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Microorganism that causes disease |
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Microbe that doesn’t cause disease (in normal circumstances) |
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Entry, growth, & multiplication of a microorganism in the body that leads to symptoms & impairs health (disease) |
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Entry, growth, & multiplication of a microorganism in the body that causes no apparent clinical symptoms establishment of bact colony w/in a host |
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Ability of microorganism to cause disease |
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Characteristics of a microorganism that enhance ability to cause disease |
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Infectious disease of animals that can cause disease when transmitted to humans (but not always causing symptomatic infection) |
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Habitat where pathogen lives, grows, & multiplies -humans, animals, envir |
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Rate ppl acquire infection in pop Ex. 500 cases per month |
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Death rate from infection in pop |
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Microbes residing in host |
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All microbes & combined genomes |
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Microbes w health-promoting fxns |
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Permanent residents that can cause disease via opportunistic infections |
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pathogen expressed during certain favorable conditions like antibiotic-induced dysbiosis C diff, UPEC, UTIs |
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All transmission modes + pathogen examples |
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Direct contact: -person-to-person (touching- Grp A strep & EC o157, sexual- C trachomatis & N gonorrhoeae, droplets- M TB & B pertussis, in utero- Grp B Strep & L monocytogenes) Indirect contact: -vehicle-borne (contaminated obj/substance like food- EC O157, blood- S aureus, doorknobs- Grp A strep) -airborne (suspended in air for long periods- Legionella pneumophila) -vector-borne (mechanical = direct transfer- flies w EC O157, biological = parasite inside reservoir/vector- mosquito w malaria) |
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Chain of infection: EC O157 |
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Shiga toxin, intimin, acid resistance genes Animals-> fecal contaminated food-> mouth |
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Chain of infection: Bacillus anthracis |
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Sporulation, poly-γ-d-glutamic acid capsule, edema factor, lethal factor Soil, hides, animal blood-> inhalation, intestinal, cutaneous, injection |
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Chain of infection: Clostridium difficile |
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Sporulation, flagella, surface layer proteins, polysaccharide capsule, D-alanylation of teichoic acids, hydrolytic enzymes, toxins A & B Feces-> spores on fomites-> mouth ingestion |
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Chain of infection: Grp A Strep |
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M proteins, A capsule, pyrogenic toxin human nasopharynx-> saliva, nasal secretions-> mouth or skin break |
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Chain of infection: Mycobacterium tuberculosis |
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Ag 85 complex, cord factor, KatG, SodA, glycolipid envelope, granulocma formation, tissue damage Human respir tract-> droplet spread-> mouth |
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Chain of infection: V cholerae |
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Polar flagellum, toxin coregulated pills, cadA, biofilms, cholera toxin Feces-> Contaminated water-> mouth |
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Factors that impact host susceptibility |
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Immune status Exposure lvl (ex. Crowds) Children/elderly Behaviors (needle sharing, sexual activity, ex) Pre-existing infections Genes Pathogen characteristics Malnutrition Medications (antibiotics, chemotherapy, etc) |
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Specific & nonspecific host defenses |
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Specific: acquired, protective Abs Non-specific: innate, skin, nasal hairs, coughing reflex, cilia, enzymes in saliva & tears, low pH, phagocytes, genes |
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Ways that chain of infection can be broken to prevent disease |
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Each link is required for infection, break anywhere to control disease |
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describe & draw Koch’s postulates + experiments |
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1. Suspected pathogen is present in every case of disease 2. Pathogen can be isolated & grown in pure cultures 3. Pathogen causes same disease when put in healthy host 4. Pathogen can be reisolated from now diseased host -Then, conclude that pathogen causes the disease -Shown in B anthracis from cows to mice -Shown in TB from apes, humans, & cattle to guinea pigs -VC failed bc not all healthy hosts introduced to pathogen developed disease |
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Problems w Koch’s postulates + examples |
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1. Assumes disease symptoms are completely due to microbe (autoimmune conditions, pathogen interactions) 2. Assumes bacterium can be cultured (Mycobacterium leprae) 3. assumes bact characteristcs dont change during infection or after culture (Shiga toxin-producing EC) 4. Assumes pathogens are equal in ability to cause disease (Grp A strep variation by host susceptibility & virulence) 5. Requires experimental infection to new host (need adequate animal models) -Modified to include virulence genes-> can be modified to inactivate |
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Compare/contrast infectious disease trends (outbreak, sporadic, endemic, pandemic, etc) |
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Sporadic: isolated cases that cant be linked to others Endemic: background lvl of disease in pop Outbreak/epidemic: sudden increase in frequency in specific pop > endemic lvls Pandemic: epidemics over wide geographic area affecting high proportion of pop |
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Get E from food, absorb vitamins, regulate immune sys to recognize some microbes as self, metabolize drugs, protect against disease-causing microbes |
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Factors that influence microbial composition |
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O2, pH, water, surface T, nutrients, UV exposure Age, gender, diet, drugs, immune status, genes, race, behaviors, infections, hormones, exercise, weight, climate, skin care |
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Why some microbes more common at certain sites |
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O2, pH, water, surface T, nutrients, UV exposure Diff sites = diff conditions = favorable to diff microbes |
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Why microbes diff across ppl |
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Age, gender, genes, behaviors affect microbiome |
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Diff methods to characterize microbiome |
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16S rRNA seq: variable regions dictate phyla & # of reads dictates abundance Culturing: difficult bc 20-60% microbes non-cultivable Metagenomics: random shotgun seq of DNA, includes all viruses/phage/fungi/bact, can make predictions abt fxn Transcriptomics: random shotgun RNA seq: transcriptional active genes, predictions abt fxn Mass spec: proteomics & metabolomics, which proteins of metabolites present, metabolomics is best rep of given sys bc gives picture of full spectrum of chem rxns occurring |
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How microbes can prevent pathogens from causing infection |
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Produce inhibitory molecules Nutrient deprivation Prevent colonization Limit inflammatory responses |
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How microbiome develops & changes over t |
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Microbiome changes after birth Becomes more stable by early childhood Can change w treatments, malnutrition, obesity Older indiv have more unhealthy microbiome |
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Characteristics of healthy vs diseased microbiomes |
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Healthy: balanced level of firmicutes & bacteroidetes, high diversity Unhealthy: more proteobacteria, less diversity |
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How specific factors (ex. Antibiotics) impact microbiome & pathogenesis of bacteria (ex. C. difficile) |
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Abs decrease microbiome diversity & select for resistant bact pops that can persist-> enrichment in virulence gene abundance & enhance inflammatory responses Inflammation & deletion of some symbionts allow some pathogens to invade & proliferate |
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Pili vs fimbriae vs afimbrial adhesins |
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Pili & fimbriae: rod shaped filament our proteins on cell surface -pili = longer & thicker, “hair”, tip attaches to host cell receptors, made of pilin protein -fimbriae = shorter & thinner, “thread” Afimbrial adhesins: embedded in cell surface, not long or filamentous, proteins, mediate tight binding, often used after initial attachment by pili |
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Nonspecific vs specific adherence, diff types |
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Nonspecific: reversible attachment, “docking”, attractive Fs -HPho, electrostatic, acid-base, van der waals Specific: irreversible, “anchoring”, bonds betwn complementary molecules -adhesin + receptor |
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Structure/molecule on pathogen surfaces that mediates binding to host cells |
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Molecule on host cell surface that binds to adhesin -glycoproteins or carb residues -extracellular matrix molecules |
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Pap pili & type I fimbriae Intestinal & urogenital tracts-> feces, urine, genital secretions-> sexual contact, fecal-oral, fomites-> mouth, urogenital tract |
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Type IV pili, effector proteins, intimin Intestinal tracts-> feces-> mouth |
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Chain of infection: N go off |
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Type IV pili, Opa proteins, endothelial I would Urogenital tracts-> sex & fecal-oral-> mouth/urogenital tract |
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Adherence mechs for UPEC, EPEC, N gonorrhoeae, & EC O157 |
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UPEC: pap pili assembled via chaperone usher sys in kidneys, type I fibriae in bladder EPEC: type IV pili (bundle-forming)-> type III secretion sys inserts Tir into host cells-> initimin attachment NG: Type IV pili loose-> Opa intimate O157: Intimin protein |
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Why is adhesin specificity important & what does it predict |
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Determines site of colonization (tissue tropism) & host range (host specificity) Variability in adhesin genes dictate specificity |
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How pili are assembled via chaperone usher sys, role of diff proteins |
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Ex. Pap pili, type I fimbriae Proteins thru IM via Sec sys-> chaperone brings to FimD “usher”-> adhesive FimH tip & PapG thru 1st-> FimA forms majority of shaft |
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How phase variation works in type I fimbriae |
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Regulatory switch element: fim switch is invertable DNA element w/ promoter for fimA Recombinases fimB & E bind to inverted repeat to turn fimA transcription on/off |
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Adherence strategy/steps in UPEC vs EPEC vs N gonorrhoeae |
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UPEC: diff adhesins for diff areas during movement, colon-> urethra-> type I fimbriae in bladder-> pap pili in kidneys EPEC: type IV pili attaches to host cells & other EPEC cells-> type III secretion sys inserts Tir (tranlocated intimin receptor) into host cell-> intimin attaches to tir to trigger cell rearrangements |
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Role of type IV pili in N gonorrhoeae, how assembled, retraction, twitching motility, competence |
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Attach to host epithelial cells & each other to form microcolonies Pilin proteins translocations across IM as pre-pilins-> PilD protease cleaves N-term leader seq-> mature PilE peptide released-> extension via PilQ secretion pore-> extension & retraction by ATP conversion, proteins degraded during retraction Extension/retraction results in twitching motility along a surface Upon retraction, pseudopilus in PilQ pore w/ pore connected to Com proteins that allow DNA uptake Roles: adherence, twitching motility, natural competence |
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Enzymes (proteases & transpeptidases) that recognize pilin proteins |
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Microbial surface components recognizing adhesive matrix molecules G+ pathogens (ex. S agalactiae) Surface-associated molecules covalently attached to PG by sortases (but not pili) Important for intimate attachment, invasion, & biofilms |
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Microbes growing on surfaces encased in self-secreted EPS matrix |
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Extracellular polysaccharide substance (EPS) |
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Self-secreted matrix of biofilms Composition affects conditions of biofilm & varies by pathogen |
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Biofilms of diff microbes |
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Chain of infection: Strep agalactiae |
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Pili, MSCRAMMs, capsule, hemolysin toxin Gastrointestinal & urogenital tracts-> sex, fecal-oral, placenta |
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3 routes of invasion by S agalactiae |
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Invade membrane of host cells by 1. Pl3K & Akt 2. FAK + Paxillin 3. Rho/Rac |
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Adherence mechs for S agalactiae |
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Pili loose attachment MSCRAMMs for intimate attachment |
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3 virulence factors for S agalactiae |
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Pili loose attachment MSCRAMMs intimate attachment Rho/Rac for cellular invasion Hemolysis toxin Protective capsule |
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G+: lipoteichoic acid (LTA) anchors cell wall to IM & can be used for adherence, cross-linked PG covalently linked to teichoic acid, polysaccharide capsule, “cell wall” of thick PG G-: LPS can be used for adherence, thin PG separating IM & OM |
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Adherence in G+ vs G- bact, pathogens that use chaperone-usher vs type IV pili assembly sys vs sorta set assembly sys |
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G+: pili anchored to PG, LTA can be used for adherence, pili assembly requires sortases G-: pili anchored to OM, LPS can be used for adherence, chaperone-usher assembly, & type IV assembly thru PP, type I & IV pili |
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How sortases aid in assembly & presentation of adhesins on G+ bact |
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recognize & cleave LPXTG motif & link together pilin monomers-> pilin can be anchored to PG at peptide cross-bridges SrtA: “house-keeping”, anchors proteins to cell wall SrtC: “pious-specific”, recognizes & links pilins |
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Microbial communities vs biofilms, 5 steps of biofilm formation, why there is heterogeneity in biofilms |
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loose attachmen (pioneers) (reversible)-> intimate attachment (settlers), micro colony formation (irreversible)-> signaling & aggregation (society), proliferation (EPS production, QS, channel formation)-> community, maturation-> dispersal of planktonic bact |
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Specific components of EPS in biofilms |
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Polysaccharides: major component, gel-like, alginate promotes water retention, cellulose & poly-N-acetyl glucosamine (PNAG) provide structure proteins: enzymes digest compounds for nutrients or dispersal DNA: extracellular eDNA provides structure during early formation & horiz gene transfer water, lipids Extracellular polymeric substance |
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Why biofilms important for some pathogens, examples |
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Poor Ab recognition Avoids killing by antibiotics, phagocytes, & antibacterial peptides Contains nutrients, metabolites, & water Cell-to-cell communitarian DNA exchange Switch from planktonic to biofilm is an important virulence trait Can spread to other locations Dental plaque of cavities S aureus in wounds Catheter & implant infections UPEC UTIs Enteroaggregative EC in mucus layer (EC O104:H4 is shiga toxin-producing & biofilm-forming) |
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Factors that impact composition of microbes in biofilms |
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Oxygen & nutrient gradient |
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