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Diagnosing Viral Hepatitis An Alphabet Soup

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Icterus - yellowing of the skin and the whites of the eyes ... Primary Question 'Does Mr. Johnson Have Hepatitis' ... what is causing Mr. Johnson's hepatitis. ... – PowerPoint PPT presentation

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Title: Diagnosing Viral Hepatitis An Alphabet Soup


1
Diagnosing Viral Hepatitis -An Alphabet Soup
  • Eugene G. Martin, Ph.D.Professor of Pathology
    Laboratory Medicine
  • UMDNJ Robert Wood Johnson Medical School

Based upon slides available from the CDC
2
Whats so Important about Viral Hepatitis?
  • GLOBAL PROBLEM - Estimated 350,000,000 chronic
    carriers (HBV HBC) worldwide
  • COMMON IN THE US 1990 - 4th most communicable
    disease
  • DEADLY - 1 mortality rate
  • SEQUELAE - Primary Hepatic Carcinoma
  • PREVENTABLE Types A B

3
Viral Hepatitis Lecture Goals
  • Recognize
  • Clinical lab presentation of viral hepatitis
  • The importance of epidemiology, geography,
    presentation and clinical history in assessing a
    case of hepatitis
  • The major forms of viral hepatitis
  • The significance of acute and chronic forms of
    viral hepatitis
  • How to differentiate viral hepatitis from other
    forms of hepatitis

4
Case Study Mr. William Johnson
  • 31 Year Old Electrician complaining of
  • General Malaise
  • Rash
  • Itching
  • Right Upper Quadrant Pain
  • No Appetite
  • Weight Loss
  • He has no family members reporting exposure
  • He was born in Zaire, but immigrated to the US at
    age 10

Lets begin with a series of questions First,
what additional information should you be
interested in?
5
Physical Examination
  • Well-developed young man
  • Not in acute distress
  • Positive physical findings include
  • Icterus - yellowing of the skin and the whites of
    the eyes
  • Firm, enlarged and tender liver (tender
    hepatomegaly)
  • Now
  • How typical is jaundice in a case of hepatitis?
  • What significance can one attach to the tender
    hepatomegaly?

6
Viral Hepatitis Symptomatology
Viral hepatitis is USUALLY asymptomatic and when
symptomatic USUALLY the symptoms are non-specific.
7
Differential Diagnosis Hepatitis
  • Alcoholic Hepatitis
  • Malignancy
  • Biliary tract disease
  • Viral hepatitis
  • Toxic injury to the liver
  • Ischemic injury to the liver
  • Systemic viruses with secondary effects on the
    liver e.g. CMV, Epstein Barr
  • Immunologic disorders - Autoimmune hepatitis
  • Wilsons disease

How do you begin to sort your way through this ?
8
Medications
  • He reports that his doctor recently prescribed
    Furadantin (nitrofurantoin) for treatment of an
    e.coli related urinary tract infection.

Are medications a serious consideration when
one is considering the diagnosis of hepatitis?
9
Other Questions to Think About?
  • Can you rule out any type of hepatitis based upon
    patient complaints?
  • How important is his occupation?
  • How significant is his lack of exposure to
    individuals with jaundice or a history of drug
    abuse?
  • Primary Question Does Mr. Johnson Have
    Hepatitis. If so, what is the likelihood he has
    viral hepatitis?

10
LAB TIP
  • All patients with jaundice do not necessarily
    have hepatitis and all cases of hepatitis are not
    necessarily due to viruses.

11
Bilirubin Metabolism
12
Classification of Jaundice
  • Percentage of Conjugated to Total Bilirubin
  • Increased production eg. Hemolysis
  • Impaired uptake by the liver eg. Portacaval
    shunt
  • Defective conjugation eg. ABO incompatibility
  • 20 ?
  • Commonly seen in viral or alcoholic hepatitis
  • 50 - Conjugated Hyperbilirubinemia
  • Cholestasis
  • Intrahepatic obstruction
  • Extrahepatic obstruction

13
Classic Pattern of Viral Hepatitis
  • MARKEDLY INCREASED SGOT (AST) and SGPT (ALT)
  • (10 to 100 X normal) - indicates severe
    hepatocyte damage
  • AST Originates (liver, heart, Skeletal Muscle
    and RBCs. Non-specificity issue.
  • ALT Found primarily in liver. Most elevations
    reflect liver disease.
  • Patterns
  • Both enzymes are increased to the same degree
    VIRAL HEPATITIS
  • (ASTALT, 2X) ALCOHOLIC HEPATITIS
  • A fluctuating temporal course frequently -
    HEPATITIS C
  • Increased (GGTP) ?-glutamyl transpeptidase.
    Moderate elevations.
  • Slightly increased Alkaline Phosphatase (1-3 X
    normal) indicates mild cholestasis
  • Slightly increased Lactate Dehydrogenase (LDH)
    (1-3 X normal)
  • Normal sedimentation rate and complete blood
    count (CBC)
  • Severe liver-cell necrosis MAY RESULT in
  • Decreased serum albumin,
  • Decreased serum cholesterol,
  • Prolonged prothrombin time, and
  • Serum bilirubin 25 mg/dl

14
Bilirubinuria
  • Bilirubin levels in urine
  • Hemoglobin breakdown results in bilirubin
    production (unconjugated).
  • In the liver, bilirubin is conjugated to an acid
    to make conjugated bilirubin.
  • Conjugated bilirubin is water soluble and can be
    excreted in urine.
  • Abnormal bilirubin values
  • Pre-hepatic (unconjugated DOES NOT appear in
    urine)
  • anemia's 
  • excessive breakdown of RBC
  • Hepatic
  • hepatitis
  • cirrhosis
  • obstruction of biliary duct
  • toxic liver damage
  • Post-hepatic
  • biliary tree obstruction

15
Use of Urine Chemistry
?Gut delivery of bilirubin ? less enterohepatic
return of bilinogen
OR ? hepatocyte capacity to
take up and re-excrete bilinogen
16
Staging Acute Hepatitis
  • Anicteric phase (I)
  • ? urine bilirubin
  • ? urine urobilinogen
  • ??? SGOT (AST), ??? SGPT (ALT) - level reflects
    the severity of liver damage usually precedes
    jaundice
  • ? (WBC) count with relative lymphocytosis some
    atypical lymphocytes common
  • Normal sedimentation rate

17
Staging Acute Hepatitis
  • Icteric Phase (II)
  • Majority of patients are NOT Icteric!!
  • Increased serum bilirubin (8 mg/dl - 15 mg/d) -
    rises in 10-14 days, then declines in 2-4 weeks.
  • Slightly increased serum alkaline phosphatase
    reflects mild cholestasis.
  • Decreased urine urobilinogen absent urobilinogen
    at the peak of disease.
  • Fall in SGOT (AST) and SGPT (ALT) indicates
    diminishing liver-cell necrosis.
  • Increased sedimentation rate
  • Increased serum iron reflects release from
    damaged liver cells.

18
Staging Acute Hepatitis
  • Recovery phase (III)
  • Bilirubinuria precedes disappearance of
    bilirubinemia
  • Urine urobilinogen reappears.
  • Normal sedimentation rate
  • Slight decrease in serum albumin
  • Mild elevation in ? globulin

19
Mr. Johnsons CHEMISTRY
Urine
Blood
20
Mr. Johnson - Summary
  • Albumin Low end Nrml.
  • LDH - ? 2x
  • Alk. Phos. - ? 2x
  • GGTP (862) - ? 18x
  • ALT (4200) - ??? 70x
  • AST (3488) - ??? 63x
  • AST/ALT .83
  • Mixed Hyperbilirubinemia 5.0 Conjugated/12.4
    Total ? 40 Conjugated
  • Urobilinogen - Absent
  • Urine Bilirubin -

Conclusion Consistent with Icteric HEPATITIS,
possibly one close to resolving since
bilirubinuria OFTEN precedes the disappearance of
bilirubinemia
So now we need to know what is causing Mr.
Johnsons hepatitis.
21
Screening to a serologic diagnosis
  • Biochemical alterations tell you that an
    individual has hepatitis
  • The presence or absence of a viral antigen or
    antibody indicates the type and stage of a viral
    disease
  • Ultimately, some diagnoses are based upon
    exclusion!!

22
Causes of Hepatitis
  • Non-Viral
  • Toxic Injury
  • Drug abuse ETOH
  • Anesthetics Halothane
  • Antibiotics e.g. Nitrofurantoin
  • Acetaminophen Overdose
  • Ischemic injury
  • Metabolic Disorders
  • Wilsons disease
  • Viral
  • Primary
  • Hepatitis A ? G, Sen-V
  • Secondary
  • CMV
  • Herpes Simplex
  • Epstein Barr Inf. Mono.
  • Varicella Zoster
  • Parvo B19

23
Rule Out Toxic Hepatitis
  • In toxic hepatitis, AST 3500 U/L
  • If Yes ? Consider toxic or ischemic hepatitis
  • If No ? precede to r/o viral hepatitis,
    particularly if there is no history of drug
    exposure
  • Mr. Johnson AST is 3488 which is close. In
    addition, he was treated with a drug that could
    conceivably cause a toxic hepatitis.
  • Proceed to screen for a viral hepatitis we may
    yet conclude that he has a pharmacologic hepatitis

24
Drugs and Hepatitis
  • Chronic Active Hepatitis
  • Allopurinol (Lopurin) - Anti-gout medication
  • Dantrolene sodium (Dantrium) Muscle relaxant
  • Halothane Anesthetic
  • Isonazide (INH) - TB therapy
  • Methyldopa (Aldomet) Antihypertensive
  • Methotrexate Chemotherapeutic
  • Nitrofurantoin (Furadantin) Urinary Tract
    Infections
  • Cholestatic Hepatitis
  • Chlordiazepoxide (Librium) Anti-anxiety
  • Imipramine (Tofranil) Anti-depressant
  • Nitrofurantoin (Furadantin) Urinary Tract
    Infections

25
The single biggest error
  • When a patient presents with signs and symptoms
    of an acute hepatitis
  • More than half the time, the cause is an
    undiagnosed, non-viral cause of hepatitis - a
    reaction to a chemical or pharmacologic substance
    the most common

26
Screening Results Hepatitis B
Acute or ChronicHep. B
27

Viral Hepatitis - Overview

Type of Hepatitis
A
B
C
D
E
Source of
blood/
blood/
blood/
feces
feces
virus
blood-derived
blood-derived
blood-derived
body fluids
body fluids
body fluids
Route of
percutaneous
percutaneous
percutaneous
fecal-oral
fecal-oral
transmission
permucosal
permucosal
permucosal
Chronic
no
yes
yes
yes
no
infection
Prevention
pre/post-
pre/post-
blood donor
pre/post-
ensure safe
exposure
exposure
screening
exposure
drinking
immunization
immunization
risk behavior
immunization
water
modification
risk behavior
modification
28
Estimates of Acute and Chronic DiseaseBurden for
Viral Hepatitis, United States
HAV
HBV
HCV
HDV
Acute infections
(x 1000)/year
125-200
140-320
35-180
6-13
Fulminant
deaths/year
100
150
?
35
Chronic
0
1-1.25
3.5
infections
million
million
70,000
Chronic liver disease
deaths/year
0
5,000
8-10,000
1,000
Range based on estimated annual incidence,
1984-1994.
29
Acute Viral Hepatitis by Type, United States,
1982-1993
34
47
16
Hepatitis A
Hepatitis B
Hepatitis C
3
Hepatitis Non-ABC
Source CDC Sentinel Counties Study on Viral
Hepatitis
30
HEPATITIS A VIRUS
31
HEPATITIS A VIRUS
  • RNA Picornavirus
  • Single serotype worldwide
  • Acute disease and asymptomatic infection ONLY!
  • No chronic infection
  • Protective antibodies develop in response to
    infection - confers lifelong immunity

32
  • HEPATITIS A - CLINICAL FEATURES

Jaundice by age group 6-14 yrs
40-50
14 yrs 70-80 Rare complications
Fulminant hepatitis
Cholestatic hepatitis
Relapsing
hepatitis Incubation period Average 30
days
Range 15-50 days Chronic sequelae None

33
Acute Type A Hepatitis
University Diagnostic Laboratories 1998
34
REPORTED CASES OF HEPATITIS A, UNITED STATES,
1952-2002
Frequency declining since 1996
Source NNDSS, CDC
35
Hepatitis A Incidence, United States, 1980-2002
1995 vaccine licensure
1996 ACIP recommendations
1999 ACIP recommendations
2002 rate 2.9
2002 rate provisional
36
PERSONS AT INCREASED RISK OF HEP A INFECTION
  • Men who have sex with men (MSM) 10
  • Illegal drug users 6
  • International travelers 5
  • Daycare Child or Employee 6
  • Unknown 46

37
Mr. Johnson A serology
Interpretation
Mr. Johnson has been exposed to the Hepatitis A
virus at some point in the past, but has already
recovered from this disease. Hepatitis A is not
the cause of his current illness.
38
Hepatitis B Virus
39
Hepatitis B Overview
  • Serious Causes death from liver disease in up to
    25 of those infected at birth.
  • Cancer related Liver cancer especially prevalent
    in areas of world where hepatitis B is common.
  • Disease of refugees New arrival Southeast Asian
    refugees (1 out of 2 is immune, 1 out of 7 is a
    carrier, 1 out of 3 is susceptible).
  • Preventable Safe, effective, and affordable
    vaccination is available.

40
Geographic Distribution of Chronic HBV Infection
HBsAg Prevalence
³8 - High
2-7 - Intermediate
41
Global Patterns of Chronic HBV Infection
  • High (8) 45 of global population
  • lifetime risk of infection 60
  • early childhood infections common
  • Intermediate (2-7) 43 of global population
  • lifetime risk of infection 20-60
  • infections occur in all age groups
  • Low (
  • lifetime risk of infection
  • most infections occur in adult risk groups

42
Risk Factors Associated with Reported Hepatitis
B, 1990-2000, United States
Source NNDSS/VHSP
Other Surgery, dental surgery, acupuncture,
tattoo, other percutaneous injury
43
Hepatitis B by Year, United States, 1966 - 2000
Infant immunization recommended
HBsAg screening of pregnant women recommended
Vaccine licensed
OSHA rule enacted
Adolescent Immunization recommended
Decline among MSM HCWs
Decline among injecting drug users
Source NNDSS
44
Transmission - HBV
  • Percutaneous transmission
  • Sharing of injection drug use equipment, needle
    stick injury, ear-piercing, body piercing,
    tattooing, inadequate sterilization of medical
    equipment, scarification
  • Household transmission
  • Less risk but significant can occur in settings
    such as shared toothbrushes, razors, combs,
    washcloths
  • Concentration of HBV in body fluids
  • High Blood, serum, wound exudates
  • Medium saliva, semen, and vaginal secretions
  • Low/not detectable urine, feces, sweat, tears,
    breastmilk
  • Perinatal Transplacental transmission, rare
    (2-5)
  • Sexual transmission Unprotected sex

45
Hepatitis B Clinical Features
  • Incubation period ranges from 45-180 days
  • Average is 60-90 days
  • Onset is insidious
  • Clinical illness (jaundice) olds 30-50 for 5 yrs
  • Acute case-fatality rate 0.5-1
  • Chronic infection 5
    yrs old, 2-6
  • Premature mortality fromchronic liver
    disease 15-25

46
Acute HBV Infection with Recovery
Typical Serologic Course
anti-HBe
HBeAg
Symptoms
Total anti-HBc
Titer
anti-HBs
IgM anti-HBc
HBsAg
0
4
8
12
16
20
24
28
32
36
52
100
Weeks after Exposure
47
Acute vs. Chronic Infection
  • A chronic infection may result from an inadequate
    immunologic response to the initial infection by
    the virus

48
Outcome of Hepatitis B Virus Infection by Age at
Infection
100
100
Pool of carriers in U.S. is 1-1.25 million
persons.
80
80
Chronic Infection
60
60
Symptomatic Infection ()
Chronic Infection ()
40
40
20
20
Symptomatic Infection
0
0
Birth
1-6 months
7-12 months
1-4 years
Older Children and Adults
Age at Infection
49
The presence of HBsAg indicates an ACUTE or
CHRONIC hepatitis B infection HBsAg DOES NOT
correlate with infectivity HBeAg DOES CORRELATE
with infectivity The presence of HBeAg means the
patient is infectious!!
Progression to Chronic HBV Infection
Acute (6 months)
Chronic (Years)
HBeAg
anti-HBe
HBsAg
Total anti-HBc
Titer
  • HBsAg indicates an ACUTE or CHRONIC hepatitis B
    infection
  • HBsAg DOES NOT correlate with infectivity
  • HBeAg DOES CORRELATE with infectivity
  • HBeAg means the patient is infectious!!

CHRONIC VS ACUTE ACUTE hepatitis B IgM
antibodies to Hepatitis B core antigen (HBc
IgM) CHRONIC hepatitis B infection will NOT have
HBc IgM Both will be HBsAg
IgM anti-HBc
Years
0
4
8
16
20
24
28
36
12
32
52
Weeks after Exposure
50
Mr. Johnson Serology
Interpretation
Chronic type B Hepatitis - only moderately
infection (HBeAg Negative). He has begun
seroconversion, but it is incomplete. Worries
Doe he have any risk factors which would make
Delta hepatitis a concern? If so, screen for Hep
D.
51
  • The clinician may be EASILY misled into
    thinking that the acute illness represents
    infection with hepatitis B virus rather than
    other agents whenever the HBsAg carrier state has
    not been previously recognized.
  • Robert Perillo, M.D.
  • Gastroenterology Vol. 85, No. 1

52
The Consequence
  • This Khmer woman died of hepatoma, four months
    after arriving in a refugee camp in Thailand.

53
HBV leads to liver cancer
  • Hepatocellular Carcinoma HCC
  • Epidemiologic correlation in many populations
  • Risk for HCC is 12-300 times greater in HBsAg
    persons
  • HBV DNA is incorporated into DNA of hepatoma
    cells
  • Incidence
  • Peak incidence is in 40-60 yr olds
  • In Taiwan, 1 cause of death for men 40 yrs
  • 0.25-1 million deaths/year in the world
  • Over 1500 persons die/yr in the U.S. from HCC
  • HCC is 3-4x more common in HBsAg men than women
  • 5-year survival rate for HCC is 2.3.
  • Hepatitis B vaccine is the first vaccine to
    prevent cancer.

54
Hepatitis B Prevention
  • Hepatitis B Immune Globulin (HBIG)
  • Provides temporary passive protection
  • Indicated in certain postexposure settings
  • Hepatitis B Vaccine
  • Vaccinate all children 0-18 years of age
  • Birth dose preferred
  • Vaccinate all high-risk individuals
  • Test before vaccination
  • Hepatitis B Prenatal Testing
  • Test EVERY pregnant woman during every pregnancy

55
Hepatitis C Virus Infection

Incubation period Average 6-7 weeks Range 2-26
weeks Acute illness (jaundice) Mild (
fatality rate Low Chronic infection 60-85 Chroni
c hepatitis (usually asymptomatic) 10-70
Cirrhosis
56
Serologic Pattern Acute HCV Infection with
Recovery
anti-HCV
Symptoms /-
HCV RNA
Titer
ALT
Normal
6
1
2
3
4
0
1
2
3
4
5
Years
Months
Time after Exposure
57
Serologic Pattern of Acute HCV Infection with
Progression to Chronic Infection
anti-HCV
Symptoms /-
HCV RNA
  • If youre only looking at anti-HCV you will be
    UNABLE to differentiate Acute HCV with recovery
    FROM Chronic HCV without recovery!!!

Titer
ALT
Normal
6
1
2
3
4
0
1
2
3
4
5
Years
Months
Time after Exposure
58
Hepatitis C Virus Infection, United States
  • New infections per year 1985-89 242,000
  • 2001 25,000
  • Deaths from acute liver failure Rare
  • Persons ever infected (1.8) 3.9 million
    (3.1-4.8)
  • Persons with chronic infection 2.7 million
    (2.4-3.0)
  • HCV-related chronic liver disease 40 - 60
  • Deaths from chronic disease/year 8,000-10,000
  • 95 Confidence Interval

59
Sources of Infection for Persons With Hepatitis C
Injecting drug use 60
Sexual 15
Transfusion 10 (before screening)
Occupational 4
Other 1
Unknown 10
Iatrogenic perinatal
Source Centers for Disease Control and Prevention
60
Reported Cases of Acute Hepatitis C by Selected
Risk Factors, United States, 1982-2001
Injecting Drug Used
Sexual
Health related work
Transfusion
1982-1990 based on non- A, non-B hepatitis
61
Chronic Hepatitis C Factors Promoting
Progression or Severity
  • Increased alcohol intake
  • Age 40 years at time of infection
  • HIV co-infection
  • Other
  • Male gender
  • Chronic HBV co-infection

62
Injecting Drug Use and HCV Transmission
  • Highly efficient
  • Contamination of drug paraphernalia, not just
    needles and syringes
  • Rapidly acquired after initiation
  • 30 prevalence after 3 years
  • 50 after 5 years
  • Four times more common than HIV

63
Occupational Transmission of HCV
  • Inefficient by occupational exposures
  • Average incidence 1.8 following needle stick
    from HCV-positive source
  • Associated with hollow-bore needles
  • Case reports of transmission from blood splash to
    eye one from exposure to non-intact skin
  • Prevalence 1-2 among health care workers
  • Lower than adults in the general population
  • 10 times lower than for HBV infection

64
Perinatal Transmission of HCV
  • Transmission only from women HCV-RNA positive at
    delivery
  • Average rate of infection 6
  • Higher (17) if woman co-infected with HIV
  • Role of viral titer unclear
  • No association with
  • Delivery method
  • Breastfeeding
  • Infected infants do well
  • Severe hepatitis is rare

65
Sexual Transmission of HCV
  • Occurs, but efficiency is low
  • Rare between long-term steady partners
  • Factors that facilitate transmission between
    partners unknown (e.g., viral titer)
  • Accounts for 15-20 of acute and chronic
    infections in the United States
  • Sex is a common behavior
  • Large chronic reservoir provides multiple
    opportunities for exposure to potentially
    infectious partners

66
Post-exposure Management for HCV
  • Immunoglobulin, antivirals are not recommended
    for prophylaxis
  • Follow-up after needlesticks, sharps, or mucosal
    exposures to HCV-positive blood
  • Test source for anti-HCV
  • Test worker if source anti-HCV positive
  • Anti-HCV and ALT at baseline and 4-6 months later
  • For earlier diagnosis, HCV RNA at 4-6 weeks
  • Confirm all anti-HCV results with RIBA
  • Refer infected worker to specialist for medical
    evaluation and management

67
Mr. Johnson HCV serology
Interpretation
Mr. Johnson has no evidence of exposure to
hepatitis C Hepatitis C is not likely to be the
cause of his current illness.
68
HCV Infection Testing Algorithmfor Diagnosis of
Asymptomatic Persons
STOP
Negative
Screening Test for Anti-HCV
Positive
OR
Negative
NAT for HCV RNA
RIBA for Anti-HCV
Negative
Positive
Positive
Indeterminate
STOP
Additional Laboratory Evaluation (e.g. PCR, ALT)
Medical Evaluation
Negative PCR, Normal ALT
Positive PCR, Abnormal ALT
Source MMWR 199847 (No. RR 19)
69
Medical Evaluation and Managementfor Chronic HCV
Infection
  • Assess for biochemical evidence of Chronic Liver
    Disease
  • Assess for severity of disease and possible
    treatment, according to current practice
    guidelines
  • 40-50 sustained response to antiviral
    combination therapy (peg interferon, ribavirin)
  • Vaccinate against hepatitis A
  • Counsel to reduce further harm to liver
  • Limit or abstain from alcohol

70
Hepatitis D (Delta) Virus
d antigen
HBsAg
RNA
71
(No Transcript)
72
Geographic Distribution Hepatitis Delta
Taiwan
Pacific Islands
HDV Prevalence
High
Intermediate
Low
Very Low
No Data
73
Hepatitis Delta
  • CLINICAL FEATURES
  • Coinfection
  • severe acute disease
  • low risk of chronic infection
  • Superinfection
  • usually develops chronic HDV infection
  • high risk of severe chronic liver disease
  • MODES OF TRANSMISSION
  • Percutanous exposures
  • injecting drug use
  • Permucosal exposures
  • sex contact

74
HBV HDV Co-infection Tupical Serologic Course
Symptoms
ALT Elevated
anti-HBs
Titer
IgM anti-HDV
HDV RNA
HBsAg
Total anti-HDV
Time After Exposure
75
HBV - HDV Superinfection
Typical Serologic Course
Jaundice
Symptoms
Total anti-HDV
ALT
Titer
HDV RNA
HBsAg
IgM anti-HDV
Time After Exposure
76
Mr. Johnson Delta serology
Interpretation
Mr. Johnson has evidence of chronic Hepatitis B
AND evidence of a super-infection with the Delta
Hepatitis virus. Upon further discussion, Mr.
Johnson admits that he is an intravenous drug
user. He has a high risk of serious, long term
liver disease. If you didnt look you wouldnt
know!
77
Hepatitis E Virus
78
Clinical Features Hepatitis E
  • Most outbreaks are associated with fecally
    contaminated drinking water
  • Minimal person-to-person transmission
  • U.S. cases usually have history of travel to
    HEV-endemic areas
  • Incubation Period 40 Days (range 15-60 Days)
  • Case Fatality Rate 1- 3
  • EXCEPT PREGNANT WOMEN 15-25 !!
  • Illness severity Increases with age!
  • No Chronicity

79
Hepatitis E Infection
Symptoms
ALT
IgG anti-HEV
IgM anti-HEV
Titer
Virus in stool
0
1
2
3
4
5
6
7
8
9
10
11
12
13
Time After Exposure - weeks
80
Geographic Distribution of Hepatitis E
Outbreaks or Confirmed Infection in 25 of
Sporadic Non-ABC Hepatitis
81
Hepatitis
  • The End

82
Prevention and Control Measures
  • Avoid drinking water (and beverages with ice) of
    unknown purity, uncooked shellfish, and uncooked
    fruit/vegetables not peeled or prepared by
    traveler
  • IG prepared from donors in Western countries does
    not prevent infection
  • Unknown efficacy of IG prepared from donors in
    endemic areas
  • Vaccine?

83
RISK FACTORS - HEPATITIS A, 1990-2000, UNITED
STATES
Source NNDSS/VHSP
84

Hepatitis D - Prevention
  • HBV-HDV Coinfection
  • Pre or post-exposure prophylaxis to prevent HBV
    infection
  • HBV-HDV Superinfection
  • Education to reduce risk behaviors among persons
    with chronic HBV infection
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