VIRAL HEPATITIS

                                                                                VIRAL HEPATITIS
                                                                 

(By Dr.S.UMA DEVI.M.D)

Viral hepatitis specifically refers to a primary infection of the liver by one of the five etiologically
associated viruses
(the number is now believed to be seven including type F and G)
These five types of hepatitis include
TYPE  A:  Synonyms:infectious hepatitis,epidemic jaundice,short incubation period hepatitis
Type B:  Serum or transfusion hepatitis
TYPE  C:
TYPE  D: caused by defective virus;has no independent existence;depends on HBV: drug abusers are
prone for it.
TYPE E : Epidemically prone,Enterically transmitted.

Method of transmission

Hepatitis A and E :    feco oral’
Hepatitis B:    via 1)contaminated blood 2)Contaminated syringes/needles 3)unsafe sex 4)traspalcental
Hepatitis C and D : Thr’ contaminated syringes,thr’ blood and blood products

HAV versus HAB virus infection

  Similarities:  Both infections are similar in clinical picture
Differ in
1.Incubation period
2. Route of entry
3.Immunity conferred
4. Onset

CLINICAL PICTURE (USUAL CLINICAL PICTURE)

 TYPE A AND TYPE B
1.Prodromal period  1 week (flu like picture)
2. Icteric phase 2weeks (jaundice,tender hepatomegaly)
3. Convalascent period 3 wks
4. Biochemical recovery later ( after 6 months)

DIFFERENTIATING FEATURES TYPE  A  TYPE B

(.MNEMONICS for Differentiating features-AEIOU-Age,entry,incubation.onset course)

What are the unusual modes of presentation of hepatitis A?
1. Fulminant hepatitis
2. Pronounced cholestasis simulating obstructive jaundice

FIG 1.Sequence of serological markers in acute hepatitisA

What is fulminant hepatitis?
Severe hepatitis with massive hepatic necrosis resulting in hepatic coma and death.
Occurs in 0.5 to1% of viral hepatitis(type A to E)

Yes
Yes
Yes
Other causes:drugs and toxins,Shock.CAH,Bud-chiari,Wilsons syndrome,Baterial,parasitic
What is an- icteric hepatitis?
Jaundice is not clinically evident but tender hepatomegaly +
These patients usually suffer from CAH etc

              HBV Hepatitis

Etiology:


Hepatitis B virus
Hepatitis B is 50 -100 times more infective than HIV.
Antigens of HBV:
• Surface antigen—HBS Ag
• Core antigen---HBCAg  (enclosed by outer coat of HBs Ag
• HB E Ag -----Additional antigen found in some cases along withHBSAg

HBE Ag is specific for HBV.
ANTIBODIES
• For HBS Ag-   Anti HBSAg
• FOR HBCAg-AntiHBCAg          
• For HBEAg-Anti HBE Ag

Fig.2.Hepatitis B antigens   nasirmicrobiologist.yolasite.com

Lab diagnosis of Hepatitis B
Depends on many serological markers
SIX---  HBS Ag-  and  Anti HBSAg
HBCAg-AntiHBCAg
HBEAg-Anti HBE Ag
How are serological markers useful?
1. To know the stage of the disease
2. Degree of infectivity
3. Prognosis
4.Immune status of the patient

I.Stage of the disease
HBS AGg appears first and then the  anti HBC antibody
So, if HBS AGg is present and Anti HBC is absent it means very early infection in non vaccinated
2. Infectivity of the patient
Presence of antigen HBE correlates with abundance of Dane particles in circulation
Such situation indicatesincreased risk of transmission of HBV infection via various routes

3.Prediction of development of carrier state
Persistance of HBS Ag at 3
rd
 month and persistence of HBS Ag at 6
 month,
Indicates carrier state
th
4.Prediction of recovery
Presence of antibodies againstHBE i.e. presence of antiHBE indicates  recovery is under way.

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25% of adults chronically infected in childhood ,later die from cirrhosis or liver cancer.
PREVENTION OF HEPATITIS B INFETION
Active immunization with HepatitisB vaccine containing HBSAg
Passive immunization with hyper immune serumwith hepatitis immunoglobulin(HBIG)
TYPES OF VACCINE
(HepatitisB vaccine is 92% effective)

Plasma derived
Yeast derived
Dose and schedule of vaccine-(Plasma derived)
3 doses –o,1st mth and 6
th
 monthparenteral

HBV vaccination is indicated in whom?
1. Health care workers
2. Doctors and nurses in dialysis unit and hemophilia centers
3. Immuno deficient patients
4. Spouses of patients with acute hepatitis and spouses on carriers of HBV.
What is NON A,Non B virus?
2 important types
1.Blood born NonA NON B virusinfection caused by hepatitis C
WaterbornNonA nonB :  caused byHepatitisE virus(HEV)

Features of Hepatitis C infection
Incubation period
50 days
Route of infection:parenteral -90%post trasfusional
Carrier state is described

DELTA  HEPATITIS-HDV
Features
Causes HDV hepatitis
HDV is a defective virus ;canot exist independently.
It requires HBV for multiplication and transmission
Two types of infection of HDV
Coinfection-infection simultaneous with HBV
2.Super infectio-infecting a patient already infected with HBV

 Summary

MAIN METHODS OF
TRANSMISSION

Contamination of food, etc. with fecal
matter from infected person
Contaminated blood transfusions; shared
needles associated with intravenous drug
use

COMMON OUTCOME

Often resolves completely after 4 to 8 weeks; usually
does not become chronic
Often less favorable than type A; can be fatal in 10 to
10% of cases in the elderly and after blood
transfusions; can become chronic in 10 to 15% of
cases

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C (HCV, hepatitisC)

Shared needles or contaminated blood
transfusion; sexual transmission rate low
but possible
D (delta agent) This virus is closely associated with
HBV
Irregular course; patient is often asymptomatic for
years; can lead to chronic hepatitis
Exists only concurrent with hepatitis B; causes
extremely severe symptoms; may be an important
cause of hepatitis worldwide

Investigations in Acute Hepatitis
Urine –Bilirubin
Total count-low with neutropenia
SGOT and SGPT are raised-levels can go to 400-4000IU/LSerum bilirubin raised
Prothrombin time normal -12 sec.If markedly prolonged indicates severe liver damage.


Other viruses causing Hepatitis
EB virus
Cytomegalo virus
Coxasackie virus
Yellow fever
Herpes simplex
Other infectious agents causing Hepatitis
Leptospirosis
Toxoplasmosis
 
CHRONIC HEPATITIS

Any hepatitis lasting 6mths or longer showing chronic and persistent   liver damage.

Histological classification of Chronic hepatitis
Chronic persistent hepatitis  (CPH)
Chronic lobular hepatitis  (CLH)
Chronic active hepatitis(CAH)

Chronic persistant and chronic lobular hepatitis
Usually follow Acute hepatitis B or C
Both may be
• asymptomatic or
• cause  vague symptoms,have no clinical signs(Smtms Hepatomegaly)
         Persistantly high transaminase value
Chronic persistant hepatitis (syn Portal hepaitits) portal mononuclear inflammation
Chronic lobular hepatitis-diffuse lobular inflammation
Lobular spotty inflammation-resembles resolving acute viral hepatitis

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CHRONIC  ACTIVE HEPATITIS

Serious condition,progress to hepatic cirrhosis ,hepatic malignancy
Histologically fibrosis  present with inflammation
Other organs affected-Thyroid,eye,kidney,blood vessels –Thyroiditis,corneal ulcerations,membrano
proliferative glomerulo nephritis,vasculitic syndromes and sometimes also arthritis ,pulmonary fibrosis.

Piecemeal necrosis:

• This the hall mark of Chronic active hepatitis
• Extension of portal infiltration into hepatic lobules
• Extension of limiting plate into hepatic cells
• These cells (zone1) are surrounded by connective tissue forming “Rosettes”

Bridging necrosis

Necrosis and subsequent fibrous septa extend from portal zoneto portal zone or  portal zone to central
vein.

Etiology of chronic hepatitis

Viral—hepatitis virus –B,C,D.
Drugs-Methy dopa,INH,
Wilsons,
 Autoimmune(Lupoid)
Alpha1 antitrypsin deficiency

Clinical presentation of Chronic hepatitis

Usually with jaundice
Some present with complications of cirrhosis
Extra hepatic featuresin HBV and autoimmune etiology
-are immune complex mediated.

Treatment of CAH
Most promising treatment-alpha interferon in HBeAg/HBV Dna positive patients

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Fig 3.morphologic features of both acute and chronic hepatitis
Diagrammatic representations of the morphologic features of acute and
chronic hepatitis. Bridging necrosis (and fibrosis) is shown only for chronic
hepatitis; bridging necrosis may also occur in acute hepatitis (not shown).
http//cueflash.com


TREATMENT OF VIRAL HEPATITIS
1.Suppotive therapy for self limiting hepatitis like HAV
2.INTERFERON Most promising treatment-alpha interferon in HBeAg/HBV DNA positive patients
3.Anti viral drugs
Hepatitis B Lamivudin
Ribaverin for Hepatitis C


AUTO IMMUNE HEPATITIS
Cause: autoimmune
Clinically ;Jaundice and
 extra hepatic manifestations  like arthritis,Glomerulo nephritis,poly arteritis
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May have hepato splenomegaly
Lab test: Anti smooth muscle antibody  ANA .

 Etiology  of  Various types of Hepatitis  arranged in alphabetical order

hepatitis A  a self-limited viral disease of worldwide distribution, usually transmitted by oral ingestion ofinfected material but sometimes transmitted parenterally; most cases are clinically inapparent or havemild flu-like symptoms; any jaundice is mild.

anicteric hepatitis  viral hepatitis without jaundice.

hepatitis B  an acute viral disease transmitted primarily parenterally, but also orally, by intimate personal
contact, and from mother to neonate. Prodromal symptoms of fever, malaise, anorexia, nausea, and
vomiting decline with the onset of clinical jaundice, angioedema, urticarial skin lesions, and arthritis. After
3 to 4 months most patients recover completely, but some may become carriers or remain ill chronically.
hepatitis C  a viral disease caused by the hepatitis C virus, commonly occurring after transfusion or
parenteral drug abuse; it frequently progresses to a chronic form that is usually asymptomatic but that
may involve cirrhosis.

cholangiolitic hepatitis
cholestatic hepatitis
1. inflammation of the bile ducts of the liver associated with obstructive jaundice.
2. hepatic inflammation and cholestasis resulting from reaction to drugs such as estrogens or
chlorpromazines.

hepatitis D , delta hepatitis infection with hepatitis D virus, occurring either simultaneously with or as asuperinfection in hepatitis B, whose severity it may increase.

hepatitis E  a type transmitted by the oral-fecal route, usually via contaminated water; chronic infection
does not occur but acute infection may be fatal in pregnant women.

enterically transmitted non-A, non-B hepatitis  (ET-NANB).

hepatitis G  a post-transfusion disease caused byHepatitis G virus, ranging from asymptomatic infectionto fulminant hepatitis.
infectious hepatitis
infectious necrotic hepatitis  black disease
A fatal disease of sheep ,sometimes of humans in US and Australia due to clostridium Novyi marked by
necrotic areas in the liver.
lupoid hepatitis  chronic active hepatitis with autoimmune manifestations.
neonatal hepatitis  hepatitis of uncertain etiology occurring soon after birth and marked by prolonged
persistent jaundice that may progress to cirrhosis.

non-A, non-B hepatitis  a syndrome of acute viral hepatitis occurring without the serologic markers of

hepatitis A or B, including hepatitis C and hepatitis E.

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posttransfusion hepatitis  viral hepatitis, now primarily hepatitis C, transmitted via transfusion of blood

or blood products, especially multiple pooled donor products such as clotting factor concentrates.

serum hepatitis .

transfusion hepatitis  post transfusion hepatitis.

viral hepatitis  Hepatitis A,B,C,D and E.
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