VIRAL HEPATITIS

Contents:
 Introduction
 Types
 Etiology
 Clinical Features
 Mode of transmission
 Investigations
 Treatment
 Conclusion
 References

Introduction:
 Viral hepatitis is a systemic disease with primary administration in the liver.
 It is of particular concern to the dental practitioner because of the potential for
infection of the dentist and dental staff
 Dentists in US are approximately 3-5 times more likely to be exposed to Hepatitis B
virus than general people

Types:
 Hepatitis A
 Hepatitis B
 Hepatitis C
 Hepatitis D
 Hepatitis E
 Hepatitis F
 Hepatitis G
Hepatitis A
 It is also called as Infectious Hepatitis
 It is a sub acute disease occuring mainly in children and young adults.
 Morphology:
 Belongs to picornavirus family
 HAV is 27nm, non-enveloped single stranded RNA virus with isosahedral symmetry.
 Etiology : - Hepatitis A virus
 Mode of transmission: Through oral route
 The large majority of infections are asymptomatic
Clinical Features: The clinical disease has two stages – prodromal and icteric.
 Syptoms: fever, malaise, anorexia, nausea, vomiting, liver tenderness, myalgia.
 Prodromal phase may last only a few days as long as two weeks.
 Incubation Period: It ranges from 2-6 weeks
 Icteric Phase: starts with appearance of jaundice and other symptoms include
darkening of urine,whitish stools.
 It lasts about 4-6 weeks.
Laboratory Diagnosis:
It can be made by
 a) Demonstration of virus
 b)Detection of antibody
 c)Biochemical tests
a)Demonstration of virus: By 1. Immunoelectron Microscopy (IEM) 2. Enzyme linked
Immunosordent assay (ELISA) – HAV can be detected by faeces by ELISA 3. Isolation:
It is not possible to grow virus proteinly from faeces of the patient.
b)Detection of antibody: ELISA kits for detection of IgM and IgG antibodies are
available.
c)Biochemical Tests: Liver function tests such as ALT and bilirubin supplement the
diagnosis.
 Treatment:
 As route of administration Hepatitis A is oro-faecal, there is no significant risk of
infection in clinical dentistry practice.
 However close contact with saliva may transmit infection if saliva contains the virus.

Hepatitis B:
 It is also called as Serum Hepatitis.
 Morphology: It belongs to Hepadnaviridae family, Genome-DNA, icosehadral
envelope.
 It is 42nm double shelled particle
 Etiology: Hepatitis B virus
 Mode of transmission: It is through :
a)parentral,
b)perinatal and
c)sexual.
Clinical Features:
 Onset is slow.
 Incubation period – 75 days
 It is divided into
a)Preicteric
b)Icteric
c)Convalescent
a)Preicteric: malaise, anorexia, nausea, vomiting, myalgia.,weakness.
b)Icteric : Patient develops jaundice, pale stools, dark urine (Bilirubiumia)
c)Convalescent: It is long and drawn out with malaise and fatigue.
In some patients,there is serum-sickness like reaction with fever, skinrash and arthralgia.
Laboratory Diagnosis:
 Acute Hepatitis B:
Average incubation period HBV infection is 75 days.
Approximately 4-6 weeks before onset of syptoms.
HBsAg appears in serum,followed by HBeAg and their titres begin to rise.
 Thereafter serum ALT and AST levels start to increase
Late in incubation period, Anti HBC appears and rises in titer.
Usually HBsAg titer and the serum ALT and AST levels continue to climb through the
prodromal phase and peak in the early icteric.
HBeAg and the serum ALT and AST level begin to rise during icteric phase.
HBsAg is no longer detectable in serum within 4 months after the appearance of
symptoms.
In convalescent phase, liver enzyme levels return to normal and zero conversion from
HBsAg to anti-HBs occurs.
There is a variable time after HBsAg is no longer detectable before appearance of
anti-HBs. This time is referred as “WINDOW PERIOD”.
In apparent Hepatitis B, HBsAg,HBeAg may appear in the serum after a short time
Serum ALT and AST levels are mildly elevated but soon returned to normal.
 Chronic active Hepatitis B
 In Chronic active Hepatitis B, HBsAg fails to seroconvert to anti-HBs.
 HBcAg continues to be present.
 Anti-HBc raises to high titres
 Serum ALT and AST levels remain elevated , through usually < 10 times normal.
Treatment:
 Immunization
a)Passive Immunization
b)Active Immunization
a)Passive Immunization: It may be employed following any accidental exposure to
Hepatitis B infection.
Hepatitis B immunoglobulin [HBIG] is prepared from donors titres of anti-HBs
Given in doses 0f 300-500 IV IM
It may not prevent the infection but protects against illness and development of carrier
state.
b)Active Immunization: Following vaccines are available
(i) Plasma Derived Vaccine: It is prepared by purifying 22nm particle of HBsAg from
plasma of healthy carriers.
Particles are inactivated by Formaldehyde
Vaccine is immunogenic and safe.
 (ii) Recombinant yeast Hepatitis B vaccine:
It is produced by a recombinant DNA in yeasts in which a plasmid containing the
gene of HBsAg has been incorporated.
HBsAg particles produced are extracted and purified for use as vaccine.
The vaccine is as immunogenic as plasma derived vaccine.
Both vaccines are adsorbed with aluminium hydroxide
a) Adjuvant
3 doses a 0,1 & 6 months are administered IM into detailed muscle

Hepatitis C:
 It was formerly known as blood-borne ,non A, non B Hepatitis.
 It belongs to the family – flaviviridae
 Etiology: RNA virus
 Mode of transmission: a) Parental route
b) Transmitted by needle stick injuries, use of contaminated needles and syringes,
transfusion of infected blood and blood products , and sexual intercourse.
 Clinical Features: It is generally less severe ,with milder symptoms, absent or less
marked jaundice.
Incubation period- 6 to 8 weeks
Laboratory Diagnosis: ALT and AST has elevated but are usually lower than in
Hepatitis B.
1st and 2nd generation serologic antibody tests are available for identification of HCV
infection.
These include – EIA-1,EIA-2 and RIBA-1 & RIBA-2.
Viral genome [HCV RNA]can be detected by PCR and by immunofluorescence.

Hepatitis D:
 It is a defective virus as it is dependent on helper function of HBV for its replication
and expression.
 It belongs to Deltavirus.
 Morphology: Spherical,36-38nm diameter,RNA particle surrounded by HBsAg
envelope.
 Etiology: It is caused by hepatitis deltavirus[HDV] a defective RNA agent.
  Mode of transmission: Parenterally
 Clinical Features: It can occur in presence of HBV under 2 situations.
(i)Simultaneous infection with both HBV and HDV (coinfection)
(ii)superinfection of an HBsAg carrier by HDV
 Laboratory Diagnosis: It is made by detecting IgM anti-delta antibody in serum.
ELISA & RIA kit are commercially available for detection of antibodies to HDV.
HDAg is 10 expressed in liver cell nuclei, it can be detected by immuno-fluorescence.
Prophylaxis: No, specific prophylaxis exists,but immunisation with hepatitis B
vaccine is effective.
Screening of blood donors of HBsAg will also limit blood borne HDV infection.

Hepatitis E:
 The virus(es) formerly recognized as causing enterically transmitted non-A, non-B
hepatitis has been isolated and coded as hepatitis E virus (HEV), an RNA virus.
Trans- mission commonly occurs through fecally contaminated drinking water, and
outbreaks have occurred in developing countries in Africa, Asia, and Latin America.
Epidemics have not occurred in Canada and the United States, and only occasionally
cases have been seen in the 7 United States. The disease usually follows a benign
pattern like HAV, with a mortality rate of 1% to 2%, which increases to 20% to 40%
in pregnant women. Serologic tests such as EIA and polymerase chain reaction assays
of RNA are now available for HEV.

Hepatitis F and G:
 There is some evidence of the existence of other unidentified hepatitis viruses,
perhaps other enterically transmitted non-A, non-B agents, and these have been
arbitrarily assigned as F and G.

Dental Implications:
 A comprehensive medical history is important for identifying patients with histories
of viral hepatitis or may elicit symptoms of acute disease. Furthermore, understanding
the epidemiologic factors can aid in determining the type of viral hepatitis that the
patient had (e.g., perhaps a localized outbreak. associated with intravenous drug abuse
at summer camp, or perhaps the viral hepatitis followed multiple blood transfusions).
If a history of hepatitis B is suspected and the patients medical records are not
available. a screening test for HBsAg should be ordered.
  Regional examination of the sclera and oral mucosa, particularly the lingual frenum,
may reveal mild jaundice in a patient with an unremarkable past medical history and
nonspecific symptoms of malaise, anorexia, weight loss. and fever. If acute viral
hepatitis is suspected, no elective dental treatment should be performed until after
medical consultation and resolution of the acute disease
 During dental treatment of a patient with acute or chronic viral hepatitis, universal
precautions must be used. Gloves, mask, and protective eyeglasses are mandatory,
Aerosol production should be minimized by using a Slow-speed handpiece as much as
possible, working under a rubber dam, using high-speed evacuation. and judiciously
using the air syringe, Strict aseptic technique is essential and should include
sterilization of all instruments and handpieces,
 thorough postoperative disinfection, use of disposable smocks and drapes, and
proper disposal Of contaminated materials, Scheduling these patients late in the day
eliminates the immediate use Of the equipment by another patient. Other
considerations include obtaining a preoperative prothrombin time before dental
Surgery (a platelet count may also be necessary if splenomegaly is a complicating
factor), modifying the chair position to the sitting or semireclining position for
patients with ascites, and avoiding the use of drugs metabolized by the liver.

Medical Management:
 Treatment protocols for acute viral hepatitis are supportive, and there is no consensus
on the value or need to provide antiviral therapy during an acute infection, For
chronic viral hepatitis. the decision on how and when to institute therapy is complex
and must be based on factors such as patient interest, clinical and laboratory findings,
risk of disease progression without intervention, odds of therapeutic success. risk of
therapeutic adverse effects and the overall health of the patient.
 Approved drug therapies to treat chronic HBV include interferon-α2b, pegylated
interferon-α2a, adefovir dipivoxil lamivudine, and entecavir. Since these drugs do not
eradicate HBV, therapeutic protocols tend to be prolonged.
 Interferon-α2b and pegylated interferon-α2a are biologic response modifiers that
enhance the host's natural immune response. Adefovir dipivoxil, lamivudine, and
entecavir are nucleoside analogues that inhibit HBV DNA synthesis. The emergence
of resistant HBV strains is of particular concern for lamivudine, reaching 32% after 1
year and 70% after 5 years of therapy. Overall about two thirds of patients who
qualify for antiviral therapy enter an inactive phase, marked by HBeAg
seroconversion and a drop in HBV DNA viral load below 3 log10 IU/mL. However,
20% will suffer relapse later in life. Current therapeutic strategies to control chronic
HDV infection are ineffective. Drugs available for the treatment of HCV pegylated
interferon-α and ribavarin.
 TV Preventive measures to reduce viral hepatitis spread include aggressive
vaccination protocols (for HBV): adequate screening and handling measures for
donated blood and tissues; the implementation of proven infection control measures in
 the health care setting; and promotional/educational efforts to reduce the practice of
unsafe injection drug use and/or high-risk sexual practices. Approximately of healthy
adults and 95% of infants, children. and adolescents produce protective antibodies
against HBV after vaccination. An adequate response is defined as a serum level Of
anti-HBs antibody of > 10 mIU/ml„ Although some waning of the anti-HBs response
may occur over time, clear guidelines regarding the need for booster immunization
have yet to be established. Unfortunately, there exists no vaccine against HCV.

Conclusion:
 VH is a huge burden on lives and economies of people Collaboration of different
parties are needed to prevent and control VH. As a non-commercial, informal and
voluntary collaboration, the VHN seeks to bring together representatives from the
various sectors World Health Organization

References:
 Dr. C P Baveja
 BURKETS
 WOOD And GOAZ