logging in or signing up Viral Hepatitis A B C D E G doctorrao Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 7719 Category: Science & Tech.. License: All Rights Reserved Like it (5) Dislike it (0) Added: November 25, 2008 This Presentation is Public Favorites: 3 Presentation Description Viral Hepatitis continues to infect millions of people in the world, Basic understanding about the spread, and early diagnosis can save several individuals in the world Comments Posting comment... By: felix234 (7 month(s) ago) pls i wuld like to have a copy of dat Saving..... Post Reply Close Saving..... Edit Comment Close By: doctorrao (12 month(s) ago) Dear Dr Rammurugan I am grateful to you for the invitation, I did several programmes with the support of freinds like you, I have only academic interest to make the Medical Microbiology to teach and learn a pleasure At present I am in transition to a New job, I will be in touch with you yours sincerely Dr.T.V.Rao Mob 9742140985 Saving..... Post Reply Close Saving..... Edit Comment Close By: rammurugan (12 month(s) ago) Temple city (Madurai)welcomes to see you sir. I am expecting positive reply from you sir. Dr.Ram Murugan Saving..... Post Reply Close Saving..... Edit Comment Close By: doctorrao (12 month(s) ago) Dear Doctor Rammurugan Thanks for the support, be in touch on my mail doctortvrao@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: rammurugan (12 month(s) ago) Sir, Excellent Presentations,I am expecting Newer Antibiotics Profile and Newer detection Methods. Dr.N.Ram Murugan.MD(MICRO),D.O Saving..... Post Reply Close Saving..... Edit Comment Close loading.... See all Premium member Presentation Transcript VIRAL HEPATITISA,B,C,D,E G …….. : VIRAL HEPATITISA,B,C,D,E G …….. Dr.T.V.Rao MD What Is Hepatitis? : What Is Hepatitis? The word "hepatitis" means inflammation of the liver. Toxins, certain drugs, some diseases, heavy alcohol use, bacterial and viral infections can all cause hepatitis. Hepatitis is also the name of a family of viral infections that affect the liver; the most common types in the United States are hepatitis A, hepatitis B, and hepatitis C. Hepatitis : Hepatitis Hepatitis (plural hepatitides) implies injury to the liver characterized by the presence of inflammatory cells in the tissue of the organ. The name is from ancient Greek hepar or hepato, meaning liver, and suffix -itis, meaning "inflammation" (c. 1727) Viral Hepatitis : Viral Hepatitis A group of viruses known as the hepatitis viruses cause most cases of liver damage worldwide. Hepatitis can also be due to toxins (notably alcohol), other infections. Common viruses cause hepatitis include A,B,C,D,E. G ………. Acute hepatitis Viral Hepatitis: Hepatitis A through E (more than 95% of viral cause), Herpes simplex, Cytomegalovirus, Epstein-Barr, yellow fever virus, adenoviruses. Slide 5: A “Infectious” “Serum” Viral hepatitis Enterically transmitted Parenteraly transmitted F, G, TTV ? other E NANB B D C Viral Hepatitis - Historical Perspectives : Source of virus feces blood/ blood-derived body fluids blood/ blood-derived body fluids blood/ blood-derived body fluids feces Route of transmission fecal-oral percutaneous permucosal percutaneous permucosal percutaneous permucosal fecal-oral Chronic infection no yes yes yes no Prevention pre/post- exposure immunization pre/post- exposure immunization blood donor screening; risk behavior modification pre/post- exposure immunization; risk behavior modification ensure safe drinking water Type of Hepatitis A B C D E Hepatitis A : Hepatitis A Hepatitis A is an acute liver disease caused by the hepatitis A virus (HAV), lasting from a few weeks to several months. It does not lead to chronic infection. Slide 9: Hepatitis A Virus Hepatitis A Virus : Hepatitis A Virus Naked RNA virus Related to enteroviruses, formerly known as enterovirus 72, now put in its own family: heptovirus One stable serotype only Difficult to grow in cell culture: primary marmoset cell culture and also in vivo in chimpanzees and marmosets 4 genotypes exist, but in practice most of them are group 1 Nature of HAV virus : Nature of HAV virus HAV is a 27 – 30 nm spherical particle with cubic symmetry Contain linear single stranded RNA genome with size of 7.5 kb. Only one serotype HAV characters : HAV characters HAV are stable to treatment with 20% ether,acid and heat at 600c for 1 hour. The virus are destroyed by autoclaving at 1210c for 20 minutes, boiling in water for 5 minutes Treatment with chlorine 1 ppm for 30 minutes Heating food > 850c for 1 minute destroys Culturing HAV virus : Culturing HAV virus Various primate cell lines will support grwoth of HAV,though fresh isolates of virus are difficult to adapt and grow. Usually to cytopathic effects are apparent Pathology in Viral Hepatitis : Pathology in Viral Hepatitis Indicates inflamation of liver. Microscopically there is spotty parenchymal cell degeneration, with necrosis of Hepatocytes, with disruption of liver cell cords The parenchymal changes are accompanied by Reticuloendothelial ( KUFFER) cell hyperplasia,periportal infiltration by monoculear cells and cell degeneration. Causes liver damage : Causes liver damage Localised areas of necrosis are frequently observed Later accumulation of macrophages near degenerating Hepatocytes Transmission Of Hepatitis A : Transmission Of Hepatitis A : Ingestion of food or water contaminated with faecal matter, Even in microscopic amounts, From close person-to-person Slide 17: Close personal contact(e.g., household contact, child day care centers) Contaminated food, water(e.g., infected food handlers, raw shellfish) Blood exposure (rare)(e.g., injecting drug use, transfusion)Not transmitted by Transplacental route Hepatitis A Virus Transmission Slide 18: Endemicity Disease Rate Peak Age of Infection Transmission Patterns High Low to High Early childhood Person to person; outbreaks uncommon Moderate High Late childhood/ young adults Person to person; food and waterborne outbreaks Low Low Young adults Person to person; food and waterborne outbreaks Very low Very low Adults Travelers; outbreaks uncommon Global Patterns of Hepatitis A Virus Transmission Clinical Manifestations : Clinical Manifestations Incubation period 2 – 6 weeks May be asymptomatic Overt illness in 5% Present as two stages, 1 Preicteric 2 Icteric Clinical features : Clinical features Malaise Anorexia Nausea, omitting liver tenderness Onset of Jaundice Recovery in 4-6 weeks Mortality 0.1 – 1 % Slide 21: Complications: Fulminant hepatitis Cholestatic hepatitis Relapsing hepatitis Chronic sequelae: None Hepatitis A - Clinical Complications Laboratory Diagnosis : Laboratory Diagnosis Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA. Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA. Cell culture – difficult and take up to 4 weeks, not routinely performed Direct Detection – EM, RT-PCR of faeces. Can detect illness earlier than serology but rarely performed. Slide 23: Fecal HAV Symptoms 0 1 2 3 4 5 6 12 24 Hepatitis A Infection Total anti-HAV Titer ALT IgM anti-HAV Months after exposure Typical Serological Course Treatment : Treatment No specific antiviral drug is available Treatment is symptomatic Specific passive prophylaxis by pooled normal human immunoglobulin given before exposure or in early incubation period can prevent or attenuate clinical illness. Slide 25: Many cases occur in community-wide outbreaks no risk factor identified for most cases highest attack rates in 5-14 year olds children serve as reservoir of infection Persons at increased risk of infection travelers homosexual men injecting drug users Hepatitis A Vaccination Strategies Epidemiologic Considerations Vaccination for HAV : Vaccination for HAV Hepatitis A vaccination is recommended for all children starting at age 1 year, travellers to certain countries, and others at risk. A safe and effective formalin inactivated alum conjugated vaccine containing HAV grown in human diploid cell culture is available A full course containing two intramuscular injections of the vaccine Protection starts after 4 weeks after injection and lasts for 10 – 20 years Slide 27: Many cases occur in community-wide outbreaks no risk factor identified for most cases highest attack rates in 5-14 year olds children serve as reservoir of infection Persons at increased risk of infection travelers homosexual men injecting drug users Hepatitis A Vaccination Strategies Epidemiologic Considerations Epidemiology : Epidemiology A major communicable disease in the Devloping world. Well cooked food and sanitary water supply will protect the individual living Community hygiene is important in schools, hostels and jails, as overcrowding and poor sanitation favour the spread Prevention of Hepatitis A Infection : Prevention of Hepatitis A Infection Pre-exposure travelers to intermediate and high HAV-endemic regions Post-exposure (within 14 days) Routine household and other intimate contacts Selected situations institutions (e.g., day care centers) common source exposure (e.g., food prepared by infected food handler) Hepatitis B Infection : Hepatitis B Infection Most Important Infectious Disease : Most Important Infectious Disease There are more than 350 million carriers 25% of them will develop chronic active hepatitis. World wide 1 million deaths a years are attributed to HBV related liver disease and Hepatocellular Carcinoma Hepatitis B : Hepatitis B Hepatitis B is a liver disease caused by the hepatitis B virus (HBV). It ranges in severity from a mild illness, lasting a few weeks (acute), to a serious long-term (chronic) illness that can lead to liver disease or liver cancer. Slide 33: Hepatitis B Virus Blumberg in 1965 discovers, names as Australia antigen. 1968 identified with association in serum hepatitis. Surface component of HBV called as surface antigen. HBV Viruses Under Electron Microscope : HBV Viruses Under Electron Microscope Spherical particles 22 nm in diameter Filamentous or tubular 22 nm with varying length Called as HBs Ag surface components which are produced in excess. Third type double walled spherical structure 42 nm diameter called HBV Called as Dane particle HBV – Surface antigens : HBV – Surface antigens Enveloped proteins on surface of virions and surplus 22 nm diameter spherical and filamentous particles constitute the B surface antigens HBs Ag consists two major polypeptides and is glycolated Structure 0f Hepatitis B virus : Structure 0f Hepatitis B virus HBV shows antigenic diversity : HBV shows antigenic diversity HBV shows antigenic diversity, two different antigenic components and common group reactive antigen a Two contain specific antigens d y w r Only one member of each pair being present at a time Divided into four Major antigenic subtypes adw, adr, ayw, and ayr Geographic distribution : Geographic distribution ayw – common in Europe,Australia,and America. adr - Prevalent in south, East India and Far east, ayr - very rare Core antigen HB c ag Be HBe is a soluble non particle nucelocapsid protein Both Hbc and Hbe are coded by same genes Replication : Replication The RNA dependent DNA synthesis takes place within the newly assembled Virion core in the cytoplasam. Hepadnaviruses the only virus that produce genome DNA by reverse transcription with mRNA as the template Pathogenesis of HBV infection : Pathogenesis of HBV infection Disease is Immune mediated Hepatocytes carry viral antigen Immune response subject to antibody dependent. N K cell and cytotoxic T cell attack In the absence of adequate immune response HBV infection may not cause hepatitis. But lead to carrier state. Infection – Immunodeficient person are likely to because asymptomatic carrier followed infection Slide 42: Incubation period: Average 60-90 days Range 45-180 days Clinical illness (jaundice): <5 yrs, <10% 5 yrs, 30%-50% Acute case-fatality rate: 0.5%-1% Chronic infection: <5 yrs, 30%-90% 5 yrs, 2%-10% Premature mortality fromchronic liver disease: 15%-25% Hepatitis B - Clinical Features What are the clinical symptoms of Hepatitis B?? : What are the clinical symptoms of Hepatitis B?? Spectrum of Chronic Hepatitis B Diseases : Spectrum of Chronic Hepatitis B Diseases 1Chronic Persistent Hepatitis - asymptomatic 2. Chronic Active Hepatitis - symptomatic exacerbations of hepatitis 3. Cirrhosis of Liver 4. Hepatocellular Carcinoma Slide 45: Symptoms HBeAg anti-HBe Total anti-HBc IgM anti-HBc anti-HBs HBsAg 0 4 8 12 16 20 24 28 32 36 52 100 Acute Hepatitis B Virus Infection with Recovery Typical Serologic Course Weeks after Exposure Titre Slide 46: IgM anti-HBc Total anti-HBc HBsAg Acute (6 months) HBeAg Chronic (Years) anti-HBe 0 4 8 12 16 20 24 28 32 36 52 Years Weeks after Exposure Titre Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course Slide 47: High (>8%): 45% of global population lifetime risk of infection >60% early childhood infections common Intermediate (2%-7%): 43% of global population lifetime risk of infection 20%-60% infections occur in all age groups Low (<2%): 12% of global population lifetime risk of infection <20% most infections occur in adult risk groups Global Patterns of Chronic HBV Infection Slide 49: High Moderate Low/Not Detectable blood semen urine serum vaginal fluid feces wound exudates saliva sweat tears breastmilk Concentration of Hepatitis B Virus in Various Body Fluids How Hepatitis B is transmitted : How Hepatitis B is transmitted Contact with infectious blood, semen, and other body fluids from having sex with an infected person, sharing contaminated needles to inject drugs, or from an infected mother to her newborn. Slide 51: Sexual - sex workers and homosexuals are particular at risk. Parenteral - IVDA, Health Workers are at increased risk. Perinatal - Mothers who are HBeAg positive are much more likely to transmit to their offspring than those who are not. Perinatal transmission is the main means of transmission in high prevalence populations. Hepatitis B Virus Modes of Transmission Diagnosis : Diagnosis A battery of serological tests are used for the diagnosis of acute and chronic hepatitis B infection. HBsAg - used as a general marker of infection. HBsAb - used to document recovery and/or immunity to HBV infection. anti-HBc IgM - marker of acute infection. anti-HBcIgG - past or chronic infection. HBeAg - indicates active replication of virus and therefore infectiveness. Anti-Hbe - virus no longer replicating. However, the patient can still be positive for HBsAg which is made by integrated HBV. HBV-DNA - indicates active replication of virus, more accurate than HBeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy. Treatment : Treatment Patients with Hepatitis needs supportive treatment Recombinant Interferon alfa therpay is beneficial in HBV and HCV Treatment : Treatment Interferon - for HBeAg +ve carriers with chronic active hepatitis. Response rate is 30 to 40%. alpha-interferon 2b (original) alpha-interferon 2a (newer, claims to be more efficacious and efficient) Lamivudine - a nucleoside analogue reverse transcriptase inhibitor. Well tolerated, most patients will respond favorably. However, tendency to relapse on cessation of treatment. Another problem is the rapid emergence of drug resistance. Adefovir – less likely to develop resistance than Lamivudine and may be used to treat Lamivudine resistance HBV. However more expensive and toxic Entecavir – most powerful antiviral known, similar to Adefovir Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA, and seroconversion to HBeAg. High Risk Individuals : High Risk Individuals Medical and Dental surgeons Pathologists Physicians Laboratory technicians Blood bank personnel HBV is common in : HBV is common in Patients undergoing Dialysis Staff of Hem dialysis Units Vaccination Genetically Engineered : Vaccination Genetically Engineered Vaccination - highly effective recombinant vaccines are now available. Vaccine can be given to those who are at increased risk of HBV infection such as health care workers. It is also given routinely to neonates as universal vaccination in many countries. Hepatitis B Immunoglobulin : Hepatitis B Immunoglobulin Hepatitis B Immunoglobulin - HBIG may be used to protect persons who are exposed to hepatitis B. It is particular efficacious within 48 hours of the incident. It may also be given to neonates who are at increased risk of contracting hepatitis B i.e. whose mothers are HBsAg and HBeAg positive Blood screening is Mandatory : Blood screening is Mandatory Other measures - screening of blood donors, blood and body fluid precautions is mandatory in majority of Countreis Universal Precautions : Universal Precautions Universal precautions," as defined by CDC, are a set of precautions designed to prevent transmission of human immunodeficiency virus (HIV), hepatitis B virus (HBV), and other blood borne pathogens when providing first aid or health care. Universal Precautions : Universal Precautions Under universal precautions, blood and certain body fluids of all patients are considered potentially infectious for HIV, HBV and other blood borne pathogens. Hand washing Minimal health precaution to Medical and Paramedical staff : Hand washing Minimal health precaution to Medical and Paramedical staff Hepatitis C Infection : Hepatitis C Infection Hepatitis C Virus Non A, non B Hepaci virus What is Hepatitis C Virus : What is Hepatitis C Virus Hepatitis C virus also known as Non A or Non B virus found while doing experiments on Chimpanzees. HCV infections are seen only in humans The epidemiology is like HBV infection. HCV Virology : HCV Virology The virus is not been grown in culture The virus is 50- 60 nm with linear single stranded RNA genome surrounded by an enveloped carrying glycoprotein spikes Now classified as Hepacivirus in the family of Flaviviridae Six genotypes are identified, with high mutability Slide 66: hypervariable region capsid envelope protein protease/helicase RNA-dependent RNA polymerase c22 5’ core E1 E2 NS2 NS3 33c NS4 c-100 NS5 3’ Hepatitis C Virus Hepatitis C Virus : Hepatitis C Virus Genome resembled that of a flavivirus positive stranded RNA genome of around 10,000 bases 1 single reading frame, structural genes at the 5' end, the non-structural genes at the 3' end. enveloped virus, virion thought to 30-60nm in diameter Morphological structure remains unknown Hepatitis C virus : Hepatitis C virus Genotype 1 and 4 has a poorer prognosis and response to interferon therapy, In Hong Kong, genotype 1 accounts for around 67% of cases and genotype 6 around 25%. Now 6 genotypes are identified. Terminology : Terminology Family Genus Species Genotype Subtype Quasispecies Pathogenesis : Pathogenesis Slide 71: Incubation period: Average 6-7 wks Range 2-26 wks Clinical illness (jaundice): 30-40% (20-30%) Chronic hepatitis: 70% Persistent infection: 85-100% Immunity: No protective antibody response identified Hepatitis C - Clinical Features How HCV transmitted : How HCV transmitted Blood transfusions Transplantation of organs Injectable drug abusers Immunocompromised Sexual transmission ? Less important Vertical transmission is possible Clinical features : Clinical features Overt Jaundice is seen in 5% of patients About 50 – 80% patients progress to chronic hepatitis May progress to Cirrhosis, or Hepatocellular carcinoma Chronic Hepatitis C Infection : Chronic Hepatitis C Infection The spectrum of chronic hepatitis C infection is essentially the same as chronic hepatitis B infection. All the manifestations of chronic hepatitis B infection may be seen, albeit with a lower frequency i.e. chronic persistent hepatitis, chronic active hepatitis, cirrhosis, and hepatocellular carcinoma. Transmission of HCV : Transmission of HCV Percutaneous IV drugs Clotting factors before viral inactivation Transfusion, transplant from infected donor Therapeutic (contaminated equipment, unsafe injection practices) Occupational (needle stick) Per mucosal Perinatal Sexual HCV - Occupational Transmission : HCV - Occupational Transmission Inefficiently transmitted Average incidence 1.8% following needle stick from HCV-positive source 10 times lower than HBV infection Hollow-bore needles Case reports from blood splash to eye No reports from skin exposures to blood Prevalence 1-2% among health care workers Lower than in the general population Slide 77: Transfusion or transplant from infected donor Injecting drug use Hemodialysis (yrs on treatment) Accidental injuries with needles/sharps Sexual/household exposure to anti-HCV-positive contact Multiple sex partners Risk Factors Associated with Transmission of HCV Slide 78: Symptoms anti-HCV ALT Normal 0 1 2 3 4 5 6 1 2 3 4 Hepatitis C Virus Infection Typical Serologic Course Titre Months Years Time after Exposure Laboratory Diagnosis : Laboratory Diagnosis HCV antibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. ELISA test results to be confirmed with Immunoblotting assay Molecular Methods in Diagnosis : Molecular Methods in Diagnosis HCV-RNA - various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out. Prognostic Tests : Prognostic Tests Genotyping – genotype 1 and 4 have a worse prognosis overall and respond poorly to interferon therapy. A number of commercial and in-house assays are available. Genotypic methods – DNA sequencing, PCR-hybridization e.g. INNO-LIPA. Serotyping – particularly useful when the patient does not have detectable RNA. Viral Load – patients with high viral load are thought to have a poorer prognosis. Viral load is also used for monitoring response to IFN therapy. A number of commercial and in-house tests are available. HCV Treatment : HCV Treatment α-Interferon Ribavirin Effective in about 50% of cases No vaccine Treatment : Treatment Interferon - may be considered for patients with chronic active hepatitis. The response rate is around 50% but 50% of responders will relapse upon withdrawal of treatment. Ribavirin - there is less experience with ribavirin than interferon. However, recent studies suggest that a combination of interferon and ribavirin is more effective than interferon alone. Slide 85: Screening of blood, organ, tissue donors High-risk behavior modification Blood and body fluid precautions Prevention of Hepatitis C Slide 86: Hepatitis D Delta agent Hepatitis D Virus : Hepatitis D Virus The delta agent is a defective virus which shows similarities with the viroids in plants. The agent consists of a particle 35 nm in diameter consisting of the delta antigen surrounded by an outer coat of HBsAg. The genome of the virus is very small and consists of a single-stranded RNA Slide 89: Coinfection severe acute disease. low risk of chronic infection. Superinfection usually develop chronic HDV infection. high risk of severe chronic liver disease. may present as an acute hepatitis. Hepatitis D - Clinical Features Slide 90: Percutanous exposures injecting drug use Permucosal exposures sex contact Hepatitis D Virus Modes of Transmission Slide 91: anti-HBs Symptoms ALT Elevated Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Coinfection Typical Serologic Course Time after Exposure Titre Slide 92: anti-HBs Symptoms ALT Elevated Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Coinfection Typical Serologic Course Time after Exposure Titre Slide 93: Jaundice Symptoms ALT Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Superinfection Typical Serologic Course Time after Exposure Titre Slide 95: HBV-HDV Coinfection Pre or postexposure prophylaxis to prevent HBV infection. HBV-HDV Superinfection Education to reduce risk behaviors among persons with chronic HBV infection. Hepatitis D - Prevention Slide 96: Hepatitis E infection NANB Hepatitis E Virus : Hepatitis E Virus Calicivirus-like viruses unenveloped RNA virus, 32-34 nm in diameter +ve stranded RNA genome, 7.6 kb in size. very labile and sensitive Can only be cultured recently Slide 98: Hepatitis E Virus Slide 99: Incubation period: Average 40 days Range 15-60 days Case-fatality rate: Overall, 1%-3% Pregnant women, 15%-25% Illness severity: Increased with age Chronic sequelae: None identified Hepatitis E - Clinical Features Slide 100: Symptoms ALT IgG anti-HEV IgM anti-HEV Virus in stool 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Hepatitis E Virus Infection Typical Serologic Course Titer Weeks after Exposure Slide 101: Most outbreaks associated with faecally contaminated drinking water. Several other large epidemics have occurred since in the Indian subcontinent and the USSR, China, Africa and Mexico. 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. Minimal person-to-person transmission. Hepatitis E - Epidemiologic Features Slide 103: Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler. IG prepared from donors in Western countries does not prevent infection. Unknown efficacy of IG prepared from donors in endemic areas. Vaccine? Prevention and Control Measures for Travelers to HEV-Endemic Regions Hepatitis G virus : Hepatitis G virus A new virus recently identified in Humans. Not grown in culture lines RNA genome is cloned Its role still for debate HGV RNA was found in acute, chronic, fulminant hepatitis , hemophiliacs, patients with multiple transfusions It resembles HCV In all other aspects Protect yourself : Protect yourself Medical and Paramedical staff can reduce, avoid the incidences of accidental infection with HBV,HCV,HDV,and Hepatitis G infections with, safe handling of needles Prevent needle stick injuries : Prevent needle stick injuries Report your needle stick injuries to higher authorities : Report your needle stick injuries to higher authorities Created for benefit of Medical and Paramedical Students in Developing World : Created for benefit of Medical and Paramedical Students in Developing World Dr.T.V.Rao MD Email doctortvrao@gmail.com You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.
Viral Hepatitis A B C D E G doctorrao Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 7719 Category: Science & Tech.. License: All Rights Reserved Like it (5) Dislike it (0) Added: November 25, 2008 This Presentation is Public Favorites: 3 Presentation Description Viral Hepatitis continues to infect millions of people in the world, Basic understanding about the spread, and early diagnosis can save several individuals in the world Comments Posting comment... By: felix234 (7 month(s) ago) pls i wuld like to have a copy of dat Saving..... Post Reply Close Saving..... Edit Comment Close By: doctorrao (12 month(s) ago) Dear Dr Rammurugan I am grateful to you for the invitation, I did several programmes with the support of freinds like you, I have only academic interest to make the Medical Microbiology to teach and learn a pleasure At present I am in transition to a New job, I will be in touch with you yours sincerely Dr.T.V.Rao Mob 9742140985 Saving..... Post Reply Close Saving..... Edit Comment Close By: rammurugan (12 month(s) ago) Temple city (Madurai)welcomes to see you sir. I am expecting positive reply from you sir. Dr.Ram Murugan Saving..... Post Reply Close Saving..... Edit Comment Close By: doctorrao (12 month(s) ago) Dear Doctor Rammurugan Thanks for the support, be in touch on my mail doctortvrao@gmail.com Saving..... Post Reply Close Saving..... Edit Comment Close By: rammurugan (12 month(s) ago) Sir, Excellent Presentations,I am expecting Newer Antibiotics Profile and Newer detection Methods. Dr.N.Ram Murugan.MD(MICRO),D.O Saving..... Post Reply Close Saving..... Edit Comment Close loading.... See all Premium member Presentation Transcript VIRAL HEPATITISA,B,C,D,E G …….. : VIRAL HEPATITISA,B,C,D,E G …….. Dr.T.V.Rao MD What Is Hepatitis? : What Is Hepatitis? The word "hepatitis" means inflammation of the liver. Toxins, certain drugs, some diseases, heavy alcohol use, bacterial and viral infections can all cause hepatitis. Hepatitis is also the name of a family of viral infections that affect the liver; the most common types in the United States are hepatitis A, hepatitis B, and hepatitis C. Hepatitis : Hepatitis Hepatitis (plural hepatitides) implies injury to the liver characterized by the presence of inflammatory cells in the tissue of the organ. The name is from ancient Greek hepar or hepato, meaning liver, and suffix -itis, meaning "inflammation" (c. 1727) Viral Hepatitis : Viral Hepatitis A group of viruses known as the hepatitis viruses cause most cases of liver damage worldwide. Hepatitis can also be due to toxins (notably alcohol), other infections. Common viruses cause hepatitis include A,B,C,D,E. G ………. Acute hepatitis Viral Hepatitis: Hepatitis A through E (more than 95% of viral cause), Herpes simplex, Cytomegalovirus, Epstein-Barr, yellow fever virus, adenoviruses. Slide 5: A “Infectious” “Serum” Viral hepatitis Enterically transmitted Parenteraly transmitted F, G, TTV ? other E NANB B D C Viral Hepatitis - Historical Perspectives : Source of virus feces blood/ blood-derived body fluids blood/ blood-derived body fluids blood/ blood-derived body fluids feces Route of transmission fecal-oral percutaneous permucosal percutaneous permucosal percutaneous permucosal fecal-oral Chronic infection no yes yes yes no Prevention pre/post- exposure immunization pre/post- exposure immunization blood donor screening; risk behavior modification pre/post- exposure immunization; risk behavior modification ensure safe drinking water Type of Hepatitis A B C D E Hepatitis A : Hepatitis A Hepatitis A is an acute liver disease caused by the hepatitis A virus (HAV), lasting from a few weeks to several months. It does not lead to chronic infection. Slide 9: Hepatitis A Virus Hepatitis A Virus : Hepatitis A Virus Naked RNA virus Related to enteroviruses, formerly known as enterovirus 72, now put in its own family: heptovirus One stable serotype only Difficult to grow in cell culture: primary marmoset cell culture and also in vivo in chimpanzees and marmosets 4 genotypes exist, but in practice most of them are group 1 Nature of HAV virus : Nature of HAV virus HAV is a 27 – 30 nm spherical particle with cubic symmetry Contain linear single stranded RNA genome with size of 7.5 kb. Only one serotype HAV characters : HAV characters HAV are stable to treatment with 20% ether,acid and heat at 600c for 1 hour. The virus are destroyed by autoclaving at 1210c for 20 minutes, boiling in water for 5 minutes Treatment with chlorine 1 ppm for 30 minutes Heating food > 850c for 1 minute destroys Culturing HAV virus : Culturing HAV virus Various primate cell lines will support grwoth of HAV,though fresh isolates of virus are difficult to adapt and grow. Usually to cytopathic effects are apparent Pathology in Viral Hepatitis : Pathology in Viral Hepatitis Indicates inflamation of liver. Microscopically there is spotty parenchymal cell degeneration, with necrosis of Hepatocytes, with disruption of liver cell cords The parenchymal changes are accompanied by Reticuloendothelial ( KUFFER) cell hyperplasia,periportal infiltration by monoculear cells and cell degeneration. Causes liver damage : Causes liver damage Localised areas of necrosis are frequently observed Later accumulation of macrophages near degenerating Hepatocytes Transmission Of Hepatitis A : Transmission Of Hepatitis A : Ingestion of food or water contaminated with faecal matter, Even in microscopic amounts, From close person-to-person Slide 17: Close personal contact(e.g., household contact, child day care centers) Contaminated food, water(e.g., infected food handlers, raw shellfish) Blood exposure (rare)(e.g., injecting drug use, transfusion)Not transmitted by Transplacental route Hepatitis A Virus Transmission Slide 18: Endemicity Disease Rate Peak Age of Infection Transmission Patterns High Low to High Early childhood Person to person; outbreaks uncommon Moderate High Late childhood/ young adults Person to person; food and waterborne outbreaks Low Low Young adults Person to person; food and waterborne outbreaks Very low Very low Adults Travelers; outbreaks uncommon Global Patterns of Hepatitis A Virus Transmission Clinical Manifestations : Clinical Manifestations Incubation period 2 – 6 weeks May be asymptomatic Overt illness in 5% Present as two stages, 1 Preicteric 2 Icteric Clinical features : Clinical features Malaise Anorexia Nausea, omitting liver tenderness Onset of Jaundice Recovery in 4-6 weeks Mortality 0.1 – 1 % Slide 21: Complications: Fulminant hepatitis Cholestatic hepatitis Relapsing hepatitis Chronic sequelae: None Hepatitis A - Clinical Complications Laboratory Diagnosis : Laboratory Diagnosis Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA. Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA. Cell culture – difficult and take up to 4 weeks, not routinely performed Direct Detection – EM, RT-PCR of faeces. Can detect illness earlier than serology but rarely performed. Slide 23: Fecal HAV Symptoms 0 1 2 3 4 5 6 12 24 Hepatitis A Infection Total anti-HAV Titer ALT IgM anti-HAV Months after exposure Typical Serological Course Treatment : Treatment No specific antiviral drug is available Treatment is symptomatic Specific passive prophylaxis by pooled normal human immunoglobulin given before exposure or in early incubation period can prevent or attenuate clinical illness. Slide 25: Many cases occur in community-wide outbreaks no risk factor identified for most cases highest attack rates in 5-14 year olds children serve as reservoir of infection Persons at increased risk of infection travelers homosexual men injecting drug users Hepatitis A Vaccination Strategies Epidemiologic Considerations Vaccination for HAV : Vaccination for HAV Hepatitis A vaccination is recommended for all children starting at age 1 year, travellers to certain countries, and others at risk. A safe and effective formalin inactivated alum conjugated vaccine containing HAV grown in human diploid cell culture is available A full course containing two intramuscular injections of the vaccine Protection starts after 4 weeks after injection and lasts for 10 – 20 years Slide 27: Many cases occur in community-wide outbreaks no risk factor identified for most cases highest attack rates in 5-14 year olds children serve as reservoir of infection Persons at increased risk of infection travelers homosexual men injecting drug users Hepatitis A Vaccination Strategies Epidemiologic Considerations Epidemiology : Epidemiology A major communicable disease in the Devloping world. Well cooked food and sanitary water supply will protect the individual living Community hygiene is important in schools, hostels and jails, as overcrowding and poor sanitation favour the spread Prevention of Hepatitis A Infection : Prevention of Hepatitis A Infection Pre-exposure travelers to intermediate and high HAV-endemic regions Post-exposure (within 14 days) Routine household and other intimate contacts Selected situations institutions (e.g., day care centers) common source exposure (e.g., food prepared by infected food handler) Hepatitis B Infection : Hepatitis B Infection Most Important Infectious Disease : Most Important Infectious Disease There are more than 350 million carriers 25% of them will develop chronic active hepatitis. World wide 1 million deaths a years are attributed to HBV related liver disease and Hepatocellular Carcinoma Hepatitis B : Hepatitis B Hepatitis B is a liver disease caused by the hepatitis B virus (HBV). It ranges in severity from a mild illness, lasting a few weeks (acute), to a serious long-term (chronic) illness that can lead to liver disease or liver cancer. Slide 33: Hepatitis B Virus Blumberg in 1965 discovers, names as Australia antigen. 1968 identified with association in serum hepatitis. Surface component of HBV called as surface antigen. HBV Viruses Under Electron Microscope : HBV Viruses Under Electron Microscope Spherical particles 22 nm in diameter Filamentous or tubular 22 nm with varying length Called as HBs Ag surface components which are produced in excess. Third type double walled spherical structure 42 nm diameter called HBV Called as Dane particle HBV – Surface antigens : HBV – Surface antigens Enveloped proteins on surface of virions and surplus 22 nm diameter spherical and filamentous particles constitute the B surface antigens HBs Ag consists two major polypeptides and is glycolated Structure 0f Hepatitis B virus : Structure 0f Hepatitis B virus HBV shows antigenic diversity : HBV shows antigenic diversity HBV shows antigenic diversity, two different antigenic components and common group reactive antigen a Two contain specific antigens d y w r Only one member of each pair being present at a time Divided into four Major antigenic subtypes adw, adr, ayw, and ayr Geographic distribution : Geographic distribution ayw – common in Europe,Australia,and America. adr - Prevalent in south, East India and Far east, ayr - very rare Core antigen HB c ag Be HBe is a soluble non particle nucelocapsid protein Both Hbc and Hbe are coded by same genes Replication : Replication The RNA dependent DNA synthesis takes place within the newly assembled Virion core in the cytoplasam. Hepadnaviruses the only virus that produce genome DNA by reverse transcription with mRNA as the template Pathogenesis of HBV infection : Pathogenesis of HBV infection Disease is Immune mediated Hepatocytes carry viral antigen Immune response subject to antibody dependent. N K cell and cytotoxic T cell attack In the absence of adequate immune response HBV infection may not cause hepatitis. But lead to carrier state. Infection – Immunodeficient person are likely to because asymptomatic carrier followed infection Slide 42: Incubation period: Average 60-90 days Range 45-180 days Clinical illness (jaundice): <5 yrs, <10% 5 yrs, 30%-50% Acute case-fatality rate: 0.5%-1% Chronic infection: <5 yrs, 30%-90% 5 yrs, 2%-10% Premature mortality fromchronic liver disease: 15%-25% Hepatitis B - Clinical Features What are the clinical symptoms of Hepatitis B?? : What are the clinical symptoms of Hepatitis B?? Spectrum of Chronic Hepatitis B Diseases : Spectrum of Chronic Hepatitis B Diseases 1Chronic Persistent Hepatitis - asymptomatic 2. Chronic Active Hepatitis - symptomatic exacerbations of hepatitis 3. Cirrhosis of Liver 4. Hepatocellular Carcinoma Slide 45: Symptoms HBeAg anti-HBe Total anti-HBc IgM anti-HBc anti-HBs HBsAg 0 4 8 12 16 20 24 28 32 36 52 100 Acute Hepatitis B Virus Infection with Recovery Typical Serologic Course Weeks after Exposure Titre Slide 46: IgM anti-HBc Total anti-HBc HBsAg Acute (6 months) HBeAg Chronic (Years) anti-HBe 0 4 8 12 16 20 24 28 32 36 52 Years Weeks after Exposure Titre Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course Slide 47: High (>8%): 45% of global population lifetime risk of infection >60% early childhood infections common Intermediate (2%-7%): 43% of global population lifetime risk of infection 20%-60% infections occur in all age groups Low (<2%): 12% of global population lifetime risk of infection <20% most infections occur in adult risk groups Global Patterns of Chronic HBV Infection Slide 49: High Moderate Low/Not Detectable blood semen urine serum vaginal fluid feces wound exudates saliva sweat tears breastmilk Concentration of Hepatitis B Virus in Various Body Fluids How Hepatitis B is transmitted : How Hepatitis B is transmitted Contact with infectious blood, semen, and other body fluids from having sex with an infected person, sharing contaminated needles to inject drugs, or from an infected mother to her newborn. Slide 51: Sexual - sex workers and homosexuals are particular at risk. Parenteral - IVDA, Health Workers are at increased risk. Perinatal - Mothers who are HBeAg positive are much more likely to transmit to their offspring than those who are not. Perinatal transmission is the main means of transmission in high prevalence populations. Hepatitis B Virus Modes of Transmission Diagnosis : Diagnosis A battery of serological tests are used for the diagnosis of acute and chronic hepatitis B infection. HBsAg - used as a general marker of infection. HBsAb - used to document recovery and/or immunity to HBV infection. anti-HBc IgM - marker of acute infection. anti-HBcIgG - past or chronic infection. HBeAg - indicates active replication of virus and therefore infectiveness. Anti-Hbe - virus no longer replicating. However, the patient can still be positive for HBsAg which is made by integrated HBV. HBV-DNA - indicates active replication of virus, more accurate than HBeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy. Treatment : Treatment Patients with Hepatitis needs supportive treatment Recombinant Interferon alfa therpay is beneficial in HBV and HCV Treatment : Treatment Interferon - for HBeAg +ve carriers with chronic active hepatitis. Response rate is 30 to 40%. alpha-interferon 2b (original) alpha-interferon 2a (newer, claims to be more efficacious and efficient) Lamivudine - a nucleoside analogue reverse transcriptase inhibitor. Well tolerated, most patients will respond favorably. However, tendency to relapse on cessation of treatment. Another problem is the rapid emergence of drug resistance. Adefovir – less likely to develop resistance than Lamivudine and may be used to treat Lamivudine resistance HBV. However more expensive and toxic Entecavir – most powerful antiviral known, similar to Adefovir Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA, and seroconversion to HBeAg. High Risk Individuals : High Risk Individuals Medical and Dental surgeons Pathologists Physicians Laboratory technicians Blood bank personnel HBV is common in : HBV is common in Patients undergoing Dialysis Staff of Hem dialysis Units Vaccination Genetically Engineered : Vaccination Genetically Engineered Vaccination - highly effective recombinant vaccines are now available. Vaccine can be given to those who are at increased risk of HBV infection such as health care workers. It is also given routinely to neonates as universal vaccination in many countries. Hepatitis B Immunoglobulin : Hepatitis B Immunoglobulin Hepatitis B Immunoglobulin - HBIG may be used to protect persons who are exposed to hepatitis B. It is particular efficacious within 48 hours of the incident. It may also be given to neonates who are at increased risk of contracting hepatitis B i.e. whose mothers are HBsAg and HBeAg positive Blood screening is Mandatory : Blood screening is Mandatory Other measures - screening of blood donors, blood and body fluid precautions is mandatory in majority of Countreis Universal Precautions : Universal Precautions Universal precautions," as defined by CDC, are a set of precautions designed to prevent transmission of human immunodeficiency virus (HIV), hepatitis B virus (HBV), and other blood borne pathogens when providing first aid or health care. Universal Precautions : Universal Precautions Under universal precautions, blood and certain body fluids of all patients are considered potentially infectious for HIV, HBV and other blood borne pathogens. Hand washing Minimal health precaution to Medical and Paramedical staff : Hand washing Minimal health precaution to Medical and Paramedical staff Hepatitis C Infection : Hepatitis C Infection Hepatitis C Virus Non A, non B Hepaci virus What is Hepatitis C Virus : What is Hepatitis C Virus Hepatitis C virus also known as Non A or Non B virus found while doing experiments on Chimpanzees. HCV infections are seen only in humans The epidemiology is like HBV infection. HCV Virology : HCV Virology The virus is not been grown in culture The virus is 50- 60 nm with linear single stranded RNA genome surrounded by an enveloped carrying glycoprotein spikes Now classified as Hepacivirus in the family of Flaviviridae Six genotypes are identified, with high mutability Slide 66: hypervariable region capsid envelope protein protease/helicase RNA-dependent RNA polymerase c22 5’ core E1 E2 NS2 NS3 33c NS4 c-100 NS5 3’ Hepatitis C Virus Hepatitis C Virus : Hepatitis C Virus Genome resembled that of a flavivirus positive stranded RNA genome of around 10,000 bases 1 single reading frame, structural genes at the 5' end, the non-structural genes at the 3' end. enveloped virus, virion thought to 30-60nm in diameter Morphological structure remains unknown Hepatitis C virus : Hepatitis C virus Genotype 1 and 4 has a poorer prognosis and response to interferon therapy, In Hong Kong, genotype 1 accounts for around 67% of cases and genotype 6 around 25%. Now 6 genotypes are identified. Terminology : Terminology Family Genus Species Genotype Subtype Quasispecies Pathogenesis : Pathogenesis Slide 71: Incubation period: Average 6-7 wks Range 2-26 wks Clinical illness (jaundice): 30-40% (20-30%) Chronic hepatitis: 70% Persistent infection: 85-100% Immunity: No protective antibody response identified Hepatitis C - Clinical Features How HCV transmitted : How HCV transmitted Blood transfusions Transplantation of organs Injectable drug abusers Immunocompromised Sexual transmission ? Less important Vertical transmission is possible Clinical features : Clinical features Overt Jaundice is seen in 5% of patients About 50 – 80% patients progress to chronic hepatitis May progress to Cirrhosis, or Hepatocellular carcinoma Chronic Hepatitis C Infection : Chronic Hepatitis C Infection The spectrum of chronic hepatitis C infection is essentially the same as chronic hepatitis B infection. All the manifestations of chronic hepatitis B infection may be seen, albeit with a lower frequency i.e. chronic persistent hepatitis, chronic active hepatitis, cirrhosis, and hepatocellular carcinoma. Transmission of HCV : Transmission of HCV Percutaneous IV drugs Clotting factors before viral inactivation Transfusion, transplant from infected donor Therapeutic (contaminated equipment, unsafe injection practices) Occupational (needle stick) Per mucosal Perinatal Sexual HCV - Occupational Transmission : HCV - Occupational Transmission Inefficiently transmitted Average incidence 1.8% following needle stick from HCV-positive source 10 times lower than HBV infection Hollow-bore needles Case reports from blood splash to eye No reports from skin exposures to blood Prevalence 1-2% among health care workers Lower than in the general population Slide 77: Transfusion or transplant from infected donor Injecting drug use Hemodialysis (yrs on treatment) Accidental injuries with needles/sharps Sexual/household exposure to anti-HCV-positive contact Multiple sex partners Risk Factors Associated with Transmission of HCV Slide 78: Symptoms anti-HCV ALT Normal 0 1 2 3 4 5 6 1 2 3 4 Hepatitis C Virus Infection Typical Serologic Course Titre Months Years Time after Exposure Laboratory Diagnosis : Laboratory Diagnosis HCV antibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears. ELISA test results to be confirmed with Immunoblotting assay Molecular Methods in Diagnosis : Molecular Methods in Diagnosis HCV-RNA - various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy. HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out. Prognostic Tests : Prognostic Tests Genotyping – genotype 1 and 4 have a worse prognosis overall and respond poorly to interferon therapy. A number of commercial and in-house assays are available. Genotypic methods – DNA sequencing, PCR-hybridization e.g. INNO-LIPA. Serotyping – particularly useful when the patient does not have detectable RNA. Viral Load – patients with high viral load are thought to have a poorer prognosis. Viral load is also used for monitoring response to IFN therapy. A number of commercial and in-house tests are available. HCV Treatment : HCV Treatment α-Interferon Ribavirin Effective in about 50% of cases No vaccine Treatment : Treatment Interferon - may be considered for patients with chronic active hepatitis. The response rate is around 50% but 50% of responders will relapse upon withdrawal of treatment. Ribavirin - there is less experience with ribavirin than interferon. However, recent studies suggest that a combination of interferon and ribavirin is more effective than interferon alone. Slide 85: Screening of blood, organ, tissue donors High-risk behavior modification Blood and body fluid precautions Prevention of Hepatitis C Slide 86: Hepatitis D Delta agent Hepatitis D Virus : Hepatitis D Virus The delta agent is a defective virus which shows similarities with the viroids in plants. The agent consists of a particle 35 nm in diameter consisting of the delta antigen surrounded by an outer coat of HBsAg. The genome of the virus is very small and consists of a single-stranded RNA Slide 89: Coinfection severe acute disease. low risk of chronic infection. Superinfection usually develop chronic HDV infection. high risk of severe chronic liver disease. may present as an acute hepatitis. Hepatitis D - Clinical Features Slide 90: Percutanous exposures injecting drug use Permucosal exposures sex contact Hepatitis D Virus Modes of Transmission Slide 91: anti-HBs Symptoms ALT Elevated Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Coinfection Typical Serologic Course Time after Exposure Titre Slide 92: anti-HBs Symptoms ALT Elevated Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Coinfection Typical Serologic Course Time after Exposure Titre Slide 93: Jaundice Symptoms ALT Total anti-HDV IgM anti-HDV HDV RNA HBsAg HBV - HDV Superinfection Typical Serologic Course Time after Exposure Titre Slide 95: HBV-HDV Coinfection Pre or postexposure prophylaxis to prevent HBV infection. HBV-HDV Superinfection Education to reduce risk behaviors among persons with chronic HBV infection. Hepatitis D - Prevention Slide 96: Hepatitis E infection NANB Hepatitis E Virus : Hepatitis E Virus Calicivirus-like viruses unenveloped RNA virus, 32-34 nm in diameter +ve stranded RNA genome, 7.6 kb in size. very labile and sensitive Can only be cultured recently Slide 98: Hepatitis E Virus Slide 99: Incubation period: Average 40 days Range 15-60 days Case-fatality rate: Overall, 1%-3% Pregnant women, 15%-25% Illness severity: Increased with age Chronic sequelae: None identified Hepatitis E - Clinical Features Slide 100: Symptoms ALT IgG anti-HEV IgM anti-HEV Virus in stool 0 1 2 3 4 5 6 7 8 9 10 11 12 13 Hepatitis E Virus Infection Typical Serologic Course Titer Weeks after Exposure Slide 101: Most outbreaks associated with faecally contaminated drinking water. Several other large epidemics have occurred since in the Indian subcontinent and the USSR, China, Africa and Mexico. 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. Minimal person-to-person transmission. Hepatitis E - Epidemiologic Features Slide 103: Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler. IG prepared from donors in Western countries does not prevent infection. Unknown efficacy of IG prepared from donors in endemic areas. Vaccine? Prevention and Control Measures for Travelers to HEV-Endemic Regions Hepatitis G virus : Hepatitis G virus A new virus recently identified in Humans. Not grown in culture lines RNA genome is cloned Its role still for debate HGV RNA was found in acute, chronic, fulminant hepatitis , hemophiliacs, patients with multiple transfusions It resembles HCV In all other aspects Protect yourself : Protect yourself Medical and Paramedical staff can reduce, avoid the incidences of accidental infection with HBV,HCV,HDV,and Hepatitis G infections with, safe handling of needles Prevent needle stick injuries : Prevent needle stick injuries Report your needle stick injuries to higher authorities : Report your needle stick injuries to higher authorities Created for benefit of Medical and Paramedical Students in Developing World : Created for benefit of Medical and Paramedical Students in Developing World Dr.T.V.Rao MD Email doctortvrao@gmail.com