hepatitis b and d
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Transcript of hepatitis b and d
Co infection
HEPATITIS B and DASHLY ALEX
HARISREE
HEPATITIS B
DNA Virus
Hepadnaviridae class
Hepatitis B virus is 100 times more infectiouss than HIV
virus
TRANSMISSION
• Vertical transmission : from mother to child in utero during
parturition or soon after birth is the usual means of
transmission world wide .
• It is related to the replicative state of the mother .
• 90% HbeAg + or 30% HbeAg -.
• HBV is not transmitted by breast feeding .
• Horizontal transmission :occurs particularly in children via
minor abrasions or close contact with other children .
• HBVcan survive on household articles eg toys ,tooth brushes
for prolonged periods.
• Inravenous route (infected blood or blood product
,contaminated needles etc )
• Close personal (sexual intercourse ).
• Virus can be found in semen saliva and vaginal fluids .
Clinical presentation
• Acute Hepatis B:
Loss of apetite
Nausea
Vomiting
Body aches
Dark urine
Jaundice
Ichy skin
Fulminant hepatic failure may arise. infection may be
entirely asymptomatic and may go unrecognized .
• Chronic hep B:
Asymptomatic
Or associated with chronic inflammation of liver .
• Extra hepatic manefestations are seen in 1-10 % of patients
• Serum sickness like syndrome .
• Rashes (urticaria or maculopapular rash )
• Polyarteritis nodusa
• Membranous glomerulonephritis
•
• Incubation period ranges from 45-180 days, average is
60-90 days
Onset is insidious
• Clinical illness (jaundice): <10% for <5 yr olds
30%-50% for >5 yrs
• Acute case-fatality rate: 0.5%-1%
• Chronic infection: <5 yrs old, 30%-90%
>5 yrs old, 2%-6%
• Premature mortality from chronic liver disease: 15%-25%
Pathogenesis
• Hbv virons (dane particles)bind to the host cell via preS domain of
the viral surface antigen and are internalized by endocytosis .
• preS and IgA are accused of this interaction .
• HBV preS receptors are primarily expressed on hepatocytes .
• During HBV inf the host immune response cause both
hepatocellular and viral clearence .
• Adaptive immune response ,particulary virus specific cytotoxic T
lymphocytes,contributes to most of the liver injury associated with
HBV infection .by antiviral cytokines.
Investigations
• LFT s
• Serological
• ANTIGENS :
HBsAg
HBeAg
HBV DNA
ANTIBODIES :
Anti –HBs
Anti –HBc
Anti -HBe
• Goals of Treatment in Children
Suppression of viral replication
Seroconversion from e Ag to e Ab
Reduction in long-term sequelae of
HBV-associated liver disease
TREATMENT
• Approved Antiviral Agents
• – Lamivudine*
• – Adefovir dipivoxil
• – Interferon alfa*
• – Entecavir
• – Pegylated interferon
• – Telbivud
Treatment
• Alfa interferons were the first drug approved in US for
the treatment of chronic hep B
Prevention
• Pregnant women should be tested for HBsAg during an early
prenatal visit.
• Failing that, they should be tested when admitted for delivery.
• Some women who are HBsAg-positive are treated
with lamivudine or telbivudine during the 3rd trimester, which
may prevent perinatal transmission of HBV.
Prevention
• Neonates whose mothers are HBsAg-positive should be
given 1 dose of HBIG 0.5 mL IM within 12 h of birth.
• Recombinant HBV vaccine should be given IM in a
series of 3 doses, as is recommended for all infants in the
US.) The first dose is given concurrently with HBIG but
at a different site.
• The 2nd dose is given at 1 to 2 mo, and the 3rd dose is
given 6 mo after the first.
HEPATITIS D – An Introduction
• Caused by Hepatitis Delta Virus – a defective RNA virus.
• HDV requires the help of a hepadnavirus like hepatitis
B virus (HBV) for its own replication.
• HDV is transmitted percutaneously or sexually
through contact with infected blood or blood products.
Who is at risk for
infection?
• Chronic HBV carriers are at risk for infection with HDV.
• Individuals who are not infected with HBV, and have not
been immunized against HBV, are at risk of infection
with HBV with simultaneous or subsequent infection
with HDV.
Where is HDV a problem
globally?
• The hepatitis delta virus is present worldwide and in all
age groups.
• Its distribution parallels that of HBV infection, although
with different prevalence rates.
• The natural reservoir of hdv is man.
When is a HDV infection
life-threatening?
• HDV infection of chronically infected HBV-carriers may
lead to fulminant acute hepatitis or severe chronic active
hepatitis, often progressing to cirrhosis.
• Chronic hepatitis D may also lead to the development of
hepatocellular carcinoma.
Why is there no treatment
for the disease?
• Hepatitis D is a viral disease, and as such, antibiotics are
of no value in the treatment of the infection.
• There is no hyperimmune D globulin available for pre- or
postexposure prophylaxis.
• Disease conditions may occasionally improve with
administration of a-interferon.
• Liver transplantation may be considered for cases
of fulminant acute and end-stage chronic hepatitis D.
THE DISEASE
An HDV infection absolutely requires an associated HBV
infection.
• Coinfection of HBV and HDV :
• results in both acute type B and acute type D hepatitis.
• The incubation period depends on the HBV titre of the
infecting inoculum.
• Coinfections of HBV and HDV are usually acute, self-
limited infections
• In patients with acute, self-limiting infection,
convalescence begins with the disappearance of clinical
symptoms.
• Superinfection of HBV and HDV
• causes a generally severe acute hepatitis with short
incubation time that leads to chronic type D hepatitis in
up to 80% of cases.
• associated with fulminant acute hepatitis and severe
chronic active hepatitis, often progressive to cirrhosis.
• During the acute phase of HDV infection, synthesis of
both HBsAg and HBV DNA are inhibited until the HDV
infection is cleared.
• Fulminant viral hepatitis is rare, but still about 10 times
more common in hepatitis D than in other types of viral
hepatitis.
• It is characterized by hepatic encephalopathy showing
changes in personality, disturbances in sleep, confusion
and difficulty concentrating, abnormal behavior,
somnolence and coma.
• The mortality rate of fulminant hepatitis D reaches 80%.
• Liver transplantation is indicated.
• Chronic viral hepatitis D is usually initiated by a
clinically apparent acute infection.
• Symptoms are less severe than in acute hepatitis, and
while serum ALT and AST levels are elevated, bilirubin
and albumin levels and prothrombin time may be normal.
• In chronic hepatitis D, the HBV markers are usually
suppressed.
• Progression to cirrhosis usually takes 5 - 10 yrs, but it can
appear 2 years after onset of infection.
• Hepatocellular carcinoma (HCC) occurs in chronically
infected HDV patients with advanced liver disease.
• There are 3 phases of chronic hep D :
a) an early active phase with active HDV replication and
suppression of HBV,
b) a second moderately active one with decreasing HDV and
reactivating HBV,
c) a third late one with development of cirrhosis and
hepatocellular carcinoma caused by replication of either virus or
with remission resulting from marked reduction of both viruses
• The mortality rate for HDV infections lies between 2%
and 20%, values that are ten times higher than for
hepatitis B.
Diagnosis
• Hepatitis D should be considered in any individual who is
HBsAg positive or has evidence of recent HBV infection.
• Total anti-HDV are detected by commercially available
radioimmunoassay (RIA) or enzyme immunoassay (EIA)
kits.
• The method of choice for the diagnosis of ongoing HDV
infection should be RT-PCR, which can detect 10 to 100
copies of the HDV genome in infected serum.
• Each of the markers of HDV infection, including IgM and
IgG antibodies, disappears within months after recovery.
• In contrast, in chronic hepatitis D, HDV RNA, HDAg,
and IgM and IgG anti-HD antibodies persist.
Host immune response
• Both humoral and cellular immunity are induced in
patients infected with HDV.
• Anti-HD antibodies do not always persist after acute
infection is cleared.
• The serological evidence of past HDV infection is
therefore not easy to demonstrate.
Risk groups
• Intravenous drug users using HDV-contaminated
injection needles
• Promiscuous homosexual and heterosexual groups
(although HDV infections are less frequent than HBV or
HIV infections)
• People exposed to unscreened blood or blood products
• Haemophiliacs
• Persons with clotting factor disorders
Treatment
• For infected patients, massive doses of a-interferon (9
million units three times a week for 12 months or 5
million units daily for up to 12 months) have yielded
remissions, but most patients remained positive for HDV
RNA despite the improved disease conditions.
• Liver transplantation has been helpful for treating
fulminant acute and end-stage chronic hepatitis.
Guidelines for epidemic
measures
1.) When two or more cases occur in association with some
common exposure, a search for additional cases should be
conducted.
2.) Introduction of strict aseptic techniques. If a plasma
derivative like antihaemophilic factor, fibrinogen, pooled plasma
or thrombin is implicated, the lot should be withdrawn from use.
3.) Tracing of all recipients of the same lot in search for
additional cases.