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BDS2 BAMS > Epidemiology, pathogenesis, diagnosis and dental relevance of Hepatitis Viruses > Flashcards

Epidemiology, pathogenesis, diagnosis and dental relevance of Hepatitis Viruses Flashcards

1
Q

what 2 hepatitis viruses cause the most risk to patients and dentists?

A

hep B and C

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2
Q

structure of hep A virus

A
  • simple
  • protein coat with RNA genome
  • spherical
  • some have an envelope but most don’t
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3
Q

where can hep A grow?

A

can only grow in cell

- cannot be grown on agar plate

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4
Q

transmission of hep A

A

faecal-oral route mainly

not BBV, can be person-to-person, food or water borne

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5
Q

incubation period of hep A

A

2-7 weeks
- remains viable in sea water
Can get Hep A from food poising from sea food

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6
Q

signs of hep A infection

A

mainly subclinical infections
- illness is usually brief and self-limiting
mortality is less than 0.2%
no chronic disease

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7
Q

what is a difference between hep A and hep B, C and D?

A

hep A has no chronic disease

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8
Q

how to diagnose hep A?

A

serology

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9
Q

passive immunisation

A

give pre-formed antibodies

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10
Q

active immunisation

A

give antigens and body makes antibodies; longer lasting effect

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11
Q

hepatitis A immunisation

A

Human Normal Immunoglobulin
- Short-term protection (4 months)

Vaccine

  • Formaldehyde-inactivated
  • Prepared from the GBM or HM 175 strain of hepatitis A virus
  • Single dose makes antibody for 1 year
  • Booster dose at 6 – 12 months makes immunity for 10 years
    (i. e. if go abroad frequently to a high risk area, advised to have does of vaccine after a year of first (booster))
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12
Q

viral load

A

number of viral particles per ml of blood

higher load = more infectious

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13
Q

prevalence of hep B

A

350 million people infected globally

  • Global problem
  • Most acquired the disease by vertical transmission or during preschool childhood

70% of new cases occur among people between the ages 15-39 (relatively young)

Hepatitis B is 100 times more infectious than HIV (very infectious)
- As with HIV infection, potent prolonged treatment of hepatitis B selects for variants that are naturally resistant to treatment

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14
Q

what must happen in combination with hep B vaccine?

A

blood titre

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15
Q

treatment of hep B

A

No curative treatment but new antivirals suppress viral load

  • 2 drugs approved for the treatment of chronic HBV (IFNalpha and Lamivudine) approximately 35% or less will show a long term response.
  • Isn’t ideal – doesn’t cure but supresses the viral load
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16
Q

structure of hep B

A

Partially double stranded DNA virus
- All other hepatitis are RNA

Hepadnavirus
- Liver virus

Eight different subtypes of HBV exist

  • These types specific determinants are useful in epidemiology
  • All types are protected against by vaccine
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17
Q

how many types of HBV are there?

A

Eight different subtypes of HBV exist

  • These types specific determinants are useful in epidemiology
  • All types are protected against by vaccine
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18
Q

dane particle

A

intact virus (viral coat with DNA genome)

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19
Q

long cylindrical and smaller circular forms that can be seen next to dane particle

A

Viruses produced excessive amounts of protein coat – surface antigen

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20
Q

what is the role of the outer surface protein on viruses?

A

surface protein/antigen

  • Active component of vaccine is the surface antigen made by genetic engineering
  • Make antigens against the antibody which protect you
  • Docks with liver cells
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21
Q

what is HBe antigen?

A

HBe Ag is derived from the core

If E antigen positive - then very high viral load (risk) likelihood of transmitting is greater than E antigen negative

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22
Q

geographic distribution of chronic HBV infection

A

Varied distribution

  • UK low prevalence of infection
  • Red areas higher - Africa, Asia, South America
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23
Q

Acute Hepatitis B Infection Lab Reports – England 2018

A
  • 381 acute or probable acute cases

Incidence: 0.68 / 100,000

  • Highest incidence in London: 1.23 per 100,000
  • Most cases (64.7%) in men
  • Commonest risk factor: heterosexual exposure (50%)

Cause a sub clinical infection

  • Acute - small number show clinical signs of sickness
  • Higher in certain parts (urban, men)

Many infections not recognised so not reported - unknown
- Why we need standard infection control precautions

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24
Q

Why we need standard infection control precautions

A

Many infections not recognised so not reported - unknown

- as they are sub-clinical infections but still risk of transmission

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25
Q

3 main transmission routes for HBV

A
  • bloodborne
  • sexual
  • perinatal (Mother who is a Hep B carrier can transmit to infant at birth)
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26
Q

at risk individuals of hep B

A

IV drug users

Sexually active hetero- and homosexuals

Children of immigrants from disease-endemic areas

  • Infected as a child have a larger chance at becoming a carrier
  • Potential to transmit to other
  • Long term carriers can result in serious liver disease - cirrhosis and cancer

Sexual/household contacts of infected people

Infants born to infected mothers

Healthcare workers

Haemodialysis patients

  • Easy to transmit BBV if conditions right
  • Strict screening and infection control needed
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27
Q

epidemiology of hep B virus

A

depends on location

non endemic area (adults)

  • 80% inapparent disease
  • 20% acute hepatitis
  • – 95% recovery and 5% chronicity

endemic areas (infants)

  • mostly inapparent disease
  • — 5-20% recovery; 80-95% chronicity

both chronic infections can lead to cirrhosis and liver cancer

28
Q

hep B infections in developed (non-endemic areas)

A

developed countries where the prevalence of the virus is low, infection commonly occurs during adulthood primarily through sex or injecting drug use. Here the majority of infections are again subclinical with most patients developing an adequate immune response and consequent recovery.

29
Q

hep B infections in non-developed (endemic) areas

A

developing countries in sub-Saharan Africa and the Far East, HBV is endemic.
New borns and infants are primarily infected either by an infected mother at birth or through close contacts during the first few years of life.
The infection is usually inapparent and most children become chronic carriers with about 40% developing cirrhosis and cancer

30
Q

chronic HBV infections

A

HBV is not directly cytopathic.

The mechanism for the infection and destruction of hepatocytes is immune mediated.

When the viral antigens are expressed on liver cell surfaces in conjunction with HLA class I molecules, they are recognized by cytotoxic (CD8+) lymphocytes (CTL), which kill the infected hepatocytes.

Patients who clear HBV have a strong CTL response; patients unable to clear HBV become chronic carriers due to a very weak CTL response.

31
Q

Risk of Chronic HBV by Age of Acquisition and Immune Status

A

Neonates: 90-100%
Children: 20-40%
HIV-positive: 21%
Adults: <5%

  • Neonates have a high risk of becoming a carrier, unable to shift the infection
  • HIV positive are immunosuppressed so have a higher risk for carriage
32
Q

possible outcomes of HBV infection

A

Significant proportion have sub clinical
- recovery with immunity is the norm in UK

Very small number die from fulminant hepatitis
- serious acute infection that can’t recover

Some become carriers
- persistent infection
(HBV + for more than 6 months and haven’t developed antibodies for it then carrier)

Will at some point spontaneously clear virus – but unknown when

Some will go onto have chronic active hepatitis and severe liver disease

33
Q

when are you classed as HBV carrier

A

HBV + for more than 6 months and haven’t developed antibodies for it then carrier

34
Q

normal recovery of HBV infection

A
  • Symptoms - sick or sub clinical (no symptoms)

Anti-bodies develop

  • IgM first formed in human immune response
  • Anti-HBe is important - far less infectious

Last to develop is antibody to surface protein - but if vaccinated will be in blood

35
Q

chronic carriage of HBV infection

A

Continue to carry surface and HBe antigens in blood for months and years
- No antigens made to them

Risk for transmission and risk of developing disease

36
Q

passive immunisation of HBV infection

A

Hepatitis B immunoglobulin
- From pooled plasma

Main use: single acute exposure in non-immune individual
- Used for someone who is a non-responder (3 doses, no antibodies developed remain at risk)

Sharps injury from someone who is a carrier need to give them hep B immunoglobulin in short space of time

  • Stops virus latching the virus onto liver cells
  • Administer within 48 hours
37
Q

if an individual has responded to the hep B vaccine then they are….

A

highly immunogenic
- Developed an acceptable level of antibodies

No booster doses required for persons who have responded to HBV vaccine
- Even if dies down a bit immune memory will kick in to protect them so no booster required

38
Q

active HBV immunisation

A

\Vaccine: hepatitis B surface antigen (HBsAg) adsorbed on aluminium hydroxide adjuvant
- Produced by recombinant DNA technology

Protection: good

Response: not always good – check antibody levels
- Titre is integral part

Vaccine administration is intramuscular
- Three doses:
(Time zero; one month; six months)

Post immunisation: test for antibody response 2-4 months after vaccination course complete (titre)

39
Q

hep B virus post exposure prophylaxis

A

Average volume of blood inoculated during a needlestick injury with a 22 gauge needle is 1ul - may contain 100 infectious doses of HBV

  • If a non-responder to vaccine has a needlestick injury they have a 1 in 3 chance of infection
40
Q

who needs hep B virus post exposure prophylaxis?

A

Vaccine responders: none required

Vaccine non-responders: in the occupational setting, hepatitis B immune globulin (HBIG) provides an estimated 70% - 75% protection from HBV infection

41
Q

treatment of chronic HBV infection

A

Goal of Therapy: sustained viral suppression
(Trying to break the phases of viral replication cycle to stop it)

Agents available:

  • Immunomodulatory agents: interferon-alpha and pegylated interferon
  • Nucleoside analogues: lamivudine, telbivudine and entecavir
  • Nucleotide analogues: adefovir and tenofovir

Doesn’t cure but effective at viral suppression – reduce viral load so no longer a risk to patient and can return to work

42
Q

goal of HBV treatment

A

sustained viral suppression

43
Q

agents of HBV infections (3)

A
  • Immunomodulatory agents: interferon-alpha and pegylated interferon
  • Nucleoside analogues: lamivudine, telbivudine and entecavir
  • Nucleotide analogues: adefovir and tenofovir

Doesn’t cure but effective at viral suppression – reduce viral load so no longer a risk to patient and can return to work

44
Q

when was hep C discovered?

A

1989

- previously called non-A, non-B hepatitis

45
Q

what family of viruses does hep C belong to?

A

flavivirus

46
Q

how many genotypes of hep C virus are there?

A

1-6

  • Genotypes behave differently - issue
  • No protection from Hep B vaccine
47
Q

prevalence of hep C

A

200 million people infected worldwide
- For every 1 person infected with HIV, four are infected with HCV
Quite prevalent

  • North Africa and Asia: high
  • UK: moderate
  • USA: lower
48
Q

vaccine and treatment of hep C

A

No vaccine available

Treatments improved greatly but expensive
- Curable infection

49
Q

structure of hep C virus

A
  • enveloped RNA virus
  • diameter 30-38nm

cannot be grown in tissue culture (agar plate)
- diagnosis by serology

50
Q

Hepatitis C Laboratory Reports (England and Wales, 1992-2004)

A

Early 1990s discovered as an agent

  • Can then develop tests to screen
  • Big public health problem as numbers on the rise initially

2015: 143,000 people in England with chronic HCV
2018: 113,000 people in England with chronic HCV
- Figures are coming down
- Messages about prevention and availability of prevention

Need to push testing for those who are potentially at risk once treat people no longer a risk

51
Q

main risk factor for hep C infection developed countries

A

intravenous drug use

52
Q

hep C diagnosis (4)

A

Serological

  • Anti-HCV test: detects presence of antibodies - indicates exposure to HCV
  • HCV-RNA test: identifies presence of virus in blood – indicates active infection
    (main test for active on going infection)

Viral load / Quantitative HCV test: measures the number of viral particles in peripheral blood

Viral genotyping: determines the type of HCV present

  • additional test for hepatitis C - Certain genotypes respond better than other to certain medication types
  • Can target
53
Q

incubation for hep C

A

6-12 weeks

54
Q

type of infection from hep C

A

most patients have sub-clinical infection

jaundice in 25% of patients

55
Q

chronic hepatitis C frequency

A

60% - very high

most cases preceded by clinically inapparent infection

  • unaware of their disease and infectivity
  • Risk for dental treatment as patients unaware they are carriers

indolent and slowly progressive for 20+ years

progression from mild hepatitis to cirrhosis and liver cancer and disease

56
Q

natural history of HCV infection

A
  • Can be called silent infection

Can take 20-25 years to progress
- Sometimes only find out positive when get liver problems and then screened

57
Q

treatment of chronic hep C infection (2 types)

A

Has to be self-injected (not pleasant, tough, can cause depression)

Interferon alpha (pegylated) in combination with

  • Ribavirin – improves outcome slightly
  • Plus boceprevir or telaprevir (HCV protease inhibitors) for Genotype 1 -improves outcome even more
Second generation protease inhibitors: 
- Sofosbuvir 
- Ledipasvir
Newer treatment - better
(Virus needs to make new protein coat; Proteases break up protein chain. Drugs stop this so cannot break up chains so no new virus proteins coats)
58
Q

what treatment is better for chronic hep C infection

A

Second generation protease inhibitors:

  • Sofosbuvir
  • Ledipasvir

(Virus needs to make new protein coat; Proteases break up protein chain. Drugs stop this so cannot break up chains so no new virus proteins coats)

59
Q

effectiveness of hep C treatment

A

Not suppression of viral load it is cure

If individual is Hep C RNA positive not allowed to work

  • Treatments that are 98% effective means can have recovery
  • Long term sequelae of liver issues are stopped

Curable infection almost for all Hep C variants

60
Q

characteristics of hep D (delta agent)

A
  • Defective virus
  • RNA virus

Can only replicate when Hep B present too
- Delta agent relied on Help B making its protein coat

61
Q

2 ways of hep D infection

A

Can be independently transmitted but cannot cause infection without Hep B

co infection
- both present simultaneously

super infection
- already have help B and D comes along later

62
Q

co infection of hep D

A

both hep B and D present simultaneously

63
Q

super infection of hep D

A

already have help B and D comes along later

64
Q

way to protect against hep D

A

vaccination against hep B protects against hep D as cab’t get B so no D infection

65
Q

difference in recovery of hep D infection if co-infection Vs super infection

A

co infection has a far higher (90-95%) recovery rate than super infection (5-10%)

both infection types carry the same chronic infection risk (cirrhosis and liver cancer)

66
Q

hep E mimicks….

A 
hep A
(structure - spherical non-enveloped RNA virus, no chronic disease, cannot be grown in tissue culture, faecal oral main transmission)
67
Q

hep E and preganancy

A

Women infected in pregnancy there is a mortality rate a

- Significant immunosuppression in pregnancy is a possible link

BDS2 BAMS (54 decks)

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