HEPATITIS

Dr. Amany A. Ghazy

 Hepatitis
v Hepatitis" means inflammation of the liver.
v It is injury to the liver characterized by the presence of
inflammatory cells in the liver tissue.
v It can be caused by:
Toxins (aflatoxins)
certain drugs,
heavy alcohol use,
bacterial and viral infections.
 Viral Hepatitis
v It is liver inflammation due to a viral infection.
v Viral hepatitis may be acute (recent infection, relatively
rapid onset) or chronic forms.
v Common viruses cause hepatitis include:
Hepatitis A,B,C,D,E viruses (> 95% of viral cause),
Herpes simplex,
Cytomegalovirus,
Epstein-Barr virus,
adenoviruses.
Viral Hepatitis - Historical
Perspectives
Infectious A Enterically
E
transmitted

Viral NANB
hepatitis

Parenteral
Serum B D C y
transmitte
F, d
G,
 Types of Viral Hepatitis

A B C D E

Type of ssRNA dsDNA ssRNA ssRNA ssRNA

virus

prevalence Very high High Highest law rare

(0.5-10%) up to 20%

Chronic no yes yes yes no

infection

Oncogenicity no yes yes yes rare

& HCC
 Types of Viral zepatitis

A B C D E

Source of feces blood/ blood/ blood/ feces

virus blood-derived blood-derived blood-derived
body fluids body fluids body fluids

Route of fecal-oral percutaneous percutaneous percutaneous fecal-oral

transmission permucosal permucosal permucosal

fulmination may Some rare rare Yes, especially

occur pregnant females

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
 Hepatitis A virus (HAV)
v Hepatitis A is acute liver disease caused by HAV, lasting from a few
weeks to several months. It does not lead to chronic infection.
v Most common.
v Type of virus: RNA virus.
v Mode of transmission: (feco-oral route)
Close personal contact (household contact, child day care centers)
Contaminated food, water (e.g., infected food handlers, raw shellfish)
Not transmitted by Trans-placental route
Prevalence
 Hepatitis A virus (HAV)
v Causes of liver damage:
Localized areas of necrosis are frequently observed.
Later accumulation of macrophages near
degenerating hepatocytes.
v Clinical Manifestations:
Incubation period 2 6 weeks
Malaise, Anorexia
Nausea, vomitting, liver tenderness
Onset of Jaundice
Recovery in 4-6 weeks
Mortality 0.1 1 %
 Hepatitis A Infection
Typical Serological Course

Sympt Total anti-

oms HAV

Titer ALT

Fecal
HAV IgM anti-HAV

0 1 2 3 4 5 6 1 2
2 4
Months after exposure
 Hepatitis A virus (HAV)
v Laboratory Diagnosis:
Acute infection is diagnosed by the detection of HAV-IgM in
serum by EIA.
Past Infection i.e. immunity is determined by the detection of
HAV-IgG by EIA.
v Treatment:
No specific antiviral drug is available
Treatment is symptomatic (should get plenty of rest and eat a
nutritious diet).
Also ensure not to spread HAV by washing their hands after
using the toilet and before preparing food.
 Hepatitis B virus (HBV)
v Hepatitis B is a liver disease caused by HBV.

v It ranges in severity from a mild illness, lasting a few weeks

(acute), to a serious long-term (chronic) illness that can lead
to liver cirrhosis or liver cancer (HCC).

v It is the Most Important Infectious Disease because:

There are more than 350 million carriers

25% of them will develop chronic active hepatitis.

It attributes to 1 million deaths a years, world wide.

 Hepatitis B virus (HBV)

v HBV has many important

Ag:
Surface component of
HBV called as surface
antigen (HBs Ag).
HBc Ag.
HBe Ag.
Pathogenesis (LIFE CYCLE)
Prevalence
 Modes of Transmission
v Contact with infected blood, semen& other body fluids via:
Sexual: heterosexual or homosexuals.

Parenteral: IVDA, tattoo or body piercing with dirty needles.

Perinatal: Mothers who are HBeAg positive ..

v High Risk Individuals:

Health care providers (Physicians, surgeons, technicians)

Addicts, Sexual workers.

Babies of infected mothers (high prevalence populations).

Patients undergoing Dialysis

 Concentration of Hepatitis B
Virus in Various Body Fluids

Low/Not
High Moderate Detectable

blood semen urine

serum vaginal fluid feces
wound exudates saliva sweat
tears
breastmilk
Clinical Features
 Acute Hepatitis B Virus Infection with Recovery
Typical Serologic Course
Symptoms
HBeAg anti-HBe

Total anti-HBc
Titre

HBsAg IgM anti-HBc anti-HBs

0 4 8 12 16 20 24 28 32 36 52 100
Weeks after
Progression to Chronic Hepatitis B Virus Infection
Typical Serologic Course
Acute Chronic
(6 months) (Years)
HBeA anti-HBe
g HBsAg
Total anti-
Titr HBc
e

IgM anti-HBc

0 4 8 1 1 2 2 2 3 3 5 Yea
6 0 4after
2Weeks 8 2Exposure
6 2 rs
 Diagnosis
v Serological tests used for the diagnosis of HBV infection:
HBsAg: used as a general marker of infection.

HBsAb: used to document recovery or immunity to HBV infection.

anti-HBc IgM: marker of acute infection.

anti-HBcIgG: past or chronic infection.

HBeAg: indicates active replication of virus (infectiveness).

HBV-DNA: indicates active replication of virus, more accurate than

HBeAg. Used mainly for monitoring response to therapy.
 Treatment
v Supportive treatment.
v Recombinant Interferon alfa therpay is beneficial in HBV
and HCV
v Antiviral drugs:
Lamivudine: most patients will respond favorably. But, relapse on
cessation of treatment or drug resistance.
Adefovir: less resistance but more expensive and toxic
v Successful response to treatment result in disappearance of
HBsAg & HBV-DNA.
 MCQ
v In hepatitis B infected patients, the most important
indicator of active virus replication and risk of
transmissibility is:
HBsAg

HBeAg

HBcAg

HBsAb
 Hepatitis C virus (HCV)
v HCV also known as Non A or Non
B virus.
v HCV infections are seen only in
humans.
v The virus has single stranded RNA
genome surrounded by an
enveloped carrying glycoprotein
spikes.
Prevalence
 Pathogenesis

vClick to edit Master text styles

Second level
Third level
vFourth level
vFifth level
 Mode of Transmission
v Blood transfusions

v Transplantation of organs from infected donor.

v Percutaneous:
injectable drug abusers

Therapeutic (contaminated equipment, unsafe injections)

Occupational (needle stick)

v Sexual transmission ? Less important

v Vertical transmission is possible.

 Clinical features
v short, mild, flu-like illness.

v Nausea, vomiting & diarrhoea.

v loss of appetite & weight loss.

v jaundice seen in 5% of patients (yellow skin, eyes &urine) .

v itchy skin.

v About 50 80% patients progress to chronic hepatitis

v May progress to Cirrhosis, or Hepatocellular carcinoma

 Hepatitis C Virus Infection
Typical Serologic Course
anti-
HCV
Sympt
oms
Titr
e

ALT

Norma
l
0 1 2 3 4 5 6 1 2 3 4
Mont Years
hs
Time after
Exposure
 Laboratory Diagnosis
v HCV antibody: used to diagnose HCV infection.
Not useful in acute phase as it appears 4 weeks after infection.
v HCV-RNA: detected by PCR and branched DNA.
used to diagnose HCV infection in acute phase. However, its
main use is in monitoring the response to antiviral therapy.
v Prognostic Tests:
Genotyping: genotype 1 and 4 have a worse prognosis overall
and respond poorly to interferon therapy.
Viral Load: high viral load means poor prognosis.
 HCV Treatment
v Combination of antiviral drugs (-interferon & ribavirin)
The antiviral drugs may cause significant side effects as
headaches , flu-like symptoms, nausea ,tiredness, body aches
,Depression ,skin rashes

v Effective in about 50% of cases

v No vaccine
 Hepatitis D virus (HDV)
(Delta agent)
v It is a defective RNA virus need to be
surrounded by outer coat (HBsAg).

So it needs HBV to cause infection.

v Modes of Transmission:
Percutanous: injecting drug use.

Permucosal exposures.

sexual contact.
Prevalence
 Clinical Features

v Coinfection:
severe acute disease.
low risk of chronic infection.
v Superinfection:
usually develop chronic HDV infection.
high risk of severe chronic liver disease.
may present as an acute hepatitis.
 HBV - HDV Coinfection
Typical Serologic Course

Sympto
ms
ALT
Elevated
Titre
anti-
IgM anti- HBs
HDV

HDV RNA

HBsAg
Total anti-
HDV

Time after
 HBV - HDV
Superinfection
Typical Serologic
Course
Jaund
ice Sympto
ms
Total anti-
Titre ALT HDV

HDV RNA
HBsAg

IgM anti-
HDV
Time after
Exposure
 Hepatitis E virus (HEV)
v Un-enveloped RNA virus.

v Most outbreaks are associated with faecally

contaminated drinking water.

v Minimal person-to-person transmission.

v It causes swelling of the liver, but no long-

term damage.
Prevalence
 Hepatitis E Virus Infection
Typical Serologic
Course
Sympt
oms IgG anti-HEV
ALT

Titer IgM anti-HEV

Virus in stool

0 1 2 3 4 5 6 7 8 9 1 1 1 1
0 1 2 3
Weeks after
 Hepatitis G virus
v A new virus recently identified in Humans.

v Not grown in culture lines

v RNA genome.

v HGV RNA was found in acute, chronic, fulminant

hepatitis & patients with multiple transfusions

v It resembles HCV In all other aspects

 Preventive & Control
measures for Hepatitis
Viruses
v Immunization: (for infants & high risk persons)
Hepatitis A vaccination is recommended for all children starting
at age 1 year & travellers to endemic countries (2 injections,
protection starts 4 weeks after injection and lasts for 10 - 20
years).

Hepatitis B vaccination, 3 injections are given over 3-6 months,

immunity for at least 5 years.
 Other preventive
measures
v Preventive Measures for HAV & HEV (water &food hygiene):
Wash hands well after using any washroom.
Eat only freshly cooked foods.
Drink only commercially bottled water or boiled water in
endemic places where sanitation & water supply are questionable.
v Preventive Measures for HBV, HCV & HDV:
Cover open wounds, don't share razors, manicure tools or needles.
Practice safe sex.
Don't allow yourself to be pierced with non-sterile equipment.
Screening of blood, organ, tissue donors.
 Blood screening is
Mandatory
v Screening of blood donors,
Click to edit Master text styles
blood and body fluid Second level
Third level

Fourth level
precautions is mandatory in Fifth level

majority of Countries.
 MCQ

v Acute phase HCV infection can be diagnosed by:

HCsAg
HCV-RNA
HCV antibody
HCeAg
HBcAg