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Medicine Year 1 - Semester 2 - Part 2 > Bloodborne Pathogens > Flashcards

Bloodborne Pathogens Flashcards

1
Q

What are blood borne infections ?

A

Infectious diseases caused by pathogenic micro-organisms which exist in blood and other bodily fluids.

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2
Q

What causes blood borne infections ?

A

Over 20 possible organisms (malaria, syphilis, brucellosis, VHFs etc.)

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3
Q

State some key viral pathogens

A

Hepatitis B (HBV)
Hepatitis C (HCV)
Human Immunodeficiency virus (HIV)

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4
Q

State some routes of transmission of blood-borne viruses

A

Blood-to-blood

Other bodily fluids

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5
Q

Blood-to-blood transmission causes

A

Injecting drug use
Needlestick & wound injury

Tattoos and piercing
Contaminated blood products

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6
Q

Bodily fluids transmission causes

A

Sexual & Genitourinary fluids (semen and vaginal secretions)

Birth canal (mother to child)

Other biological samples
- CSF
- Synovial / Pleural / Peritoneal fluid

Saliva / household utensils

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7
Q

Why are blood-borne viruses important ?

A

There is a risk of occupational transmission for healthcare workers (e.g. needle stick injury)

Often BBV infections are asymptomatic, BUT they can have serious long-term health consequences if not detected and managed.

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8
Q

Prevention of occupational exposure to BBVs

A

Standard universal precautions (wear gloves)

Disposal of sharps and hazardous waste

Hepatitis B vaccination

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9
Q

Management of any exposure to BBVs

A

Immediate 1st aid
Report and Test

Consider HIV post-exposure prophylaxis

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10
Q

What are viruses ?

A

Sub-microscopic infectious agents
- 80-1400nm diameter

Obligate intracellular parasites

Can be classified by nucleic acid content

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11
Q

Obligate intracellular parasites meaning

A

Rely on the metabolic processes of host cells

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12
Q

How are viruses identified ?

A

Identified based on:

  • protein antigens or antibodies to them
  • detection and amplification of nucleic acid (PCR)
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13
Q

Diagnostics for BBVs

A

Doing an antigen test - looking for presentation of protein

Look for antibodies of the protein

PCR testing - to amplify DNA / RNA

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14
Q

Main transmission of Hep B

A

Mother to child

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15
Q

Main transmission of Hep C

A

Blood to Blood contact

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16
Q

Main transmission of HIV

A

Sexual contact

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17
Q

Treatment of HBV - Hep B

A

Long-term anti-viral treatment can control chronic HBV infection

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18
Q

Treatment of HCV - Hep C

A

Anti-viral treatment
May clear (cure ?) HCV

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19
Q

Treatment of HIV

A

Anti-viral treatment can control chronic HIV infection

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20
Q

Vaccination / immunity for

  • HBV
  • HCV
  • HIV
A

HBV
- 95% of infected children/babies develop chronic HBV
- 95 of infected adults naturally clear HBV and are then immune
- there is an effective vaccine

HCV
- 20% of infected adults naturally clear, but are not immune
- no vaccine

HIV
- not cleared naturally
- no vaccine

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21
Q

Diagnosis for BBVs

A

Serology

HepB:
- HBV-DNA

HepC:
- HCV-RNA & genotype

HIV:
- Ag/Ab test, HIV-RNA

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22
Q

Global burden of disease - BBVs

A

Most common BBV - Hep B

Hep C - lowered numbers : more effective treatment

HIV

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23
Q

Why is there overlap between BBVs ?

A

As they are all transmitted in similar way.

So they cluster amongst population groups where risk of exposure occurs.

Some people get more than one BBV.

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24
Q

Hepatitis B: epidemiology

A

Most HBV transmission worldwide is from mother to child (during birth/early life)

This is preventable by vaccination.

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25
Q

Statistics involving Hep B

A

296 million people living with HBV
~ 1.5 million new infections /year
~ 820,000 deaths/year

68% living in Western Pacific /Africa

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26
Q

Hepatitis B virology

A

HepaDNAvirus

Hepatitis B can cause:
- acute & chronic hepatitis
- cirrhosis
- heptocellular carcinoma

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27
Q

Describe the structure of a HBV viral particle

A

HBsAg - surface antigen
HBcAg - core antigen
HBeAg - circulates in the bloodstream

DNA polymerase
HBV DNA

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28
Q

Acute infection of HBV

A

Short duration
Cleared within 6 months

  • asymptomatic
  • acute viral hepatitis
  • acute liver failure
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29
Q

Chronic infection of HBV

A

Long duration
> 6 months infected

  • Chronic hep B
  • Cirrhosis : compensated
  • Cirrhosis : decompensated

RISK OF HEPATOCELLULAR CARCINOMA

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30
Q

What does the outcome of Hep B depend on ?

A

Depends largely on age at the time of infection.

Younger the age at infection :
- greater the risk of chronic infection
- lower the risk of being symptomatic during the initial phase

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31
Q

Hep B - infants

A

Most asymptomatic

> 90% progression to chronic infection

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32
Q

Hep B - >5years esp adults

A

More likely to have symptoms

> 90% clear acute infection

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33
Q

Acute Hepatitis B: Clinical Course

A

Incubation 6 weeks- 6 months

Prodrome (few days)
Icteric phase (<6 weeks)

Convalescence (gradual recovery)
OR
Acute liver failure (<6 weeks)

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34
Q

Prodrome phase - acute hep B

A

few days

  • fatigue
  • fever
  • malaise
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35
Q

Icteric phase - acute hep B

A

< 6 weeks
- jaundice

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36
Q

Acute liver failure

A

<6 weeks

Encephalopathy
Bleeding

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37
Q

Management of acute hep B

A

Anti-viral drugs and Transplantation in severe (fulminant) liver failure

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38
Q

Chronic Hepatitis B : Clinical Course

A

Immune tolerant phase
Immune active phase
Immune control phase
Immune clearance phase

Reactivation phase

39
Q

What do symptoms and disease state of Chronic HBV depend on ?

A

The balance between HBV and host immune response.

40
Q

HBsAg

A

Positive during acute and chronic infection

41
Q

Anti sAb

A

Marker of immunity - positive following previous infection and vaccination

42
Q

HBcAg

A

Not present in blood

43
Q

Anti- HBc IgM

A

Positive during acute infection
(sometimes in chronic flares)

44
Q

Anti HBc IgG

A

Positive during chronic infection
Positive during recovery

45
Q

HBeAg

A

Positive during acute and some chronic infection; indicates high viral replication and transmissibility

46
Q

Anti eAb

A

Often indicates reduced viral replication & transmissibility in chronic infection

47
Q

HBV-DNA

A
  • detection of virus
    Quantifies viral load
48
Q

Hep B diagnosis

A

Only ~ 10% of people living with HepB worldwide are aware of their diagnosis

49
Q

Describe antigens in Acute Hep B

A

For acute Hep B:

The surface antigen goes up and comes down.

The surface antibody goes up and stays up.

The core antibody stays up.

50
Q

Describe antigens in Chronic Hep B

A

For chronic Hep B:

The surface antigen remains because you haven’t cleared it.

So, no surface antibody made really.

Core antibody comes and stays.

The e-antigen is initially positive but then becomes negative, as you move into the immune control phase

51
Q

Treatment of acute hepatitis B

A

Usually no specific treatment

Supportive care & avoid hepatotoxins

Rarely antiviral drugs & transplantation in fulminant liver failure

52
Q

Treatment of chronic hepatitis B

A

Anti-viral drugs may be used to reduce HBV-DNA & liver inflammation

Tenofovir or entecavir are 1st line

Often lifelong after initiation

Aim to reduce the risk of cirrhosis and hepatocellular carcinoma.

53
Q

Prevention of Hep B

A

Babies are vaccinated against Hep B @ 8,12 and 16 weeks

54
Q

Reasons to vaccinate against Hep B

A

Uninfected household contacts

Occupational or travel risk

People who inject drugs

Co-existing medical conditions

55
Q

Hep C epidemiology

A

Globally ~58 million people have chronic HCV

Most common in Eastern Mediterranean region.

56
Q

Hepatitis C: Virology

A

Enveloped single stranded RNA virus

Classified into genotypes 1-6

Rapid emergence of variants has prevented vaccine development

57
Q

Describe the structure of Hepatitis C

A

Core
Viral RNA
Envelope glycoproteins
Envelope

58
Q

Why is there no vaccine for hep C ?

A

Rapid emergence of variance

59
Q

Acute HCV

A

Resolved infection (~25%)
Persistent infection (~75%)

60
Q

Resolved HCV infection

A

Anti-HCV positive
HCV RNA negative

61
Q

Persistant HCV infection

A

Anti-HCV positive
HCV RNA positive

62
Q

Chronic HCV

A

Persistence of infection >6 months

63
Q

Acute HCV

A

Usually asymptomatic
Mild-non-specific symptoms

Jaundice in ~15% of patients

Serum ALT/AST may be high

64
Q

Clinical course : HCV - Hep C

A

Infection persistent
Chronic hepatitis with MILD fibrosis
Chronic hepatitis with SEVERE fibrosis

Liver cirrhosis (~20% in 20 years)
Liver cirrhosis (decompensated)

DEATH

65
Q

HIV and HCV

A

HIV co-infection accelerates disease progression

66
Q

Hepatitis C: diagnosis and severity assessment

A

Anti-HCV: current / past infection

HCV-RNA: active infection

Liver biopsy / fibroscan to stage disease

67
Q

Treatment for Hepatitis C

A

Direct acting antivirals

Highly effective new treatment
Treatment duration is shorting

Some regimens - now only 8 weeks
Cure achieved in 95%

68
Q

Hepatitis C : Prevention - for occupational reasons

A

There is no vaccine

Safe handling of blood-contaminated materials

Safe and appropriate use of healthcare injections

Testing donated blood

69
Q

Hepatitis C prevention

A

Harm reducing services for people who inject drugs

Prevention of exposure to blood during sex

Antiviral treatment of those who are infected

70
Q

HIV epidemiology

A

2/3rd of cases African region

37 million people living with HIV

71
Q

HIV: Virology

A

RNA-RT retrovirus

Enters host immune cells (CD4 cells)

Reverse Transcriptase action

72
Q

Reverse transcriptase - HIV

A

Makes a DNA copy of the viral RNA

Viral DNA is integrated into the host cell genome

This pro-virus DNA is transcribed & translated into viral proteins

Host immune cells are killed by invading virus, so the host becomes dangerously immune-suppressed.

73
Q

HIV: what is necessary for cell entry ?

A

env gp120
env gp41

74
Q

Enzymes involved in HIV

A

Reverse transcriptase
Integrase
Protease

75
Q

HIV: function of reverse transcriptase

A

Drug Target

Converts RNA –> DNA

76
Q

HIV: function of integrase

A

Integrates viral DNA to host chromosome

77
Q

HIV: function of protease

A

Helps process viral proteins

78
Q

HIV: clinical course

A

Deterioration linked to loss of CD4 cells

79
Q

Function of HIV diagnosis

A

Early HIV diagnosis can:

  • Save lives
  • Stop transmission
80
Q

HIV diagnosis and severity assessment

A

Serology (HIV antibody detection)

Antigen-Antibody tests

HIV-Viral load CD4 count

81
Q

Serology (HIV antibody detection)

A

Can be done in blood or oral fluid

Available as rapid (& self-tests)

Window period for seroconversion ~90 days

82
Q

Antigen-Antibody tests - HIV

A

Done on blood (usually from a vein)

‘Window’ period ~18-45 days

83
Q

HIV- Viral load CD4 count

A

Monitor treatment response and immune-suppression

84
Q

What to do if the initial test is negative after exposure ?

A

Re-test at the end of the window period

85
Q

HIV treatment : therapy

A

Anti-retroviral therapy (ART) is NOT curative but allows long healthy lives

86
Q

HIV treatment : drugs

A

Typically give 3 drugs from more than 1 class:

e.g.

  • 2 reverse transcriptase inhibitors
    (tenofovir, emtricitabine)
  • 1 integrase inhibitor
    (dolutegravir)
87
Q

Describe ART

A

ART is lifelong one initiated

Previously - “defer ART until low CD4 count”

Now - early ART initiation improve long term outcomes

88
Q

Reasons to be proactive in testing

A

Early ART initiation improves long term outcomes

Reduction in sexual and vertical transmission of HIV

Restore and preserve immunological function

89
Q

HIV: reasons for prevention

A

Safer sex
Often harm reduction
Focus on testing

90
Q

Uses of ART : Anti-retroviral therapy

A

Prevention of mother to child transmission

U=U

Pre-exposure prophylaxis
Post-exposure prophylaxis

91
Q

Key point about : HBV

A

Vaccine preventable

92
Q

Key point about : HCV

A

NO vaccine but potentially curable

93
Q

Key point about : HIV

A

No vaccine or cure

Can be controlled by long-term medication

Medicine Year 1 - Semester 2 - Part 2 (53 decks)

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