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ESA 3 > Infection 6 > Flashcards

Infection 6 Flashcards

1
Q

Describe the basic features of the HIV virus

A

Retrovirus

Genus: lentivirus

Enveloped, spherical, 80-100nm diameter

Diploid ss+ RNA virus, non-segmented, linear

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2
Q

Compare HIV1 and HIV2

A

HIV1 is most common

HIV2 confined to W. Africa (mostly)

HIV1 is more virulent

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3
Q

How can HIV be transmitted?

A

Sexually

Blood and body fluids

Mother to child (Pregnancy and birth)

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4
Q

Describe HIV pathogenesis from infection to death

A

Viral DNA transcribed to ssDNA and integrated into host genome

Antigenic variation is rapid

Incubation period 2-3 weeks (up to 10 yrs) delaying seroconversion for weeks

Seroconversion = the development of HIV antibodies

Seroconversion can cause servoconversion illness, but is largely asymptomatic

Progressive loss of CD4+ T cells leads to immunodeficiency (AIDS)

Eventually exposes patient to opportunistic infection, kaposi sarcoma and malignancies

These invariably lead to death of the patient

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5
Q

Describe the classification of HIV

How does the existence of multiple types, groups and subtypes of HIV affect treatment?

A

Classification:

HIV can be split into types 1 and 2

Type one can be further grouped into M, N, O, P

M group has 9 subtypes, A, B, C, D, E, F, G, H, J, K

Treatment:

Treatments are broadly similar

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6
Q

Describe the infection of a cell with HIV and the subsequent generation of new viral particles

A

HIV virion fuses with host cell membrane via viral gp120/41 attachment and fusing with CD4/CCR5 complex

Release of diploid RNA with reverse transcriptase into host cytoplasm

Reverse transcription produces dsDNA

Integrase enzymes integrate viral dsDNA with host genome

Transcription occurs and viral RNA is produced that is translated into viral proteins

Viral proteins assemble around viral RNA

Immature virus pushes out of the cell taking some of the cell membrane (Budding)

Protein chains in the new virus are cut with protease enzymes and produce a working virus

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7
Q

Describe seroconversion illness

A

50-70% of patients have this acute syndrome lasting 2-6 wks after aquisition of HIV

25% of these are severe enough to seek medical attention

Symptoms:

Fever, Malaise

Arthralgia, headache

Sore throat and lymphadenopathy

Non-specific symptoms typical of acute viral infection

Early invasion of the nervous system may lead to meningitis, encephalitis, peripheral neuropathy or myelopathy

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8
Q

Describe the Seroconversion rash

A

Seen in about 25% of acute HIV patients

Non-specific erythrematous maculopapular rash (can involve palms/soles)

Usually resolves within 2-3 wks

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9
Q

How can HIV be identified via labratory diagnostic methods?

A

Virus can be cultured from circulating mono-nuclear cells

Genome detection by PCR and p24 antigen detected prior to seroconversion

ELISA used for antibody screening (post-seroconversion)

Confirmation of ELISA result w/western blotting

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10
Q

Describe a typical regimen of screening for HIV to make and confirm diagnoses.

For each screen, give what is identified by that screen

A

1st screen:

4th generation EIA (Enzyme immunoassay)

Can detect HIV antibody, IgMs and p24 antigen

Allows pre and post seroconversion detection

2nd screen (to confirm):

Second generation EIA

Can detect viral particles, purified HIV antigens or recombinant virus

3rd screen (further confirmation):

Nucleic acid testing (NAT)

Pooled samples tested via amplification of viral RNA via PCR

If positive, individual samples tested

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11
Q

Give some classes of antiretroviral drugs

A

Nucleoside reverse transcriptase inhibitor

Non-Nucleoside reverse transcriptase inhibitor

Protease inhibitors

Fusion inhibitors

Integrase inhibitors

Co-receptor/Entry inhibitors

All pretty self explanatory

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12
Q

Outline the principles of HIV treatment

A

Highly active antiretroviral treatment (HAART):

Use of a combination of antiretroviral drugs of different classes

Resistance often develops to these drugs and so drugs must be switched periodically

New resistances will occur, however sometimes these weaken old resistance, opening previously used lines of treatment

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13
Q

Give a basic description of the Hepatitis B virus

A

Genus: Orthohepadnavirus

Enveloped, pleiomorphic, 24-48nm diameter

Circular partially ds DNA

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14
Q

How many HB carriers are estimated worldwide?

What regions have high prevalence of HB?

A

400 million

Africa, Western Pacific, Asia

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15
Q

What are the possible ill effects of chronic HB infection?

A

Chronic Hepatitis

Cirrhosis

Heptacellular carcinoma

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16
Q

Bywhat mechanism does HBV replicate?

A

Reverse transcriptase

17
Q

Outline HBV prophylaxis

A

Vaccination:

Wild type HB surface antigen (HBsAg) based

sAg mutants reduce vaccine effectiveness

If testing for HBsAg, mutant can give false negative

Hyperimmunoglobulin:

Post exposure prophylaxis

Newborns or needlestick injury

18
Q

Give the lifetype risk of infection and distribution of HBV in high, intermediate and low risk groups

A

High:

Lifetime risk = >60%

Neonatal and early childhood infection common

Intermediate:

Lifetime risk = 20-60%

Infections occur in all ages

Low:

Lifetime risk = <20%

Most infections in adult risk groups

19
Q

What are the routes of transmission for HBV?

A

Vertical - Mother to infant

Sexual

Percutaneous (blood, IV drugs, Sharp injury, tattoo)

20
Q

What are the clinical features of acute HBV infection?

A

Incubation:

2-6 months

Symptoms:

Fever, Malaise, Jaundice

Acute case fatality:

0.5 - 1%

21
Q

Give the rates of symptomatic infection in children and adults that aquire HBV

A

Children:

<10%

Adults:

30-50%

22
Q

Compare rates of chronic infection in those infected with HBV between sex and age groups

A

Sex:

Male > Female

Age:

Infant - 90%

Child - 30%

Adult - <3%

23
Q

What are the outcomes of chronic HBV infection?

A

Asymptomatic carrier:

​Can later progress to chronic persistent hepatitis or liver cancer

Chronic persistent hepatitis:

Can lead to chronic active hepatitis and liver cancer

Chronic acitive hepatitis:

Can lead to liver cancer or cirrhosis

24
Q

Compare the transmissibility of HIV and HBV via blood to blood event

A

HIV viraemic patient (HIV RNA+) = 1:300

HBV viraemic patient (HBeAg+) = 1:3

25
Q

What immediate actions should be taken after an exposure event such as needlestick injury?

A

Wash the wound with soap and water (Hibiscrub and betadine not recommended)

Encourage bleeding

Report the incident to manager

Ask a colleague to approach patient about a blood sample, have a blood sample taken yourself

Make a risk assessment on the need for post-exposure prophylaxis (can consult on-call virologist/microbiologist)

26
Q

How might you carry out a risk assessment for the need for post-exposure prophylaxis after a transmission event?

A

Seriousness of injury

Risk:
Blood to blood > Blood to mucous membrane > non-blood fluid to blood > fluid to mucous membrane

Were gloves worn? (Wiping effect on needle)

Patient status:

Is patient likely to have a blood borne virus?

Assess lifestyle, history, admission DDx, drug history

27
Q

Outline HIV post exposure prophylaxis

A

Triple antiretroviral therapy

Combination depends on local background resistance prevalence

28
Q

What is CRP?

A

An acute phase proteins, part of the acute phase reaction (increase or decrease in response to inflammation)

Produced by the liver

29
Q

How is the liver involved in distant inflammation?

A

Microorganism cell wall products activate macrophages and monocytes

These cells release cytokines such as:

    • Interleukin 1 (IL-1)*
    • IL-6*
    • TNF*

Cytokines, especially IL-6 circulate in the blood and reach the liver

These cytokines stimulate the liver to produce proteins, the acute phase proteins

30
Q

Give some other examples of acute phase proteins

A

Complement

Fibrinogen

31
Q

Why is CRP useful clinically?

A

Up to 1000x increase when stimulated

Rapid production (within hours)

Easy to measure!

32
Q

What is the function of CRP?

A

It is an opsonin (see wk 3)

33
Q

Give some examples of events that may trigger the acute phase reaction and hence lead to an increase in CRP

A

Infection

Trauma

Surgery

Burns

Tissue infarction

Inflammation

Cancer

34
Q

Give some other phenomena (ie. not CRP rise) that occur as a result of the acute phase reaction

A

Fever

Hormone secretion (E.g. Cortisol)

Blood changes (anaemia)

Metabolic changes

35
Q

What is the erythrocyte sedimentation rate and why is it clinically important?

A

ESR:

The rate at which erythrocytes sediment during one hour

Use:

Increased fibrinogen causes RBCs to clump and settle faster

Therefore ESR can be use as a marker for increase fibrinogen and hence inflammation etc

ESA 3 (54 decks)

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