nurses

3.  HepatitisViruses -
A,B,C,D,E
 Other viruses – Cytomegalo, EBV,
HSV,Yellow fever, Rubella,
Enteroviruses etc

4.  50% of children do
not develop Jaundice.
 Large tender liver is
common.
 30% will have
splenomegaly
 Coagulation is usually
normal

5.  Liver is enlarged,tender
 Cervical adenopathy(10-20%)
 Splenomegaly(10-20%)
 Fever is absent
 Encephalopathy :Irritability
Letargy,confusion

6.  Clinical jaundice
 Dark urine:1-5 days before
jaundice
 Patient may feel better
 Resolution of fever
 pruritus

7.  Infiltration of
mononuclear cells
 Hepatic cells necrosis
 Kupfer cells
hyperplasia
 Variable degrees of
cholestasis
 In more severe cases;
Bridging necrosis

8.  Serum bilirubin:5-20 mg/dl due to cholestasis,
abnormal biliary flow at the canalicular level
 Direct bil =indirect bil
 SGOT,SGPT=400-4000 iu due to cytopathic injury
 Alk.phosphatase :mild elevation
 Synthetic function
 PT is usually normal:
 in severe hepatitis,PT is prolonged
serum albumin
hypoglycemia

9. •Picornavirus (RNA virus)
•Enterically transmitted (fecal/oral
route)
•Often referred to as “infectious
hepatitis”
•Only a single serotype exists
•Estimated to be the cause of 40% of
acute hepatitis cases

10.  Close personal contact
(e.g., household contact,
child day care centers)
 Contaminated food,
water (e.g., infected food
handlers, raw shellfish)
 Blood exposure (rare)
(e.g., injecting drug use,
transfusion)

11.  Household contacts of infected
persons
 Persons, especially children, living
in areas with increased rates of
hepatitis
 Persons travelling to countries
where hepatitis A is common
 Sex contacts of infected persons

13.  Incubation period
average-30 days
Range 15-50 days
 Route of spread -
Ingestion
 Complications:
1)Fulminanthepatitis
2)Cholestatic hepatitis
3)Relapsing hepatitis
 Chronic sequelae: None

14.  Jaundice
 Fatigue
 Abdominal pain
 Loss of appetite
 Nausea
 Diarrhoea
 Fever

17.  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.

18. •Interruption of fecal-oral spread
•Avoidance of contaminated water or food
(undercooked shell fish)
•Proper handwashing in day care and
healthcare facilities
•Prophylaxis with immune globulin before
or early in incubation (< 2wks post
exposure) is 80 - 90% effective
•Killed vaccine is available for those at risk.
Safe and effective formalin inactivated
deployed cell grown vaccine, 2 IM doses at
2-4 week intervals

19. Viruses highly infectious as little as 0.00001 ml can transmit the disease

20.  Endemic throughout the world
 More than 2 billion people have
infection and around 350 million are
chronic carriers
 Every year 14-16 million people are
infected and 2 lakh deaths occur
 In India - 43-45 million HBsAg
carriers among which 10-12 million
have HBeAg

21.  Serum hepatitis
 Incubation period-6wks to 6months
 5-15% of cases go in for carrier state
 Persistent infection leads to CAH and
Ca liver
 Chronic infection:
<5 yrs, 30%-90%
>5 yrs, 2%-10%
 Premature mortality from
chronic liver disease-15%-25%

22. 1 Perinatal transmission
A carrier mother usually transmits hepatitis
B virus to an infant perinatally
2 Blood contact
Blood transfusion accidental contact with
an infected person's blood or body fluids through
skin cuts, abrasion, or mucosal membranes of the
eyes and mouths. Sharing injection instruments for
drug injection. Using contaminated instruments for
ear piercing, tattooing or acupuncture. Sharing
personal items such as razors, shavers or nail
trimmer which may have been contaminated with
blood
3 Sexual contact
Unprotected sexual contact with a carrier

23.  HBV – Dane particle
 HBsAg-AustraliaAg
Three types one group specific Ag Alpha and two pairs of type specific Ags d-y
and w-r (ayw,ayr,adw and adr)
Appears in the blood after a month and peak levels seen in pre icteric phase.
Anti HBsAg appears within a week of disappearance of surface Ag

24.  HBcAg –not detactable in serum but
demonstrated in liver by IF
 Anti HBcAg appears in the preicteric
phase
 HBeAg – hidden antigenic
component of the virus core.
Appears in the same time as HBsAg
but disappears soon.Directly
proportional with the no of viral
particles and degree of infectivity
 Anti Hbe-appears after the
disappearance ofAg

25. 1Chronic Persistent Hepatitis -
asymptomatic
2. Chronic Active Hepatitis -
symptomatic exacerbations of
hepatitis
3. Cirrhosis of Liver
4. Hepatocellular Carcinoma

28. Two categories based on serological markers.
1. Super carriers – HBeAg in blood – highly infectious.
-Very minute amounts of serum or blood from such carriers can transmit
the infection.
- Have high titres of HBsAg and DNA polymerase and mildly raised serum
transminase levels
- HBV may be demonstrable in their blood.
2. Simple carriers – more common type – no HBeAg.
- low level of HBsAg
- HBV and DNA polymerase are absent.
- transmit the infection only when large volumes of blood or serum are
transferred – blood transfusion.

29.  IP 2-6 months
 Onset insidious, fever is not prominent
 Rash,arthralgia, polyarthritis nodosa and
glomerulonephritis
 Some progress to chronic active hepatitis and
cirrhosis
 Primary hepatocellular Ca – late consequence
 Case fatality 0.5 –2 %

30. Serum markers.
The Ags and Abs are
detected in the serum by
ELISA,CIE,CF,RIA etc
 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.

31.  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.Detected by PCR

33.  Interferon - for HBeAg +ve carriers with chronic active
hepatitis. Response rate is 30 to 40%.
 Lamivudine - a nucleoside analogue reverse
transcriptase inhibitor. Well tolerated, most patients will
respond favorably. However, tendency to relapse on
cessation of treatment. Another problem is the rapid
emergence of drug resistance.
 Successful response to treatment will result in the
disappearance of HBsAg, HBV-DNA, and seroconversion
to HBeAg.

34.  Recombinant vaccine
 Three doses for both
children and adults.
 1ml for adults and
0.5ml for children
 0,1 and 6 months is
the dosage schedule

35.  HepatitiBImmunoglobul
in – (HBIG 200units/ml)
used to protect persons
who are exposed to
hepatitis B within 48
hours of the incident and
also can be given to
neonates whose mothers
are HBsAg and HBeAg
positive.0.5ml IM
 Other measures -
Screening of blood
donors, blood and body
fluid precautions

36.  Enveloped single stranded
RNA virus
 Common cause of post
transfusion hepatitis
 Resembles type B
hepatitis in clinical and
epidemiological features
 Inc period – average
50days
 About 150million carriers
seen in worldwide

37.  Transfusion or transplant
from infected donor
 Injecting drug use
 Hemodialysis (yrs on
treatment)
 Accidental injuries with
needles/sharps
 Sexual/household
exposure to anti-HCV-
positive contact
 Multiple sex partners
 Birth to HCV-infected
mother

38. HCV antibody
 To diagnose hepatitis C infection.
 Not useful in the acute phase as it takes at least 4 weeks
after infection before antibody appears.
HCV-RNA
 PCR and branched DNA.
 To diagnose HCV infection in the acute phase. However,
its main use is in monitoring the response to antiviral
therapy.
HCV-antigen - EIA

39. Interferon
 For patients with chronic active hepatitis.
 The response rate is around 50%
 50% of responders will relapse upon withdrawal of
treatment.
Ribavirin - Combination of interferon and ribavirin is
more effective than interferon alone.

40.  Screening of blood,
organ, tissue donors
 High-risk behavior
modification
 Blood and body
fluid precautions

41.  antigen
HBsAg
RNA
Hepatitis D (Delta) Virus

42.  Percutanous exposures
injecting drug abusers
 Permucosal exposures
 sex contact

43.  HBV-HDV
Co infection
Pre or post exposure
prophylaxis to prevent HBV
infection.
 HBV-HDV
Super infection
Education to reduce risk
behaviors among persons
with chronic HBV infection.

44.  Spherical non enveloped
single stranded RNA
virus
 Resembles HAV in clinical
course
 Often appears as
epidemics
 Inc per – average 6 weeks
 Mild and self limited

45.  Most outbreaks associated with faecally contaminated
drinking water.
 Several other large epidemics have in the Indian
subcontinent and the USSR, China, Africa and Mexico.
 In the United States and other nonendemic areas, a low
prevalence of anti-HEV (<2%) has been found in healthy
populations. The source of infection for these persons is
unknown.
 Minimal person-to-person transmission.

46.  Incubation period: Average 40 days
Range 15-60 days
 Case-fatality rate: Overall, 1%-3%
Pregnant women, 15% - 25%
 Illness severity: Increased with age
 Chronic sequelae: None identified

47.  Avoid drinking water (and beverages with
ice) of unknown purity, uncooked shellfish,
and uncooked fruit/vegetables
 IG prepared from donors in Western
countries does not prevent infection.
 Unknown efficacy of IG prepared from
donors in endemic areas.