REPORT: PATHOGENESIS, DIAGNOSTICS, TREATMENT AND PRINCIPLES OF PROPHYLAXIS OF

PARENTARAL VIRAL HEPATITIS (B-C-D-GB-TT)

Sajid Mehmood Adnan Akram Aftab Ahmed

Accident & Emergency Department. Department of Infectious Diseases. Department of Infectious Diseases.
Royal Infirmary Liverpool. University Hospital Riga. Kaunas Medical University Hospital.
United Kingdom Latvia Kaunas. Lithuania
sajid@infekcijas.eu adnan@infekcijas.eu aftab@infekcijas.eu

HBV- virus DNA (Hepadna group)

Can occur at any age
Transmission-parantaral by intravenous rout, infected blood,mainly in homosexuals, Vertical
transmission.
I.p- 1 to 6 months.

Clinics- Prodromal period 1 month generally 1-2 wks, during this time occur arthralgia mostly in
large joints and influenza like symptoms.
-May fallow serum sickness like immunological syndrome (other constitutional symptoms of
anorexia, fever law grade, malaise, vomiting, head ache). Serum sickness like symptoms may
consist of rashes eg- urticaria and macular papular rash.
-With the onset of jaundice clinical symptoms decrease.
-urine becomes dark and stools become pale.
-Liver may be enlarged, spleen may be palpable (cytolitic syndrome).

Complications – extra hepatic immune complex mediated conditions such as arthritis or

glomerular nephritis seen.
Investigations – (1) liver biochemical analysis- [A] in prodromal stage-serum bilirubin is
normal, Bilirubin urea ,urobilinogen in urine, amino transferases, ASAT and ALAT are all
increased ( ALAT >ASAT).
[b] Icteric stage- serum bilirubin reflect the level of jaundice, serum ASAT reaches max 1-2 days
after the appearance of jaundice, Alkaline phosphatase in serum mildly elevated.
(2) Blood analysis- Leukopenia and relative Lyphocytosis, prolonged PT, increased ESR
(3) Viral markers

Structure of hepatitis B virus- complete infective virion (dane particle) consist os circular
double stranded DNA, specific DNA polymarase and structural proteins, surrounded by an outer
envelop of surface proteins which is recognized serologically as HBV surface antigen (HBS
antigen).
Nucleo capcid contains 2 serologically distinct antigens the Core and E antigen ( HBC ag, HBE
ag),
a. HBS antigen- associated with the viral surface coat, it is found in serum during the 1st acute
infection, Appears usually 1-6 wks before clinical or biochemical illness develops (I.P) , and
disappears in recovery period.
Corresponding Anti HBS ab- Appears wks or months later after clinical recovery and usually
persist for life its detection indicates past HBV infection and relative immunity. (vaccination). In
chronic state or carrier state usually HBS ag persist and Anti HBS does not develop.
b. Hbc ag – Associated with viral core found in infected liver cells not in serum, corresponding
anti Hbc- appears at the onset of symptoms nearly 2 months also found in acute infections (HBS
ag +, Anti Hbc IgM+), chronic hepatitis (HBS ag +, Anti Hbc IgM negative but Anti Hbc IgG
+), Carrier state (HBS ag+, Anti Hbc IgM negative and Anti Hbc IgG+).
Therefore Anti Hbc- (IgM-Acute),(IgG-Chronic carrier state)
c. Hbe ag – viral core ag found only in HBS ag positive serum, It tends to produce viral DNA
polymerase does its presence reflects more active viral replication and associated with greater
infectivity of the blood and progress to chroni liver disease.
Corresponding Anti Hbe- points to relatively law infectivity, (Anti Hbe+, Hbe ag negative-
carrier ),(Anti Hbe negative ,Hbe ag +-chronic).

ACUTE TOTALLY CHRONIC CARRIER

RECOVERED
HBS ag + HBS ag - HB sag + Hbs ag +
Hbc Anti, IgM + Hbc anti IgM Hbc anti IgM Hbc anti IgM
negative negative negative
Hbc Anti IgG HBC anti IgG + Hbc anti IgG + Hbc anti IgG +
negative
Hbe ag + Hbe ag negative
Anti Hbc negative Anti Hbe +

Treatment – symptomatic
Prevention and profilaxis-
1.Avoid risk factors shared needles, homosexuals, multiple partners
2. Passive and active immunity- Vaccination should be given to all persons at risk

COMBINATION PRFILAXIS (vaccination + immunoglobulins) should be given to

accidental injury- needle stick, new born with HBS ag + mothers, Rgular sexual partners of Hbs
ag + who have been found HBV negative.
(500 Iu adults, 200 Iu new born i.m )
3. Chronic Hbv carriers treatment- patients who are Hbe ag+, HBS ag +, Anti Hbe negative.
Chronic state can be treated with alfa INF.

VHD - Delta virus

Incomplete RNA virus, enclosed in shel of HB ag
It is unable to replicate on its own ,and activated by presence of HBV
Route of transmission- mainly in drug users IP- 1-2mo
Any age, prodromal period nearly 1mo
During this period artharalgia, influenza like symptoms.
Clinic similar to HBV
HDV infection can occur either as a coinfection with HBV or as a superinfection in an HB sag+
patients
Coinfection of HDV and HBV clinically indistinguishable, Dg is confirmed by anti HDV
IgM+, anti HBC IgM+
Anti HDV Igm appears at 1 week and dissappear by 5-6 weeks when anti HDV IgG =
Increase serum ASAT
HDV RNA in serum and liver can be messured and is found in acute and chronic HDV
infection.chronic HDV is a severe form of liver disease
15 of dis. Progress in dev. Of cirrhosis
Treatment - alfa INF produces remission and relapses is common.

VHC
RNA virus 6 subtypes are seen Route of transmission-parenteral, post transfusion hep(blood)
Sexual contact
Mother- child IP-1-2 mo

Clinical features-prodromal period nearly 1 mo,in acute phase flue like symptoms increase in
serum transferaces,
Extra hepatic manifestations-artheritis,agranulocytosis,aplastic anemia,diffuse neurological
problems/
In HCV- acute form, chronic,Hepatic cirrhosis dev within 15-30 yrs, Hepatocellular carcinoma
dev

Diagnosis- (1)anti HCV IgM in serum (1st gen.test)

(2) 2nd gen.test-
a. ELISA, b. RIBA(recombinant immunoblotassy),c. PCR-to check viral RNA .if + then do
liver biopsy to detect chronic hepatitis and cirrhosis/
Treatment- no clear guide line, INF been used in acute phases/

VH-GB(HGBV)
RNA virus,flavi vir Parenteral-sexual contact,blood IP-180 days Characteristic chronic forms
Can occur fulfilmant form
DG-HGB ag+, Anti HGBV, PCR

VH-TT
Recently detected ,parenteral route
Mainly blood.similar to HCV and HGBV in clinics and in investigations
Viral hepatitis dg. Is based on 4 steps.
1.epidermiological 2.pre icteric( prodromal) variation 3.clinics 4. lab Data