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1. Viral Hepatitis: ABCDE NEPMU-2 Norfolk, VA (757) 444-7671

2. Objectives Describe the Clinical Syndromes of Viral Hepatitis List the modes of Transmission Understand and be able to interpret Diagnostic (laboratory) tests Know the Treatment and Occupational Impact of Viral Hepatitis List Preventive Measures for each Hepatitis type Describe Immunization protocols

3. Hepatitis Inflammation of the Liver that can be viral, chemical or drug-induced Viral Hepatitis: Systemic infection which causes inflammation of the liver Currently 5 recognized types of viral hepatitis: A, B, C, D, E All 5 viruses cause similar illness, but have distinct antigenic properties

4. Acute Hepatitis: Symptoms Malaise 76-94% Anorexia 71-96% Dark urine 65-94% Nausea 61-81% Abdominal pain 26-68% Scleral icterus 48% Vomiting 20-37%

5. Acute Hepatitis: Signs Jaundice 70-90% Hepatomegaly 14-69% Tender liver 20-86% Rash 40% Splenomegaly 3-21% Fever 1-8% High LFTs 100%

7. Estimates of Acute and Chronic DiseaseBurden for Viral Hepatitis, United States

8. Other Viruses Associatedwith Acute Hepatitis Common in U.S.* Cytomegalovirus Epstein-Barr Herpes simplex Varicella zoster Measles Rubella Coxsackie Exotic** Yellow fever Argentinean hemorrhagic fever Bolivian hemorrhagic fever Lassa fever Rift Valley fever Marburg Ebola

9. Hepatitis Laboratory Tests Liver function tests Enzymes produced by liver cells that increase when the liver is stimulated or inflamed Antigen and Antibody tests Immunology Terms ANTIBODY (Immunoglobulin, Ig, Anti- ) A protein in the blood generated in response to foreign proteins or polysaccharides. Sometimes antibodies provide protection from infection. IgM : Acute Infection IgG : Appears slightly after IgM, may persist for life Total Ig = IgM + IgG Examples: Anti-HAV, Anti-HBsAg ANTIGEN (Ag) Substances that stimulate production of an antibody, Usually protein components of an infectious agent Examples: HBsAg, HAV

10. Caused by a small RNA enterovirus of the picornavirus family Causes about 25-50% of acute hepatitis in the U.S. and other developed countries High prevalence in west Pacific, Southeast Asia, Africa and other developing countries Hepatitis A�infectious hepatitis, epidemic hepatitis�

13. Onset: usually abrupt Duration Mild lasting 1-2 weeks Severe lasting months Rarely fatal Children usually asymptomatic 5-10% jaundiced 1-2 week duration Adults are usually symptomatic Jaundiced Nausea, vomiting, & fever are common. Hepatitis A: Clinical Aspects

14. Hepatitis A: Clinical Aspects Incubation 15-45 days, average 30 days Greatest infectivity 2 wks before jaundice appears Fecal viral shedding Greatest during late incubation and prodrome Diminishes rapidly after jaundice occurs

15. Hepatitis A: Transmission PERSON TO PERSON (Fecal-Oral Routes) Poor personal hygiene Intimate contact Contaminated food or water Poor sanitation NOT transmitted by sharing utensils, cigarettes, kissing Transmission of HAV generally occurs as a result of ingestion by a susceptible person of virus shed in the feces of an infected person. Close personal contact is the most common mode of HAV transmission as demonstrated by high rates of infection among household and sex contacts of persons with hepatitis A and among children in day care center outbreaks. Contaminated food and water can also serve as vehicles of HAV transmission; the vehicles of transmission in foodborne outbreaks are most often uncooked foods or foods touched by human hands after cooking, but outbreaks have been reported in association with foods contaminated before wholesale distribution. Because HAV can survive for 12 weeks to 10 months in water, infection can occur by ingestion of a variety of raw shellfish harvested from sewage-contaminated areas. Waterborne outbreaks have also been reported both in association with drinking focally contaminated water and with swimming in contaminated swimming pools and lakes. In addition, HAV transmission can occur as a result of blood exposures such as injecting drug use or blood transfusion because viremia can occur prior to onset of illness in infected persons; however, such transmission is rare. Transmission of HAV generally occurs as a result of ingestion by a susceptible person of virus shed in the feces of an infected person. Close personal contact is the most common mode of HAV transmission as demonstrated by high rates of infection among household and sex contacts of persons with hepatitis A and among children in day care center outbreaks. Contaminated food and water can also serve as vehicles of HAV transmission; the vehicles of transmission in foodborne outbreaks are most often uncooked foods or foods touched by human hands after cooking, but outbreaks have been reported in association with foods contaminated before wholesale distribution. Because HAV can survive for 12 weeks to 10 months in water, infection can occur by ingestion of a variety of raw shellfish harvested from sewage-contaminated areas. Waterborne outbreaks have also been reported both in association with drinking focally contaminated water and with swimming in contaminated swimming pools and lakes. In addition, HAV transmission can occur as a result of blood exposures such as injecting drug use or blood transfusion because viremia can occur prior to onset of illness in infected persons; however, such transmission is rare.

16. Concentration of Hepatitis A Virusin Various Body Fluids Feces can contain up to 108 infectious virions per ml and are the primary source of HAV. Viremia occurs during the prodromal phase of illness and HAV has been transmitted on rare occasions by transfusion. Virus has also been found in saliva during the incubation period in experimentally infected animals, but transmission by saliva has not been reported to occur. Feces can contain up to 108 infectious virions per ml and are the primary source of HAV. Viremia occurs during the prodromal phase of illness and HAV has been transmitted on rare occasions by transfusion. Virus has also been found in saliva during the incubation period in experimentally infected animals, but transmission by saliva has not been reported to occur.

17. Hepatitis A: Diagnosis Acute symptoms Elevated LFTs Confirmation: IgM anti-HAV, appears early and remains detectable for 4-6 months Total anti-HAV (combination of IgM & IgG) is detectable early and persists lifelong. It is not diagnostic of acute Hepatitis A. About 1/3 of the US population has anti-HAV IgG

19. Sources of Hepatitis A Virus Infection byMutually Exclusive Groups, United States, 1983-93

20. Hepatitis A produces occasional mortality, with an estimated 100 deaths each year in the United States due to fulminant hepatitis A. The overall case-fatality rate is approximately 0.4%; the highest case-fatality rate is among persons >49 years of age (17.5 per 1000). In this age group, preexisting chronic liver disease appears to be associated with an increased risk of death from acute hepatitis A. Hepatitis A produces occasional mortality, with an estimated 100 deaths each year in the United States due to fulminant hepatitis A. The overall case-fatality rate is approximately 0.4%; the highest case-fatality rate is among persons >49 years of age (17.5 per 1000). In this age group, preexisting chronic liver disease appears to be associated with an increased risk of death from acute hepatitis A.

21. Hepatitis A: Prevention Immunization Sanitation & Education Safe food, water and ice Good personal hygiene Standard Immune globulin prophylaxis (IG) 80 - 90% effective if given within two weeks of exposure Immunization 2 weeks prior eliminates need Indications: Close personal contacts Day Care center outbreaks Fellow food handlers Restaurant patrons if deficiencies in hygiene or if handler prepared unheated food IG provides protection against HEP A through passive transfer of AB. It is given intramuscularly for the prevention of HAV. When used for pre-exposure prophylaxis a dose of .02ml/kg of IGIM confers protection for <3 months, and a dose of .06 ml/kg IM confers protection for <=5 months. When administered within 2 weeks following an exposure to HAV (.02 ml/kg IM), IG is >85% effective in preventing HEP A.IG provides protection against HEP A through passive transfer of AB. It is given intramuscularly for the prevention of HAV. When used for pre-exposure prophylaxis a dose of .02ml/kg of IGIM confers protection for <3 months, and a dose of .06 ml/kg IM confers protection for <=5 months. When administered within 2 weeks following an exposure to HAV (.02 ml/kg IM), IG is >85% effective in preventing HEP A.

22. Hepatitis A Vaccine Two dose series: Initial plus booster in 6-12 months All Active duty and Select Reserves 95% protection after first dose Four week period for antibody development HAVRIXR OR VAQTAR, interchangeable TWINRIXR (Hepatitis A&B combination vaccine) Three dose series Interchangeability: dose 1 with TwinrixR - give 2nd dose of HAVRIXR OR VAQTAR A and 2 & 3rd dose of HEP B vaccine Dose 1 and 2 with TwinrixR � Another dose of HAVRIXR OR VAQTAR not necessary, give dose 3rd dose of HEP B vaccine Recommended Doses and Schedules of Hepatitis A Vaccine HAVRIX� (by SmithKline Beecham Biologicals) & VAQTA (by Merck & Co)�Note: VAQTA pediatric dose is now good to up to 18 y/o also. Doses  Children and adolescents 2-18 years Adults >18 years HAVRIX EL.U.* (ml) 720 El U (.5 ml) at 0, 6-12 mo 1440 ELU (1ml) at 0, 6-12 VAQTA UNITS 25 U (.5 ml) 0, 6-18 mo 50 U (1ml) at 0, 6  The vaccine should be given by intramuscular injection into the deltoid muscle. Recommended Doses and Schedules of Hepatitis A Vaccine HAVRIX� (by SmithKline Beecham Biologicals) & VAQTA (by Merck & Co)�Note: VAQTA pediatric dose is now good to up to 18 y/o also. Doses Children and adolescents 2-18 years Adults >18 years HAVRIX EL.U.* (ml) 720 El U (.5 ml) at 0, 6-12 mo 1440 ELU (1ml) at 0, 6-12 VAQTA UNITS 25 U (.5 ml) 0, 6-18 mo 50 U (1ml) at 0, 6

23. Hepatitis A and Food Workers High potential for outbreaks Verify Diagnosis Evaluate food related duties, types of food & preparation methods Some food related work low-risk Wearing gloves reduces risk Fellow food handlers are more at risk than diners If a food handler is diagnosed with HEP A, IG should be administered to other food handlers at the same establishment. Because common-source transmission to patrons is unlikely, IG administration to patrons is usually not recommended but can be considered if: During the time when the food handler was likely to be infectious, the food handler both directly handled uncooked foods or foods after cooking and had diarrhea or poor hygienic practices and: Patrons can be identified and treated within 2 weeks after the exposure. In settings where repeated exposure to HAV might have occurred (ex. Institutional cafeterias), stronger considerations of IG use might be warranted. In the event of a common-source outbreak, IG should not be administered to exposed persons after cases have begun to occur because the 2-week period during which IG is effective will have been exceeded.If a food handler is diagnosed with HEP A, IG should be administered to other food handlers at the same establishment. Because common-source transmission to patrons is unlikely, IG administration to patrons is usually not recommended but can be considered if: During the time when the food handler was likely to be infectious, the food handler both directly handled uncooked foods or foods after cooking and had diarrhea or poor hygienic practices and: Patrons can be identified and treated within 2 weeks after the exposure. In settings where repeated exposure to HAV might have occurred (ex. Institutional cafeterias), stronger considerations of IG use might be warranted. In the event of a common-source outbreak, IG should not be administered to exposed persons after cases have begun to occur because the 2-week period during which IG is effective will have been exceeded.

25. Hepatitis E Symptoms similar to hepatitis A: Malaise, lethargy, anorexia, nausea and vomiting, followed by dark urine, pale stools, and jaundice Caused by Calicivirus Produces symptoms mostly in 15-40 year olds Children usually have sub-clinical infection Outbreak potential 15-60 day incubation period, usually 5-6 weeks No chronic carriers: self-limited Severely affects pregnant women with a the mortality rate of 10-20% Overall mortality rate is 0.5-3%

26. Incubation period: Average 40 daysRange 15-60 days Case-fatality rate: Overall, 1%-3% Pregnant women, 15%-25% Illness severity Increased with age Chronic sequelae: None identified Notes:The incubation period following exposure to HEV ranges from 15 to 60 days (mean, 40 days). Typical clinical signs and symptoms of acute hepatitis E are similar to those of other types of viral hepatitis and include abdominal pain anorexia, dark urine, fever, hepatomegaly, jaundice, malaise, nausea, and vomiting. Other less common symptoms include arthralgia, diarrhea, pruritis, and urticarial rash. The period of infectivity following acute infection has not been determined but virus excretion in stools has been demonstrated up to 14 days after illness onset. In most hepatitis E outbreaks, the highest rates of clinically evident disease have been in young to middle-age adults; lower disease rates in younger age groups may be the result of anicteric and/or sub clinical HEV infection. No evidence of chronic infection has been detected in long-term follow-up of patients with hepatitis E. Incubation period: Average 40 daysRange 15-60 days Case-fatality rate: Overall, 1%-3% Pregnant women, 15%-25% Illness severity Increased with age Chronic sequelae: None identified Notes:The incubation period following exposure to HEV ranges from 15 to 60 days (mean, 40 days). Typical clinical signs and symptoms of acute hepatitis E are similar to those of other types of viral hepatitis and include abdominal pain anorexia, dark urine, fever, hepatomegaly, jaundice, malaise, nausea, and vomiting. Other less common symptoms include arthralgia, diarrhea, pruritis, and urticarial rash. The period of infectivity following acute infection has not been determined but virus excretion in stools has been demonstrated up to 14 days after illness onset. In most hepatitis E outbreaks, the highest rates of clinically evident disease have been in young to middle-age adults; lower disease rates in younger age groups may be the result of anicteric and/or sub clinical HEV infection. No evidence of chronic infection has been detected in long-term follow-up of patients with hepatitis E.

27. Outbreaks of hepatitis E have occurred over a wide geographic area, primarily in developing countries with inadequate environmental sanitation. The reservoir of HEV in these areas is unknown. The occurrence of sporadic HEV infections in humans may maintain transmission during interepidemic periods, but a nonhuman reservoir for HEV is also possible. In the United States and other nonendemic areas, where outbreaks of hepatitis E have not been documented to occur, a low prevalence of anti-HEV (<2%) has been found in healthy populations. The source of infection for these persons is unknown. Outbreaks of hepatitis E have occurred over a wide geographic area, primarily in developing countries with inadequate environmental sanitation. The reservoir of HEV in these areas is unknown. The occurrence of sporadic HEV infections in humans may maintain transmission during interepidemic periods, but a nonhuman reservoir for HEV is also possible. In the United States and other nonendemic areas, where outbreaks of hepatitis E have not been documented to occur, a low prevalence of anti-HEV (<2%) has been found in healthy populations. The source of infection for these persons is unknown.

28. Hepatitis E: Diagnosis Serologic test available History: Evaluate risk factors, exposure history Rule out hepatitis A IgG WILL NOT PROTECT No serologic tests to diagnose HEV infection are commercially available in the United States. However, several diagnostic tests are available in research laboratories, including enzyme immunoassays and Western blot assays to detect IgM and IgG anti-HEV in serum, polymerase chain reaction tests to detect HEV RNA in serum and stool, and immunofluorescent antibody blocking assays to detect antibody to HEV antigen in serum and liver. No serologic tests to diagnose HEV infection are commercially available in the United States. However, several diagnostic tests are available in research laboratories, including enzyme immunoassays and Western blot assays to detect IgM and IgG anti-HEV in serum, polymerase chain reaction tests to detect HEV RNA in serum and stool, and immunofluorescent antibody blocking assays to detect antibody to HEV antigen in serum and liver.

29. Prevention of hepatitis E relies primarily on the provision of clean water supplies. Prudent hygienic practices that may prevent hepatitis E and other enterically transmitted diseases among travelers to developing countries include avoiding drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruits or vegetables that are not peeled or prepared by the traveler. No products are available to prevent hepatitis E. IG prepared from plasma collected in non-HEV-endemic areas is not effective in preventing clinical disease during hepatitis E outbreaks and the efficacy of IG prepared from plasma collected in HEV-endemic areas is unclear. In studies conducted to date with prototype vaccines in animals, vaccine-induced antibody attenuated HEV infection, but did not prevent virus excretion in stools. If a vaccine is developed, the epidemiology of hepatitis E needs to be further defined in order to determine whether vaccination strategies could be effectively used to prevent this disease. Prevention of hepatitis E relies primarily on the provision of clean water supplies. Prudent hygienic practices that may prevent hepatitis E and other enterically transmitted diseases among travelers to developing countries include avoiding drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruits or vegetables that are not peeled or prepared by the traveler. No products are available to prevent hepatitis E. IG prepared from plasma collected in non-HEV-endemic areas is not effective in preventing clinical disease during hepatitis E outbreaks and the efficacy of IG prepared from plasma collected in HEV-endemic areas is unclear. In studies conducted to date with prototype vaccines in animals, vaccine-induced antibody attenuated HEV infection, but did not prevent virus excretion in stools. If a vaccine is developed, the epidemiology of hepatitis E needs to be further defined in order to determine whether vaccination strategies could be effectively used to prevent this disease.

31. Hepatitis B Virus Structure

32. Hepatitis B�serum hepatitis, post-transfusion hepatitis� Double shelled DNA hepadnavirus Spread by sex, blood, and body fluids Severe disease Prolonged illness Chronic problems in ~ 10%

34. Hepatitis B: Clinical Aspects Incubation period: 45-180 days, average 60-90 days Onset insidious (subtle and treacherous) Symptoms more severe Malaise, arthralgias, rash, nausea & vomiting Often hospitalized One in 200 die from acute disease Chronic liver disease kills ten times as many

35. Hepatitis B: Transmission Virus present in blood, semen, saliva Percutaneous Contaminated needles (tattoos, piercing, drugs, etc) Blood transfusion Perinatal Permucosal Sexual contact Continuous close contact

36. Notes:HBV is transmitted by percutaneous or permucosal exposure to infectious blood or body fluids from persons who have either acute or chronic HBV infection. The highest concentrations of virus are in blood and serous fluids; lower concentrations are found in semen, vaginal fluid, and saliva. Therefore, blood exposure and sex contact are relatively efficient modes of transmission. Saliva can be a vehicle of transmission through bites; however, transmission has not been documented to occur as a result of other types of exposure to saliva, including kissing. HBsAg has also been detected in low concentrations in other body fluids, including tears, sweat, urine, feces, breast milk, cerebrospinal fluid, and synovial fluid; however, these fluids have not been associated with transmission. Notes:HBV is transmitted by percutaneous or permucosal exposure to infectious blood or body fluids from persons who have either acute or chronic HBV infection. The highest concentrations of virus are in blood and serous fluids; lower concentrations are found in semen, vaginal fluid, and saliva. Therefore, blood exposure and sex contact are relatively efficient modes of transmission. Saliva can be a vehicle of transmission through bites; however, transmission has not been documented to occur as a result of other types of exposure to saliva, including kissing. HBsAg has also been detected in low concentrations in other body fluids, including tears, sweat, urine, feces, breast milk, cerebrospinal fluid, and synovial fluid; however, these fluids have not been associated with transmission.

37. Hepatitis B: Diagnosis Symptoms Elevated LFTs Confirmed by serology IgM anti-HBc (IgM core antibody) HBsAg (surface antigen) HBsAb/anti-HBs (antibody to surface antigen ) HBcAb/anti-HBc (antibody to core antigen) HBeAg (E antigen) HBeAb/anti-HBe (antibody to E antigen)

38. Hepatitis B Serology IgM anti-HBc (core antibody) Appears early Persists for 6 months HBsAg (surface antigen) Detectable 30-60 days after exposure May indicate chronic carrier status HBsAb (antibody to surface antigen) Develops after resolved infection Indicates long term immunity

39. Hepatitis B Serology Anti-HBc/HBcAb (antibody to core antigen) Develops in all HBV infections HBeAg (E antigen) Indicates HBV replication Correlates with high infectivity Present in acute or chronic infection Anti-HBe (antibody to E antigen) Develops in most HBV infections Correlates with lower infectivity

40. Notes:Serologic markers of HBV infection vary depending on whether the infection is acute or chronic. The first serologic marker to appear following acute infection is HBsAg, which can be detected as early as 1 or 2 weeks and as late as 11 or 12 weeks (mode, 30-60 days) after exposure to HBV. In persons who recover, HBsAg is no longer detectable in serum after an average period of about 3 months. HBeAg is generally detectable in patients with acute infection; the presence of HBeAg in serum correlates with higher titers of HBV and greater infectivity. A diagnosis of acute HBV infection can be made on the basis of the detection of IgM class antibody to hepatitis B core antigen (IgM anti-HBc) in serum; IgM anti-HBc is generally detectable at the time of clinical onset and declines to sub-detectable levels within 6 months. IgG anti-HBc persists indefinitely as a marker of past infection. Anti-HBs becomes detectable during convalescence after the disappearance of HBsAg in patients who do not progress to chronic infection. The presence of anti-HBs following acute infection generally indicates recovery and immunity from re-infection. Notes:Serologic markers of HBV infection vary depending on whether the infection is acute or chronic. The first serologic marker to appear following acute infection is HBsAg, which can be detected as early as 1 or 2 weeks and as late as 11 or 12 weeks (mode, 30-60 days) after exposure to HBV. In persons who recover, HBsAg is no longer detectable in serum after an average period of about 3 months. HBeAg is generally detectable in patients with acute infection; the presence of HBeAg in serum correlates with higher titers of HBV and greater infectivity. A diagnosis of acute HBV infection can be made on the basis of the detection of IgM class antibody to hepatitis B core antigen (IgM anti-HBc) in serum; IgM anti-HBc is generally detectable at the time of clinical onset and declines to sub-detectable levels within 6 months. IgG anti-HBc persists indefinitely as a marker of past infection. Anti-HBs becomes detectable during convalescence after the disappearance of HBsAg in patients who do not progress to chronic infection. The presence of anti-HBs following acute infection generally indicates recovery and immunity from re-infection.

41. 90% of infants 30% of 5 year olds 6% of adults Risk of chronic infection is lower after acute illness Chronic Carrier State

42. Chronic Carrier State 10% / yr lose HBeAg - become noninfectious 1-2% / yr lose HBsAg - become non-carriers 25 % will develop chronic active disease 20% will develop cirrhosis 5% will develop hepatocellular cancer HBV causes 85% of primary liver cancer worldwide

43. Chronic Carrier State 2 positive HBsAg tests 6 months apart or Positive HBsAg with Negative anti-HBc IgM

44. Chronic Carriers Active duty Navy or Marine Corps HBV carriers, who do not have evidence of chronic persistent or recurrent active hepatitis not restricted from full duty Asymptomatic HBV carriers need annual evaluation HBV carriers with persistent symptoms or elevated LFTs, need periodic evaluation Medical Department personnel who are chronic carriers are not restricted

45. Notes:In patients with chronic HBV infection, both HBsAg and IgG anti-HBc remain persistently detectable, generally for life. HBeAg is variably present in these patients. The presence of HBsAg for 6 months or more is generally indicative of chronic infection. In addition, a negative test for IgM anti-HBc together with a positive test for HBsAg in a single serum specimen usually indicates that an individual has chronic HBV infection. Notes:In patients with chronic HBV infection, both HBsAg and IgG anti-HBc remain persistently detectable, generally for life. HBeAg is variably present in these patients. The presence of HBsAg for 6 months or more is generally indicative of chronic infection. In addition, a negative test for IgM anti-HBc together with a positive test for HBsAg in a single serum specimen usually indicates that an individual has chronic HBV infection.

46. Hepatitis B is an STD Many prostitutes in the Philippines, Thailand, and developing countries are hepatitis B carriers Sexual activity is #1 risk factor in U.S.

48. Hepatitis B Prevention Education Needles, sex, universal precautions Vaccine Pre-exposure, active immunity HBIG Post-exposure Passive immunity

49. Hepatitis B Vaccine Recombivax-HER or Engerix-BR Interchangeable - 3 dose series Day zero, day 30, 6 months 1/2 dose (0.5 ml) OK for under age 30 If a dose missed, continue where with next scheduled dose: DO NOT RESTART SERIES Recombivax-HER, Engerix-BR or TwinrixR: all are three-dose series

50. Hepatitis B Vaccine Required All recruits Health care workers Hospital Corps & dental techs New Medical Department officers Patients with STDs Public safety workers Correctional facility workers Compliance with OSHA regulations

51. Hepatitis B Vaccine Pre-vaccination screening Not recommended Post-vaccination testing Identify non-responders in high risk jobs Non-responders receive one additional 3-dose series of hepatitis B vaccine, but not a third

52. HBIG (Hepatitis B immune globulin) Post-exposure prophylaxis Passive immunity High concentration of anti-HBs Indications Perinatal exposure to HBsAg+ mother Percutaneous or permucosal exposure to HBsAg+ blood Sexual exposure to HBsAg+ person Also need 3 dose vaccine series

54. Hepatitis D Virus-like particle Defective RNA virus Requires HBV co-infection to replicate ANYONE WHO IS HBsAg(+) IS AT RISK

55. Hepatitis D: Transmission Similar to Hepatitis B No fecal-oral transmission Highest rates in Italy, Venezuela, Africa, Romania, central Asia and the Middle East

56. Hepatitis D: Diagnosis Serologic test for hepatitis D antibody

57. Hepatitis D: Complications 10-15% develop cirrhosis within two years 70% eventually develop cirrhosis 2-20% fatality rate 25-50% of fulminant liver failure in hepatitis B actually due to hepatitis D co-infection Hepatitis D Prevention: Hepatitis B vaccine

58. Hepatitis C �transfusion related non-A, non-B hepatitis� Caused by RNA flavivirus Accounts for 16% acute hepatitis in U.S. Transmission similar to hepatitis B Blood, sex, body fluids Usually asymptomatic or mild disease Chronic infection very common 20% of community acquired hepatitis 90% post-transfusion hepatitis Blood banks started screening in 1990: <1% risk now

59. Hepatitis C Diagnosis 1. Symptoms Elevated LFTs Rule out other causes of hepatitis Confirmed by serology Serologic test detects HCV antibody Positive in chronic cases May not be positive in acute phase Rule out other causes of acute hepatitis Submit MER on acute cases only

60. Hepatitis C: Typical Serologic Course

62. Hepatitis C Virus Epidemiology, U.S. New infections (cases)/yr 1985-89: 242,000 (42,000) 1998: 40,000 (6,500) Deaths from acute liver failure: Rare Persons ever infected (1.8%): 3.9 million Persons with chronic infection: 2.7 million Percent of chronic liver disease - HCV-related 40% - 60% Deaths from chronic disease/year 8,000-10,000

63. Transmission of HCV Percutaneous Injecting drug use Clotting factors before viral inactivation Transfusion, transplant from infected donor Therapeutic (contaminated equipment, unsafe injection practices) Occupational (needle stick) Permucosal Perinatal Sexual

64. Sources of Infection forPersons with Hepatitis C

65. Post-transfusion Hepatitis C Responsible for 90% of post-transfusion hepatitis in U.S. prior to 1990 1960s: 25% 1970s: 7-12% post-transfusion risk 1980s: 1-4% risk (ALT screening 1986) 1990s: < 1% risk in (screening started 1990) Most cases now community acquired Problem among Viet Nam veterans

68. Routine HCV Testing Not Recommended(Unless Risk Factor Identified) Ever injected illegal drugs Received clotting factors made before 1987 Received blood/organs before July 1992 Ever on chronic hemodialysis Evidence of liver disease Children born to HCV-positive women Healthcare, emergency, public safety workers after needle stick/mucosal exposures to HCV-positive blood

69. Medical Evaluation and Management for Chronic HCV Assess for biochemical evidence of chronic liver disease Assess for severity of disease and possible treatment Vaccinate against hepatitis A and B Counsel to reduce further harm to liver and prevent transmission to others Refer to support group

70. Hepatitis C Prevention Screening of blood, organ, tissue donors Blood and body fluid precautions Education High-risk behavior modification Same risk factors as hepatitis B Blood > sex > Perinatal No vaccine IG does not protect

71.

72. Review

73. Review: Disposition of Carries/Chronic Infections Hepatitis A/E Enteric precautions for first 2 weeks but no more than one week after jaundice Hepatitis B No restrictions on chronic carriers including medical personnel HBeAg positive Medical personnel need expert review before performing invasive procedures Hepatitis C No restrictions on chronic carriers

74. Case #1 22 y/o Food handler Positive for HBsAg Negative for Anti-HBs Negative for HAV antibody Normal LFTs No Symptoms Is galley work permitted?

75. Case #2 22 y/o HM3 Positive for HBsAg Negative for anti-HBs Negative for anti-HAV Normal LFTs No Symptoms Can the HM3 work in the blood bank?

76. Case #3 CHT worker Exposed to human sewage while repairing pipes Is hepatitis B vaccine needed? Is immune globulin needed? Does spouse need shots?

77. Case #4 24 y/o Mess specialist Chronic fatigue for past 4 wks Abdominal pain 3-4 weeks ago -- resolved LFTs not elevated Positive for anti-HAV DOES EVERYONE IN THE CREW NEED IgG?

78. Case #5 30 y/o Sailor Abdominal pain for 2 wks Now has yellow eyes LFTs significantly elevated Positive anti-HBs Negative HBsAg Negative anti-HAV What is the diagnosis?

79. Case #5 Additional info: Negative for HEP C antibody No history of unsafe sex in past 6 months No history of tattoos or other needle use No history of alcohol abuse PPD converter Taking INH for past 2 months

80. Questions?