Hepatitis – b , d ,e INDIA epidemiology I.S.M CENTRAL CAMPUS

1. Hepatitis – B , D ,E

2. • The causes of hepatitis are varied and include viruses, bacteria,
and protozoa, as well as drugs and toxins (eg, isoniazid, carbon
tetrachloride, and ethanol). The clinical symptoms and course
of acute viral hepatitis can be similar, regardless of etiology, an
determination of a specific cause depends primarily on the use
of laboratory tests.
• Hepatitis may be caused by at least five different viruses• Non-
A, non-B hepatitis is a term previously used to identify cases of
hepatitis not due to hepatitis A or BWith the discovery of the
hepatitis viruses C, E, and G, virtually all the viral etiologies of
non-A, non-B disease can be specifically identifiedOther
viruses, such as Epstein-Barr virus and cytomegalovirus, can
also cause inflammation of the liver, but hepatitis is not the
primary disease caused by them
Hepatitis viruses

3. Number of reported hepatitis outbreaks (N = 291), by state — India, 2011–2013

4. • Hepatitis B virus is an enveloped DNA virus belonging to the family Hepadnaviridae
• The complete virion is a spherical particle that consists of an envelope around a core.
The core comprises a nucleocapsid that contains the DNA genome
• Other components of the core are a hepatitis B core antigen (HBcAg) and the
hepatitis B e antigen (HBeAg), which is a low-molecular-weight glycoprotein
• The envelope of the virus contains the hepatitis B surface antigen (HBsAg).
• Transmission
• It has become clear that the major mode of acquisition is through close personal
contact with body fluids of infected individuals
• HBsAg has been found in most body fluids, including saliva, semen, and cervical
secretions
• Under experimental conditions, as little as 0.0001 mL of infectious blood has
produced infection Transmission is therefore possible by vehicles such as
inadequately sterilized hypodermic needles or instruments used in tattooing and ear
piercing
Hepatitis B Virus

5. Number of hepatitis cases reported, number tested, and number confirmed for hepatitis A and
hepatitis E* — India, 2011–2013

6. • The clinical picture of hepatitis B is highly variable The incubation period may be as brief as 7
days or as long as 160 days (mean, approximately 10 weeks)
• Liver injury appears to occur from a cell-mediated immune system attack on HBV. Viral antigens
on the surface of infected hepatocytes are targets for cytotoxic T-cells
• Immune complexes of antibody and HBsAg can deposit in tissues and activate the immune
system, resulting in arthritis, as well as skin and kidney damage
• Patients who have immunosuppressed states, such as malnutrition, AIDS, and chronic illness,
are more likely to be asymptomatic carriers because their immune system does not attack.
• Acute hepatitis B is usually manifested by the gradual onset of fatigue, loss of appetite, nausea
and pain, and fullness in the right upper abdominal quadrant With increasing involvement of
the liver, there is increasing cholestasis and, hence, clay-colored stools, darkening of the urine,
and jaundice
• HBV can cause acute and chronic hepatitis The following are disease states caused by HBV:1)
Acute hepatitis2) Fulminant hepatitis: Severe acute hepatitis with rapid destruction of the
liver3) Chronic hepatitis :a ) Asymptomatic carrier: The carrier patient never develops
antibodies against HBsAg (anti-HBsAg) and harbors the virus without liver injury. There are an
estimated 200 million carriers of HBV in the worldb) Chronic-persistent hepatitis: The patient
has a low-grade "smoldering" hepatitisc) Chronic active hepatitis: The patient has an acute
hepatitis state that continues without the normal recovery (lasts longer than 6-12 months)
Pathogenesis and clinical
manifestation

7. • Many antigens and antibodies are simpler than they
seem, as follows:1) HBsAg: The presence of HBsAg
always means there is LIVE virus and infection, either
acute, chronic, or carrier.
• When anti-HBsAg develops, HBsAg disappears and the
patient is protected and immune .a ) HBsAg = DISEASE
(chronic or acute)b) Anti-HBsAg = IMMUNE, CURE, NO
ACTIVE DISEASE!!!
Lab Diagnosis

9. • Primary hepatocellular carcinoma: With chronic
infection the HBV DNA becomes incorporated into the
hepatocyte DNA and triggers malignant growth.
• There is a 200X increase in the risk of developing
primary hepatocellular carcinoma in HBV carriers as
compared to non carriers .
• Cirrhosis: Infection with HBV can result in permanent
liver scarring and loss of hepatocytes
Complications

10. • Administration of HBIG soon after exposure to the virus greatly reduces the
development of symptomatic disease Post exposure prophylaxis with HBIG
should be followed by active immunization with vaccine.
• Safe sex practices and avoidance of needle stick injuries or injection drug
use are approaches to diminishing the risk of hepatitis B infection
• Serologic tests on donor blood to remove HBV contaminated blood from the
donor pool
• Active immunization: The vaccine is a recombinant vaccine. The gene
coding for HBsAg is cloned in yeast and used to produce mass quantities of
HBsAg, used as vaccine. There is no risk of developing disease from the
vaccine because it contains only the surface envelope and proteins (HBsAg =
no DNA or capsid)
• The HBV vaccine is now given to all infants at birth, 2, 4, and 15 months
• It is also given as 3 injections to adolescents and high-risk adults (health
care workers, IV drug users, etc.)
Prevention

11. • Hepatitis D is found only in hepatitis B-infected persons•
• HDV uses HBsAg for assembly
• Hepatitis D virus is a small single-stranded RNA virus with
helical nucleo capsid
• Infection occurs in 2 ways:
• 1) Co-infection: HBV and HDV both are transmitted
together parenterally (IV drug use, blood transfusions,
sexual contact, etc.) and cause an acute hepatitis similar to
that caused by HBV. Antibodies to HBsAg will be protective
against both, ending the infection.
Delta Hepatitis (Hepatitis D)

12. • 2) Super infection: HDV infects a person who has chronic
HBV infection (like the 200 million worldwide HBV
carriers)This results in acute hepatitis in a patient already
chronically infected with HBV. This HDV infection is often
severe, with a higher incidence of fulminant hepatitis,
cirrhosis, and a greater mortality (5-15%)
• Diagnosis is made most commonly by demonstrating IgM
or IgG antibodies, or both, to the delta antigen in serum
IgM antibodies appear within 3 weeks of infection and
persist for several weeks. IgG antibodies persist for years.
Hepatitis D

13. • Hepatitis E is a small, single-strand, non-enveloped
RNA virus that is similar to but distinct from calici
viruses
• Transmission is by the faecal -oral route.
• Outbreaks occur after contamination of water supplies
or food. It is found in Asia, Africa and Central America.
It usually causes a self-limiting hepatitis of varying
severity
• Diagnosis is by IgM or NAAT . Infection is prevented by
hygiene measures.
Hepatitis E

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