Hepatitis Viruses

1. Hepatitis Viruses Etiology, epidemiology, pathogenesis, classification

2. Hepatitis viruses (HV)- group of anthroponosis diseases with different mechanisms of transmition, which are accompanied by intoxication and disorders of liver function, quite often by an icterus. Distinguish HV-A, B, C, D, E, G, each of which has its own agents. The secondary hepatitis do not belong to this group, they are caused by the viruses of cytomegalo, herpes, Epstein-Barr and adenoviruses.

3. Electronic microscopy ( negative contrast) Hepatitis virus A (d=27nm).

4. Etiology of VHA • Agent VHA was first discovered in 1973 by Feinstone. This is RNA - containing virus. • VHA is sensitive to formaldehyde, may remain preserved for a period of few months or even years during temperature + 4° C, some weeks - during room temperature. Complete inactivation of virus takes place during 85 ° C in a period of 5 minutes. VHA is resistant to chlorine, in comparison with other viruses of this group and may enter through barriers of water cleaning stations.

5. Electronic microscopy ( negative contrast).patient ‘s serum with HV B .A-tubular part В – Deyna partС – spheric part A B C

6. Etiology of VHB • VHB in natural condition is revealed in sick people and carriers. This is DNA-containing virus is pathogenic for human and few types of primates. Causes acute and persistent infection, damages primarily liver. • Virus consists on antigenic structure: HBsAg - surface, HBcAg - internal (care), HBeAg - reflects infectiouness of virus. • Towards these antigens in organism of patients antibodies are produced: anti-HBs; anti-HBc; anti-HBe.

7. Etiology of VHB • HBsAg is revealed in majority of patients in incubation stage • Presence of HBsAg in human organism testifies as presence of acute and latent proceeding infection • Prolonged conservation HBsAg may testify about transformation of the process into chronic form • HBcAg is practically not determined in blood and fixed in directly by DNA-polymerize reactions, falling positive in acute period of disease, as well as after many months and years in carriers • HBeAg is revealed in early stages of disease, which is then changed by anti-HBe.

8. Etiology of VHC • Virion of virus of hepatitis C consists on nucleus and lipid external membrane. Genome is represented by single chain RNA. VHC is resistant in external medium, particularly in biological fluids such as preparations of blood, sperm and others. Sensitive to chloroform, other desinfective solutions and high temperatures (100° C and more). • Antigenic structure of VHC is less studied.

9. Etiology of VHD • Virus represents defective virus particle, contains internal antigen (HDAg), made up of small circular RNA and surface covering, which is HBsAg VHB. It is considered that reproduction of virus is possible only during presence of HBsAg in organism of patient, therefore hepatitis D proceeds always as a coinfection or superinfection, joining with VHB.

10. Etiology of VHE • Virus of hepatitis E has been isolated from feces of patients with jaundice. Spherical particles similar to virus were able to discover due to the method of immune electronic microscopy.

11. Epidemiology of VHA • Viral hepatitis A - antroponosis. The source of disease is sick person in prejaundice period and in 15 - 20 days of acute period of the disease. • Primary localization of virus is gastrointestinal tract. Mechanism of transmission is faecal-oral. Virus is excreted from the organism of sick person with feces. • Specific final factors of transmission of hepatitis A virus are water and food. Spreading depends on conditions of water supply and its relation with fecal contamination. Important factors of transmission are flies, dirty hands. • Susceptibility to the disease is high. Mainly children and adults up to 30 year fall sick.

12. Epidemiology of VHB • The source of VHB is sick person with acute or chronic form, healthy carrier. • Mechanism – contact (wound). • Ways of transmission: parenteral, sexual, through placenta from sick mother to fetus (vertical or transplacentar). • Factors: blood, sperm, vaginal secret, milk of mother • Susceptibility to the disease is high. • Risk group: drug addicts, homosexualists, prostitutes, medical personnal

13. Anatomic pathology • Morphological changes take place in all tissual components of liver - parenchyma, connective tissue, reticuloendothelium, in bile pathways. • Dystrophic and single necrotic changes, massive and submassive necroses of liver parenchyma. • Three variants of changes: mesenhymal inflammation, cholestatic and cytolitic

14. Macro-preparation: massive hepatonecrosis

15. Pathogenesis • Entrance gates • The agent approaches regional lymphatic glands, where its massive reproduction takes place • Organism replies on this negative influence by immunological reaction of reticular tissue of the lymphatic gland (primary virusemia) • Virus continue to enter from lymphatic glands into blood in a large quantities (clinical period) • Secondary virusemia

16. Pathogenesis of VHB • explained from viral-immunogenetic position, because it is known that power of immune response is genetically determinated • Immune reaction may be strong (in fulminate form of hepatitis), flabby and adequate. Only adequate immune reaction promotes cyclic course and favorable outcomes of the disease

17. Classification hepatitis viruses (IDC XX WHO) Hepatitis viruses (В15-В19) Conclusions:cytomegalovirus (В25.1) herpes viral (herpes simplex) hepatitis (В00.8) out comes of viral hepatitis (В94.2) В15 Acute hepatitis В15.0 Hepatitis A with hepatic coma В15.9 Hepatitis A without hepatic coma В16 Acute hepatitis В В16.0 Acute hepatitis В with delta-agent (co-infections) and hepatic coma В16.1 Acute hepatitis В with delta-agent (co-infections) without hepatic coma В16.2 Acute hepatitis В without delta-agent accompanied by hepatic coma В16.9 Acute hepatitis В without delta-agent and without hepatic coma

18. В17 Other acute viral hepatitis В 17.0 Acute delta (super infection) infection in hepatitis B В17.1 Acute hepatitis C В 17.2 Acute hepatitis E В17.8 Other confirmed acute viral hepatitis В18 Chronic viral hepatitis B B18.0 Chronic viral hepatitis B with delta-agent В18.1 Chronic viral hepatitis B without delta-agent В18.2 Chronic viral hepatitis С В18.8 Other chronic viral hepatitis В18.9 Chronic viral hepatitis, without confirmation В19Unconfirmed viral hepatitis В19.0 Unconfirmed viral hepatitis with coma В19.9Unconfirmed viral hepatitis without hepatic coma

19. Classification of viral hepatitis(Hepatites virosae) (В15-В19) According to infectious agent:А (В15), В (В16), С (В17.1), D (В17.0), Е (В17.2), G (В17.8), not confirmed (В19). Clinical forms:jaundice, cholestatic, without jaundice, sub-clinical (asymptomatic), fulminant. Duration:Acute, prolonged, chronic (В18). Degree of severity:mild degree, moderate degree, severe degree, very severe degree.

20. Complications:Acute hepatic encephalopathy (І, ІІ, ІІІ, ІV stages) (В15.0; В16,0; В16.2; В19.0), exacerbation (clinical, fermented), functionaland general diseases of biliary tracts. Results:recovery, remaining symptoms ( astenovegitativ syndrom, hepatomegaly), difficult recovery, hyperbilirubinemia, chronic hepatitis (В18), liver cirrhosis, primary liver cancer.