Viral hepatitis

Hepatitis
 Inflammation of the liver • Viruses attack the hepatocytes
 Can be caused by: ATTACK • It will present abnormal CHON: MHC class I molecule
o Virus
• Immune cells will try to see what’s wrong with the liver.
o Autoimmunity RECOGNIZ • CD8+ T-CELL – recognize that the cells were infected.
E
o Drugs/ Medications
• Cytotoxic Killing
o Alcohol APOPTOSIS • COUNCILMAN BODY – hepatocytes undergoing apoptosis.
o Non-alcoholic cause – fats
Liver INFLAMED
• HEPATITIS
 largest internal organ that supports almost
every other organ in your body • LIVER DAMAGE
DAMAGE
 reddish-brown appearance and feels rubbery
to the touch
 largest gland in the human body
General Signs and Symptoms
 It is bigger in human males (around 10.5cm)
than that in females.(about 7 cm)  Fever
 The liver weight is also different in different  Malaise
genders. Normal liver weighs about 1.2 to 1.5  Nausea
kg in females and males, respectively.  hepatoMEGALY
 RUQ Pain
 Jaundice
 Weight Loss
 Dark Urine (due to ↑Bilirubin & ↑
Urobilinogen in urine)
 ↑↑Alanine aminotransferase/ ALT
 ↑ Aspartate aminotransferase/AST
 ↑Atypical Lymphocytes

*Note: it can also be asymptomatic.

Hepatitis A
Functions  formerly known as infectious hepatitis or
 Purify the body from different harmful epidemic jaundice
substances, for example, toxins  acute infectious disease caused by
 Secretes chemicals in the form of bile or Hepatitis A virus (HAV).
liver juice. Bile contains salts that neutralize
the acidic food coming from stomach. Non-specific signs and symptoms
Meanwhile, the bile juice also helps in the  Fever
digestion of fats.  Chills
 Processing Nutrients and Storage of  Headache
Vitamins, Iron and Minerals  Fatigue
 Blood Reservoir  Generalized
 Restoration of Glucose Level weakness and
 Synthesis of Blood Clotting Factors & Other pains
-Plasma Proteins  Anorexia
 Detoxification of Poisons and Drugs, Lipid  Nausea and
Metabolism and Alcohol Metabolism vomiting
 Destruction of Old RBCs  Dark urine
 Jaundice
**The disease is benign with complete recovery in
several weeks.

CAUSATIVE AGENT: Hepatitis A virus (HAV)

 is an enterovirus of the Picornaviridae
family.
 It multiplies only in hepatocytes.

RESISTANCE
 The virus is fairly resistant to heat and
chemicals.
 Withstands heating to 600 C for 1 hr.
 Not affected by chlorine in doses usually
employed for chlorination.
  Formalin is stated to be an effective o RT PCR (Reverse Transcription Polymerase
disinfectant. Chain Reaction) of feces
 The virus is inactivated by ultraviolet rays
and by boiling for 5 minutes or autoclaving. Preventions:
 hygienic measures and sanitation
RESERVOIR OF INFECTION  passive immunization
 The human cases are the only reservoir of o Human IgG given before exposure to
infection. virus or early during the incubation
period, will prevent or attenuate a
PERIOD OF INFECTIVITY clinical illness.
 The risk of transmitting HAV is greatest  active immunization
from 2 weeks before to 1 week after the o Several inactivated or live attenuated
onset of jaundice. vaccines against hepatitis A have been
developed.
INFECTIVE MATERIAL
 Mainly man’s feces. Treatment
 nospecific, dietary food and long rest
VIRUS EXCRETION
 HAV is excreted in the feces for about 2 Hepatitis B
weeks before onset of jaundice and for up
 formerly known as serum hepatitis
to 2 weeks thereafter.
 is an acute systemic infection with major
pathology in the liver, caused by hepatitis B
Host Factors:
virus.
 acute illness causes liver inflammation,
 AGE
vomiting, jaundice, and, rarely, death.
o Infection with HAV is more frequent
 Chronic hepatitis B may eventually cause
among children than in adults. However,
cirrhosis and liver cancer.
people from all ages may be infected if
 endemic throughout the world, especially in
susceptible.
tropical & developing countries.
 SEX
o Both sexes are equally susceptible.
Causative Agent
 IMMUNITY
 Hepatitis B Virus (HBV)
o Immunity after attack probably
 complex, 42 nm double-shelled
lasts for life.
DNA virus originally known as
―Dane Particle
 replicates in liver cell
Mode of Transmission:
 Incubation period 10-50 days (usually 25
to 30 days)
 FECAL-ORAL ROUTE
o Major route of transmission.
o by contaminated water, food or
milk.
 PARENTERAL ROUTE (Rarely)
o By blood and blood products or by
skin penetration through
contaminated needles.
 SEXUAL TRANSMISSION
o May occur mainly among  RESERVOIR OF INFECTION
homosexual men because of oral-  Men is the only reservoir of infection
anal contact. which can be spread either from
carriers or from cases.
Diagnostic Tests:  Infective material
 Demonstration of Virus in feces, blood, bile by  Contaminated blood is the main
Immunoelectron microscopy source
 Virus Isolation  Virus has been found in body secretion
 Detection of Antibody by ELISA such as saliva, vaginal secretion &
 Anti-HAV IgM and IgG semen in infected material.
 Blood test:  Resistance
o Alanine aminotransferase (ALT  Readily destroyed by sodium
o Bilirubin hypochlorite as is by heat sterilization
o Protein in an autoclave for 30-60 min.
 Molecular Diagnosis
Host Factors
 Acute hepatitis B:
o 90% resolve by themselves
o <1% develop fulminant hepatic
failure
o occurs in approximately:
 perinatal: 1%
 Childhood: 10% (1-5yo)
 Late infection: 30% (>5yo)
 Chronic hepatitis B
o 2-10% progress to chronic state
o occur in approximately:
 Perinatal: 95%
 Childhood: 80%
 After 5 yr. of age: 5-10%
High Risk Group:
o People from endemic regions
o Babies of mothers with chronic HBV
o Intravenous drug abusers
o People with multiple sex partners
o Hemophiliacs and other patients requiring
blood and blood product treatments
o Health care personnel who have contact with
blood
o Patients who are immunocompromised.
Humoral and cellular response:
 HBV has 3 distinct antigen:
 HBsAg – surface Ag
 HBcAg – core Ag
 HBeAg - envelope Ag
 They stimulate production of corresponding
antibody.
Mode of Transmission
Incubation Period: 45-180 days (usually 60-90 days)
 Parenteral
 IV drug abusers, health workers are
at increased risk.
 Sexual
 sex workers and homosexuals are
particular at risk.
 Perinatal (Vertical)
 mother (HBeAg+) →infant
 Mothers who are HBeAg positive
are much more likely to transmit to
their offspring than those who are
not.
 Perinatal transmission is the main
means of transmission in high
prevalence populations.
Diagnostic Tests
 Serology
 Liver Chemistry tests AST, ALT, ALP,
and total Bilirubin
 Histology
 Immunoperoxidase staining
 HBV Viral DNA
 Most accurate marker of viral DNA
and detected by PCR
 Liver Biopsy
 to determine grade (Inflammation)
and stage (Fibrosis) in chronic
Hepatitis
Prevention
 Vaccination
 highly effective recombinant
vaccines
 Hepatitis B Immunoglobulin (HBIG)
 exposed within 48 hours of the
incident/ neonates whose mothers
are HBsAg and HBeAg positive.
 Other measures
 screening of blood donors, blood
and body fluid precautions.
Treatment
 Interferon Alfa (Intron A)
 Response rate is 30 to 40%.
 Lamivudine (Epivir HBV)
 relapse ,drug resistance
 Adefovir dipivoxil
 Hepsera
Hepatitis C
 an infectious disease affecting primarily the
liver, caused by the hepatitis C virus (HCV).
 The infection is often asymptomatic
 Chronic infection → scarring of the liver
(cirrhosis)
 Can lead to chronic hepatitis
Causative Agent: HCV
 50-60 nm virus with a linear, single
stranded RNA genome, enclosed with in a
core and surrounded by an envelope,
carrying glycoprotein spikes.
 member of the Hepacivirus genus in the
family Flaviviridae.
 half life of the virus particles in the serum is
around 3 hours and may be as short as 45
minutes.
 In addition to replicating in the liver the
virus can multiply in lymphocytes.
Mode of Transmission
 Incubation Period: 40-120 days
 Intravenous Drug Use
 Healthcare Exposure
 Blood Transfusion, transfusion of
Blood products, Organ Transplant
without HCV screening carry
significant risk of infection.
 Hemodialysis
 Accidental injuries with needles/sharps
 Sexual/household exposure to anti-HCV-
positive contact
 Multiple sex partners
 Vertical Transmission
 Vertical transmission of hepatitis C
from an infected mother to her
child
Diagnostic Tests
 HCV antibody
 ELISA
 Not useful in the acute phase as it
takes at least 4 weeks after
infection before antibody appears.
 HCV-RNA
 PCR
 branched DNA
 used to diagnose HCV infection in
the acute phase.
 main use is in monitoring the
response to antiviral therapy.
 HCV-antigen
 EIA for HCV antigen
 It is used in the same capacity as
HCV-RNA tests but is much easier to
carry out.
Prevention
 General Prophylaxis:
 blood, tissue, organ screening, is
possible.
 No specific active or passive immunizing
agent is available.
Treatment
 Interferon - may be considered for patients
with chronic active hepatitis.
 Ribavirin - there is less experience with
ribavirin than interferon. However, recent
studies suggest that a combination of
interferon and ribavirin is more effective
than interferon alone.
Hepatitis D
 classified as Hepatitis delta virus
 is a disease caused by a small circular
enveloped RNA virus.
 HDV is considered to be a subviral satellite
because it can propagate only in the
presence of the hepatitis B virus (HBV).
Causative Agent: HDV + HBV
 VIRION: spherical, 36-38 nm particle with an
outer coat composed of the HBsAg
surrounding ssRNA genome.
 Satellite virus : replicates only in the
presence of HBV
Mode of Transmission
 Incubation Period:
 2-12 weeks
 The primary MOT are believed to be similar
to those of HBV, though HDV does not
appear to be sexually transmitted disease.
Clinical Features
 Infection is dependent on HBV replication
 HBV provides an HBsAg envelop for
HDV
 Two types of infection:
 Coinfection, delta and HBV are
transmitted together at the same
time
 Superinfection, delta infection
occurs in a person already infected
with HBV.
Diagnostic Test
 Immunofluorescence
 For delta antigen expression
 ELISA
 For anti-delta antibodies found in
serum
 IgM antibody appears 2-3 weeks
after infection and is soon replaced
by the IgG antibody in acute delta
infection.
Prevention
 HBV-HDV Coinfection Pre or post exposure
prophylaxis to prevent HBV infection
 Screening of blood donor for HBsAg
 HBV-HDV Superinfection Education to
reduce risk behaviors among persons with
chronic HBV infection.
 Hepatitis E
GENERAL INTERVENTIONS
 Caused by hepatitis E virus (HEV
 Encourage the pt to eat small frequent
 often causes an acute and self-limiting
meals, ↓fat&CHON,↑Carbs&fluid
infection (in that it usually goes away by
 Provide supportive care.
itself and the patient recovers) with low
 Encourage the pt to have a proper hygiene
mortality rates.
practice
 It bears a high risk of developing chronic
 Brief the family about the pt’s dse
hepatitis in immunocompromised patients
 Use gloves when making contact with the
with substantial mortality rates.
pt’s blood and other body fluids
 occasionally develops into an acute, severe
 Proper handwashing
liver disease, and is fatal in about 2% of all
 Always treat the linen and utensils as
cases.
infectious
 In pregnant women the disease is more
 Give the pt his own bedpan/urinal and
often severe and is associated with a clinical
cutlery
syndrome called fulminant hepatic failure.
 Isolation is continued for the 1st 2weeks of
the illness and 1 week after the onset of
Causative Agent: HEV
jaundice.
 HEV is spherical non-enveloped virus, 29-
 Don’t let the pt drink alcohol or take over-
nm to 32 nm in diameter, with a ssRNA
the-counter drugs w/o consulting the
genome.
doctor.
 The surface of the virion shows indentation
and spikes. ü The Virus is very labile.
GENERAL COMPLICATIONS
 It has been classified in the genus Herpes
 Cirrhosis (scarring→liver malfunction)
virus under the family Caliciviridae.
 Hepatocellular carcinoma
 Liver failure
 Emotional pain

Host Factor
 Animal Reservoir: Pigs

Mode of Transmission

 Incubation Period: 2-9 weeks

 spread mainly by the fecal-oral route due to
fecal contamination of water supplies or
food
 person-to-person transmission is
uncommon

Diagnostic Test
 ELISA
 IgG and IgM antibodies
 use recombinant and synthetic
peptide antigens
Prevention

 Sanitation: Avoid drinking water of

unknown purity, uncooked shellfish and
meat, and uncooked fruit/vegetables not
peeled or prepared by traveler.