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HEPATITIS vS- —> REPATITIS A WRUS (HAY) + There is neihing tile Cuepatotroric) HEPATITIS B viRUT (HEY) Hepatitis ¢ virus, but werAtits © wiRUSs (HU) HEPATITIS G yIRUS HEPATITIS D virus (HY) exists | HEPATITIS € viRUS (HEV) — DTWMER anmuses C cause HEfatITiC =~ incidental MARouRG V- LAssA PeveR U- Epstein Gare Vv. (sy) cmv Le HeePés Viruses sv (2a) VZv Coxsacue v- (ricordavinus) Merstes v. 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Virus multiplies in the GIT + SPREADS vin BOD Jo [Hiren L infeck MEPATOCYTES ---» Attacked by % celle ImmuN€ RESPONSE = ———> ee INITIALLY | 1-3 weeus OF : | Fevea LATER “Aworexia 4 (ureconG PRotection ) ~ al DAYS “wun — “Vomiting MO CARRIER/GROMC srATE “Taunue 9 MO RSW GF HEPATOCEWUAQ Ca- a mostry ASYMPTOMATIC 7 RESOINE MosTLy in 2-H WEERS Laea : i SEROLOLY MAINSTAY OF DX- 7 Tym Ab agains} wav | eush 774 fold fin Taq Dy ce cucrure =: lt ic the OULY CULTIUAGLE WiAUS > not done for routiene diagno ris a IMP ENTYME © DNA POLYMERASE DNA. dependent Rwa - dependent DNA POLYMERASE Reverse TRAWSERIPTALE + 4 GENES in GENOME . l SS 1 L L x THouaHT To ‘i . PLAY A Role for DNA for Core SURFACE Ag WSx protein ATION + » (el Powmeeasé * (HBs ag / Activates viRM RNA (eng) & AusTRALIA ) reccont (ong) “PP — Mensenify S wmacivane pS Awticen protein * e@° microscopy of serum of infected people :- t ‘ + t OV- few 420m @ one @ spreres Vik ions FRAMENTS (22 nm) Crvu wauses) / (2 am uside) . PANE PARTICLES Mucn More in = wave dua (infectious) AUMBER THAN DANE PARTICLES = AOTH of THESE Consti TUTE Aerae > DOESNT HAVE DA (Mot-1ecctious) + TPTLERFS RENAMENTS _ 1000 Ratio oF . DANE PARTICLES a Heche =» Bon NUELEOCAPSID Crone) Lo poesnt appear on seavm RAmoRE Assticens Weeny —» SOLweEtE A CPRECORE) -» RELEASED Frovn INFECTED CELLE » ANTIGENS =F ULSI of Hae vives 2 SEROTYPE = 3 Ags ft ¢t common GRovP Q PMIRE oF TYPE-SPECIFIC "t am A 2 a 1 REACTIVE "4 5 + dla w/e oe (Y) in wa A cevobeper : ad t+ in Eumore, AUSTRALIA .AmeRICA (rich areas) L ads +, worth & West INoiA imuusaelty aye 4+ SoutH & cart indiA depends on ‘o" Sux ankgen ( ONLY WATURAL HOsts - MAN ~ No AnimaAt REeERVOIR \ — (0 Genotypes (AT) > MODE Of INFECTION: F t t + @ trenshu" op @ Sexual @ pea @ Pereutansoug inFecked blood & intercourse o Risk oF INFEC™ AE TER, blood prod: weeoue STICK ingURy uBv | 2e/- > TRANSPLACENTAL transmission is VERY RARE! crew | 3 / ~ no evidence of transmiss” eceuas durin breast? aw | 3 > PERMUATAL TRansmiss 0) feeding be duning NaOGINAL Dettveny nes Ag carrier + Wy > 90-/- Ly determined be Haag) 4" Hoe Ag ® moter TRANSMIT v to easy Perinatal transmission : LMF inigeetian ty | enrriées = 7? 10 -15-f HAV | HBV] ew HOV ueév onti MBe a mothers transmit’ u' (3) + +tt - + 5 +e GASY max CARRIERS: people ¢ detectable HBs Ag in serum fox 6 monster Ce) 4 3-10 7: ADuLts ( canter x _! ) + 20-7 of KIDS state fra, = WW */- NEONATES v v CIMPLE CARRIERS < SUPER CARRIERS . With TIME | in bectivity > TRE GF HBs Ag Ty Anti- HBc Ab : Ad agains+ cove " C nee ne) + Oppears wittuin 1-2 weeks after appearance of HGsng A LASTS FOR 3-6 Months > inntiauy (acute fRecemt inseec!) : Tym anti HBe gemote wvpec™ : i anti 4Bc t Anti- HBs Ab: appears on disappecmance of HB 2 by Protective Ab u only MARKER @® in waccinaten peores tworearive oF Recovery /tmmunats/ wos wy Anti -HBe Ab: cad appears z disappearance of He A br INDUATES Low ImFectiMITy 2 L viger Repre™ Wy Hev-pnA * bs @ QUANTITATIVE IOICATOR OF HBV REPLICATION IN HEPATOYTES pin Des Z panewss] i) F wmv PEQOD = Time bj disappearance st Bs 4 and appearance of Anti nBs A a (yeaa | 4 | + cha, a - Acute HBV infec” iW ingfect + * + Tg 4 a - CHRONIC HOV infect 4 iehectiy * _ T] 4 - +/- | curowic wav inte” ty TCENARIOS > inf 5 carrier - +/- Tym = +|- UNNDOW PERIGD - - y4 4]- +/- | oro/eemote nev - - oS + — VACCINATED > non-infeetrour 4 infectious presi domains Sem « M protein \ My + «—___— $ protein 10 ~<— L protein core protein partially ds DNA 42 nm Incubation Prodrome, Convalescence period acute disease Early Late HBsAg Anti- Anti-HBs HBsAg} (anti-HBc) | HBc (anti-HBc) n i 1 1 1 1 1 1 0 1 2 3 4 5 6 7 8 DNA polymerase Pee —) at uk a ee HBV particles f Anti-HBc / windew period wo Ant H@e Ab @ >>¥7> HBsAg Anti HBe Ab @ Titer —> Equivalence zone (window period) a -® Anti-HBe 0 1 2 3 4 5 6 7 8 Months after exposure W» Tie |: neuce WEY = Ay ANTIVIAAL THERAPY cnromie WV : TeNofoulR & Tasivudine [ooe] TéwofoviR & emtRicitARine: for wiv-Hev coinfee* be ofw AL eeathons : Vascuuitis Maiw cause oF Aatnaatcin ESSENTIAL mixed Purpura CRrocweuLinemire mPa (aes) T> seavioay > Ab by cLish (194) L Ns 3 ard geo cuca ws 4 aT specificity Cab againel) ws S a t TLL cove a m tveafter & weees of tneec Ty RECOMAMANT IMmUNDBLOT A ASSAY (RIGA) » based on WESTERN Biot L, not done now Ty cv cove Ag ASSAY : Ly less expencive %& ke consuming. than HCV -RNA PCR my MAOLECULAR MetHODS : 7 Real time RT - PER eee DIRECT ACTING ANTIVIRAL Acemts = Hos- pereetive viRNUS | + dependant on uBv for Reeucation . since it doesnt have qe fo make itr envelope + 4 SERDTYPE 3 NO ANIMAL RESERVaR + MOOES OF TRANCMISSION = 4 € T [Becuary [Pio RIT pRopucTs (Pie IWATALYY + v pers. octuas ina patent already infec” simnultanrously infeed = HOV = wav & HDV Course GRAVE COURSE “MILDER CovRse 7 Fchances of preg: to fulm. Heoaritit & chronic infec" Dx- 44 anti HBe gm ant HBC + + igm anh HOV Tyra ant HOY Ge : WDv = ———» IFN . boas be ZOONOTIC PATHOLEN I N> ouneys > TRANSMISSION : FAECO- ORALLY plas 2 cif: ~ to HAV a CFR: 1-2] but 10-20) in PREGNANT/ EXPECTANT motkeRs *CHARACTERISTic Fearune uw CHOLESTASIS Seen \ > recently classified under Hepeviruc farm (wesembtes caveivieus) > Wo canter / CHRomic STATE > No Awtiviene tf - Be]: Igm anti nev Ceusa) > Funvivigus (Like tev’) L, alse known at © GB- virus ‘¢* + unlike oll other vivur : it doesnt come ese] chronic HEPATITIS 7 ROLE NOT UNDERSTOOD FULLY | —~ FLAT, UNSEGMENTEP BODY ( CEstopes ——» FLAT, SEGMENTED BOPY) ~/ © SEXES ARE SEPARATE in SCHISTOSOMES [scwrstosomes are dioecious] Fluuet whose ooulk worms vetide in diver bile dutt/ BOTH —~ 2 imMP-UVER Fruces r + FASCIOLA HEPATICA CLONORGHIe SINENSIS FASCTOLA HEPATICA => Ms. COMMON LIVER FLUKE a fs) Steer LIVER FLUKE Disease : Fasciounsis | :zoonohe ds. + RESIDENCE : < ox Bie suc = DH: SHEEP) HUMANS a — wy: sth: swat att. WATERPLANTS L have qt METACERCARIAE LARVAL ~ MODE OF INFECTION: INGESTION of AMUATIc WATERPLANITS & wipe evere containing METACERCARIA 4 METACERCARIA exeuptt in duodenum ‘ immature fuke enter RILIRRY DUCTS & become Apuits | ' OPERCULATED CEG , rane Faeces ON ENTERING WATER 7 ee) Ye 60%490 + BILE STAINED * OVAL SHAPED é 50Lm_« yemBrvo NATED S MIRACIDIUM LARVA ESCAPES OUT | minacipium inaetted ey swan (52H) EouS EMBRYONATE in WATER Sponocyst ist aeNeRY REDIA J and gener” REDIR 4 CeRcARIA FREC SWIMMING CERCARIA escare en SNAIL inte 1,0 wan { we ENCYSTATION — f eaten 4 on AQUATIC snece VEGETATION Ppatnocenesis & c/F P. 2 FeW DAYS To Few MoNnTHS T ACUTE DISEASE = 1-2 WEEKS ofter iMEec™ (auaing MIGRATION of 4 METACERCARIAE ) * EevER, * RIGHT UPPER QUADRANT PRIN +H mecary 7 ADULTS stay in Common Bre: duct Cor Panc- Duct) of Lumans * etuer domethe animals Cou) L EGC) . FLASK -SHAPED E44 DETECTED in: - EASTERN ASIA - CHINA Ant: -\——— opereutum © - KOREA )) . 2 ——> noe - JAPAN Post™ oxo ¥ BILE -STAINED - 4SiAR GG Du > Humans awe: 8: snpits infective form : METACERCARIA LARUAE an. sich MoM GE INFECTION : ingestion of Heh COTM metacercaniag Larvae ENCYSTED in the SCALES OF THE FISH, —_— Bie BY —, metacercaRia = wy excy sis in / DuUcPENUM ADULTS WORM in BNE DUCT Life cycle of CLoNoRcHis (ané ru) rorRAcIDIUM CERCARIA PENETRATES into SLALES hatches in midgut of sna) of Fisn & DEVELOP into METACERCARIA \ FREE SWITHINING ceacanig een RED a deny Rein cebcaria Patnouenesis 4 Cir » b worm purdin : ASYMPtomMaATic + ® worm burden / chronic infec’ . + CHOLANGITIS 2 DILATION OF BILE DUETS . 3° . Clonerchis : e-g- of CARCINOG Ewe + Gite OUcT canciNomA/ sinensis worm p . uu! CHOLANGIOCARCI NOMA occuss evpeney People c 1° SCLEROSTANG (are) CHOLANGITIS Z SPECIMENS © FAECES , BlovD Ey) FAECES mx: TO Loox FOR EGaS wy Abs in SERUM: ty €usa TH 49 Arde” in SeRUM = by ELISA Ly INMitATes ACUTE INFECTION yY PER : | mmuLTiPLex PCR [bee ] : Genet avantec> IM PORTANT Notes + Amoebic Trophoroites are only found in LAST FEW DROPS OF PUS since the mgoniem MULTIPLIES IN THE WALL of ABSCESS. COMPUCATIONS OF AMoEGIC [7 ABSCESS : ) RiGUT SIDED LiveR ABSCESS may vuphur may vupture inte PLEURA exhan +o SKIN Amoesie Pulmonary Gronuloma cubs PLEDRITIS amoebiasis | co TROPHOTOITES ® in SPUTUM » RUPTURE Of ARSCESS BELOW THE DIAPHRACIY) + 4 SUGPHRENIC ABSCEMS + GENERALIZED PERITONITIS xy Leet sipen [27 nascess J may RUPTURE INTO a I Stomach eet PERICARDIAL (amvebic PLEURA cau poricnadity) 4 HEMATOLENOUS SPREAD can occur jem 7 afjecting : Lunas ? SPLEEN BRAIN Kion i] LAB DIAGNoss oF AMOEBIC [7 ABSCESC 7 MuURoCcory oF PUS: can deteLt trophozeites (nod tysts ) b onty as/- SensiTwlt7 4p SToor curturRe: — how sensi fvily C4ar¥-) L GOLO STANDARD a > Aq DETECTION : - Lectin oA In sea - Lectin vi) in Laver pus 4 Ab detechon: - CLS - Indiveet how. agatustr! poss wen - UF apter cuRE aC} 1 FT cannot dujjerentiot yew RECENT & OLD ingee” sy PER af pus otpirated py CS ~ loo-/ specificity - 10 -100'f Sensitnt? > HPE: Trophersites in put con be shoum ra BRE stains «q PAS stan — Bright pint trophoroites im Green hacwaround Treatment] - METRONIDAZOLE / TiNIDA OLE 
