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Objectives. Describe the Clinical Syndromes of Viral HepatitisList the modes of Transmission Understand and be able to interpret Diagnostic (laboratory) testsKnow the Treatment and Occupational Impact of Viral HepatitisList Preventive Measures for each Hepatitis typeDescribe Immunization protocols.
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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?