Approach to hepatitis
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This document summarizes key details about several types of viruses including incubation period, transmission method, potential for chronic infection or fulminant disease, and age effects. It provides information on hepatitis A, B, C, D, and E viruses such as their RNA genomes, typical incubation periods ranging from 14 to 180 days, modes of transmission including fecal-oral, parenteral, sexual or perinatal, and chronic infection risks. It also outlines recommendations for hepatitis A vaccination dosages and schedules based on age at infection or medical status.
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Approach to hepatitis
- 5. Viruses Type Incubation period (days) Transmission Chronic infection Fulminant disease HAV RNA 15-19 Faeco-oral No Rare HBV DNA 60-180 Parenteral, sexual, perinatal Yes Yes HCV RNA 14-160 Parenteral, sexual Yes Rare HDV RNA 21-42 Parenteral, sexual, perinatal Yes Yes HEV RNA 21-63 Faeco-oral No Yes
- 22. Age at infection Acquire infection perinatally: Poor prognosis 30 % children, 5 % neonates full recovery Adults or older children: Good prognosis 95% full recovery Older age: Poor prognosis
- 32. AGE EXPECTED EXPOSURE DURATION DOSE < 1 year <3 months 3-5 months > 5 months 0.02 ml/kg 0.06 ml/kg 0.06 ml/kg ,ti repaeated every 5 months ≥ 1 year Healthy Immunocompromised / chronic liver disease HAV vaccine HAV vaccine + 0.02 ml/kg
Editor's Notes
- transmission
- virion consisting of a 42-nm spherical, double-shelled particle composed of small spheres and rods and with an average width of 22 nm. It is an exceedingly resistant virus, capable of withstanding extreme temperatures and humidity. The S gene encodes the viral envelope. The core antigen, HBcAg, is the protein that encloses the viral DNA., initiating a cellular immune response. The e antigen, HBeAg, which is also produced from the region in and near the core gene, is a marker of active viral replication. It serves as an immune decoy and directly manipulates the immune system; it is thus involved in maintaining viral persistence. The role of the X gene is to encode proteins that act as transcriptional transactivators that aid viral replication. Evidence strongly suggests that these transactivators may be involved in carcinogenesis.
- The natural course of chronic HBV infection consists of 4 phases. The immune tolerance phase is characterized by the presence of HBeAg, high HBV DNA levels, and persistently normal ALT levels, but no evidence of active liver disease. The immune clearance phase is characterized by the presence of HBeAg and high/fluctuating HBV DNA and ALT levels. An outcome of the immune clearance phase is HBeAg seroconversion. Most patients then enter the inactive HBV carrier phase, which is characterized by the absence of HBeAg and the presence of anti-HBe, low or undetectable HBV DNA levels (<2000 IU/mL), normal ALT levels, and no/minimal inflammation on liver biopsy. The reactivation phase is characterized by the absence of HBeAg, intermittent/persistently increased ALT and HBV DNA levels, and inflammation on liver biopsy.
- Because the symptoms of acute HBV infection and the laboratory indicators of hepatocellular dysfunction are indistinguishable from those of other forms of viral hepatitis,
- HBV surface antigen (HBsAg) appears before the onset of symptoms, peaks during overt disease, and then declines to undetectable levels in 3-6 months. Acute HBV infection is characterized by the presence of HBsAg in the serum. Hepatitis B e antigen HBeAg, HBV DNA, and DNA polymerase appear in the serum soon after HBsAg, and all signify active viral replication. Measuring HBV DNA with quantitative DNA polymerase chain reaction (PCR) is ideal for monitoring disease progression and effect of treatment Immunoglobulin M (IgM) anti-HBc becomes detectable in serum shortly before the onset of symptoms, concurrent with the onset of elevation of serum aminotransferases. Over months, the IgM antibody is replaced by immunoglobulin G (IgG) anti-HBc. Detection of IgM HBcAb is diagnostic of acute HBV infection, IgG anti-HBc does not rise until the acute disease is over and is usually not detectable for a few weeks to several months after the disappearance of HBsAg. Anti-HBs may persist for life, conferring protection; During recovery from acut phase , HbBsAg level falls before the symtpoms wane, IgM HBcAg may be the only marker of infection Hepatitis B surface antibody (HBsAb), but not hepatitis B core antibody (HBcAb), is detected in persons who have received the hepatitis B vaccine The carrier state is defined by the presence of HBsAg in the serum for 6 months or longer after its initial detection. During convalescence, HBsAg and HBeAg are cleared, and IgG antibodies to HBsAg, HBcAg, and HBeAg develop.f HBsAg in the serum for 6 months or longer after its initial detection.
- Seroprevalence – level of pathogen in a population
- HCV – most likely virus to cause chronic infection < 15 % clear the virus Rest develop chronic hepatitis Chronic HCV infection is usually clinically silent until a compliation develops Serum aminotransferases fluctauates and are sometimes normal but histologic inflammation is universal 20 % ultiamyte;y cirrhosis Extra hepatic manifestations – mainly adults – curaneous vasculitis, membranoproliferative GN, peripheral vascultitis
- Biopsy – recommended only before starting any treatment and to rule out other causes of overt liver disese Histology - In patients with chronic HCV infection, inflammatory cells accumulate in the portal tracts. They may also have foci of inflammation accompanied by necrosis in the parenchyma.
- Co infection – HDV along with HBV Super infection – HDV in a person already infected with HBV
- Candidates for postexposure prophylaxis include household and sexual contacts of infected patients, contacts in childcare centers during outbreaks, and, if the patient is a food handler, others who work at the same establishment Vaccine – 720 ELISA untis and aluminuium hydroxide is the adjuvant. Efficacy of 95-100% Cathc up – if seron negative fro HAV > 13 yr – give adult vaccine 1440 units
- Spep – serum protei electrophoresis