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Viral hepatitis A

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viral hepatitis A

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Viral hepatitis A

  1. 1. HEPATITIS RAJALEKSHMY. P. R DEPT OF SWASTHAVRITTA AMRITA SCHOOL OF AYURVEDA 1
  2. 2. • It is the largest gland of the body. • Located behind the ribs in the right upper quadrant, from 5th-12th rib. • It weighs 1800gms in men and 1400gms in women. • It is divided into 4 lobes and multiple lobules. • It is connected to two large blood vessels, the hepatic artery and the portal vein. • These blood vessels subdivide into small capillaries known as liver sinusoids, which then lead to a lobule. LIVER: A GLANCE..... 2
  3. 3. LOBULE • The lobules are roughly hexagonal, and consist of plates of hepatocytes radiating from a central vein. • The central vein joins to the hepatic vein to carry blood out from the liver. • A distinctive component of a lobule is the portal triad, which can be found running along each of the lobule's corners. 3
  4. 4. Portal triad • Branch of the hepatic artery • branch of the hepatic portal vein • Bile duct 4
  5. 5. BLOOD SUPPLY • The hepatic portal vein delivers approximately 75% of the liver's blood supply, and carries venous blood drained from the spleen, gastrointestinal tract, and its associated organs. • The hepatic arteries supply arterial blood to the liver, accounting for the remaining quarter of its blood flow. • Blood flows through the liver sinusoids and empties into the central vein of each lobule. • Central vein hepatic vein inferior vena cava 5
  6. 6. Functions • Glucose metabolism • Protein metabolism • Fat metabolism • Vitamin and iron storage • Drug metabolism • Bile formation • Bilirubin excretion 6
  7. 7. HEPATITIS • Inflammation of the liver. • Hepatitis is acute when it lasts less than six months and chronic when it persists longer. • Acute hepatitis can be self-limiting can progress to chronic hepatitis, or, rarely, can cause acute liver failure. • Chronic hepatitis may have no symptoms, or may progress over time to fibrosis (scarring of the liver) and cirrhosis (chronic liver failure). • Cirrhosis of the liver increases the risk of developing hepatocellular carcinoma. 7
  8. 8. CAUSES Toxins Certain drugs Some diseases Heavy alcohol use Bacterial and viral infections 8
  9. 9. CLASSIFICATION Viral Non-viral Auto immune Bacterial Parasitic 9
  10. 10. VIRAL HEPATITIS Viral hepatitis is a systemic disease with primary inflammation of the liver by any one of a heterogeneous group of hepatotropic viruses. 10
  11. 11. CONTD….. •The most common causes of viral hepatitis are the five unrelated hepatotropic viruses - Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E. •In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include Herpes simplex, Cytomegalovirus, Epstein–Barr virus, Yellow fever or Rubella virus. 11
  12. 12. Viral Hepatitis A Viral Hepatitis B Viral Hepatitis C Viral Hepatitis D Viral Hepatitis E Agent Hepatitis A virus (HAV); ssRNA Hepatitis B virus (HBV); dsDNA Hepatitis C virus (HCV); ssRNA Hepatitis D virus (HDV); ssRNA Hepatitis E virus (HEV); ssRNA Route of Transmission Fecal-oral Parenteral, Vertical, Sexual. Parenteral Parenteral Fecal-oral Age affected Children Any age Adults Any age Young adults Carrier state Nil Common Present Nil (only with HBV) Nil Incubation period 10-50 days (avg. 25-30) 50-180 days (avg. 60-90) 40-120 days 2-12 weeks 2-9 weeks Chronic infection No Yes Yes Yes No Specific Ig and Ig and Nil HBV vaccine Nil 12
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  14. 14. INTRODUCTION • Hepatitis A refers to liver inflammation caused by infection with the hepatitis A virus(HAV). • HAV has been known as infectious jaundice since 1912. • Acc. To WHO, HAV had many names in the past: • Epidemic hepatitis • Epidemic jaundice • Infectious hepatitis • Catarrhal jaundice • HA and type A hepatitis 14
  15. 15. HISTORY • HAV is referred to as one of the oldest diseases known to mankind by the WHO. • It was recognized as a separate entity from other types of hepatitis during world war II. • It was discovered in1973 by Steven. M. Feinstone as a non enveloped, spherical, positive stranded RNA virus. • HAV was an unidentified viral disease prior to this discovery. 15
  16. 16. EPIDEMOLOGY • Globally, symptomatic HAV infections are believed to occur in around 1.5 million people a year. • In 2010, acute hepatitis A resulted in 102,000 deaths, which is slightly up from 99,000 in 1990. • Hepatitis A is much more common in countries with underdeveloped sanitation systems and, thus, is a risk in most of the world. • HAV is a common infection in developing nations of Africa, Asia, and Central and South America. 16
  17. 17. 17 INDIA • Largest outbreak occurred in Delhi in 1955-56, when more than 40000 people were affected, because of the contamination of river Yamuna with the sewage. • Even though, mortality is very low, incapacitation is very high resulting in great loss of human resource. • Another epidemic in Delhi in 1970 due to contamination of Okhla water supply.
  18. 18. Areas with high levels of infection • In developing countries with poor sanitation and hygiene, children are infected before age of 10 yrs. • Symptomatic disease rates are low. • Outbreaks are rare. Areas with intermediate levels of infection • In developing countries, countries with transitional economies and regions where sanitary conditions are variable, children escape infection in childhood. • Higher susceptibility in old age groups. • Higher disease rates • Large outbreaks can occur. Area with low levels of infection • In developed countries with good sanitary and hygienic condns: infection rates are low. • Disease may occur among adolescents and adults in high risk groups such as injecting drug users, homo sexual men, people travelling to areas of high endemicity and in isolated population such as closed religious community. 18
  19. 19. DENSITY OF HEPATITIS A INFECTION 20
  20. 20. INTEGRATED DISEASE SURVEILLANCE PROJECT 2010 21
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  24. 24. HEPATITIS A VIRUS • Naked RNA virus • Previously known as enterovirus(type 72). • One stable serotype only. • 7 genotypes exist(four human & three simian) • Difficult to grow in cell culture. • Human and vertebrates serve as natural hosts. • Replication in hepatocytes. 25
  25. 25. CONTD….. • Fairly resistant to low pH, heat and chemicals. • Survives more than 10 weeks in well water. • Resistant to heat at 60 degree Celsius for 1 hr. • Not affected by chlorination. • Formalin-effective disinfectant. • Virus inactivated by UV rays, boiling(5 mts) or autoclaving. • Viral particles first demonstrated in liver cells by workers in Phoenix laboratory in Arizona- hence called phoenix antigen. 26
  26. 26. RESERVOIR •Human reservoir(active clinical case or sub clinical case or a carrier-healthy/incubatory). •Subclinical cases and carriers are responsible for the endemicity of the disease in community. •No evidence of chronic carrier state. •Asymptomatic infections are common in children. 27
  27. 27. PERIOD OF INFECTIVITY • Risk of transmitting HAV is greatest from 2 weeks before to 1 week after the onset of jaundice. • Infectivity falls rapidly with the onset of jaundice. 28
  28. 28. INFECTIVE MATERIAL • Mainly man’s faeces • Blood, serum and other fluids(during stage of viraemia) 29
  29. 29. VIRUS EXCRETION • HAV is excreted in faeces for about 2 weeks before onset of jaundice and for upto 2 weeks thereafter. • Also excreted in urine. 30
  30. 30. HOST FACTORS Age Frequent among children than adults. People from all ages get infected (if susceptible). Severity increases with age. Anicteric : icteric 1:3(adults) 12:1(children) Sex Both sex are equally susceptible. Immunity Acquired after an infection. Immunity after attack lasts for life. Second attack reported in about 5% patients. 31 Pregnancy VHA during pregnancy carries a high mortality. No transplacental transmission
  31. 31. ENVIRONMENTAL FACTORS • Can occur throughout the year • In India, associated with heavy rainfall. • Poor sanitation and over crowding favours spread of infection. 32
  32. 32. TRANSMISSION • Faecal oral route • Direct contact(person to person) • Indirect- contaminated water, food or milk • In developed countries, foodborne outbreaks are frequent. • Eg. Consumption of salads, vegetables and raw or inadequately cooked shellfish cultivated in sewage polluted water. 33
  33. 33. • Parenteral route • Occur during the stage of viremia • Rare; mode is of minor importance. • Eg. By blood or blood products or skin penetration through contaminated needles • Sexual transmission • Occurs in homo sexual men • Oral anal contact Unknown 52% Intl travel 5% Household/ sexual 25% Outbreak 3% Day care 15% 34
  34. 34. INCUBATION PERIOD • 10-50 days( usually 14-28 days). • Length of incubation period proportional to dose of virus ingested. 35
  35. 35. PATHOGENESIS 36
  36. 36. •After ingestion, the HAV survives in gastric acid, moves to the small intestine and reaches the liver via the portal vein. •Replicates in hepatocyte cytoplasm. •Degeneration and necrosis of hepatocytes. •Affects liver functions- hyperbilirubinaemia-jaundice •Inflammation of liver-hepatomegaly-pressure effects on other organs. 37
  37. 37. CLINICAL FEATURES 38 Pre-icteric stage • Sudden onset of fever, chills, fatigue, malaise, head ache and body ache • Within a day or two, develops gastro intestinal symptoms • High coloured urine, light coloured stools lasting for about of 3 to 5 days. Icteric stage • Onset of jaundice • With onset of jaundice, fever subsides. • Sclera looks yellow and skin looks lemon tinged. • Nausea and vomiting decreases. • High coloured urine continues for several days. • Jaundice usually reaches maximum by 2 weeks and decreases steadily thereafter. • Stage lasts for 4 to 6 weeks.
  38. 38. 39 Convalescent stage • After about 6 to 8 weeks, inflammatory process comes down, there is regeneration of cells. • Appetite improves • Icterus disappears • Urine and stools become normal • Stage lasts for 2 to 6 weeks.
  39. 39. • Resolves in 98% cases but relapse of symptoms noted in 3-20% cases. Outcome Children Adults Sub clinical infection 80-95% 10-25% Icteric disease 5-20% 75-90% Complete recovery > 98% > 98% Chronic disease None None Mortality rate 0.1% 0.1% 40
  40. 40. 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Week Response Clinical illness ALT IgM IgG HAV in stool Infection Viremia EVENTS IN HEPATITIS A VIRUS INFECTION 41
  41. 41. CONCENTRATION OF HEPATITIS A VIRUS IN VARIOUS BODY FLUIDS Source: Viral Hepatitis and Liver Disease 1984;9-22 J Infect Dis 1989;160:887-890 Feces Serum Saliva Urine 100 102 104 106 108 1010 BodyFluids Infectious Doses per mL 42
  42. 42. COMPLICATIONS • Fulminant hepatitis A/acute liver failure is a rare but devastating complication of HAV infection. • HAV liver parenchymal cells release of toxins • The cell then produces new viral components that are released into the bile capillaries hepatic necrosis. • The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells. • Fulminant hepatic failure can also lead to encephalopathy and cerebral oedema. 43
  43. 43. DIAGNOSIS • Demonstration of HAV particles in the faeces, bile or blood. • HAV is detected in the stool from about 2 weeks prior to the onset of jaundice and 2 weeks thereafter. • Anti HAV appears in IgM fraction during acute phase. • Anti HAV IgM usually declines to non detectable level within 3-6 months. • Anti HAV IgG appears more slowly and persist for decades. • Acute infection is diagnosed by the detection of HAV-IgM in serum by (enzyme immunoassay)EIA. • Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA. 44
  44. 44. CONT…. • Detection of Antibody: By ELISA • Biochemical tests: • i) Alanine aminotransferase (ALT) • ii) Bilirubin • Demonstration of viral particles in the stools by electron microscopy. 45
  45. 45. PREVENTION Control of reservoir • Complete bed rest • Disinfection of faeces and fomite Control of transmission • Promote simple measures of personal and community hygiene • Eg. Hand washing before and after toilet • Sanitary disposal of excreta • Purification of community water supply 46
  46. 46. Control of susceptible population Passive immunization-human normal immunoglobulin Prepared from pooled plasma of multiple donors. Agent/condition Target population Preparation Dose Hepatitis A Family contacts Institutional outbreaks IG 0.02 ml/kg of body weight(3.2 mg/kg of body weight) Travellers exposed to unhygienic conditions in tropical or developing countries IG 0.02-0.05 ml/kg of body weight(3.2-8.0 mg/kg of body weight) Once in 4 months 47
  47. 47. VACCINATION • Formaldehyde inactivated vaccine • Live attenuated vaccines Produced in several countries World wide used Manufactured in China Available in several countries 48
  48. 48. INACTIVATED VACCINE • Cell cultured liquid vaccine • Hepatitis virus of HM-175 strain( F strain) is propagated on human diploid cells, purified by ultra filtration technique and inactivated by formaldehyde and adsorbed on aluminium hydroxide. • Dose: adults-1 ml; children-0.5ml given IM in deltoid region. • Licensed for use in children above 12 months of age. • Interval between the first and second booster dose: 6-12 months 49
  49. 49. • Immunity lasts for 15-20 yrs. • Marketed as HAVRIX. • Storage temp: 2-8˚ C • A combination vaccine containing inactivated Hepatitis A and Hepatitis B vaccine has been licensed since 1966 for children in several countries. • Schedule of combined vaccine is 0, 1 and 6 months. • Combination of hepatitis A and B, hepatitis A and typhoid vaccine are developed for travellers. 50
  50. 50. LIVE VACCINE • Live attenuated freeze dried vaccine containing H2 strain of hepatitis A virus. • Single dose of 0.5ml is administered subcutaneously in deltoid region for all above one year of age. • Safe, immunogenic with good tolerability • No booster dose required. • Storage temp: 2-8˚C. • Recommended for both pre exposure prophylaxis of high risk individuals and post exposure prophylaxis. • Marketed as Biovac-A. 51
  51. 51. WHO SHOULD BE VACCINATED? • All children at age 1 year (i.e., 12–23 months) • Children and adolescents ages 2–18 who live in states or communities where routine Hepatitis A vaccination has been implemented because of high disease incidence • Persons traveling to or working in countries that have high or intermediate rates of Hepatitis A. • Homo sexuals • Users of illegal injection • Persons who have occupational risk for infection • Persons who have chronic liver disease. 52
  52. 52. VACCINES IN INDIA No Brand Name Manufacturers Type 1 Avaxim Aventis Pasteur India Ltd Injection 2 Avaxim 80U Paediatric Aventis Pasteur India Ltd Injection 3 Havrix Glaxo Smithkline Pharmaceuticals Ltd. Injection 4 Havrix (360) Glaxo Smithkline Pharmaceuticals Ltd. Injection 5 Havrix (720) Glaxo Smithkline Pharmaceuticals Ltd. Injection 53
  53. 53. THANK YOU 54

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