1. Viral hepatitis Prepared by: Assist. Prof. Samir Mahmood
9/19/2018
Viral hepatitis
Prepared by:
Assist. Prof. Samir Mahmood
MBChB, MSc., PhD
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2. Introduction
To date at least six main types hepatitis virus have been identified including the following:
A-B-C-D-E-G
Acute hepatitis may also occur as part of the clinical course of a number of viral infections, including: CMV, EBV, HSV, YFV, and Rubella
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3. Clinical Features Majority of infections are asymptomatic.
Common clinical features include:
Anorexia, nausea, vomiting, right upper quadrant pain, raised liver enzymes (AST and ALT).
Jaundice is the hallmark of infection.
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4. 9/19/2018
Hepatitis A
Hepatitis A is an inflammatory liver disease caused by infection with the hepatitis A virus (HAV), which is a single-stranded 27 nm non-enveloped, RNA virus.
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5. Epidemiology: World-wide distribution. Endemic in most countries.
An estimated 1.4 million cases of HAV infections occur each year.
Infection with HAV occurs predominantly in areas of lower socio-economic status and reduced hygienic standards, especially in developing, and tropical countries.
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6. Transmission
Large numbers of virus particle are excreted in stools, before the onset of symptoms.
Case to case, via faeco-oral route.
Contamination of food or water with sewage.
Infected food handlers
Polluted water.
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7. Clinical Features
Most infections in children are either asymptomatic or unrecognized, while 70% of adults develop clinical symptoms of hepatitis with jaundice and hepatomegaly.
The incubation period ranges between 15 and 49 days with a mean of approximately 30 days.
There is no chronic form of disease.
Complications: Fulminant hepatitis is rare: 0.1% of cases.
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8. Diagnosis Detection of anti-HAV IgM antibodies or HAV RNA.
The presence of HAV IgG antibodies can indicate acute or previous HAV infection.
HAV IgM and IgG antibodies also become positive early after vaccination.
Elevated Liver enzymes (ALT and AST) and serum bilirubin can be found in symptomatic patients.
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9. Control
High standards of personal and environmental hygiene, for example proper sewage disposal, safe drinking water.
If patients are in hospital they should, if possible, be barrier nursed as for any faeces-carried infection.
Food handlers should not resume work until 3 weeks after recovery.
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10. Control Immunization Inactivated HAV vaccine:
2 doses of vaccine; Second dose 6–18 months after first. It induces antibodies in over 90% of individuals within 2 weeks and protects against infection.
HIG: It is useful in protecting family contacts during epidemics.
Recovery from a clinical attack creates a lasting active immunity.
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11. Treatment
There is no specific antiviral therapy for treatment of hepatitis A.
The disease usually takes a mild to moderate course, which requires no hospitalization, and only in fulminant cases is initiation of symptomatic therapy necessary.
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12. Hepatitis E Caused by Calicivirus containing RNA genome.
Incubation period: days
Acute, self limiting hepatitis, no chronic carrier state.
Complication: Fulminant hepatitis in pregnant women. (Mortality rate up to 40%).
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13. Case to case transmission to household contacts uncommon.
The main source of infection is contaminated drinking water.
The peak age specific sero-prevalence in endemic countries is in the over-16 years group.
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14. In recent years, some of these outbreaks have occurred in areas of conflict and humanitarian emergencies, such as war zones, and in camps for refugees or internally displaced populations (IDP).
An estimated 20 million infections and 3.3 million acute cases occur annually worldwide with an estimated 56 600 deaths.
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15. Diagnosis Detection of HEV-specific antibodies.
IgG antibodies indicate acute and past HEV infections,
IgM antibodies can only be found in patients with acute infections
To prove current infection the detection of HEV RNA by PCR has been established
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16. Control As for HAV, provision of - safe drinking water and
- sanitary disposal of faeces is required to prevent the infection.
Recently a study from Germany investigated the use of Ribavirin in immunocompetent individuals with acute HEV infection and immunocompromised patients with chronic HEV infection
No vaccine is as yet available.
In 2011, the first vaccine to prevent hepatitis E infection was registered in China. Although it is not available globally, it could potentially become available in a number of other countries.
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17. Hepatitis B A major cause of morbidity and mortality worldwide.
It is estimated that more than two billion people have been, or are currently infected with hepatitis B virus (HBV) and >1 million deaths annually worldwide.
HBV infections is the most common cause of chronic hepatitis, liver cirrhosis and primary liver cancer worldwide.
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18. Hepatitis B Virus Structure
The virus is stable at 37°c for 60 minutes and remains viable after being dried and stored at 25°c for at least one week.
HBsAg is not destroyed by ultraviolet irradiation and viral infectivity may also resist such treatment .
Hypochlorite or 2%Gluteraldehyde
For 10 min. will inactivate the virus
Anti-HBs: Past Infection, Vaccine
Anti-HBc: (IgM)=Acute Infection, (IgG)= Chronic or previous exposure
Anti-HBe: Low Infectivity of virus
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19. Epidemiology
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20. Risk Groups of HBV infection
High risk group
Immigrants and refugees from areas of high HBV endemicity
Clients in institutions for the developmentally disables
Users of illicit parentral drugs
Homosexual active men
Household contacts of HBV carriers
Patients of haemodialysis unit
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21. Intermediate risk group
Health care workers who have frequent blood contact
Prisoners (male)
Staffs of institutions for the developmentally disabled
Heterosexuals with multiple partners
Low risk group
Health care workers with no or infrequent blood contact
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22. Complications
Following acute infection, approximately 5% of infected individuals fail to eliminate the virus completely.
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23. Modes of transmission
A Quantity of blood as small as 0.05 ml is enough to transmit HBV infection.
Percutaneous or mucosal exposure to infected blood and various body fluids, as well as through saliva, menstrual, vaginal, and seminal fluids. or parentral transmission: (intravenous drug use)
Sexual transmission:
Maternal-neonatal transmission
Vertical transmission/
Perinatal transmission
Horizontal transmission (sharing sharp personal utensils)
Nosocomial transmission: (including needle-stick injury)
Organ transplantation.
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24. Prevention & Control 1. Stopping the spread of HBV.
A. General hygienic measures:
B. Environmental measures:
This is mainly inside the hospitals.
C. Specific measures: These includes special
health education programs.
2. Active immunization.
3. Passive immunization.
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25. Prevention & Control Active immunization
Serum derived-purified HBsAg from serum of HBV carriers.
Recombinant HBsAg- made by genetic engineering in yeasts.
Passive immunization (HBIG)
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26. Drug Treatment
Immune modulator interferon α : standard or pegylated interfe on (PEG-IFN α2a) as well as
Nucleoside or nucleotide analogs, which act as reverse transcriptase inhibitors of the HBV polymerase.
Nucleoside analogs lamivudine (LAM), Telbivudine (LdT), Entecavir (ETV) and
Nucleotide analogs Adefovir dipivoxil (ADV) and Tenofovir disoproxil fumarate (TDF) are available
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27. Most guidelines now recommend antiviral treatment for patients with HBV DNA levels >2,000 IU/mL (corresponding to >10,000 copies/mL) together with a sign of ongoing hepatitis which can either be elevated ALT levels or liver fibrosis demonstrated by liver histology.
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28. Hepatitis C
The major cause of parenterally transmitted non A non B hepatitis. (post-transfusion hepatitis)
Virology: Belong to Togavirus related to Flavi and Pesti viruses.
Has RNA genome.
Does not grow in cell culture.
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29. Epidemiology
Hepatitis C is a disease with a significant global impact.
According to the WHO there are million people infected with the hepatitis C virus (HCV), corresponding to 2-2.5% of the world’s total population.
There are considerable regional differences. In some countries, e.g., Egypt, the prevalence is as high as 22% .
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30. Clinical Features Incubation period 6-8 weeks.
Cause a milder form of acute hepatitis than does hepatitis B
50% individuals develop chronic infection, following exposure.
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31. Transmission: Blood transfusion, blood products Organ donation
Community acquired: mechanism unclear.
Vertical transmission. (?)
Sexual transmission.
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32. Diagnosis Serology: By ELISA; Anti-HCV Ab detection
PCR detects viral genome in patients serum.
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33. Control Screening of blood donors . Health education.
No vaccine is currently available.
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34. Treatment
Interferon is now generally prescribed for the treatment of chronic hepatitis associated with HCV infection.
The current treatment recommendations for acute and chronic hepatitis C are based on HCV genotyping and on HCV RNA load determination before, during and after antiviral therapy.
Dual combination therapy (PEG-IFN + Ribavirin)
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35. Hepatitis D
Defective virus which requires Hepatitis B as a helper virus in order to replicate. Infection therefore only occurs in patients who are already infected with Hepatitis B.
Virus particle 36 nm in diameter
Encapsulated with HBsAg
RNA genome
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36. Clinical Features and Epidemiology
Increased severity of liver disease in Hepatitis B carriers.
Mode of transmission: Mainly blood and blood products.
Control
HBV vaccination also protects against HDV.
Screening of blood has reduced the risk of infection.
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37. Thank You
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