Blood bourne diseases - Hepatitis , HIV Flashcards
What are Blood borne viruses ?
Viruses carried in the blood
ex -
Most prevalent
0 HIV
0 HEPT B
0 HEPT C
hept b and
C - Blood
borne
viruses
causing
hepatitis ,
disease of
the liver.
Can be spread from person to person by infected blood or bodily fluid. s
salvia
pleural fluid
amnotic fluid etc.
- sexual contact
- during birth from mother to child
- sharing hypodermic needles
Symptoms of Hepatitis ?
- muscle and joint pain
- Fever
- feeling and being sick
- Fatigue
- a general sense of feeling unwell
- loss of appetite
- tummy pain
- dark urine
- pale, grey-coloured poo
- itchy skin
- yellowing of the eyes and skin (jaundice)
What is hepatitis ?
Liver inflammation
Types
Viral Hepatitis (can then cause autoimmune hepatitis.
* HEP
A,B,C,D E.
- HEPT C - contact with contaminated blood
- HEPT D is
not a
standalone
infection
cannot
happen
without
HEP B
infection
HEP A - disease of sanitation, spread through contaminated faeces.
Secondary hepatitis - cause by alcohol , drugs , toxins.
Autoimmune heaptitis
What is an acute and chronic hepatitis B vaccination ?
acute > 6 months
Chronic > 6 months
Difference between Hept B and C
hept B - DNA virus - double stranded with polymerase molecule
- 1Attachement -. Attach to liver cell via c receptors and surface proteins on virus cell.
2. Endocytosis - Enter into cell - shed viral envelope and begin to shed capsid
3. Double stranded circular DNA migrate into nucleus.
4. Transcription DNA transcribed into cccDNA ( covalently closed circular DNA. )
cccDNA has a long half life , very stable - very hard to destroy. It persist for very long time.
- translation of cccDNA to make viral proteins and secrete these ,effecting other cells. -
Hept C - RNA virus - single stranded
- Attachement
- Endocytosis
- Replication - single stranded RNA stays in cytosol and replicates , hijacking host translation machinery - assemble new virus proteins.
Major difference - HEP B goes into nucleus and creation of cccDNA. HEP C - single RNA stays in cytosol.
how does Hept C avoid immunity ?
- Impairs dendritic activation —-> CD4 T helper cells not activated ——> other immune cells not activated
- Inhibit MHC 1 presentation(does not show that it is infected) ——> CD8 T cell regcognition is prevented (dont kill the infected cell so virus ploiferates. ) ———> NK cells remain activated causing cytopathic effects
( no MHC 1 to inhibit NK cells so there are allowed to run rampant cause chronic inflammation , Fibrosis cirrhosis and hepatocarcinoma. )
- Distraction - release extra antigens so that antibodies attack them instead of virus.
Hiding
INDIRECT METHODS
1 virus produces surface binding proteins that are highly variable —– > difficult to make antibody / CD8 T cell response —–> cd8 cells deplete because they are constantly being made for outdated cells and the surface binding proteins keep changing.
Effect of Hept B and C on immune system ?
NK cells not deactivated so cause cytopathic effects - leads to :
- Fibrosis
- Cirrhosis
- hepatocarnimona
Indirect
Excess antigens due to virus pumping it out to distract immune system
* these extra antigens form complexes with antibodies - (immune complexes - cryoglobulinemia)
GET DEPOSITED IN THE BV and joints and body attacks them .
Causes Vasculitis (inflammation of BV )
- Depletion of CD8 t cells - Vulnerable to secondary infection.
How is Hept C diagnosed ?
Antibody test - indicates if person has ever been in infected
HCV ribonucleic test (RNA ) test if HCV infection is active
- genotype analysis.
0 When you get a positive result repeat to confirm diagnosis. With negative resukt ocnsider repeating if person is of high risk.
0 active hepatitis C if they have a positive HCV antibody test and positive HCV RNA test
0 If you have a positive antibody test but a negative HCV RNA test- you previously had HCV infection but it is resoved and is not active.
- However not immune from future HCV - prevent reinfection.
Needle stick injury when dealing with patients with HEP B OR c
0 HCV antibody testing at 12 and 24 weeks
0 HCV RNA testing at 6, 12, and 24 weeks. This should be arranged through their Occupational Health department.
How is HEP B diagnosesd
Presence (elevation ) or certain serological markers.
Intial testing should at least test for HBsAG and anti -HBc
HBsAG - Hepatitis B surface antigen — indicates presence of viral envelope. Elevated levels can indicated HBV infection.
HBeAG - Hepatitis B e antigen - associted with high levels of viral replication.
* people with chronic HBV tend t be more infectious if HeAG is dected.
0(anti-HBc) Antibody to HBcAg — indicates current or previous
HBV infection.
0 (anti-HBc IgM)- IgM antibody to hepatitis core antigen - indicates HBV infection in last 6 months
0(anti-HBc IgG) - IgG antibody to hepatitis core antigen - present for life - indicates past infection.
What markers are used to determine vaccination response in HBV ?
Antibody to HBsAg (anti-HBs)
* indiactes recovery and immunity .
0 anti - HBs without presence of anti -HBcs ( indiactes current or previous HBV infection) - indicates immunity.
anti - HBs quantified to measure vaccination response.
What markers would determine a chronic or acute infection in HEP B ?
postive HBsAG + Postive anti - HBc IgM —- acute infection
Positive HBsAG + Postive anti - HBc IgG or total with negative anti - HBc IgM 0 indiactes chronic infection.
Differential diagnosis for HEP B ?
Viral hepatitis caused by other viruses - HEP A, C, D, E, Epstein’’s BARR VIRUS , cytomegalovirus
- cytomegovirus (free blood - given in blood transfusion if patient has never been infected by it before).
- Hepatitis caused by bacteria
0leptospirosis
0 coxiella
burnetii - Autoimmune hepatitis (90 % occurs in women)
- Drug induced liver disease - suspect in patient with history of paracetamol overdose or therapeutic use of paracetamol with alcohol misuse )
- Non - fatty liver disease.
Granulomatous disorders - inherited primary immunodeficiency disease - increased susceptibility to infection.
Treatment of hep B
Vaccination - pre / pro exposure prophylaxis
- can be given at 0 , 1 and 2 months (3 doses )
or
Over 21 days for rapid protection , needlestick injury , travel to endemic areas.
- HEPT B Immunoglobulin prophylaxis given at same time upon exposure to infected bodily fluids etc- if no proven immunity.
(* given intramuscular;y , ideally within 48 hours with first dose of vaccine)
PEGINTERFERON ALFA
Peginterferon Alfa - interferon- alpha2a - stimulate the immune system
Reverse transcriptase inhibitors - prevent viral replication.
Effective vaccine
Treatment for HEPT C
0 15 - 45 % of infected clear spontaneously within 6 months without treatment
01st line- Antiviral treatment - (DAA - direct acting antivirals ) started promptly if infection not spontaneously cleared.
CHRONIC - considered for antiviral therapy
Protease inhibitors
RNA synthesis inhibitors .
no vaccine.
