Hepatitis infection community medicine.pptx

Hepatitis

1. Viral Hepatitis Dr. Jasmine Assistant Professor Department of Community Medicine 1

2. Viral Hepatitis Viral hepatitis is a term commonly used for several clinically similar yet etiologically and epidemiologically distinct diseases. It is caused by five different viruses with transmission either through contaminated food or water (hepatitis A and E) or through exposure to blood or body fluids (hepatitis B, C and D). 2

3. Hepatitis A Geographical areas can be characterized as having high, intermediate or low levels of hepatitis A infection Areas with high levels of infection: In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) have been infected with the hepatitis A virus before the age of 10 years. Areas with intermediate levels of infection: In developing countries, countries with transitional economies, and regions where sanitary conditions are variable, children often escape infection in early childhood. Areas with low levels of infection : In developed countries with good sanitary and hygienic conditions, infection rates are low. 3

4. Epidemiology- Agent Agent : T he hepatitis A virus, is an enterovirus of the Picornaviridae family Resistance : F airly resistant to low pH, heat and chemicals. Reservoir of infection : The human cases are the only reservoir of infection Period of infectivity : G reatest from 2 weeks before to 1 week after the onset of jaundice. Infective material: Mainly man’s faeces . Blood, serum and other fluids are infective during the brief stage of viraemia Virus excretion : HAV is excreted in the faeces for about 2 weeks before the onset of jaundice and for up to 2 weeks thereafter 4

5. Epidemiology Host factors : Age : More frequent among children than in adults. However, people from all ages may be infected if susceptible. In young children, infections tend to be mild or subclinical; the clinical severity increases with age. Sex: Both sexes are equally susceptible Immunity : Immunity after attack probably lasts for life, second attacks have been reported in about 5 per cent of patients Environmental factors: Poor sanitation and overcrowding favour the spread of infection, giving rise to water-borne and food-borne epidemics. 5

6. Mode of transmission Faecal -oral Route : This is the major route of transmission. It may occur by direct (person-to-person) contact or indirectly by way of contaminated water, food or milk. Parenteral Route : Hepatitis A is rarely, if ever, transmitted by the parenteral route (i.e., by blood and blood products or by skin penetration through contaminated needles). Sexual Transmission : As a sexually transmitted infection hepatitis A may occur mainly among homosexual men because of oral-anal contact Incubation period : 1 0 to 50 days (usually 14-28 days). 6

7. Clinical spectrum The onset of jaundice is often preceded by gastrointestinal symptoms such as nausea, vomiting, anorexia, and mild fever. Jaundice may appear within a few days of the prodromal period, but anicteric hepatitis is more common. Hepatitis A resolves completely in 98 per cent of cases but relapse of symptoms are noted in 3-20 per cent cases 7

8. Diagnosis Tests for abnormal liver function, such as serum alanine aminotransferase (ALT) and bilirubin, supplement the clinical, pathologic, and epidemiologic findings A specific laboratory diagnosis of hepatitis A can be obtained by : a. Demonstration of HAV particles or specific viral antigens in the faeces , bile and blood. HAV is detected in the stool from about 2 weeks prior to the onset of jaundice, up to 2 weeks after. b. Anti-HAV appears in the IgM fraction during the acute phase, peaking about 2 weeks after elevation of liver enzymes. Anti-HAV IgM usually declines to non-detectable levels within 3-6 months 8

9. Prevention and Containment Control of reservoir Complete bed rest and disinfection of faeces and fomites. The use of 0.5 per cent sodium hypochlorite has been strongly recommended as an effective disinfectant Control of transmission: The best means of reducing the spread of infection is by promoting simple measures of personal and community hygiene Control of susceptible population Vaccines : Formaldehyde inactivated vaccines - produced in several countries and which are most commonly used worldwide. Live attenuated vaccines Human immunoglobulin 9

10. Hepatitis B Agent : Hepatitis B virus Reservoir of Infection: Man Infective material : Contaminated blood, saliva, vaginal secretions and semen Resistance: 7 days on environmental surfaces Period of communicability: The virus is present in the blood during the incubation period (for a month before jaundice) and acute phase of the disease 10

11. Host factors Age : Acute hepatits B occurs in approximately 1 per cent of perinatal, 10 per cent of early childhood (1-5 years of age), and 30 per cent of late (>5 years age) HBV infections. High risk groups : The annual incidence of HBV infection in surgeons is estimated to be 50 times greater than that in the general population, and is more than twice that of other physicians Hepatitis B a nd HIV Infection : It is estimated that 10 per cent of the 40 million people infected with HIV worldwide are coinfected with HBV Humoral and c ellular r esponses : Hepatitis B virus has three distinct antigens - a surface antigen, also known as ‘’Australia antigen” (HBsAg), a core antigen ( HBeAg ), and an “e” antigen 11

12. Mode of transmission Parenteral route : Hepatitis B is essentially a blood-borne infection Perinatal transmission: Spread of infection from HBV carrier mothers to their babies Sexual transmission : Various body fluids including saliva, vaginal, menstrual and seminal fluids have been implicated as vehicles of human transmission Other routes : Transmission from child-to—child, often called horizontal transmission Incubation period : 30 to 180 days 12

13. Clinical picture Carrier state and chronic liver disease In some people, CHB is inactive and does not lead to significant liver disease. In others, it may cause progressive liver fibrosis, leading to cirrhosis with end-stage liver disease, and markedly increased risk of hepatocellular carcinoma 13

14. Diagnosis The assays that detect the presence of either antigens or antibodies, typically in serum or plasma but also in capillary blood and oral fluid. These include rapid diagnostic tests (RDTs), and laboratory-based immunoassays, e.g. enzyme immunoassays (EIAs), chemiluminescence immunoassays (CLIAs), and electrochemiluminescence immunoassays (ECLs). 14

15. Prevention and Containment Hep B vaccine: The dose for adults is 10-20 micrograms initially (depending on the formulation) and again at 1 and 6 months. Children under 10 years of age should be given half of the adult dose at the same time intervals. Hepatitis B immunoglobulin (HBIG): The recommended dose is 0.05 to 0.07 ml/kg of body weight (22)\ two doses should be given 30 days apart Passive-active immunization: The simultaneous administration of HBIG and hepatitis B vaccine is more efficacious than HBIG alone Other measures: All blood donors should be screened for HBV infection, and those positive for HBsAg also known as Australia antigen should be rejected 15

16. Treatment There is no specific treatment for acute hepatitis B. Care is aimed at maintaining comfort and adequate nutritional balance, including replacement of fluids lost from vomiting and diarrhoea. 16

17. Hepatitis C Agent : Hepatitis C virus Transmission: R eceipt of contaminated blood transfusions, blood products and organ transplants; I njections given with contaminated syringes and needle-stick injuries in health-care settings; I njection drug use; and B eing born to a hepatitis C-infected mother. Incubation period : 2 weeks to 6 months 17

18. Hepatitis C Symptoms : Those people who are acutely symptomatic may exhibit fever, fatigue, decreased appetite, nausea, vomiting, abdominal pain, dark urine, grey coloured faeces , joint pain and jaundice Diagnosis : The hepatitis C virus recombinant immunoblot assay (RIBA) and hepatitis C virus RNA testing are used to confirm the diagnosis. Treatment : Ribavarin , Direct antiviral agents (DAA) 18

19. Prevention Primary prevention Hand hygiene: Safe and appropriate use of health care injections; Safe handling and disposal of sharps and waste, Provision of comprehensive harm-reduction services to people who inject drugs including sterile injecting equipment; Testing of donated blood for hepatitis B and C, Training of health personnel; and Promotion of correct and consistent use of condoms. Secondary and tertiary prevention Education and counselling on options for care and treatment; Immunization with the hepatitis A and B vaccines to prevent coinfection Early and appropriate medical management including antiviral therapy if appropriate; and Regular monitoring for early diagnosis of chronic liver disease 19

20. Hepatitis E The infection caused by the hepatitis E virus Transmission : Faecal -oral route, Food-borne transmission from ingestion of products derived from infected animals, Transfusion of infected blood products; and vertical transmission from a pregnant woman to her foetus . Incubation period : 40 days Symptoms : D isease is mostly asymptomatic or causes a very mild illness without jaundice that goes undiagnosed. The typical symptoms are jaundice, loss of appetite, abdominal pain and tenderness, nausea and vomiting, fever and enlarged and tender liver. 20

21. Hepatitis E Diagnosis: Diagnosis of hepatitis E infection is, therefore, usually based on the detection of specific IgM and IgG antibodies to the virus in the blood Treatment: Hepatitis E is usually self-limiting. Hospitalization is required for fulminant cases and in symptomatic pregnant women. Prevention Maintaining hygienic practices such as hand washing with safe water, particularly A voiding drinking water and/or ice of unknown purity; A dhering to WHO safe food practices. 21

22. Hepatitis D Hepatitis D is caused by hepatitis D virus that requires HBV for its replication. Hepatitis D cannot occur in the absence of HBV. Route of transmission : The route of HDV transmission are the same as for HBV Diagnosis : HDV infection is diagnosed by high titres of Immunoglobulin G (IgG) and Immunoglobulin M (IgM) anti-HDV, and confirmed by detection of HDV RNA in serum. Treatment: There is no specific treatment for acute or chronic HDV infection. Persistent HDV replication is the most important predictor of mortality and the need for antiviral therapy Prevention : Prevention and control of HDV infection requires prevention of HBV transmission through hepatitis B immunization, blood safety, injection safety, and harm reduction services. 22

23. Hepatitis G Hepatitis G virus HGV was discovered in 1996. The prevalence of this infection is still not known 23

24. Thank you 24