55 phylaofbacteriaon humans o Skin o But diversitywithin4-6phyla o Oral tract o Firmicutes o Upperrespiratorytract o Actinobacteria Gram+ o Gastrointestinaltract o Bacteroidetes o Urogenitaltract o Proteobacteria Gram-  ExternalEpithelia  Archaea o Epithelialtissue:coversallsurfaces o Methanogens:oraltract, GI tract of tissues o Ammoniaoxidizers:skin o Wherethemicrobeslive  Fungi(Fewspeciesonskin,oral,GItract) o Antimicrobialfunctions(immune  Protists (FewspeciesonGItract) activity,mucussecretionin  Animals(Helminths(worms)andmites) mucosalsurfaces,rapidturnover  Viruses(thehumanvirome) of cells) o Highpopulationofresident microbes How do we acquire ourmicrobes?  Microbe-freesites: o Internalorgans,tissues  Traditional: initialmicrobiotafrombirth(mother) o Centralnervoussystem  Changesas mature o Circulatorysystem(blood,lymph)  Relativelystableonceadult  Elderly=differentcommunitythanadult Rolesof Microbiota  Nutritional o Fooddigestion/vitaminprovision  Barrier o Physical o Colonizationresistance o Reinforcehostepithelialbarrierfunctions  Immune o Educatingimmunesystem  Community o Alterhostsurfacesandfunctions o Interactwithothermicrobes Howdowe knowaboutnormal microbiota?  Usingmodelsystems:germ-freeanimals(ex:mice) o Takeconventional,germmice(healthy) Germ-free/Sterilemice(lesshealthy?)  Gnotobiotic:knownbiota o Addspecificmicrobiotatogerm-freeanimal(knowexactmicroorganisms) o Lesshealthy healthier?  Dysbiosis:disruptionofnormalmicrobiotamaycause disease(vs.infectionfrompathogen) o Emergingconcept o “OldFriendsHypothesis”  Many commonmoderndiseases=partlydueto microbiotachange  Rapidincreaseinmetabolicandimmunediseasesinindustrializedsocieties Pathogens  GermTheoryof Disease o Invisibleorganismscausedisease o 1600: Frascatoro proposed“contagium”bygerms o 1835: Bassiidentified“crust”ascauseof silkwormdisease,canbetransmittedto healthyworms o Was initiallyrejected o 1884: RobertKoch  Linkedspecificmicrobestospecificdisease(proved/developedGermTheory)  ShiftinperspectiveofGermTheory  CreatedKoch’sPostulates(identifynewmicrobialdiseases) o Koch’s Postulates 1. Microbemust befound–allcases ofdisease,butabsentfromhealthy populations 2. Microbe– isolatedfromdiseasedhostandgrown–pureculture 3. Whenmicrobe=introducedintohealthyhost,samediseaseoccurs 4. Samestrainof microbe=obtainedfromnewlydiseasedhost o Koch’sPostulatesstillused–definepathogenandassociateddisease o May havetoadjustpostulates(somemicrobescan’tbegrowninpureculture,require multiplehosts,onlyhumanhosts,etc.)  Viruses:difficulttofollowpostulatesb/ccan neverhavepurecultureofvirus (mustmodifypostulates)  Infectiousdisease–globalimportance o 25% deathsworldwide=dueto infectiousdiseases  Majorpathogens:bacteria,viruses,protists,helminths o Notfungi(stillcausedisease,butnotmajorworldwide) Whatis disease?  Colonization:Microbeslivingonyou(termusedforcommensals)  Infection:Microbeslivingonyou(usedforpathogens)  Disease:damage/injury–impairsfunction  CarrierState: colonization/infectionwithoutdisease  Pathogen:ability–causedamage(disease)  Virulence:Quantitativemeasureofseverityofdisease  VirulenceFactor: feature–contributestovirulence(ex:toxins,capsules,LPS,pili,degradative enzymes)  Attenuated:Pathogen–lostabilitytocausedisease(formerpathogen) o Importantroleinvaccines The Disease Cycle 1. Exposure to pathogens 2. Adherence to skin/mucosa 3. Invasion through epithelium 4. Colonization and Growth Reservoir Furxpersu(Production of virulence factors) Toxins Invasiveness (local/systemiceffects) (furthergrowthat originalanddistantsites) Transmission Tissuedamage (disease)  Reservoir o Sitewherepathogencanreside/remainviable&fromwhichinfectioncanoccur 1. Soil,plants, water  Can surviveinfree-livingstate  InfectionoflivinghostNOTrequired  Ex: Clostridiumtetani(livesinsoil) 2. Animals(besideshumans)–zoonosis  Largestcategory  Pathogenforthat animalORcarriedcommensallyw/osymptoms  Humans= usuallyincidentalhosts  Transmittedtous through:directcontact,contactwithanimal products (meat,milk,droppings,fur),transmissionbyvector  Ex: AIDS,influenza,plague 3. Humans only  Most pathogensdon’tproducesymptomsinallinfectedpeople (asymptomatic)  Carriers:maintain/transmitpathogenbefore/aftersymptomsappear  Chroniccarriers:maintain/transmitpathogenforlongperiods  General:highercarrierrateforpathogens(keepusaliveforreservoir)  Ex: smallpox,poliovirus,typhoidfever 4. Hospital:nosocomialinfections  Uniqueenvironment(susceptiblepeople,movementofhealthcarepersonnel patient-to-patient,invasiveprocedures,antibiotics)  Oftendifferentsetofpathogens/diseasesthanincommunity  Now:healthcareassociatedinfections(notjusthospitals)  Transmission Indirect Direct Indirect viaVector  Persontoperson  Bodilysecretions(sneezing,  Vector:livingorganismthatisintermediary blood,saliva,urine,feces,etc.)  MechanicalVector:movesmicrobespottospot(ex:  Directskincontact flies)  Intimateperson-personcontact  BiologicalVector:microbecanreplicate (STI:sexuallytransmitted o Sometimes=essentialpartofmicrobiallife infections) cycle o Ex: ticks,fleas,mosquitos Indirect viaFomites  Fomite:inanimateobject–can transmitdisease  Ex: kitchenutensils,bedding,pens,hones,etc.and surfaces:doorknobs,tables,etc.  Pathogenintroducedtofomitebyinfectedperson  Mmust beableto surviveextendedperiodsoutside host(endospores,fungi,etc.)somoredifficultfor pathogens Ex: Staphylococcus Aureus Indirect viaFood  Reservoir: Humans  Foodharbors pathogens  Gram + firmicute o Alreadyinfoodorintroducedduring  Virulence: toxins (proteins) processing  Grows in wide range of conditions o Introducedduringprep(oftenhandler)  Contaminatedbyfoodhandler,growsinfood o In waterused–cook/prepareutensils  Secretes Staphylococcal Enterotoxins (toxins  Food Intoxication – stable to temperatures and pH’s) o Microbesgrow infood, notbody o Are superantigens: activate immune o Microbesproducetoxininfood,thenperson system ingestsfood  Rapid onset, usually quickly resolved  FoodborneInfection o Microbesinfood o Personingestsfood,thenmicrobesgrow in Ex: Listeria Monocytogenes body  Reservoir:soil,plants  Gram + Firmicute Indirect viaWater  Transmission:foodcontamination  Psychrotolerant(grows– normal  Waterharborspathogens temperatures,butalsocaninlowtemp.s o Alreadyinwater (fridge)) o Fecal-OralRoute:Introducedbyinfected  Virulence:generallyonlyseriousin individual,notremovedbeforenextperson compromisedindividuals  DomesticWater(drinking,cooking,bathing)  Ability–cross epithelial/cellularbarriers o Waterpurification/wastetreatment and entertissues(canbedangerous:brain,  RecreationalWater fetus) o “natural”water:microbesnaturallyinlakes  Listeriosis:presentinfood,butgrow/spread o Artificialwater:ponds,hottubs,spas,etc. in body  Adhesionand Colonization o Adhesion:Canbeveryspecificforhostand microbe(lock&key)  Determines:hostrangeandtissuesaffected o Colonization:persistenceandgrowthat site  Growth inHost o Access propersite (crossepithelialbarrierorcross cellularbarrier–intracellular) o Growth  Replication(initialdosenotusuallysufficient)  Neednutrients o Avoid Immunesystem  Many anti-immunefunctions o Manyproduce toxins(molecule:damage/killcell)  Killedcellsreleasenutrients&can’tcontrolpathogens  Exotoxins:secretedproteins(proteins=most commontoxin)  Many differentpossiblefunctions  Can alsobepeptides,smallmolecules,LPS,peptidoglycanfragments,etc.  Endotoxins:LPS(lipopolysaccharide–makesupouterhalfof outermembraneof gram- microbes)  Heat stable,releasedupondisruptionofcellenvelope  Interactswithimmunesystem:inducefever,activateclottingfactors, activatecomplement(proteinsystem),causevasodilation  Sepsisanddeathmayresult o Produce DegradativeEnzymes(causedamage/promoteinvasion)  Attack hostECM (extracellularmatrix)orcellmembranes,facilitateinvasion,and nutrientaccess  Collagenase,nuclease,lipase,sialidase/neuraminidase,protease,hyaluronidase o Bacterial “effectorproteins”  Effectorproteins:proteinsdirectlyinjectedbyTypeIIIorTypeIV secretionsystem  Directlydeliveredtotargetcell,proteinsdisrupthostcellfunctions Specific Pathogens CommensalPathogenExample: Helicobacterpylon  Gram- Proteobacterium  Reservoir:humans  Transmission:directcontact  Siteof colonization:stomach;50% world’spopulation(most=asymptomatic)  Virulence:survivalinstomach o Productionofadhesions,toxins,anddegradativeenzymes  VirulenceFactors o BabA &HpaA:adhesions o VacA,NAP,&CagA:toxins o Urease:producesammoniaandcarbonatefrom urea(degradativeenzyme)  Causesulcersandstomach cancer o Diseasesnotthoughttobemicrobialcouldinfact bemicrobial o Now:manymore diseasethought–havemicrobialcomponent PrimaryPathogen Example:Corynebacteriumdiptheriae  Gram+ Firmicute  Reservoir:humans  Transmission:directcontact w/ respiratorysecretions  Siteof colonization:upperresp.tract, skin  Disease o Diphtheria o Asymptomaticinfection  Virulence:diphtheriatoxin(inblood) o An ABtoxin(A= active,B= binding) o Bbindsto acellsurfaceprotein(HB-EGF) o A subunitmodifiesEF-2,essentialforproteinsynthesis o A singleAsubunitcankillcell OpportunisticPathogen Example:PsuedomonasAeruginosa  Gram- Proteobacterium  Reservoir:soil  Transmission:directcontact (wounds),inhalation  Siteof colonization:skin,lungs  Rangeof susceptiblehosts o Burn victims,cysticfibrosispatients,nosocomial  Virulence:Capsule,toxins,degradativeenzymes,effectorproteins


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