Viral Hepatitis

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INTRODUCTION  

Hepatitis – causes inflammation of LIVER Primarily attack HEPATOCYTES

Healthy Liver

Inflammation of the liver

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TYPES 

Different types of Hepatitis virus  Hepatitis A Virus (HAV)  Hepatitis B Virus (HBV)  Hepatitis C Virus (HCV)  Hepatitis D Virus (HDV)  Hepatitis E Virus (HEV)  Hepatitis F Virus (HFV)  Hepatitis GVirus (HGV)

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Clinical features are similar but Hepatitis B & C are also responsible for Hepatocellular carcinoma INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

HEPATITIS B VIRUS INTRODUCTION HBV 

1960s – Blumberg & his collegues observed an antigen in haemophiliacs from Australian and named Australia antigen (Au)

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1968 – this antigen associated with acute & chronic hepatitis

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named as HBV INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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MORPHOLOGY

Family – Hepadnavirida  Icosahedral, spherical, enveloped, complex 42nm double shelled particle 

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ANTIGENIC STRUCTURE

Envelope contains – HB surface antigen (HBsAg)  Core contains HB core antigen (HBcAg) (antibodies produce against HBcAg during primary infection)  HBe antigen – not a viral particle, translated from RNA (reliable marker for infectivity) 

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Under Electron microscope HBsAg has three parts

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Spherical – 22nm in diameter

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Tubular or Filamentous – 22nm in diameter

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Dane particle – double shelled 42nm in diameter resembles original HBV structure INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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SOURCE  Blood and blood

products  All secretions (saliva, sweat, vaginal etc)  All fluids (CSF, semen etc) 

MODE OF TRANSMISSION  Sexual

contact  Vertical transmission  Injecting drug users  Nosocomial exposure  Community used razor and tooth brushes INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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SUSCEPTIBLE HOST

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Health care personnel IV drug users Haemophiliacs Renal dialysis patients Infants born to infected mothers

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SECRETIONS

BLOOD

FLUIDS

HBV PATHOGENESIS LIVER

PRIMARY

CHRONIC

IMMUNE COMPLEX

TISSUE DAMAGE

SERUM SICKNESS

NECROTIC FOCI

POLYARTERITIS NODOSA

HEPATOMEGALY

RECOVERY CIRRHOSIS HEPATOCELLULAR CARCINOMA

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MGN

HEPATOCELLULAR CARCINOMA

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CLINICAL FEATURES  

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Incubation period – 40 to 180 days Manifestation:  Primary Hepatitis  Chronic Hepatitis  Combined Hepatitis Primary hepatitis: Signs & symptoms begin 60 to 110 days after exposure to HBV INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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SIGNS –Fever, urticaria, arthralgia, arthritis, rashes.

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SYMPTOMS – Fever, anorexia, malaise, vomitting, headache, intense itching.

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Many patients are anicteric; some develop hepatomegaly Adults – recover in 4 to 7 weeks Children – recover about 2 weeks Death is rare Associated with HDV coinfection

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CHRONIC HEPATITIS

About 1 to 10 % of adults & 80 to 95 % of infants recover from primary hepatitis will become chronically infected - CPH or CAH  Chronic persistent hepatitis (CPH) – patients develop no liver damage  Chronic active hepatitis (CAH)– continuous regenerative type of liver damage leads to cirrhosis, hepatocellular carcinoma or both

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COMBINED INFECTION

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HBV associated with HDV infection Patient develop single episode of combined infection (HBV&HDV) HBV disease followed by HDV Co–infection or super infection is more severe & mortality rate is high (20 %)

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CARRIER STATE 

Two types of carriers – simple & super carriers

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Simple carriers – have surface antigens of HBV

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Super carriers – have both surface and early antigen of HBV

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LAB DIAGNOSIS  

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By clinical data Liver function test  Alanine amino transferase – gradual rise with longer duration indicates HBV infection  Bilirubin & serum globulin increases; serum albumin decreases. SEROLOGY  Surface antigen – ELISA, Latex agglutination test  Antigens – immunoflourescent test

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SEROMARKERS  Recent infection – HBsAg & IgM antibodies to HBcAg (3-5 wks before onset of symptoms)  Chronic infection – anti HBcAg  Past infection – IgG antibodies

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MOLECULAR TECHNIQUES  detection and quantitation of viral DNA by PCR

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DEMONSTRATION OF HBV (not in routine diagnosis)  Human & Simion cells are used  Produce cytopathic effect INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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TREATMENT  Alpha interferon + Lamivudin

PREVENTION Prevented by administration of immune prophylaxis - VACCINATION  Plasma derived vaccine / pooled hyper immune sera Prepared from donors with high titre of anti HBsAg 

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Recombinant DNA vaccine -Produced by cloning HBsAg in yeast cells ( Saccharomyces cerivasiae)   

Administered in three doses (0 month, 1 month after 1st dose and 6 months after 1ST dose) Children – (0.5 ml three doses) 0m, 1m, 6m Adult – (1 ml three doses) 0m,1m, 6m INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

Who should be vaccinated?  Post exposure prophylaxis (PEP)  Haemodialysis patients  Homosexually active men  Drug user  Infants born to infected mother  Personal contact with HBV patients  Other high risk population like health Care workers  Now it is part of the regular immunization schedule for children INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

UNIVERSAL PRECAUTION HEALTH CARE WORKERS      

Wear personal protective equipment (gloves, gowns etc) Hand hygiene Use disposable and sterile needles Do not recap the used needles Avoid mouth pipetting Always transport the specimen with BioHazard sign INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

Other prevention methods:  Pre-screening of blood, blood products and donors for organ or tissue transplant for HBV,HCV, HIV is mandatory 

Change in life style - ie avoid exposure to HBV carriers or patients

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Avoid sharing personal hygiene products

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Use sterile and disposable needles

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HEPATITIS C VIRUS 

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Parenterally transmitted non A – non B Hepatitis (NANB) Small, enveloped,35 to 60 nm in size contains positive sense,single stranded RNA virus Related to human Flaviviruses Placed in the genus Hepatitis C Virus

TRANSMISSION  Same as HBV  Verticle & sexual transmission is less than HBV

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INCUBATION PERIOD – 5 to 12 weeks  Peak onset of disease 7 to 8 wks after infection CLINICAL MANIFESTATION  80 % are asymptomatic in acute phase  Symptoms – Fatigue, loss of appetite, jaundice, abdominal pain, itching, hives, joint pain, nausea, vomitting  Chronic infection cause above symptoms + weakness, severe fatigue  Serious complication of HCV include  Cirrhosis of liver & progressive liver damage  Increased risk of liver cancer

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DIAGNOSIS  By clinical data 

Liver function test  ALT shows fluctuating rise

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Serology  Detection of anti HCV antibodies by ELISA & Recombinant Immuno Blot Assay (RIBA)  Detection & quantitation of genetic material from the viruses by RT-PCR

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Hepatitis C Virus Infection Typical Serologic Course anti-HCV

Titer

Symptoms

ALT

Normal 0

1

2

3 4 Months Months

5

6

1

2 3 Years

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4

TREATMENT  Recombinant alpha interferon is the only therapeutic agent approved by US  No vaccine is available PREVENTION  Tranfusion of safe blood & blood products  All HCV positive persons – infectious  Do not allow HCV positive persons or carriers to donate blood or organs  Other control measures are same as HBV

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HEPATITIS A VIRUS INTRODUCTION   

Also known as Infectious Hepatitis Family – Picornaviridae Genus – Enterovirus type 72

HAV

MORPHOLOGY  

Icosahedral, spherical, naked virus of 27 nm in diameter. Virus contains ssRNA as genome.

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SOURCE  Sewage

contaminated water,  Contaminated food. 

MODE OF TRANSMISSION  *Feco-oral route.  *Affect food handlers &

in area with poor sanitation.

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PATHOGENESIS FOOD

WATER INGESTION INTESTINE BLOOD PARENCHYMAL

KUPFFER

LIVER REPLICATION BILE

STOOL

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CLINICAL MANIFESTATION 

SUB CLINICAL – anicteric, undiagnosed.

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CLINICAL – preicteric and icteric Incubation period – 2 to 6 weeks (mean – 28 days)

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Preicteric : fever, chills, nausea, vomitting, abdominal discomfort.

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Icteric :  appearance of dark colour urine,  clay coloured stool,  jaundice of sclera & skin,  hepatomegaly (right quadrant abdominal pain) INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

DIAGNOSIS  

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By clinical data Liver function test (Biochemical analysis)  Alanine amino transferase – sharp rise with short duration  Bilirubin increases upto 5 – 20 mg/dl  Serum albumin increases& globulin decreases. Serology  Antigen detection – Immunoflourescent test  Antibody (IgM) detection – ELISA  Presence IgG indicates past infection

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TREATMENT  No specific drug is available

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PREVENTION  Personal hygeine  Good sanitation

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VACCINE  Formalin inactivated cell culture derived vaccine  Recommended for – children at 1 yr of age and  high risk population

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HEPATITIS E VIRUS

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STRUCTURE    

Small round non enveloped virus Contains positive ssRNA genome Size 29nm Belongs to the family Calcivirus

SALIENT FEATURES  Resembles HAV  Adults are morre infected  Occurs as outbrreaks  No vaccine is available INVISIBLE YET INVINCIBLE © http://medicalmicro.blogspot.com

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Mortality rate is high if women affected in third trimester stage of pregnancy SOURCE faecally contaminated water

MODE OF TRANMISSION Oro faecal route  PATHOGENESIS  Not clear 

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LAB DIAGNOSIS

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Detection of IgM or IgG antibodies – ELISA HEV detectiion by PCR is under development.

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TREATMENT & CONTROL No specific treatment Prevented by safe drinking of water No vaccine available

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