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MD2002 > Bloodborne Pathogens > Flashcards

Bloodborne Pathogens Flashcards

1
Q

What are different ways in which bloodborne pathogens can be transmitted ?

A
  • Direct contact with infected blood fluids
  • Infection via contaminated needles, syringes, or other unsterilised instruments
  • Direct infection into the bloodstream by arthropod vectors (e.g. mosquitoes)
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2
Q

What is the difference between HIV and AIDS ?

A

HIV (=Human Immunodeficiency Virus) is the virus

AIDS (=Acquired Immunodeficiency Syndrome) is a condition

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3
Q

What area of the world is most affected by HIV ?

A

Sub-Saharan African

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4
Q

How many people worldwide are affected with HIV infection ? How many new cases were there in 2014 ?

A

37 Million

2.0 Million

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5
Q

What are the main transmission routes of HIV ?

A

– Via blood/blood products or contaminated needles
– Sexually (virus is present in semen and vaginal secretions)
– Perinatally (transplacentally during delivery, ingestion of breast milk)

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6
Q

What is the family and genus of HIV ?

A

Family: retroviridae
Genus: lentivirus

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7
Q

What are the subtypes of HIV ? Which is more common and which is more virulent ?

A

HIV-1 and HIV-2 pathogenic for humans

HIV-1 - most common and more virulent

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8
Q

What are the main morphological features of the HIV virus ?

A
  • Spherical (80-100nm)
  • Enveloped
  • RNA genome
  • Surface proteins, v antigenic (elicit strong immune response) including gp120
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9
Q

Why is RNA called a retrovirus ?

A

Because it uses reverse transcriptase to make DNA copy from viral RNA

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10
Q

What are the stages of replication of the HIV virus (including any major enzymes used for some steps) ?

A
  1. Virus binds to cell (HIV can only bind to CD4 positive T cell)
  2. Fuses with membrane of the cell
  3. Starts replicating its genome using machinery of host cell
  4. Makes DNA (reverse transcriptase)
  5. Can integrate viral DNA into host DNA (use integrase)
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11
Q

Describe the Time course of HIV infection with regards to viral load, CD4 cells, and Antibody to gp120.

A

Huge increase in viral load
Within 1 week, body makes antibody to gp120
Within 2 weeks, increase in CD4 T cells
As antibodies and CD4 T cells increase, viral load decreases
Without treatment or intervention, viral load starts going back up, CD4 cell count goes down
With therapy, viral load decreases and CD4 T cell count increases

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12
Q

Describe the progression from Exposure of HIV to AIDS ?

A
  • Exposure to HIV
  • Seroconversion
  • Asymptomatic
  • Persistent generalised lymphadenopathy
  • AIDS-related clinical features
  • AIDS
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13
Q

State some AIDS-defining conditions.

A
  • Recurrent Pneumonia
  • Invasive cervical carcinoma
  • Kaposi’s Sarcoma
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14
Q

True or False: AIDS = HIV positive + one of these conditions or HIV positive + certain amount of CD4 T cells

A

True

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15
Q

Which percentage of people with
1. <1,500 copies
2. >55,000
of viral DNA/ml blood will develop AIDS within 9 years ?

A
  1. 13%

2. 93%

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16
Q

Describe treatment options for HIV infection.

A

MINIMISING VIRAL REPLICATION

1) Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
2) Non-nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
3) Protease Inhibitors (PIs)

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17
Q

What is HAART ? What does the initial treatment usually contain ?

A

HIGHLY ACTIVE ANTI-RETROVIRAL THERAPY

Initial treatment often contain:
– 1 NRTI + 1 PI
or
– 2 NRTIs + 1 NNRTI

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18
Q

What are some ways to diagnose HIV ?

A
  1. DIAGNOSIS OF HIV SPECIFIC ANTIBODIES
    - ELISA
    - Western Blotting
  2. VIRAL RNA DETECTION IN SERUM
    - Nucleic Acid Amplification Test (including quantitative NAAT test to measure viral load)
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19
Q

Which steps of diagnosis must counselling be provided at ?

A

Before testing

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20
Q

Is there a vaccine available against HIV ?

A

No

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21
Q

Describe some of the morphological features of the Hepatitis B virus.

A 
• Double-stranded DNA genome
• Enveloped
• 3 main antigen groups: 
E antigen (HBeAg)  = pre-core antigen
Surface antigen (HBsAg)
Core antigen (HBcAg)
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22
Q

What is the family of the Hepatitis B virus ?

A

Family: Hepadnavirus

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23
Q

Differentiate between the different kinds of surface antigens in the Hep B virus ?

A

HBsAg:
– Indicates infectivity
– Anti-HBsAg provides immunity & appears late

HBcAg:
– Appears early in infection

HBeAg:
– Indicates high transmissibility

24
Q

How is the HBV transmitted ?

A
  • Blood or blood products
  • Contaminated needles and equipment used by intravenous drug users
  • Association with tattooing, body piercing and acupuncture
  • Sexual intercourse
  • Intra-uterine, peri- and post-natal infection
  • Contaminated haemodialysis equipment
25
Q

What are the stages of infection of HBV ?

A
  1. Long incubation period - up to 6 months
  2. Development of acute hepatitis
  3. Possible development of chronic active hepatitis
    Possible death (especially if fulminant disease)
26
Q

What is the percentage of deaths due to fulminant hepatitis B ?

A

1-2 %

27
Q

What is the percentage of Hep B patients develop chronic active hepatitis ?

A

50 %

28
Q

Identify conditions associated with chronic active hepatitis B.

A

Cirrhosis

Hepatocellular carcinoma

29
Q

Describe the progression in levels of the following, during acute Hep B infection.

  • Surface antigens
  • Core antigens
  • Anti-HBc
  • Anti-HBe
  • Anti-HBs
A

INITIALLY:
Surface antigens and core antigens rise

THEN:
Anti-HBc (antibody to the core antigen) increase
Also, anti-HBe (antibody to the e antigen) increases
Also, anti-HBs (antibody to the s antigen) increases

30
Q

Describe the progression in levels of the following, during chronic Hep B infection.
-Surface Antigens

A

Surface Antigens stays up the whole time due to lack of antibodies to it

31
Q

What are the main clinical stages of Hep B ?

A

Pre-Icteric stage and Icteric stage

32
Q

Describe the main clinical features in each of the main two clinical stages of Hep B.

A 
PRE-ICTERIC STAGE: 
– Malaise
– Anorexia
– Nausea
– Pain in right upper quadrant (tender liver)

ICTERIC STAGE:
– Jaundice
– Dark urine (bilirubin)

33
Q

What parts of the body does jaundice affect ?

A

– Skin
– Sclerae
– Other mucous membranes

34
Q

What is the cause of jaundice ?

A

hyperbilirubemia

35
Q

What is the treatment for HBV ?

A

PEGYLATED INTERFERON OR ALPHA INTERFERON
-Suppress replication of virus (Pegylated is better at sustaining suppression of virus)

NUCLEOSIDE ANALOGUES (e.g. oral lamivudine)

  • Have antiviral activity
  • May be successful even in chronic patients
36
Q

How may Hep B be prevented ?

A
  • HBsAg vaccine (3 injections over 6 months)
  • Blood screening
  • Post-exposure prophylaxis: HBV immunoglobulin
  • Needle exchange programmes
  • Sexual health education
37
Q

What proportion of non-A non-B cases of hepatitis were accounted for by Hepatitis C ?

A

Accounted for 90% of non-A non-B cases of hepatitis

38
Q

Describe some of the morphological features of the Hepatitis C virus.

A
  • Single-stranded RNA genome

* Enveloped

39
Q

What is the family of the Hepatitis C virus ?

A

Flavivirus

40
Q

Where does Hep C virus mostly replicate ?

A

In hepatocytes

41
Q

Can the Hep C virus be cultured ?

A

No

42
Q

Which kinds of cells does Hep C destroy ?

A

Liver cells

43
Q

How is Hep C transmitted ?

A
  • Blood and blood products
  • Tattooing, body piercing and acupuncture
  • Haemodialysis
  • Sexual transmission uncommon
  • Vertical transmission uncommon
44
Q

What are the clinical features of Hep C virus ?

A
  • Usually asymptomatic
  • Fatigue
  • Nausea
  • Weight loss
  • May rarely progresses to cirrhosis
  • Small proportion may develop hepatocellular carcinoma
45
Q

How is Hep C treated ?

A

INTERFERON

  • Reduces liver transaminases in 80% of patients
  • Ribavirin works well in combination with pegylated α-interferon
COMBINATION THERAPY
-Often one of these in addition to ribavirin and pegylated α-interferon
Sofosbuvir (nucleotide analogue)
Boceprevir (protease inhibitor)
Telaprivir (nucleotide analogue)
Daclatasvir (inhibits NS5A)
46
Q

Is there a vaccine for Hep C ?

A

No

47
Q

How is HCV Screening achieved ?

A

-NAAT on blood samples

48
Q

What area of the world is most affected by Malaria ? What percentage of Malaria cases does this area account for ?

A

Sub-Saharan Africa

80%

49
Q

How many people worldwide are affected by Malaria ?

A

200 Million

50
Q

What is the cause of malaria ?

A 
5 species of the genus Plasmodium cause infection (Zoonotic disease) : 
– P. falciparum
– P. vivax
– P. ovale
– P. malariae 
– P. knowlesi

Female Anopheles mosquito injects sporozoa into the bloodstream

51
Q

Where does the malaria virus replicate ?

A

In the liver

52
Q

What happens following replication of the malaria virus in the liver ?

A

The virus may become Hypnozoites (dormant form in the livere)
Virus may also become merozoites (active and infects RBCs and gets to the brain (cerebral malaria)

53
Q

What are clinical features of malaria ?

A

• Fever
• Flu-like symptoms
• P. falciparum infection can rapidly progress to death
• P. falciparum affects every organ – wide range of complications e.g.
– Cerebral malaria
– Circulatory shock
– Hepatitis

54
Q

How is malaria diagnosed ?

A
  • At least 3 blood films (both thick and thin) obtained from different times for microscopy
  • NAAT – useful for detecting drug resistance
55
Q

How is Malaria treated ?

A
  • Chemotherapy kills blood stages of parasite
  • IF RESISTANCE, treatment advice should be changed regularly
-Combination therapy, including: 
– Quinine
– Chloroquine
– Doxycyclin
– Proguanil
– Malarone® (= proguanil + atovaquone) 
– Artemether
56
Q

How is malaria prevented ?

A
  • Sleep under bed nets
  • Cover exposed skin between dusk and dawn
  • Use of mosquito repellants
  • Prophylaxis
  • Vaccines currently being developed
57
Q

What are preventative measures against HIV infection ?

A
  • Screening of blood products
  • Needle exchange programmes
  • Anti-retroviral prophylaxis for needlestick injuries
  • Avoiding high-risk sexual partners
  • Use of barrier contraception
  • Elective caesarian section

MD2002 (77 decks)

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