Hepatitis A, B, C, D, & E PDF

Mycology and Virology | MLS-415 F1: Hepatitis A, B, C, D, & E Professor: Thynee Tago, MSMT Date: April 27, 2024 HEPATITIS A CLASSIFICATION: Genus: Hepatovirus Family: Picornaviridae STRUCTURE: 27 to 32 nm spherical particle Cubic symmetry A linear single stranded RNA 7.5 kb CONTENT: Capsid Viral Pro...

Mycology and Virology | MLS-415 F1: Hepatitis A, B, C, D, & E Professor: Thynee Tago, MSMT Date: April 27, 2024 HEPATITIS A CLASSIFICATION: Genus: Hepatovirus Family: Picornaviridae STRUCTURE: 27 to 32 nm spherical particle Cubic symmetry A linear single stranded RNA 7.5 kb CONTENT: Capsid Viral Protein Genome PEOPLE W/ INCREASED RISK OF HEPATITIS A: Hepa A = Infection of the Liver through ingestion of contaminated Fecal material Natural host → HUMANS Eyes may appear Jaundiced due to it being a liver disease Incubation: 10-50 days; Averaging 25-30 People w/ occupational risk for exposure to Hepa A People in developed countries adopting children from underdeveloped countries People w/ Chronic Liver Diseases Most prominent Sign and Symptom: YELLOWING of the SKIN/SCLERA For some there could be fever, stomach pain, darkened urine and stool is light colored Joint pain may also occur (They feel tired) Children may appear ASYMPTOMATIC; Adults are usually SYMPTOMATIC Symptoms develop and appear 2-7 weeks after infection which may last < 2 months but for some it can reach up to 6 months (the longevity depends on the stability of the immune system) Travels Internationally Men who have Sex with Men (MSM) Users of injection and Non-injection drugs Homeless people People w/ Hepa B/C or with HIV Laboratory Diagnosis Serologic assays: ○ PCR ○ ELISA HAV in Stool – Usually detected 1st ; Basically, 2 weeks before and after the onset of jaundice, HAV can be detected in the stool. Anti-HAV IgM – Usually peaks 2 weeks after the elevation of LIVER ENZYMES Anti-HAV IgG – Usually detected AFTER the onset of disease and could persist for a long time Treatment, Prevention and Control TREATMENT No specific treatment – usually you are advised to rest or have an adequate nutrition; fluids also are needed since the virus itself is self-limiting; Does not usually progress to Chronic Liver Disease unless the patient has an underlying condition on the liver. COPY FOR: ORIT, ANNE CHELSEA R. | 1 VIRUS INACTIVATION Heating food to above 85 deg C for at least 1 minute ○ The longer, the better ○ Also depends on the quality of the food Surface disinfection with Sodium Hypochlorite or Bleach (1:100) VIRUS DESTRUCTION Autoclaving Boiling in water Dry heat (180 deg C for 1 hour) or (160 deg C for 2 hours) Ultraviolet Irradiation (1 min at 11 watts) Treatment with FORMALIN or treatment with CHLORINE (10-15 ppm for 30 mins) ○ Formalin (1:4000) 3 days @ 37 deg C Natural Host → HUMANS Can survive OUTSIDE the body and can remain infectious for at least 7 days Most people with chronic HBV infection are ASYMPTOMATIC and have no evidence of liver disease or injury Average of 90 days or Weeks up to 6 months (could be longer) TRANSMISSION: Sexual Intercourse Sharing of Needles/ Syringes Through birth Contact w/ contaminated blood PREVENTION AND CONTROL Vaccination of Hepatitis A - Best prevention method ○ Specially for Frontliners, Staffing for child care, Food handlers, Military personnel, etc. Practicing Good Hand Hygiene HEPATITIS B Enveloped dsDNA; Icosahedral capsid 3 forms: ○ Spherical (22nm) ○ Tubular/ Filamentous (22-200nm) ○ Dane Particle (42nm) Complete virion (w/ genome) CLASSIFICATION: Genus: Orthohepadnavirus Family: Hepadnaviridae CONTENTS: Hepatitis B surface antigen (HBsAg) Hepatitis B core antigen (HBcAg) Viral DNA genome Clinical Manifestations PEOPLE W/ INCREASED RISK OF HEPATITIS B: Infants born from mothers w/ Hepa B Sex with someone who has HBV MSM Patients that are constantly exposed to needles (Dialysis indiv.) Users of injection and Non-injection drugs Healthcare workers MOST COMMON SYMPTOMS: Jaundice, Loss of Appetite, Nausea and Vomiting, Fever and Fatigue Laboratory Diagnosis & Identification HEPATITIS B ANTIGENS HEPATITIS B ANTIBODY Hepatitis B surface antigen (HBsAg) 1st to appear in the SERUM (once there is Hepatitis B surface antibody (anti-HBs) infxn) Hepatitis B core antigen (HBcAg) CANNOT be detected in the serum but can be detected through LIVER BIOPSY Found inside HEPATOCYTES Total hepatitis B core antibody (anti-HBc) Means that the virus is actively multiplying in the liver (Viral Replication) Perform Immunohistochemistry COPY FOR: ORIT, ANNE CHELSEA R. | 2 Treatment, Prevention and Control TREATMENT There is no medication available Rest, adequate nutrition and fluids Patients with more severe symptoms may need to be hospitalized Take medication indefinitely (under the guidance of the attending physician) ○ To avoid damaging the liver PREVENTION AND CONTROL Getting vaccinated Proper handwashing Never share needles, syringes or even water Follow universal precautions Use birth controls to prevent the spread of sexually transmitted disease Hepatitis B envelope antigen (HBeAg) Appears in the serum Hepatitis B envelope antibody (anti-HBe) Presence indicates INFECTIVITY of the individuals (Viral Infection) Used to identify whether the patient has Acute or Chronic HBV infection Also used to identify immune status of the individual (either susceptible or Immune) Interpretation HEPATITIS C HBsAg (+) Acute infection → (+) for IgM and Total Anti-HBc Chronic infection → (+) ONLY for Total Anti-HBc ○ Meaning only IgG is detected, and the body stopped producing IgM anti-HBc HBsAg (-) Immune due to PREVIOUS INFECTION → (+) for Anti-HBs and Total Anti-HBc ○ Patient has Core Antigen, meaning the virus got into the patient which produced HBcAg Immune due to VACCINATION → (+) ONLY for Anti-HBs ○ Patient has no Core Antigen, meaning the virus did not reach the patient → no HBcAg → no Anti-HBc Susceptible → (-) for BOTH Anti-HBs and Total Anti-HBc Acute Infection Acute Infection w/ (↑) Infectivity Convalescent Immune due to previous infection HBsAg + + + - HBeAg - + - - Anti-HBs - - - + Anti-HBe - - + + CLASSIFICATION: Genus: Hepacivirus Family: Flaviviridae STRUCTURE: Single-stranded RNA genome surrounded by icosahedral capsid with envelope. COPY FOR: ORIT, ANNE CHELSEA R. | 3 Non-cytopathic virus; usually enters the liver cell and undergoes replication simultaneously causing cell necrosis by several mechanisms, like Immune mediated cytolysis and other phenomena such as: ○ Hepatic steatosis, ○ Oxidative stress ○ Insulin Resistance Natural Host → HUMANS TRANSMISSION: Sexual Intercourse Sharing of Needles/ Syringes Through birth Contact w/ contaminated blood Sharing of Toothbrush or Razors for shaving EIA → RIBA → PCR If both positive for EIA and RIBA then proceed to PCR testing PEOPLE W/ INCREASED RISK OF HEPATITIS C: People with HIV People who is in Hemodialysis People who donated/Received blood or from Organ transplants Healthcare and emergency medical and public safety personnel Medtechs (constant exposure to needles) Mucosal exposures Children who are born from mothers with HCV infxn. CLINICAL MANIFESTATIONS People with newly acquired HCV infection usually are ASYMPTOMATIC The average period from exposure to symptom onset is 2-12 weeks Most people with Chronic HCV infection are asymptomatic ○ May also lead to diseases that is not only related to the liver such as: Diabetes Glomerulonephritis Porphyria Cutanea Tarda Non-Hodgkin's Lymphoma SIGNS & SYMPTOMS Loss of appetite Nausea vomiting Joint pain Jaundice Fever fatigue Dark urine Clay-colored stool Abdominal pain CONFIRMATORY TESTING: Qualitative and Quantitative assays for HCV RNA: RT-PCR or Recombinant Immunoblot Assay (RIBA) HCV genotyping Serologic testing Liver Biopsy – to determine the degree of liver damage; chronic HCV TREATMENT PEGylated interferon combined with ribavirin ○ PEG + Interferon + Ribavirin ○ Polyethylene Glycol will serve as a VESICLE/ CONTAINER for the interferon ○ Ribavirin is an antiviral drug Antiviral therapy Telaprevir and boceprevir Sofosbuvir Orthotopic liver transplantation People living with Hepatitis C should: Be vaccinated against hepatitis A and Hepatitis B Avoid alcohol Check with their doctor taking any prescription pills, herbs, supplements or over the counter medications (Medicol; ibuprofen) Be tested for HIV PREVENTION AND CONTROL Safe and appropriate use of healthcare injections; Safe handling and disposal of sharps and waste; Provision of comprehensive harm reduction services to people who inject drugs Testing of donated blood for HBV and HCV (as well as HIV and syphilis) Training of health personnel Prevention of exposure to blood during sex LABORATORY DIAGNOSIS SCREENING TESTS FOR ANTIBODY to HCV (anti-HCV): Enzyme Immunoassay (EIA) ○ In low-risk patients w/ (+) EIA, they will have to undergo confirmatory testing using RIBA COPY FOR: ORIT, ANNE CHELSEA R. | 4 HEPATITIS D CLINICAL MANIFESTATION More severe than the other type of Hepatitis viruses ○ Can run either acute or chronic course 3-7 weeks of incubation period ○ Fatigue ○ Lethargy ○ Nausea ○ Anorexia Symptoms last for about 3-7 days Jaundice occurs in the next phase of symptoms ○ Fatigue and nausea continues ○ Abnormal Serum Bilirubin Level ○ Clay-colored stool ○ Dark urine Left: Hepatitis D virus sans the capsid as it borrows structures from HBsAg, Right: Hepatitis B virus CLASSIFICATION: Genus: Deltavirus (hence the letter D) Family: Kolmioviridae SMALLEST virus known to infect animals, therefore it is not really a full virus, but considered a SATELLITE VIRUS/SUBVIRAL AGENT. Why? ○ Because of its special structure STRUCTURE: Small, Spherical, Single-stranded, enveloped particle with Hepa B surface antigen, and negative-sense RNA molecule Genetic material is wrapped in HBsAg ○ Usually present if Hepatitis B is primarily present (Coexisting infection) PATHOGENESIS The production and transmission of HDV is ENTIRELY DEPENDENT on HBV to provide HBsAg Replicates only in the hepatocytes HDV antigens ○ Small delta antigen – usually produced in the early stages of infection ○ Large delta antigen – produced in the later stages of infection High Risk of Infection: People with Chronic HBV, Injection-drug users, commercial sex workers, Men-having-sex with men ➔ ➔ ➔ ➔ ➔ Transmission: Broken skin Contact with infected blood ◆ E.g. blood transfusion, sharing of syringes, sharp objects, etc. Mother to child (Rare case) (at birth) Unprotected Sexual Intercourse Sharing toothbrushes, razors, etc. Complications HDV is known to occur either as a co-infection or a superinfection Co-infection Superinfection occurs when both HDV and HBV contracted simultaneously Acute HDV & HBV infection occurs when Chronic HBV carriers are infected with HDV Severe acute hepatitis and Chronic Hepatitis D infection in 80% of the cases LABORATORY DIAGNOSIS & IDENTIFICATION The diagnosis of Hepatitis D infection is made following serologic tests for the virus Radioimmunoassay (RIA) & Enzyme Immunoassay (EIA): Detects the total anti-HDV antibodies Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR): To monitor any ongoing HDV infection Detects 10-100 copies of HDV genome in infected serum TREATMENT No specific treatment for HDV PEGylated interferon alpha PREVENTION AND CONTROL Prevention of Hepatitis D virus is based on prevention of Hepatitis B virus Co-infection: the HBV or post exposure prophylaxis can be used to prevent the infection Superinfection: educate chronic HBV carriers about transmission and risky behaviors; proper health infection COPY FOR: ORIT, ANNE CHELSEA R. | 5 HEPATITIS E Other names: Enteric Hepatitis; Self-limiting Hepatitis; Most common cause of Acute Hepatitis ○ Acquired through contaminated water or food that is not properly cooked Replication only occurs in the LIVER ○ Incubation may go from 20-40 days (slow) Reactivation is possible CLASSIFICATION Genus: Hepevirus Species: Hepeviridae STRUCTURE: Small, nonenveloped virus with a single-stranded RNA genome; 4 genotypes Transmission Fecal-Oral; vertical transmission is possible; zoonotic transmission; breastfeeding Disease Hepatitis similar to that caused by hepatitis A virus except for extraordinarily high case fatality rate (10%-20%) among pregnant women Diagnosis Serology Treatment Supportive Prevention Avoid contact with the virus PATHOGENESIS Characteristics Genotype 1 Genotype 2 Genotype 3 Genotype 4 Geographic location Africa and Asia Mexico, West Africa Developed Countries China, Taiwan, Japan Transmission route Waterborne fecal-oral; person-to-person Waterborne fecal-oral Food-borne Food-borne Groups at high risk for infection Young adults Young adults Older Adults (>40 years) and males, Immuno-compromis ed persons Young adults Zoonotic transmission NO YES Chronic infection Occurrence of Outbreaks Common Smaller scale outbreaks YES NO Uncommon Uncommon CLINICAL MANIFESTATIONS When they occur, the signs and symptoms of Hepatitis E are similar to those of other types of acute viral hepatitis and liver injury Fever Fatigue Loss of appetite Nausea Vomiting Abdominal pain Jaundice LABORATORY DIAGNOSIS AND IDENTIFICATION Diagnosis can be confirmed only by testing for the presence of antibody against HEV or HEV RNA Liver function tests ○ Increased levels of serum bilirubin (↑) ○ Increased AST (↑) ○ Increased ALT (↑) CONFIRMATORY TEST: Nucleic acid testing is recommended to confirm positive serology results in areas where HEV is not endemic TREATMENT AND MANAGEMENT Hepatitis E usually resolves on its own without treatment (Typically advised to rest) There is no specific antiviral therapy for acute hepatitis E Patients who do develop fulminant liver failure need liver transplantation PREVENTION & CONTROL Good sanitation COPY FOR: ORIT, ANNE CHELSEA R. | 6 VACCINE No FDA-approved vaccine for hepatitis E is currently available Clean Drinking Water Boiling and Chlorination of Water Avoiding raw pork and venison VIRUS FAMILY NUCLEIC ACID TRANSMISSION INCUBATION (DAYS) Hepatitis A Picornaviridae Single-strand RNA; Nonenveloped Fecal-oral 15-502 Hepatitis B Hepadnavirus Double-strand DNA Parenteral; sex 30-1808 >90% Infants