mohsen alijani md .taums infectious diseases department
TRANSCRIPT
Mohsen alijani MD .TAUMS infectiouus diseases department
Imp
Ovre 500 million peOne out of three haOne out of three haIf not treated may eAIDS fear but more annually because ofHCC is the 2nd mosViral hepatitides areViral hepatitides areHCC risk factor(350
ortance
ople live with HBV&HCVs been in contacts been in contactnd to cirrhosis & HCCthan1.5million die
f HBV & HCVt deadly cancer
e the most prevalente the most prevalent 0000/year)
Ch i h titi iChronic hepatitis is If symptomatic mosSo it is important togroups status(IDUsg p (HBV+mothers,HBVpartners,hemodialysp yblood products,priso
tl t timostly asymptomaticstly irreversibleo recognize high risk ,Infants borne to +sexual sis pts.,those who take poners…)
AT LEAST FIVHEPATITIS
TYPE A (HAV)TYPE B (HBV)( )TYPE C (HCV)TYPE DELTA (HDVTYPE DELTA (HDVTYPE E (HEV)
VE TYPES OF VIRAL ARE RECOGNIZED
V)V)
ANNUAL INDEATH R
5 MILLION AMERI5 MILLION AMERIHCV) ARE CHRONWITH THREE FORWITH THREE FOR
MORE THAN 15,0FROM COMPLICAT
NFECTION and RATE in U. S.
CANS(0 4% HBV&1 3%CANS(0.4% HBV&1.3% NICALLY INFECTED RMS OF HEPATITISRMS OF HEPATITIS
00 DIE EACH YEAR TIONS OF HEPATITIS
ANNUAL INDEATH R
INFECTSINFECTSHAV 7,500 HBV 200,000 HCV 150,000HCV 150,000 HDV 13,000 HEV ?HEV ? - DIFFICULT T
NFECTION and RATE in U. S.
DEATH RATEDEATH RATERare
4,000 - 5,0008,000 - 10,000 8,000 10,000
TO DIAGNOSE
REGARDLESS OAGENT INVOLVAGENT INVOLVCLINICAL PICTU
ASYMPTOMATIC ANIWITHOUT JAUNDICE
MILD SYMPTOMATICCLASSIC ICTERIC INCLASSIC ICTERIC IN
WITH JAUNDICE
FULMINANT HEPATITFULMINANT HEPATIT
OF THE SPECIFIC VED A VARIABLEVED, A VARIABLE URE MAY OCCUR
ICTERIC INFECTION
C ANICTERIC INFECTIONNFECTIONNFECTION
TISTIS
DIFFERENTIAACUTE VIR
VIRAL ILLNESSES (MVIRAL ILLNESSES (MSPIROCHETAL DISE(SECONDARY SYPHIL(SECONDARY SYPHIL
RICKETTSIAL DISEADRUG INDUCED -TOSEX HORMONES) HYP)HALOTHANE, CHLORP
AL DIAGNOSIS FOR RAL HEPATITISMONONUCLEOSIS)MONONUCLEOSIS)
EASES LIS)LIS)ASES (Q FEVER)
OXIC RXN (ETOH, APAP, ERSENSITIVITY RXN -ROMAZINE, METHYLDOPA)
THREE P“CLASSIC”
PRODROMAL PHFlu like symptomsFlu-like symptoms
ICTERIC PHASE J diJaundice
CONVALESCENTRecovery
PHASES OF ” HEPATITIS
HASE
T PHASE
PRODROMPRODROM
MALAISE HEADAMALAISE, HEADAMYALGIA, ARTHFATIGABILITY
UPPER RESPIRATUPPER RESPIRATANOREXIAAVERSION TO CIGAVERSION TO CIG
MAL PHASEMAL PHASE
ACHE FEVERACHE, FEVER, HRALGIA, EASY
TORY SYMPTOMSTORY SYMPTOMS
GARETTESGARETTES
ICTERIICTERI
UPPER RIGHT QUADRAUPPER RIGHT QUADRAHEPATOMEGALYSPLENOMEGALYJAUNDICEINCREASED UROBILINO
RESULTS IN DARK URRESULTS IN DARK UR
IC PHASEIC PHASE
ANT PAINANT PAIN
OGEN -RINERINE
CONVALESCONVALES
INCREASED SENSE
RETURN OF APPET
DISAPPEARANCE ODISAPPEARANCE OABDOMINAL PAIN,
SCENT PHASESCENT PHASE
E OF WELL BEING
TITE
OF JAUNDICEOF JAUNDICE, AND TENDERNESS
LAB TLAB TAST AND AL
ELEVATION INDICATDAMAGE / NECROSIS10 TO 100 FOLD INCEXPECTEDIF ALT IS DISPROPOCOMPARED TO AST,IS MORE LIKELY THA
TESTSTESTSLT RESULTSTES HEPATIC CELL SREASE CAN BE
ORTIONATELY LOW ALCOHOLIC HEPATITIS
AN VIRAL HEPATITIS
LAB TSERUM A
PHOSPHPHOSPHEXHIBITS LITTLEEXHIBITS LITTLEIN VIRAL HEPAT
A LARGE INCREAA LARGE INCREAIMPAIRED BILE AS CHOLESTAT
TESTSALKALINE HATASEHATASEE OR NO CHANGEE OR NO CHANGE TITISASE IS SEEN INASE IS SEEN IN EXCRETION SUCH
TIC HEPATITIS
LABSERUM B
RISE AFTER OCCURRERISE AFTER OCCURRELEVELS MUST APPROAMANIFEST AS JAUNDIMANIFEST AS JAUNDI
WHY MOST CASES AREJAUNDICE OFTEN FIRSJAUNDICE OFTEN FIRSOFTEN COMPLAIN OF S
B TESTSBILIRUBIN
ENCE OF LIVER DAMAGEENCE OF LIVER DAMAGEACH 3mg/100ml TO ICEICEE ANICTERICST MANIFESTS IN SCLERAST MANIFESTS IN SCLERASEVERE ITCHING (PRURITUS)
LABBLOO
WBC COUNT MAY BWBC COUNT MAY BRELATIVE LYMPHOATYPICAL CELLS MATYPICAL CELLS M
LIKE INFECTIOUS MHIGHER THE PROTHHIGHER THE PROTHMORE SEVERE THE
B TESTSOD TESTS
BE SLIGHTLY ELEVATEDBE SLIGHTLY ELEVATEDOCYTOSISMAY BE PRESENTMAY BE PRESENT
ONONUCLEOSISHROMBIN TIME (PT) THEHROMBIN TIME (PT), THE E HEPATIC DAMAGE
HEPATITISHEPATITIS AGENT A 27nm SINGVIRUS (NO ENVELO
GENUS HEPATOVIRGENUS HEPATOVIRFAMILY PICORNAV
SPREAD MAINLY BYSPREAD MAINLY BYROUTE
SEXUAL TRANSMISSEXUAL TRANSMIS
TYPE A (HAV)TYPE A (HAV)GLE-STRANDED RNA OPE)RUS WITHIN THERUS WITHIN THE VIRIDAEY ORAL-FECALY ORAL FECAL
SION MAY OCCURSION MAY OCCUR
HH
CONDITIONS WHICONDITIONS WHISPREAD OF HAV
CROWDING, i.e. SINSTITUTIONS, DAINSTITUTIONS, DA
POOR SANITATIOCONTAMINATIONCONTAMINATION
HAVHAV
CH PROMOTECH PROMOTE :
SCHOOLS, MILITARY, AY CARE CENTERSAY CARE CENTERS
ON RESULTING IN WATER
HH
IN INFECTED INDIVIDUAIN INFECTED INDIVIDUAVIRUS IS PRESENT INBLOOD AND STOOLSBLOOD AND STOOLSDAYS BEFORE ONSET OJAUNDICEJAUNDICE
VIRUS IN STOOLS S S ODISAPPEARS BEFORE P
LIVER ENZYME ELEVATJAUNDICE ONSETJAUNDICE ONSET
HAVHAV
ALS,ALS, N S 14-21S 14 21 OF
PEAK TION OR
HHACTUAL LIVER DAMIMMUNOLOGICAL RXIMMUNOLOGICAL RXREPLICATION30 40% U S ADULT30-40% U.S. ADULTTO HAVINCUBATION PERIOINCUBATION PERIOPRODROME, IF PREMAY MIMIC INFLUENMAY MIMIC INFLUEN
HAVHAVMAGE PROBABLY A XN NOT SIMPLE VIRALXN, NOT SIMPLE VIRAL
S HAVE BEEN EXPOSEDS HAVE BEEN EXPOSED
D 15-50 DAYSD 15-50 DAYSSENT, IS SUDDEN AND
NZA OR GASTROENTERITISNZA OR GASTROENTERITIS
HHUSUALLY DISEAS
ASYMPTOMATICASYMPTOMATICADULT PATIENT W
MANIFEST JAUNDILLNESS USUALL
RECOVERY IS CONO EVIDENCE OFNO EVIDENCE OF
CARRIER STATE O
HAVHAVSE OF YOUNG, OFTEN
WILL COMMONLY DICELY SELF-LIMITING MPLETE
F CHRONIC FORM ORF CHRONIC FORM OR OF HAV
HAVHAV Usual formRelapsing hepatitis
Wks-mths after apparReccurence of symptIncrease of aminotranOccasionally jaundiceFecal excretion of HAeca e c et o o
Cholestatic hepatitisProtracted cholestaticProtracted cholestatic
variantsvariants
rent recoveryoms
nsfraseseAV
c jaundice&pruritusc jaundice&pruritus
PREVENTIONPREVENTION
WASH HANDS BEWASH HANDS BEPREPARING FOODTHE BATHROOMTHE BATHROOM, OR CLEANING SUCONTAMINATED WCONTAMINATED WDON’T EAT UNCO
SUCH AS RAW OY
N STRATEGY - HAVN STRATEGY HAV
EFORE EATING OREFORE EATING OR D, AND AFTER USING CHANGING A DIAPERCHANGING A DIAPER, RFACES
WITH FECESWITH FECESOOKED SHELLFISH, YSTERS AND CLAMS
HH
TWO-DOSE VACCINETWO DOSE VACCINE6 MONTHS APARTAVAILABLE SINCE 1994
HEALTH CARE PROVINTERNATIONAL TRINTERNATIONAL TR
INFECTION - ARE ENCOMPLETE SERIES BCOMPLETE SERIES B
HAVHAV
EE
VIDERS -RECOMMENDEDRAVELERS AT RISK FORRAVELERS AT RISK FOR
COURAGED TO HAVE BEFORE TRAVELBEFORE TRAVEL
PostexposurePostexposure
Cl l t tClose personal contact Daycare center attendee&School,hosp.workplace coFoodborne sourceFoodborne source
Within 2weeks of exp After 2weeks of expAfter 2weeks of exp.
After common source outbH b tHave begun to occur
ISG :Immunocompromised
e phx. For HAVe phx. For HAV
ISG0 02 l/k ISG0.02ml/kg&employee =ontact none
ISG0.02ml/kgNone None
break None
d,<12mth,chronic liver dis
HEPATITHEPATIT
HB VIRUS STRUCTUHB VIRUS STRUCTUCOMPLEX THAN HACLASSIFIED IN HEPCLASSIFIED IN HEP
FAMILYCAN CAUSE A WIDECAN CAUSE A WIDE
CHRONIC AND EXTRAND A CHRONIC CAAND A CHRONIC CA
TIS B (HBV)TIS B (HBV)
URALLY MOREURALLY MORE AVPADNAVIRIDAEPADNAVIRIDAE
E VARIETY OF ACUTE /E VARIETY OF ACUTE / RAHEPATIC DISEASES, ARRIER STATEARRIER STATE
HH
HBV IS SYNTHESHBV IS SYNTHESHEPATOCYTE
HBcAg MADE IN NHBsAg MADE IN C
40 - 180 DAY INCUMANY CASES AR
MOST ARE ANICT
HBVHBV
SIZED ONLY IN THESIZED ONLY IN THE
NUCLEUSCYTOPLASMUBATION PERIOD
RE SUBCLINICAL AND TERIC
WHO IS AT GFOR HBV
IV DRUG ABUSERIV DRUG ABUSERBLOOD PRODUC
ACCOUNTS FOR 5-1HEPATITIS
HEMODIALYSIS PPEOPLE FROM S
COUNTRIES (70-80
GREATEST RISKINFECTION?
RSRST RECIPIENTS0% POSTRANSFUSION
PATIENTSOUTHEAST ASIAN 0%)
WHO IS AT GFOR HBV
LAB PERSONNELLAB PERSONNELBLOOD PRODUCTSEXUALLY ACTIVPERSONS WITH
FREQUENT SEX CMEDICAL/DENTAMEDICAL/DENTA
GREATEST RISKINFECTION?
L WORKING WITHL WORKING WITH TSVE HOMOSEXUALSMULTIPLE AND
CONTACTSAL PERSONNELAL PERSONNEL
HH
LIKE HAV ACTUALIKE HAV, ACTUAPROBABLY IMMU
IMMUNE RXN TO IMMUNE RXN TO DNA POLYMERASDNA POLYMERASSERUM
HBVHBV
AL LIVER DAMAGEAL LIVER DAMAGE NOLOGICAL RXNHBcAg IN LIVERHBeAg, DANE PARTICLE,
SE AND HB A IN THESE, AND HBcAg IN THE
ExtrahepaticExtrahepatic
HBVHBVPapular acrodermSERUM SICKNESSERUM SICKNESMEMBRANOUS GPAN EMCPAN,EMC
RELATED TO CIRCOMPLEXES (HBCOMPLEXES (HB
HCV ass.with:EMC
c manifestationsc manifestations
matitis of childhoodSS-LIKE SYNDROMESS LIKE SYNDROMEGLOMERULONEPHRITIS
RCULATING IMMUNE sAg ANTI HBs)sAg, ANTI-HBs)
C,PCT,LICHEN PLANUS
cryoglocryogloobulinemiaobulinemia
Viral HepatitViral HepatitRarely
PancreatitisMyocarditisAtypical pneumoniaAplastic anemiaTransvers myelitisPeripheral neuropath
cirrhosisHepatocellular carciHepatocellular carci
tis complicationstis complications
hy
nomanoma
HH“CORE ANTIBOD
PERIOD DURING EVIDENCE OF HBONLY MARKER A
HBc TITERPATIENT IS INFE
TIMETIME
HBVHBVDY WINDOW” IS THE WHICH THERE IS NO
BsAg OR ANTI-HBsAT THIS TIME IS ANTI-
ECTIOUS DURING THIS
Acute Hepatitis B Virus Acute Hepatitis B Virus Typical SeroTypical Sero
Symptoms
HBeAg
TiterTiter
IgM HBsAg
Weeks afteWeeks afte0 4 8 12 16 20 24
Infection with RecoveryInfection with Recoverylogic Courselogic Course
anti-HBe
Total anti HBcTotal anti-HBc
anti-HBc anti-HBs
er Exposureer Exposure28 32 36 52 100
OTHER CHARAHBV IN
DISEASE OF YOUDISEASE OF YOUPARENTERALLY
MORE LIKELY TO DISEASECLINICAL ONSET
MORE INSIDIOUS WITHOUT HEADA
ACTERISTICS OF NFECTION
UNG ADULTSUNG ADULTSACQUIRED INFECTION PRODUCE CLINICAL
T SIMILAR TO HAVAND PROTRACTED
ACHE OR FEVER
CHRONICCHRONIC
CHRONIC FORMS OAND HCV INFECTION
FOR HEALTH CAREHBV CAUSES GREAHBV CAUSES GREAHAS BEEN MOST ST
C HEPATITISC HEPATITIS
OF HBV, HBV / HDV, NS ARE RECOGNIZED
E PROVIDER, CHRONIC ATEST CONCERN ANDATEST CONCERN AND TUDIED
Progression to Chronic HProgression to Chronic HTypical SeroTypical Sero
Acute(6 months)
HBeAg
TiterTiter
IgM anti
Weeks after ExposureWeeks after Exposure0 4 8 12 16 20 24 28 32 36
Hepatitis B Virus InfectionHepatitis B Virus Infectionlogic Courselogic Course
Chronic(Years)
Total anti HBc
HBsAg
g anti-HBe
Total anti-HBc
-HBc
52 Years
CHROCHRO
A CARRIER IS DEFA CARRIER IS DEFPERSISTENCE OF
CARRIERS DEVELCARRIERS DEVELAND THUS REMAIN
HAVE SUSTAINEDAND HBeAg(>3mthAND HBeAg(>3mthMore in neonates,Dhemodialysis immuhemodialysis,immu
ONIC HBVONIC HBV
FINED BY SEROLOGICFINED BY SEROLOGIC HBsAg FOR 6 MONTHS
LOP LITTLE ANTI HBLOP LITTLE ANTI-HBs N HBsAg- POSITIVE
D LEVELS OF ANTI-HBc h)h)Down syn.chronic unocompromised(HIV)unocompromised(HIV)
CHROCHROCARRIERS DEVELO
ASYMPTOMATIC SUBMORE LIKELY TO BE
THEY ARE MORE INCONTAGIOUS = GRECONTAGIOUS = GRETRANSMITTING THE
1 MILLION HBV CAR
ONIC HBVONIC HBVOPING AN
BCLINICAL INFECTION E HBsAg POSITIVEg
NFECTIOUS AND EATER RISK OFEATER RISK OF
DISEASE
RRIERS IN U.S.!
CHROCHRO
MAY BE GENETIC BMAY BE GENETIC BDEVELOPING THE C(AUTOSOMAL RECE(AUTOSOMAL RECE
GREATER SOUTHEPROGRESSION TOPROGRESSION TO AFTER ANICTERIC GREATER IN MEN TGREATER IN MEN T
ONIC HBVONIC HBV
BASIS FORBASIS FOR CARRIER STATE ESSIVE)ESSIVE)
EAST ASIANS, 3RD WORLDHBV CARRIER GREATERHBV CARRIER GREATER THAN ICTERIC INFECTION
THAN WOMENTHAN WOMEN
CHROCHROCARRIERS MAY BE
CHRONIC DISEASE“HEALTHY” CARRI
AND IS MONITOREDCHRONIC DISEASECHRONIC DISEASE
HBeAg, HBV DNA, ↑LEVELS, ↑ RISK OFLEVELS, ↑ RISK OF
TX WITH INTERFERO
ONIC HBVONIC HBVE HEALTHY OR EXHIBIT
ER ONLY HAS ↑ HBsAg gDE CARRIER HAS ↑ HBsAg,E CARRIER HAS ↑ HBsAg,
SERUM LIVER ENZYME CIRRHOSIS/HEPATOMACIRRHOSIS/HEPATOMAON ALPHA-2b
HEPATITHEPATIT
FORMERLY KNOWFORM NON-A NON30 TO 60 nm RNAFAMILY FLAVIVIRFAMILY FLAVIVIRSPREAD MAINLY
ROUTEROUTE
TIS C (HCV)TIS C (HCV)
WN AS PARENTAL N-B HEPATITISA VIRUSRIDAERIDAEY BY PARENTAL
HH
ACCOUNTS FORACCOUNTS FOR TRANSFUSION HERISK OF SEXUAL
LOWER THAN FORRISK THROUGH C
LOW
HCVHCV
90 95% OF POST90-95% OF POST EPATITISL TRANSMISSION R HBVCASUAL CONTACT
HHVERTICAL TRAN
RISK INCREASEDFOR HCV RNARISK INCREASEDPOSITIVE
OVERALL PREVAAT 1AT 1
HCVHCVNSMISSION POSSIBLED IF MOTHER IS POSITIVE
D IF MOTHER IS HIV
ALENCE ESTIMATED .4%.4%
WHO IS AT GFOR HCV
IV DRUG ABUSERSIV DRUG ABUSERSBLOOD PRODUCT
b f 1992 (ANTI HCbefore1992 (ANTI-HCGREATLY REDUCEHEMODIALYSIS PALAB PERSONNEL W
PRODUCTS
GREATEST RISKINFECTION?
S (even noninjection)S (even noninjection)RECIPIENTS CV SCREENING HASCV SCREENING HAS D RISK)
ATIENTSWORKING WITH BLOOD
WHO IS AT GFOR HCVFOR HCV
SEXUALLY ACTIVSEXUALLY ACTIVPERSONS WITH M
FREQUENT SEXUAFREQUENT SEXUAMEDICAL/DENTA
VIA NEEDLESTICKPATIENT)Infants of HCV+moHIV infected pts.HIV infected pts.Sexual partners of
GREATEST RISKINFECTION?INFECTION?
VE HOMOSEXUALSVE HOMOSEXUALSMULTIPLE AND AL CONTACTSAL CONTACTSL PERSONNEL (3-10%
K FROM INFECTED
others
f HCVab+
OTHER CHARAHCV IN
APPEARS TO BEAPPEARS TO BECELLS30 180 DAY INCU30-180 DAY INCUUP TO 80% ARE A
ASYMPTOMATICASYMPTOMATICANTI-HCV IS NOTDEVELOPDEVELOPUP TO 90% = CH
ACTERISTICS OF NFECTION
CYTOPATHIC TO LIVER CYTOPATHIC TO LIVER
UBATION PERIODUBATION PERIODANICTERIC AND
T PROTECTIVE AND SLOW TO
HRONIC CARRIERS
OTHER CHARAHCV IN
SEROLOGIC DEMSEROLOGIC DEMANTI-HCV DOES NWEEKS TO MONTWEEKS TO MONTPROVIDES A PRO
UNDETECTED WINTHE PATIENT CONINFECTIOUS
ACTERISTICS OF NFECTION
MONSTRATION OFMONSTRATION OF NOT OCCUR FOR HSHS
OLONGED NDOW DURING WHICH NTINUES TO BE
Serologic Pattern of Ai h Rwith Re
Symptoms +/Symptoms +/-
HCV RNA
Tite
r
A
Normal
0 1 2 3 4 5
Time after EMonths
Acute HCV Infection ecovery
anti-HCV
ALT
6 1 2 3 4
ExposureYears
OTHER CHARAHCV IN
CHRONIC HCV PACHRONIC HCV PAHAVE FEW CLINICDISEASEDISEASEHOWEVER, PERS
INFECTION CAN PLATER HEPATIC FHEPATOCELLULA
ACTERISTICS OF NFECTION
ATIENTS USUALLYATIENTS USUALLY CAL SIGNS OF LIVER
SISTENT VIRAL PREDISPOSE TO:FAILUREAR CARCINOMA
OTHER CHARAHCV IN
PRESENCE OF ANTIPRESENCE OF ANTI-DISTINGUISH BETWECHRONIC HCVCHRONIC HCVPOSITIVE IMMUNOGCANNOT DISCRIMINAPERSON WHO HAS RFROM ONE WHO IS A
ACTERISTICS OF NFECTION
HCV DOES NOT-HCV DOES NOT EEN ACUTE OR
GLOBULIN TEST ATE BETWEEN A RECOVERED FROM HCV A CHRONIC CARRIER
HCV NOT EASILIN HEALTHIN HEALTH
POTENTIAL TRANSMISSION RISPOTENTIAL TRANSMISSION RIS
CONC/ml PATHOGEN SERUM/PLASMAPATHOGEN SERUM/PLASMA
HBV 1000 - 100 000 000HBV 1000 - 100,000,000
HCV 10 - 1,000,000
HIV 10 - 1000
BP LANBP LAN
LY TRANSMITTED CARE SETTINGCARE SETTING
SK TO HEALTH CARE WORKERSSK TO HEALTH CARE WORKERS
TRANSMISSION RATE (%)POST NEEDLESTICK INJURYPOST NEEDLESTICK INJURY
6 0 - 30 0 6.0 - 30.0
2.7 - 6.0
0.31
NPHEAR: EPIDEMIOL REV 16:437 1994NPHEAR: EPIDEMIOL REV 16:437, 1994.
PrecautioPrecautio
N f i f t fNone for infants of mothers(including
Barrier method conmultiple sex partne
ons for HCVons for HCV
f HCV +f HCV +ve breast feeding)
ntraception only in p yers&those with STIs
CHROCHRO
2-3 MILLION CARRIE2 3 MILLION CARRIEDIAGNOSIS BASED
HCVHCVPRESENCE OF ↑ LIV
RNA INDICATES MORNA INDICATES MONATURAL PROGRE
QUITE VARIABLEQUITE VARIABLE
NIC HCVNIC HCV
ER OF HCV IN U.S.ER OF HCV IN U.S.D ON PRESENCE OF ANTI-
VER ENZYMES AND HCV RE ACTIVE DISEASERE ACTIVE DISEASE
ESSION OF CHRONIC HCV
Serologic Pattern of AcProgression to CProgression to C
Symptoms +/Symptoms +/-
HCV RNA
Tite
r
Norm
0 1 2 3 4 5
Time after EMonths
cute HCV Infection with Chronic InfectionChronic Infection
anti-HCV
ALT
mal
6 1 2 3 4
ExposureYears
CHRON
RISK OF CIRRHORISK OF HEPATOMANY PATIENTSMANY PATIENTS
INDOLENT COURSMILD CASES AREMILD CASES AREMORE ACTIVE DIS
INTERFERON ALPINTERFERON ALP
IC HCV
SIS 20-30%OMA UNDER 20%
EXPERIENCE ANEXPERIENCE AN SEE MONITOREDE MONITOREDSEASE TREATED WITH
PHA 2bPHA-2b
HEPATITHEPATIT
HIGHLY PATHOGHIGHLY PATHOGHEPATITIS (Delta)LOW MOLECULA
GENOME ENCLOSCOATED WITH HB35-37 nm DIAMET
TIS D (HDV)TIS D (HDV)
GENIC FORM OF VIRALGENIC FORM OF VIRAL
AR WEIGHT RNA SED IN PARTICLE BsAgTER
HH
IT IS A DEFECTIVIT IS A DEFECTIVNEEDS HBV TO RS O OG C SSEROLOGIC TES
EXISTS BY AVAILWORLD WIDE DIS
GREATER IN MEDLOW IN SOUTHEA
HDVHDV
VE VIRUS WHICHVE VIRUS WHICH REPLICATES OST FOR ANTI-HDAg
ABILITY LIMITEDSTRIBUTIONDITERRANEAN BASINAST ASIA
HH
HDV A i i ilHDV Ag is primarilyAntiHDV IgM in serinfection after 30-40AntiHDV (IgM&IgG)( g g )HDV infection
HDV Ag in liver&HDg
HDVHDV
i h t t l iy exp.in hepatocyte nucleirum during acute HDV 0 days) in serum during chronic ) g
DV RNA in serum&liver
HH
TRANSMISSION STRANSMISSION SPROBABLY CYTO
HEPATIC CELLSHEPATIC CELLSTWO PATTERNS
DESCRIBED (C i fDESCRIBED (Coinfe
BOTH HAVE INCRCOMPARED TO HCOMPARED TO H
HDVHDV
SIMILAR TO HBVSIMILAR TO HBVOPATHIC TO
OF INFECTION ti & S i f ti )ection & Superinfection)
REASED MORBIDITY HBVHBV
HDV INFECTHDV INFECT
COINFECTIONCOINFECTIONACUTE SIMULTANHBV AND HDVHBV AND HDVOFTEN BUT NOT IN MORE SEVEREIN MORE SEVERE SURVIVORS RAREINFECTION (< 5%)INFECTION (< 5%)CASE FATALITY RAT
TION PATTERNSTION PATTERNS
NEOUS INFECTION WITH
NECESSARILY RESULTS INFECTIONINFECTIONELY DEVELOP CHRONIC
TE 5%
HDV INFECTSUPERINFECTIONSUPERINFECTION
RESULTS IN HDV SHB A CARRIER (CHBsAg CARRIER (CCAN OCCUR ANYTDISEASEDISEASEUSUALLY RESULTPROGRESSIVE SUBPROGRESSIVE SUBHEPATITISSUBSTANTIAL INCSUBSTANTIAL INCFULMINANCY&DEAChronic HDV :greatChronic HDV :greatmortality 2times mo
TION PATTERNSNNSUPERINFECTION IN AN CHRONIC HBV)CHRONIC HBV)TIME DURING CHRONIC
TS IN RAPIDLY BACUTE OR CHRONICBACUTE OR CHRONIC
REASE INREASE IN ATH RATE#20%ter risk of HCC 3times &ter risk of HCC 3times & ore than chronic HBV
Anti HDVtesH
S &f l i t hSevere &fulminant he
Chronic HBV with acu
Multiple percutaneous
In endemic areas for
sting in pts with HBV
titiepatitis
ute exacerbation
s exposure
HDV
HEPATITHEPATIT
FORMERLY KNOWFORMERLY KNOWOF NON-A NON-B UNCLASSIFIED VENDEMIC TO Sou
ASIA, FORMER SOAND MEXICO (None
NO SEROLOGIC T
TIS E (HEV)TIS E (HEV)
WN AS ENTERIC FORMWN AS ENTERIC FORM HEPATITIS
VIRUSuthEast AND CENTRAL OVIET UNION, AFRICA e in US)
TEST AVAILABLE
HH
INFECTION FOLLOWINFECTION FOLLOWHAV INFECTION6 8 WEEK INCUBAT6 - 8 WEEK INCUBATFECAL-ORAL ( water
TRANSMISSIONTRANSMISSIONMILD CLINICAL COUFATALITY RATE APP
WOMEN IN 3RD TRIM
HEVHEV
WS PATTERN SIMILAR TOWS PATTERN SIMILAR TO
TION PERIODTION PERIODr/food borne)
URSE (MORTALITY < 1%)
PROACHES 20% FOR MESTER OF PREGNANCY
FULMINAHEP
RARE AND OCCURSRARE AND OCCURSICTERIC HEPATITIS ISEVERE, PROGRES
OF VIRAL HEPATITISCAUSES EXTENSIVE
NECROSIS
ANT VIRAL ATITIS
S IN LESS THAN 1% OFS IN LESS THAN 1% OF INFECTIONS
SSIVE MANIFESTATION SE LIVER CELL
Poor prognosPoor prognos
Hi hHigher agesSerious underlying Early presenting sig
AscitesPeripheral edemaHepatic encephalopHepatic encephalop
stic signs in HBVstic signs in HBV
diseasegns of:
pathypathy
Severe hepatoneeding
Hi h PTHigh PTLow AlbLow glucoseVery high BilirubinVery high Bilirubin
ocellular disease admission:
FULMINANTFULMINANT
LIVER MAY SUDDENLIVER MAY SUDDEN
MARKED ↑ IN PROTTHAT DOES NOT IMPTHAT DOES NOT IMP
FATALITY APPROAO
IF THEY SURVIVE, RCHRONIC DISEASECHRONIC DISEASE
VIRAL HEPATITISVIRAL HEPATITIS
NLY BECOME SMALLERNLY BECOME SMALLER
THROMBIN TIME (PT), PROVE WITH VITAMIN KPROVE WITH VITAMIN K
ACHES 80%C S 80%
RARELY DEVELOPS
PREVENTIOIMMUNOPR
ACTIVE IMMUNITACTIVE IMMUNITBY STIMULATINGPROTECTION AFTPROTECTION AFTLONG-TERM IMM
CAN BE ACCOMPACTUALLY HAVINSUCCESSFUL IMM
ON THROUGH ROPHYLAXIS
TYTYG OWN IMMUNE RESPONSETER LATENT PERIODTER LATENT PERIODUNITY IS PROVIDEDPLISHED BY:NG DISEASEMUNIZATION
PREVENTIOIMMUNOPR
PASSIVE IMMUNITYPASSIVE IMMUNITYTRANSFERRING PREFROM AN IMMUNIZEDFROM AN IMMUNIZEDNEED OF IMMUNITYPROTECTION IS TRAPROTECTION IS TRAIMMEDIATE
INJECTION OF IMMUINJECTION OF IMMU
ON THROUGH ROPHYLAXIS
YYEFORMED ANTIBODIES D HOST TO A PERSON IND HOST TO A PERSON IN
ANSITORY BUT ONSET ISANSITORY, BUT ONSET IS
UNE GLOBULIN (HBIG)UNE GLOBULIN (HBIG)
HEPATITISHEPATITIS
PLASMA DERIVEPLASMA-DERIVEHEPTAVAX-BTHREE SEPARATINTRAMUSCULARFIRST TWO 1 MOFIRST TWO 1 MOTHIRD AT 6 MONT96% YOUNG ADU96% YOUNG ADU
S B VACCINES B VACCINE
ED VACCINEED VACCINE
TE 20- µg R INJECTIONSONTH APART AND THEONTH APART AND THE THSLTS SEROCONVERTLTS SEROCONVERT
HEPATITISHEPATITISRECOMBINANT D
RECOMBIVAX HBENGERIX - B
PRODUCED BY RTECHNOLOGY USTECHNOLOGY USSEROCONVERT
20-29 YEARS OLD20-29 YEARS OLDResponse rate30-55% 75% >90%55%,75%,>90%res
S B VACCINES B VACCINEDNA VACCINESB
RECOMBINANT DNA SING YEASTSING YEAST99% HEALTHY ADULT
DD-
t l i 3 dspectevly in 3 doses
DecreaseDecrease
A 40Age over 40Renal faliureHIV infectionDiabetesDiabetesChronic liver diseasOb itObesitysmoking
ed responseed response
se
VaccDOSE&I
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cination INTERVAL
oid) at 0-2,1-4,4-6mthshronic suppresed pts,:40mcg(2ml)
years
HEPATITISBOTH PROTECT A
HEPATITIS
HEPATITIS B, ASYMCARRIER STATE, ASEROLOGIC TEST
AFTER COMPLETINDIFFERENTIATE THAND FAIL TO RESP90-95% EFFECTIVE
S B VACCINEAGAINST ACTIVE
S B VACCINE
MPTOMATIC HBV, THE AND HDVTING WITHIN 6 MONTHS NG SERIES CAN HOSE THAT RESPOND POND TO VACCINEENESS
HEPATITISHEPATITIS
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VACCINE NON-RESUSCEPTIBLE TO RESPONDER WITDETECTABLE ANTPROTECTED AGA
S B VACCINES B VACCINE
O IS NEGATIVE FORO IS NEGATIVE FOR EN 1-5 YEARS AFTER
AN BE:AN BE:ESPONDER AND STILL
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POST-TPOST T
NEED POST TESNEED POST TESOF COMPLETING GGREATER THAN
DIFFICULT TO INTREVACCINATION
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TESTINGTESTING
ST WITHIN 6 MONTHSST WITHIN 6 MONTHS PRIMARY SERIES6 O S S S 6 MONTHS RESULTS
TERPRET N IS SUCCESSFUL FOR RS ~ 50%
ANTIBODY AND BO
70% WHO DEVEO70% WHO DEVEOMAINTAIN DETECT7 YEARS (S7 YEARS (Some sayTHOSE THAT RES
DETECTABLE ANTDEMONSTRATED ANAMNESTIC RES
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SPONSE
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CDC REVIEWING DCDC REVIEWING DBOOSTER DOSERECOMMEND TITERECOMMEND TITETO DATE, NO ONE
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R DRAWN (HbSAb)R DRAWN (HbSAb)WHO HAS RECEIVED A
CCINECCINE, DEVELOPED ANTI-
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HEPATITISHEPATITIS
2 VACCINES HA2 VACCINES - HABOTH DERIVED F
HAVSTIMULATE IMMU
PRODUCE ANTIBO
S A VACCINES A VACCINE
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UNE SYSTEM TO ODIES TO THE VIRUS
HEPATITISHEPATITIS
GIVEN IN DELTOIGIVEN IN DELTOITWO DOSES - SE
MONTHS TO 1 YEADOSEFULL COURSE - C100% OF PATIENTNO GUIDELINES F
S A VACCINES A VACCINE
D MUSCLED MUSCLEECOND ONE GIVEN 6 AR AFTER THE FIRST
CONFERS IMMUNITY IN TSFOR BOOSTERS YET
PREVENTIHBVHBV
PRACTICE SAFE SPRACTICE SAFE SCLEAN BLOOD SPILDON’T SHARE RAZ
NAIL CLIPPERS or NWHEN GETTING A MA
HAVING A BODY PARTTHE INSTRUMENTS AR
ION STRATEGY -V HCV HDVV, HCV, HDV
EXEXLLS WITH BLEACHZORS, TOOTHBRUSHES, NEEDLESANICURE, TATTOO, or T PIERCED, MAKE SURE ,RE STERILE
PREVENTIONPREVENTION
WHEN TRAVELING:WHEN TRAVELING:DRINK ONLY BOILEDTREATED WATER (THTREATED WATER (TH
DON’T EAT UNCOOKEUNCOOKED FRUITS andUNCOOKED FRUITS andHAVEN’T BEEN PEELEDDON’T SWIM OR BATHDON T SWIM OR BATHCONTAMINATED WATE
STRATEGY - HEVSTRATEGY HEV
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D SHELLFISH or d VEGTABLES THATd VEGTABLES THAT
DE IN POTENTIALLYE IN POTENTIALLY
ER
INCUBATIINCUBATI
HAV - 15 - 45 DAYHBV - 45 - 180 DAHCV - 14 - 180 DAHCV 14 180 DAHDV - 45 - 180 DAHEV 15 60 DAYHEV - 15 - 60 DAY
ION PERIODION PERIOD
AVERAGE
YS 30 DAYS
AYS 60-90 DAYS
AYS 56 DAYSAYS 56 DAYS
AYSYSYS 40 DAYS
ONON
HAV - ABHBV - INHBV INHCV - INHDV - ABHDV ABHEV - AB
NSETNSET
BRUPT NSIDIOUSNSIDIOUSNSIDIOUSBRUPTBRUPTBRUPT
CHRONICHRONI
HAV - DOES NOT DEVEHBV - CHILDREN UND
AGE ABOVE 5 HCV - 85% OR GREATHDV - DEVELOPS MOS
SUPERINFEHEV –only in solid
IC DISEASEIC DISEASE
ELOPDER 5 - 20 - 50% 5 - 10%
TERST OFTEN WHEN HDV IS A
ECTIONorgan transplant pts
CONCLRECOMM
p BEST APPRp BEST APPRGOOD BARRIGOOD BARRIPREVENTION UNIVERSAL P
LUSIONS /MENDATIONSROACHROACH
ER TECHNIQUESER TECHNIQUESWITH VACCINATION
PRECAUTIONS
سپاسگزارم شما حوصلهه شما سپاسگزارمه و صبر از صبر و حوصلهاز
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