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Medfools Bacteriology a la chart for the USMLE I

Bacteriology a la chart for the USMLE IAdapted from notes from UCLA., with additional corny mnemonics Staphylococcus aureus (virulent) (nonmotile, nonsporeforming, facultative anaerobe) Gm+ cocciDiseasesCharacteristicsHabitat/Tran smissionPathogenesisDiagnosisTreatmentPr evention*Skin infections:impetigo, cellulitis,erysipelas, abcess,furuncle, carbuncle*Bacteremia/sepsis:hematogenous spread*Acute endocarditis:DESTRUCTIVE (compareto )*Pneumonia damagingprocess, cavitations,empyema, effusions*Osteomyelitis/septicarthritis- hematogenousand traumatic spread*Food poisoning 1-8 hronset, vomiting, preformedtoxin*Tox shock syndrome-fever, vomiting, diarrhea,diffuse erythematous rashGm + cocci ingrapes/clustersCatalase +coagulase +Ubiquitous inenvironment; normalflora of skin/noseSpread through lesions,fomitesEnterotoxin- vomiting,diarrhea, heat resistant,(actually released in gut)TSST-1 tampon use,wounds, superantigenExfoliatin- scalded skinTISSUE SPREAD:Alpha toxin(lechthinase)-ski

www.medfools.com 1 Medfools Bacteriology a la chart for the USMLE I Adapted from notes from UCLA., with additional corny mnemonics Staphylococcus aureus (virulent) (nonmotile, nonsporeforming, facultative anaerobe) Gm+ cocciDiseases Characteristics Habitat/Transmission Pathogenesis Diagnosis Treatment Prevention

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Transcription of Medfools Bacteriology a la chart for the USMLE I

1 Bacteriology a la chart for the USMLE IAdapted from notes from UCLA., with additional corny mnemonics Staphylococcus aureus (virulent) (nonmotile, nonsporeforming, facultative anaerobe) Gm+ cocciDiseasesCharacteristicsHabitat/Tran smissionPathogenesisDiagnosisTreatmentPr evention*Skin infections:impetigo, cellulitis,erysipelas, abcess,furuncle, carbuncle*Bacteremia/sepsis:hematogenous spread*Acute endocarditis:DESTRUCTIVE (compareto )*Pneumonia damagingprocess, cavitations,empyema, effusions*Osteomyelitis/septicarthritis- hematogenousand traumatic spread*Food poisoning 1-8 hronset, vomiting, preformedtoxin*Tox shock syndrome-fever, vomiting, diarrhea,diffuse erythematous rashGm + cocci ingrapes/clustersCatalase +coagulase +Ubiquitous inenvironment; normalflora of skin/noseSpread through lesions,fomitesEnterotoxin- vomiting,diarrhea, heat resistant,(actually released in gut)TSST-1 tampon use,wounds, superantigenExfoliatin- scalded skinTISSUE SPREAD:Alpha toxin(lechthinase)-skin necrosis.

2 HemolysisHyaluronidase- degradesproteoglycansFibrinolysin- lysis fibrinclotsIMMUNE EVASION:Protein A- binds IgG-Fc,blocks opsonization andcomplement fixationCoagulase- activatesprothrombinHemolysin- destroysRBCs, PMNs, M0s,plateletsLeukocidin- destroysWBCsGm + cocci in grapes,Catalase differentiatesfrom Strep. : Betahemolysis, coagulase,Yellow (Au) pigment(coagulase causescoagulation!)Coagulase neg:S. epidermidis:novobiocin sensitive sensitive skin S. saprophyticus:Novobiocin resistantBeta lactamaseproduction iscommon! Usemethicillin,nafcillin,dicloxacillinMR SA-vancomycinnoneS. epidermitis: associated w/ IV catheters, damaged/prosthetic heart valves: INSIDIOUS onset, Nosocomial, LESS culture ContaminantS.

3 Saprophyticus: Community acquired UTI in young viridans (GABHS) (nonmotile, nonsporeforming) Gm+ cocciDiseasesCharacteristicsHabitat/Tran smissionPathogenesisDiagnosisTreatmentPr evention*Pharyngitis- strep throat ,erythema, tonsillar exudate, fever*Skin/soft tissue infections-impetigo, cellulitis, necrotizingfascitis*Scarlet fever- centrifugal, redrash, erythrogenic toxin, slap cheek,strawberry tongue*Tox shock syndrome- clinicallylike Staph TSS*Rheumatic fcver- fever,myocarditis, polyarthritis, chorea,subcutaneous nodules, erythemamarginatum rash. Mitral valvedisease follows pharyngitis, NOTskin infections. Abs vs. bacteriacross react w/ joint and heartantigens*Acute GN- hypertension,hematuria, edema of both pharyngitis AND skininfections.

4 Cross reactive antigensdeposited in + cocci inchains or pairsBeta-hemolytic areclassified byLancefield groups(A,B,D) accordingto C-carbohydratesHuman throat/skin,Transmission byrespiratory dropletsHyaluronidase- degradesproteoglycans (TISSUE SPREAD)Erythrogenic toxin-scarlet fever, 0- results inbeta hemolysis, target ofASO antibodiesM protein- antibodytarget, but inhibitscomplement/phagocytosisStreptoki nase- convertsplasminogen to plasmin,dissolves fibrin clotsIgA protease HE S an MSI All Strep areCatalase Beta hemolysisand Bacitracinsensitivity point toGABHS, esp withinc. ASO topreventrheumaticfever. PenicillinDOES NOTtreat post strepdisease agalactiae (Group B strep)Neonatal menigitis, sepsispneumoniaBeta-hemolyticFemale urinary tractS.

5 Faecalis (enterococcus)Subacute endocarditis, UTI Oh crap! I ve got Heartproblems! Not hemolyticGI tractGrows in NaClS. bovis (group D)UTINot hemolyticGI tractHydrolyze esculin in presence ofbile. NOT grow in bileS. pneumoniae (pneumococcus)Lobar pneumonia, ADULT meningitis, URI (kids)Alpha-hemolyticNasopharynx85 different capsularpolysaccaridesQuellung rxn23 valent vaccine, forAIDS, elderly, asplenicsS. Mutans , mitis (Viridans group)Subacute endocarditis, (Chocolate agar, Oxidase +, kedney bean shape) Gm- cocciN. meningitidis (meningococcus)DiseasesCharacteristicsHa bitat/TransmissionPathogenesisDiagnosisT reatmentPrevention*Meningococcemia- fever,arthralgias, myalgias,petechial rash, inc.

6 Inpeople w/ complementdeficiencies*meningitis- fever,headache, stiff neck,photophobia, inCSF* Waterhouse-Friedrichsen- fever,purpura, DIC, adrenalinsufficiency due tobilateral adrenalhemorrhage, shock, death(like a badmeningococcemia)Gm cocci ,chocolate agarAirborne droplets,colonized nasopharynx,establishes carrier statesin somePolysaccharide capsule,endotoxin (LPS),IgA proteaseCapsular polysaccharidesare antigenic serve asmarkers for maltosePresumptive diagnosisby Gm stain ofpetechiae or CSFLATEX agglutinationtest b/c capsularpolysaccharidesPenicillin orCeftriaxone(G3)Chemoprophylaxiswith Rifampin(excreted intosaliva)Polysaccharidevaccine in gonnorhoeae (gonnococcus) (most common notifiable disease in US)Males- symptomaticdysuria, penile dischargeb/c of urethritis.

7 Leads toepididymitis, prostatitis,urethral stricturesFemale- asymptomatic,vaginal discharge,dyspareunia, due tocervicitis, Infertility, PID,ectopic, tubo-ovarianabcess, perihepatitis (Fitz-Hugh-Curtis syndrome),opthalmia neonatorumBoth: Septic arthritisNO CAPSULEGm cocci ,chocolate agarSexual transmissionOFTEN coexistent WITHC hlamydia ANDS yphilllis (tx w/tetracycline orchloramphenacol) Pili/fimbriae(ANTIGENIC variation)LPSOMPsIgA proteaseNO CAPSULE!Men: Gm diplococciin PMNs Does NOT fermentmaltoseNo serologic testing, nocapsule!Ceftriaxone(G3) commonErythromycineye drops innewborns (alsoprotects )No : bacterial meningitis: 0-6 months (Group B Strep, , Listeria); 6 months 3 years ( B), 3-15 years (N.)

8 Meningitidis), >15 years (S. pneumoniae) (Anaerobic, spore-forming, with Exotoxin) Gm+ RodsC. tetaniDiseasesCharacteristicsHabitat/Tra nsmissionPathogenesisDiagnosisTreatmentP reventionTetanus tetany, risussardonicus joker smile ,exaggerated reflexes,respiratory failureSpores, ubiquitous insoil, enter wounds andgerminate in anaerobicenvironment of necrotictissueTetanus toxin travelsintra axonally to CNS,blocks release ofinhibitory glycineneurotransmitter Penicillin,ventilatorysupport, musclerelaxantsTetanus immuneglobulin,preformed IgTetanustoxoid(formaldehydetreated tox)C. botulinumBotulism flaccid paralysis ,descending weakness, diplopia,flaccid paralysis, resp botulism- spores towounds, germinate, release toxinInfant botulism- ingestion ofspores in honey- floppy babySpores, in soil,inadequate sterilizationof canned veggies,smoked toxin ingestedpreformed.

9 Tox spreadsin blood, to nerves blocksAch RELEASE Toxin can be used to Txtorticollis, blepharospasmAntitoxin,ventilatory supportNOPENICILLIN!!Will burst cellsand release toxinWatch swollencans!C. perfingensGas gangrene (myonecrosis):war wounds, septic abortionsFood poisoning- ingestion ofcooking resistant spores infoods. Watery diarrhea,cramps, little vomitingResults increpitus- gasproduction andHemolysisNormal flora of colonand vaginaAlpha tox- lecithinasedegrades cell membranes-hemolyticMorphology,exudate smears,culture, sugarfermentation,organic acidproductionDebridement, O2gas, PenicillinC. difficileAntibiotic associatedpseudomembranous colitis- espin hospitalized pts. Normal flora in 3% ofpeopleSuppression of normalflora allows overgrowth,usually by clindamycin,ampicillin,cephalosporins Exotox A (severediarrheaExotox B (damage tocolonic mucosa)ID C-diff tox instoolMetronidazole-poorly absorbedorally, inc.)

10 (Aerobic, spore-forming, with Exotoxin) Gm+ RodsB. anthracisDiseasesCharacteristicsHabitat/ TransmissionPathogenesisDiagnosisTreatme ntPreventionWoolsorter s disease-pulmonary anthrax, pneumoniaLarge w/ squareends, nonmotileCommon in infected byspores on animalproducts (skins/hides)Transmission throughskin, GI tract, respiratorytractAntiphagocytic capsulemade of d-glutamate[only one w/ Aminoacids!] (not apolysaccharide)Tripartite anthraxtoxin: protectiveantigen, lethal factor,edema factor. Protectivefactor andblood agar ofanimalproducts, andvaccination (protectiveantigen) forhumans at riskB. cereusVomiting with 4 hr incubationperiod (like )- heatstable toxin-- Distinguishedfrom B.


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