The document provides an overview of viral hepatitis, particularly focusing on hepatitis B, including its causes, transmission, and clinical presentation. It outlines the prevalence of HBV infection globally and in Uganda, transmission routes, and the natural history of the disease, as well as diagnostic approaches and treatment categories based on disease severity. Preventative control measures and treatment goals are also emphasized, highlighting the importance of early diagnosis and vaccination.

1. Viral Hepatitis
Chelangat k. Ivan
MCO MSFH
Feb. 2024

2. INTRODUCTION
• Hepatitis is the inflammation of the liver,
• Hepatitis can be caused by viruses, bacteria and non infectious agents such as
toxins dugs and alcohol.
• Viral hepatitis is the inflammation of the liver caused by viruses
• The commonest causes of viral hepatitis include one of the five hetero types; A,
B, C, D, and E.
• Other viruses include CMV,HSV, EBV, Adenovirus, yellow fever viruses among
others.
• Hepatitis A and E viruses usually cause acute infections which are self limiting
• HBV and HCV infections may progress to chronic infections with long term
complications such as liver cirrhosis, liver failure and HCC
• HDV only exists in the presence of HBV

3. Hepatitis B
• Hepatitis B infection is caused by hepatitis B virus (HBV), an
enveloped DNA virus that infects the liver, causing hepatocellular
necrosis and inflammation.
• HBV infection can be either acute or chronic
• Associated illness ranges in severity from asymptomatic to
symptomatic, progressive disease
• Chronic hepatitis B (CHB) – Defined as persistence of HBsAg for
6months ore more - is a major public health concern

5. HBsAg
• Nucleocapsid is 27 nm surrounded by am outer envelope of the
surface protein (HBsAg) embedded in membranous lipid derived from
host cell
• It indicates current Hepatitis B Infection
• POSITIVE HBsAg tests can be due to recent vaccination but this
positivity is unlikely to persist beyond 14 days post-vaccination.
• It is present in sera of patients with viral hepatitis B (with or without
clinical symptoms).

6. HBcAg
• HBcAg (core antigen) is an an Hepatitis B viral protein.
• Its an indicator of active viral replication.
• This means the person infected with hepatitis B can likely
transmit the virus on to another person.
• HBcAg IS NOT SECRETED (does not circulate in blood).
• It is readily detected in hepatocytes after biopsy
• The presence of both HBcAg and HBeAg proteins together
acts as a marker of viral replication, and antibodies to these
antigens are markers of declining replication(anti-HBcAg &
anti-HBeAg).

7. HBeAg
•Can be found between icosahedral nucleocapsid core and
lipid envelope
•Its an indicator of active viral replication ; this means that the
person infected with hepatitis B can likely transmit the virus
on to another person
•HBeAg is secreted and accumulates in serum
•The presence of HBeAg in the serum of patients can serve as
marker of active replication in chronic hepatitis.

8. Prevalence of HBV infection
• About 2 billion people in the world are exposed to HBV
infection and majority of which live in sub-Saharan Africa
and southeast Asia.
• Globally 257 million people are living with chronic HBV
infection.
• In Uganda it is estimated that 4.1% of the population aged
15-64 years has chronic HBV infection (UPHIA, 2016);
• The prevalence vary in regions being highest in north and
lowest in south west.

9. Hepatitis B Transmission
• Endemic Countries
• Vertical transmission (in
utero, birth, breast feeding)
• Early childhood, close
interpersonal contact
(infected blood)
• Unsterilized medical
equipment
• Unprotected penetrative sex
• Blood transfusion
• Injection drug abuse
• Instruments used for
tattooing's/piercings/razor
• Needle stick
• Rarely – toothbrush
NOT contaminated food/water, sharing Clothes,
food/water/utensils or greeting, Kissing

10. Natural History And Consequences Of
Hepatitis B Infection
• Depending on the age of exposure, HBV can be eliminated by natural
immunity.
• Infection that is acquired in the neonatal period leads to chronicity in more
than 90% of the exposed.
• This rate drops to 30%-50% for infections acquired before 6 years of age.
• Infection acquired above 5 years of age will spontaneously be eliminated in
over 90% of the infected individuals within 6 months.
• Those that fail to eliminate the infection enter the chronic phase of disease
that has different outcomes:
• the majority will remain asymptomatic;
• a few will progress to liver cirrhosis that remains stable (compensated) and a
• small percentage may decompensate and suffer complications such as ascites,
hepatic encephalopathy, haematemesis (variceal bleeding), infections, malnutrition,
kidney failure and liver cancer that increase the risk of death.

11. Clinical Presentation
• Acute symptomatic disease (2-
3month, lasts 2-4month)
• Loss of appetite, Nausea,
Vomiting,
• Low Grade Fever
• Myalgia, arthralgia, Fatigability
• Jaundice, dark urine, and light
colored stool
• RUQ And Epigastric Pain
• Fulminant Hepatitis and CHB
• Hepatic Encephalopathy
• Somnolence
• Disturbance In Sleep Pattern
• Mental Confusion
• Coma Ascites
• GI Bleeding
• Coagulopathy
• Ascites

12. Physical exam
• Patients with acute hepatitis
are asymptomatic but
physical examination may
reveal;
• Low grade fever
• Jaundice
• Hepatomegaly (mildly
enlarged soft liver)
• Splenomegaly (5-15%)
• Chronic hepatitis
• Hepato-splenomegaly
• Muscle wasting, palmer
erythema, spider angioma
• Cirrhosis;
• Ascites, Jaundice, Peripheral
Edema, Gynecomastia,
Testicular Atrophy. Collateral
Veins.

13. Diagnosis
HBsAg POSITIVE
• Household contact/ spouses
should be screened;
• Discus the benefits of
a) Initiating treatment if eligible
b) Monitoring if not eligible
• Baseline tests to asses the
eligibility for treatment CBC,
LFTs(ALT and AST),HIV, HBV
viral load, Abd. U/S
• Baseline Before initiation of
treatment;
1. RFTs, or Urinalysis-dipstick
(proteinuria and glycosuria if
RFTs not available)
2. HBeAg;
a) if +ve at T-0, =significant active
replication. It can be used to
monitor the response to Rx. if
turns –ve and is replaced by
antibody, consider stopping Rx.
after 12month of Rx.
b) If –ve at T-0,= no significant
active replication OR mutant
virus which cannot secrete this
antigen.
3. HBV DNA
4. AFP.

14. Treatment
WHO TO TREAT
• Category 1;
I. All Patients who have clinical
evidence of cirrhosis OR adults
with APRI Score > 2
These should be treated regardless
of HBV vial load
• Category 2;
Co-infection with HBV and HIV
Regardless of WHO stage, CD4 cell
count, viral load(HBV or HIV)
• Category 3;
• All patients who do not have
clinical evidence of cirrhosis and
have APRI score <2 but have;
I. Persistent elevation of ALT after
excluding other causes of liver
enzyme elevation;
II. Viral load of more than
20,000IU/mL

15. Goals of treatment
1. Suppression of HBV
replication to undetectable
levels
2. Decrease necroinflamation
and fibrosis
3. Prevent progression to
cirrhosis, liver failure and
HCC
Treatment options
1. TDF 300mg od
2. TDF+3TC 600mg od

16. Control measures
• Immunization
• Use of condoms
• Avoid sharing sharps
• Screening of blood products
• Standard precautions
• Use of gloves
• Protective garments, mask and
gaggles
• Proper disposal of needles
• Bleach solutions to decontaminate
work surfaces
• Autoclaving for metal objects