Hepatitis Hepatitis VirusesViruses

EtiologyEtiology, , epidemiologyepidemiology, , pathogenesispathogenesis, , classificationclassification

Hepatitis viruses (HV)- Hepatitis viruses (HV)- group of antgroup of anthhroponoroponosissis diseases with diseases with differentdifferent mechanisms of mechanisms of transmitransmition, tion, which which are accompanied by intoxication are accompanied by intoxication and and disordersdisorders of liver of liver function function, quite , quite often by an icterus. often by an icterus.

Distinguish Distinguish HV-A, B, C, D, E, GHV-A, B, C, D, E, G, each of , each of which has which has its own agentsits own agents. The second. The secondaryary hepatitis do not belong to this group, hepatitis do not belong to this group, they are caused by the viruses of they are caused by the viruses of cytomegalocytomegalo, , herpesherpes, Epste, Epsteinin-Ba-Barr and rr and adenovirusadenoviruseses..

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

Etiology of VHAEtiology of VHA Agent VHA was first discovered in 1973 by Agent VHA was first discovered in 1973 by

Feinstone. This is RNA - containing virus. Feinstone. This is RNA - containing virus. VHA is sensitive to formaldehyde, may VHA is sensitive to formaldehyde, may

remain preserved for a period of few months remain preserved for a period of few months or even years during temperature + 4or even years during temperature + 4°° C, C, some weeks - during room temperature. some weeks - during room temperature. Complete inactivation of virus takes place Complete inactivation of virus takes place during 85 during 85 °° C in a period of 5 minutes. VHA C in a period of 5 minutes. VHA is resistant to chlorine, in comparison with is resistant to chlorine, in comparison with other viruses of this group and may enter other viruses of this group and may enter through barriers of water cleaning stations. through barriers of water cleaning stations.

Electronic microscopy Electronic microscopy (( negative contrast negative contrast)) ..patient ‘s serum with HV Bpatient ‘s serum with HV B . .A-tubular partA-tubular part В – В – Deyna partDeyna part С – С – spheric partspheric part

B C

A

Etiology of VHBEtiology of VHB VHB in natural condition is revealed in sick VHB in natural condition is revealed in sick

people and carriers. This is DNA-containing people and carriers. This is DNA-containing virus is pathogenic for human and few virus is pathogenic for human and few types of primates. Causes acute and types of primates. Causes acute and persistent infection, damages primarily persistent infection, damages primarily liver.liver.

Virus consists on antigenic structure: Virus consists on antigenic structure: HBsAg - surface, HBcAg - internal (care), HBsAg - surface, HBcAg - internal (care), HBeAg - reflects infectiouness of virus.HBeAg - reflects infectiouness of virus.

Towards these antigens in organism of Towards these antigens in organism of patients antibodies are produced: anti-patients antibodies are produced: anti-HBs; anti-HBc; anti-HBe.HBs; anti-HBc; anti-HBe.

Etiology of VHBEtiology of VHB HBsAg is revealed in majority of patients in HBsAg is revealed in majority of patients in

incubation stageincubation stage Presence of HBsAg in human organism testifies as Presence of HBsAg in human organism testifies as

presence of acute and latent proceeding infectionpresence of acute and latent proceeding infection Prolonged conservation HBsAg may testify Prolonged conservation HBsAg may testify

about transformation of the process into about transformation of the process into chronic formchronic form

HBcAg is practically not determined in blood and HBcAg is practically not determined in blood and fixed in directly by DNA-polymerize reactions, fixed in directly by DNA-polymerize reactions, falling positive in acute period of disease, as well falling positive in acute period of disease, as well as after many months and years in carriersas after many months and years in carriers

HBeAg is revealed in early stages of disease, HBeAg is revealed in early stages of disease, which is then changed by anti-HBe. which is then changed by anti-HBe.

Etiology of VHCEtiology of VHC

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

Antigenic structure of VHC is less studied. Antigenic structure of VHC is less studied.

Etiology of VHDEtiology of VHD

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

Etiology of VHEEtiology of VHE

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

Epidemiology of VHAEpidemiology of VHA Viral hepatitis AViral hepatitis A - antroponosis. The source of - antroponosis. The source of

disease is sick person in prejaundice period and in disease is sick person in prejaundice period and in 15 - 20 days of acute period of the disease.15 - 20 days of acute period of the disease.

Primary localization of virus is gastrointestinal Primary localization of virus is gastrointestinal tract. Mechanism of transmission is faecal-oral. tract. Mechanism of transmission is faecal-oral. Virus is excreted from the organism of sick person Virus is excreted from the organism of sick person with feces. with feces.

Specific final factors of transmission of hepatitis A Specific final factors of transmission of hepatitis A virus are water and food. Spreading depends on virus are water and food. Spreading depends on conditions of water supply and its relation with conditions of water supply and its relation with fecal contamination. Important factors of fecal contamination. Important factors of transmission are flies, dirty hands. transmission are flies, dirty hands.

Susceptibility to the disease is high. Mainly Susceptibility to the disease is high. Mainly children and adults up to 30 year fall sick. children and adults up to 30 year fall sick.

Epidemiology of VHBEpidemiology of VHB The source of VHB is sick person with acute or The source of VHB is sick person with acute or

chronic form, healthy carrier.chronic form, healthy carrier. Mechanism – contact (wound). Mechanism – contact (wound). Ways of transmission: parenteral, sexual, Ways of transmission: parenteral, sexual,

through placenta from sick mother to fetus through placenta from sick mother to fetus (vertical or transplacentar). (vertical or transplacentar).

Factors: blood, sperm, vaginal secret, milk of Factors: blood, sperm, vaginal secret, milk of mothermother

Susceptibility to the disease is high. Susceptibility to the disease is high.

Risk group: drug addicts, homosexualists, Risk group: drug addicts, homosexualists, prostitutes, medical personnalprostitutes, medical personnal

Anatomic pathologyAnatomic pathology

Morphological changes take place in all Morphological changes take place in all tissual components of liver - tissual components of liver - parenchyma, connective tissue, parenchyma, connective tissue, reticuloendothelium, in bile pathways. reticuloendothelium, in bile pathways.

Dystrophic and single necrotic changes, Dystrophic and single necrotic changes, massive and submassive necroses of massive and submassive necroses of liver parenchyma. liver parenchyma.

Three variants of changes: mesenhymal Three variants of changes: mesenhymal inflammation, cholestatic and cytoliticinflammation, cholestatic and cytolitic

Macro-preparationMacro-preparation: : massive massive hepatonecrosishepatonecrosis

PathogenesisPathogenesis Entrance gatesEntrance gates The agent approaches regional lymphatic The agent approaches regional lymphatic

glands, where its massive reproduction takes glands, where its massive reproduction takes place place

Organism replies on this negative influence by Organism replies on this negative influence by immunological reaction of reticular tissue of immunological reaction of reticular tissue of the lymphatic gland (primary virusemia) the lymphatic gland (primary virusemia)

Virus continue to enter from lymphatic glands Virus continue to enter from lymphatic glands into blood in a large quantities (clinical period)into blood in a large quantities (clinical period)

Secondary virusemia Secondary virusemia

Pathogenesis of VHBPathogenesis of VHB

explained from viral-immunogenetic explained from viral-immunogenetic position, because it is known that power position, because it is known that power of immune response is genetically of immune response is genetically determinateddeterminated

Immune reaction may be strong (in Immune reaction may be strong (in fulminate form of hepatitis), flabby and fulminate form of hepatitis), flabby and adequate. Only adequate immune adequate. Only adequate immune reaction promotes cyclic course and reaction promotes cyclic course and favorable outcomes of the diseasefavorable outcomes of the disease

Classification hepatitis Classification hepatitis viruses viruses

((IDC XX WHOIDC XX WHO))Hepatitis viruses Hepatitis viruses (В15-В19)(В15-В19)ConclusionsConclusions:: cytomegaloviruscytomegalovirus (В25.1) (В25.1) herpes viralherpes viral ( (herpes simplexherpes simplex) ) hepatitis hepatitis (В00.8) (В00.8) out comes of viral hepatitis out comes of viral hepatitis (В94.2)(В94.2)В15 В15 Acute hepatitisAcute hepatitis В15.0 В15.0 Hepatitis A with hepatic comaHepatitis A with hepatic coma В15.9 В15.9 Hepatitis A without hepatic comaHepatitis A without hepatic comaВ16 В16 Acute hepatitis Acute hepatitis ВВВ16.0 В16.0 Acute hepatitis Acute hepatitis В В with delta-agentwith delta-agent ( (co-infectionsco-infections) ) and hepatic and hepatic

comacomaВ16.1 В16.1 Acute hepatitis Acute hepatitis В В with delta-agentwith delta-agent ( (co-infectionsco-infections) ) without hepatic without hepatic

comacomaВ16.2 В16.2 Acute hepatitis Acute hepatitis В В without delta-agent accompanied by hepatic without delta-agent accompanied by hepatic

comacomaВ16.9 В16.9 Acute hepatitis Acute hepatitis В В without delta-agent and without hepatic comawithout delta-agent and without hepatic coma

В17 В17 Other acute viral hepatitisOther acute viral hepatitis В 17.0 В 17.0 Acute deltaAcute delta ( (super infection) infection in hepatitis Bsuper infection) infection in hepatitis B В17.1 В17.1 Acute hepatitis CAcute hepatitis C В 17.2 В 17.2 Acute hepatitis EAcute hepatitis E В17.8 В17.8 Other confirmed acute viral hepatitisOther confirmed acute viral hepatitisВ18 В18 Chronic viral hepatitis BChronic viral hepatitis B BB18.0 18.0 Chronic viral hepatitis B with delta-agentChronic viral hepatitis B with delta-agentВ18.1 В18.1 Chronic viral hepatitis B without delta-agentChronic viral hepatitis B without delta-agentВ18.2 В18.2 Chronic viral hepatitis Chronic viral hepatitis С С В18.8 В18.8 Other chronic viral hepatitisOther chronic viral hepatitis В18.9 В18.9 Chronic viral hepatitis, without confirmationChronic viral hepatitis, without confirmationВ19В19 Unconfirmed viral hepatitisUnconfirmed viral hepatitis В19.В19.0 0 Unconfirmed viral hepatitis with comaUnconfirmed viral hepatitis with coma В19.9В19.9 Unconfirmed viral hepatitis without hepatic comaUnconfirmed viral hepatitis without hepatic coma

Classification of viral hepatitisClassification of viral hepatitis ((Hepatites virosaeHepatites virosae) (В15-В19)) (В15-В19)

According to infectious agent:According to infectious agent: А (В15), В (В16), А (В15), В (В16), С (В17.1), С (В17.1), DD (В17.0), Е (В17.2), (В17.0), Е (В17.2), GG (В17.8), (В17.8), not not confirmedconfirmed (В19). (В19).

Clinical formsClinical forms:: jaundicejaundice,, cholestatic, without jaundice, cholestatic, without jaundice, sub-clinical (asymptomatic), fulminant.sub-clinical (asymptomatic), fulminant.

DurationDuration:: AcuteAcute, , prolonged, chronic prolonged, chronic (В18).(В18).

Degree of severityDegree of severity:: mild degreemild degree, , moderate degree, severe moderate degree, severe degree, very severe degreedegree, very severe degree..

ComplicationsComplications:: Acute hepatic encephalopathy (І, ІІ, ІІІ, І(І, ІІ, ІІІ, ІV stagesV stages) (В15.0; ) (В15.0; В16,0; В16.2; В19.0), В16,0; В16.2; В19.0), exacerbationexacerbation ((clinicalclinical, , fermentedfermented), ), functionalfunctional and and general diseases of biliary tractsgeneral diseases of biliary tracts. .

ResultsResults:: recoveryrecovery, , remaining symptoms remaining symptoms ( ( astenovegitativ astenovegitativ syndromsyndrom, , hepatomegalyhepatomegaly), ), difficult difficult recoveryrecovery, , hyperbilirubinemiahyperbilirubinemia, , chronic chronic hepatitishepatitis (В18), (В18), liver cirrhosisliver cirrhosis, , primary primary liver cancerliver cancer. .