May be caused by viruses (commonest) such as hepatitis A, B, C, D, and E viruses or autoimmunity, αlpha1-antitrypsin deficiency

1. HEPATITIS
By DR NDAYISABA CORNEILLE

2. Hepatitis
 The term hepatitis refers to any inflammatory process of the
liver.
 The liver is a vital organ that processes nutrients, filters the blood, and
fights infections.
 When the liver is inflamed or damaged, its function can be affected.
 May be caused by viruses (commonest) such as hepatitis A, B, C, D,
and E viruses or autoimmunity, αlpha1-antitrypsin deficiency
 The hepatotropic viruses are a heterogeneous group of infectious
agents that cause similar acute clinical illness.

3. Viral Hepatitis
 The clinical spectrum of disease is extraordinarily broad:
- asymptomatic
- symptomatic
- liver failure
 Viral Hepatitis CLASSIFICATION:
Enterically transmitted (HAV, HEV) ,parenterally(Bloodborne
)transmitted (HBV, HCV, HDV) and mosquito bite
transmitted(coused by yellow fever virus)
Other virus like HSV,CMV,EBV and Rubella cause acute
hepatitis as part of their systemic disease

4.  Bloodborne transmitted: are not shed in feces, may be
associated with a prolunged viremia, persistent infectivity and
progression to chronic liver disease.
 Enterically transmitted: these viruses survive exposure to bile,
are shed in feces, produce infections that are generally self-
limited although they may cause severe hepatitis and acute
liver failure; neither a viremic nor an intestinal carrier state
occurs and chronic liver disease never develops.
 Acute Hepatitis: Short-term hepatitis.
– Body’s immune system clears the virus from the body
within 6 months
 Chronic Hepatitis: Long-term hepatitis.
– Infection lasts longer than 6 months because the body’s
immune system cannot clear the virus from the body

6. Acute Viral Hepatitis
 1.HEPATITIS A :a non-enveloped RNA virus which is
classified as a picornavirus.Humans are only known hosts
 HAV infection during pregnancy or at the time of delivery
does not appear to result in increased complications of
pregnancy or clinical disease in the newborn.
TRANSMISSION
 Fecal-oral spread through
1. Close person-to-person contact with an infected person
2. Sexual contact with an infected person
3. Ingestion of contaminated food or drinks
 Parenteral transmission occurs rarely

7. Clinical features/Complications
- Fever - Malaise
- Loss of appetite - Nausea
- Vomiting - Abdominal pain
- Dark urine - Pale stool
- Joint pain - Jaundice
- Regional lymph nodes and the spleen may be enlarged,
aplastic anemia, nephritis, arthritis, vasculitis
 A person may have all, some or none of these . The
typical duration of illness is 7–14 days

8. DIAGNOSIS
 Serologic, viral polymerase chain reaction (PCR) testing for
raised ALT(alanine aminotransferase ) and AST(aspartate
aminotransferase) is required to confirm HAV.
 LFTs ;Almost all patients with acute hepatitis A have detectable
IgM anti-HAV in serum
 IgM anti-HAV can be detected from 5-10 days before the
symptoms up to 6 months after infection.
 The antibody test for total anti-HAV measures both IgG ,anti-
HAV+ve and IgM anti-HAV –ve by radioimmunoassay

9. TREATMENT
 Mainly supportive consists of :.Intravenous hydration as
needed . Antipruritic agents and fat-soluble vitamins for the
prolonged cholestatic form of disease. Serial monitoring for
signs of acute liver failure and early referral to a
transplantation center can be life saving.

10. PREVENTION
 VACCINE: Two-dose , with the 2nd dose given 6–12 mo after
the 1st dose

11. Hepatitis B
Epidemiology: the mean incubation period
is approximately 60 to 90 days (range 30-
180 days)
Only 1% to 5% of infected adults
develop chronic infection with
prolonged viremia, but 90% of
neonatal infections and about 50%
of infection acquired during infancy
result in persistent viremia.

12. Mode of transmission
Mode of transmission:bloodborne, percutaneous and sexual routes, but the
overall importance of these modes in the epidemiology of HBV
infection is ill-defined. HBsAg-positive mother can give it during
perinatal exposure
HBV is present in blood, lymph, semen, cervico vaginal secretions, saliva
and other body fluids of infected individuals.
No evidence of fecal-oral spread.
Persistent infection may lead to:
Chronic Persistent Hepatitis - asymptomatic
Chronic Active Hepatitis - symptomatic exacerbations of hepatitis
Cirrhosis of Liver
Hepatocellular Carcinoma

13. Classification
 HBV is a small, double-shelled
virus in the family
Hepadnaviridae
 Double stranded DNA virus
 contains numerous antigenic
components, including HBsAg,
hepatitis B core antigen
(HBcAg), and hepatitis B e
antigen (HBeAg).
 Humans are the only known host for
HBV
Transmission
 Contact with infectious blood,
semen, and other body fluids
primarily through:
1. Birth to an infected mother,
2. Sexual contact with an infected
person
3. Sharing of contaminated
needles, syringes, or other
injection drug equipment.

14. Clinical features
Incubation period 45-160 days (average 120 days)
The preicteric, or prodromal phase
It is nonspecific and is characterized by insidious onset of
malaise, anorexia, nausea, vomiting, right upper quadrant
abdominal pain, fever, headache, myalgia, skin rashes, and
dark urine, beginning 1 to 2 days before the onset of jaundice.
The icteric phase
it is characterized by jaundice, light or gray stools, hepatic
tenderness and hepatomegaly , Splenomegaly and
lymphadenopathy are common

15. Laboratory diagnosis
 Hepatitis B serologic test
 measurement of several hepatitis B virus (HBV)-specific antigens and antibodies.
Routine screening for HBV infection requires assay of at least three serologic
markers (HBsAg, anti-HBc, anti-HBs). HBsAg - used as a general marker of
infection.
 HBsAb - used to document recovery and/or immunity to HBv infection.
 anti-HBc IgM - marker of acute infection.
 anti-HBcIgG - past or chronic infection.
 HBeAg - indicates active replication of virus and therefore infectiveness.
 Anti-Hbe - virus no longer replicating. However, the patient can still be positive
for HBsAg which is made by integrated HBV.
 HBV-DNA - indicates active replication of virus, more accurate than HBeAg
especially in cases of escape mutants. Used mainly for monitoring response to
therapy.whereas both anti-HBs and anti-HBc are detected in persons with
resolved infection. HBeAg is present in active acute or chronic infections and is a
marker of infectivity.

16. test Results Interpretation
HBsAg
anti-HBc
anti-HBs
Negative
negative
negative
Susceptible
HBsAg
anti-HBc
anti-HBs
Negative
Positive
Positive
Immune due to natural infection
HBsAg
anti-HBc
anti-HBs
Negative
Negative
Positives
Immune due to hepatitis B vaccination
HBsAg
anti-HBc
IgM anti-HBc
anti-HBs
Positive
Positive
Positive
Negative
Acutely infected
HBsAg
anti-HBc
IgM anti-HBc
anti-HBs
Positive
Positive
Negative
negative
Chronically infected

17. COMPLICATIONS
 ALF with coagulopathy, encephalopathy, and cerebral edema
occurs more frequently with HBV than with the other
hepatotropic viruses.
 HBV infection can also result in chronic hepatitis, which can
lead to cirrhosis, end-stage liver disease complications, and
primary hepatocellular carcinoma.
 Membranous glomerulonephritis with deposition of
complement and HBeAg in glomerular capillaries is a rare
complication of HBV infection.

18. TREATMENT
 Acute HBV care is aimed at maintaining comfort and
adequate nutritional balance, including replacement of
fluids that are lost from vomiting and diarrhoea.
 Treatment of chronic hepatitis B in adults >18 yr of age
with compensated liver disease and HBV
replication:Interferon-α-2b (IFN-α2b) and lamivudine
(synthetic nucleoside analog)
 Interferon-α-2b (IFN-α2b) is for child but under the care
of a pediatric gastroenterologist

19. PREVENTION
 Hepatitis B vaccine and hepatitis B immunoglobulin (HBIG)
are available for prevention of HBV infection.
 Household, sexual, and needle-sharing contacts should be
identified and vaccinated if they are susceptible to HBV
infection.
 Children with HBV should not be excluded from school, play,
child care, or work couse not spread by breast-feeding,
kissing, hugging, or sharing water or utensils unless they are
prone to biting. A support group might help children to cope
better with their disease.

21. HEPATITIS C
– 6-7 weeks on
average (range 2-6
months);
– infectious one or
more weeks before
getting ill;
– chronic carriers
remain infectious;
Transmission
 contact with blood of an
infected person primarily
through:
 Sharing of contaminated
needles, syringes.
 Sexual contact with an
infected person
 Birth to an infected
mother
Incubation
period

22. – Nausea
– Loss of appetite
– Vomiting
– Fatigue
– Fever
– Dark urine
– Pale stool
– Jaundice
– Stomach pain
– Side pain
Symptoms
3 out of 4 persons have no symptoms and can
infect others without knowing it

23. Diagnosis
– HCV antibody: not useful in the acute phase as it takes at least 4 weeks after
infection before antibody appears.(Antibodies usually develop within 3 months)
– The most widely used serologic test is the third-generation enzyme
immunoassay (EIA) to detect anti-HCV
– The most commonly used virologic assay for HCV is a PCR assay, which
permits detection of small amounts of HCV RNA in serum and tissue samples
within days of infection.
– Screening for HCV should include all patients with the following risk factors:
history of illegal drug use,hemodialysis, idiopathic liver disease, and children
born to HCV-infected women ,….
– HIV+ persons may not develop detectable antibodies
– liver enzyme tests
– liver biopsy

24. TREATMENT&PREVENTION.
 In adults, peginterferon (subcutaneous, weekly) combined
with oral daily ribavirin is the most effective therapy;
 In children >3 years, IFN-α2b and ribavirin .
PREVENTION.
 No vaccine is available to prevent HCV.
 contact with body fluids of an Avoid infected person.
 Screening of blood, organ, tissue donors

25. HEPATITIS D
 HDV, the smallest known animal virus, is considered defective
because it cannot produce infection without a concurrent HBV
infection. The 36 nm diameter virus is incapable of making its
own coat protein; its outer coat is composed of excess HBsAg
from HBV. The inner core of the virus is single-stranded
circular RNA that expresses the HDV antigen.
 HDV can cause an infection at the same time as the initial HBV
infection (co-infection), or HDV can infect a person who is
already infected with HBV (super-infection).

26.  Coinfection
– Severe acute disease.
– Low risk of chronic infection.
 Superinfection
– Usually develop chronic HDV infection.
– High risk of severe chronic liver disease.
– May present as an acute hepatitis.
Hepatitis D should be considered in any child who
experiences acute liver failure.
Hepatitis D - Clinical Features

27. DIAGNOSIS.
 The diagnosis is made by detecting IgM antibody to
HDV; the antibodies to HDV develop ≈2–4 wk after co-
infection and ≈10 wk after a super-infection.
 A test for anti-HDV antibody is commercially available.
PCR assays for viral RNA

28. TREATMENT&PREVENTION.
The treatment is based on supportive measures once an infection
is identified.
There are no specific HDV-targeted treatments to date.
The treatment is mostly based on controlling and treating HBV
infection, without which HDV cannot induce hepatitis.
PREVENTION.
 There is no vaccine for hepatitis D.
 Hepatitis B vaccines and HBIG are used for the same
indications as for hepatitis B alone.

29. THANKS