Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 -krish finess > MICRO: Opportunistic viral infections > Flashcards

MICRO: Opportunistic viral infections Flashcards

1
Q

What are ‘endogenous’ vs ‘exogenous’ viruses?

A

Endogenous - latent viruses that reactivate in the absence of immune sysytem; acquired in past prior to immune suppression e.g. VZV

Exogenous - viruses acquired from environment; increased severity in immunosuppressed e.g. influenza, SARS-COV-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How are viruses classified?

A

Baltimore classification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List some AIDS defining illnesses with viral causes (opportunistic viral infections).

A
  • Cervical cancer, invasive
  • CMV disease
  • CMV retinitis
  • Encephalopathy HIV related
  • HSV chronic ulcers, bronchitis, pneumonitis, oesophagitis
  • Kaposi sarcoma
  • Lymphoma, Burkitt’s
  • Progressive multifocal leukoencephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What classification system is used for all viruses?

A

Baltimore classification

Consists of 7 groups that take into consideration whether the viral genome is made DNA or RNA, whether the genome is single- or double-stranded, and whether the sense of a single-stranded RNA genome is positive or negative.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do we detect viruses?

A

Not grown - this requires human cell lines and is dangerous. So instead we look for indirect or direct evidence of their presence.

Indirect detection - immune system response to the virus e.g. antibody tests = PAST infection

Direct detection - fragments of the actual viruses e.g. viral proteins (LFTs), viral genetic material (PCR) = infection NOW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the problem with using antibody levels to measure infection in the immunosuppressed?

A

Detection of antibody levels is generally used

  • IgG = gone >6 weeks
  • IgM = active/resolving infection

BUT antibodies will be lower in the immunosuppressed and serological courses may differ with different viruses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How can you overcome challenges with diagnostic virology in immunocompromise?

A
  1. Screen prior to immunocompromise - to identify previous viral exposire and guide antiviral prophylaxis
  2. Monitor using PCR - usually done monthly to detect infection and reactivation promptly so that
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Put these in order of highest risk of opportunistic viral infection.

  • Various monoclonal antibody therapies
  • DMARDs and steroids
  • Allogeneic stem cell transplant
  • Advanced HIV infection (CD4 dep)
  • Solid organ transplant
  • Cytotoxic chemotherapy
A
  1. Allogeneic stem cell transplant - HIGHEST RISK
  2. Advanced HIV infection (CD4 dep)
  3. Solid organ transplant
  4. Various monoclonal antibody therapies
  5. Cytotoxic chemotherapy
  6. DMARDs and steroids - LOWEST RISK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the sources of viral infections in transplant recipients?

A
  1. Viruses acquired from graft e.g. HBV
  2. Viral reactivation from host e.g. HSV
  3. Novel infection from infected infividual e.g. VZV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the steps to prevent viral infection at each of these stages in transplant patients?

  1. Viruses acquired from graft
  2. Viral reactivation from host
  3. Novel infection from infected individual
A
  1. Viruses acquired from graft
    • serostatus risk assessment
  2. Viral reactivation from host
    • serostatus monitoring
    • prophylaxis
    • pre-emptive therapy
  3. Novel infection from infected infividual
    • isolation-brrier nursing
    • advice for visitors
    • vaccination of contacts
    • control of diet
    • post-exposure prophylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Chronology of HSCT infections

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the challenges with anti-viral therapy in the immunocompromised?

A
  • Increased doses
  • Longer duration
  • Combination therapy
  • ↑ Opportunity antiviral resistance
  • ↑ Toxicity of antivirals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are viral infections different in the immunocompromised?

A
  • Present differently
  • Disseminated
  • Different organs
  • More severe
  • Oncogenic
  • Lack of immune mediated symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the issues with HSV 1 and 2 in immunocompromised?

A
  • Increased frequency severity with risk of dissemination
  • More organs can be involved e.g. pneumonitis, oesophagiis, hepatitis but NOT encephalitis
  • Risk of acyclovir resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the management of HSV1/2 in immunocompromised?

A

Give prophylaxis

  • BM - 1 month (until enlargement)
  • Solid organ - 3-6 months and if treated for rejection

Test for HSV IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the clinical features of VZV infection in the immunocompromised?

A

Chicken-pox - pneumonitis, encephalitis, hepatitis, purpura fulminans in neonate

Shingles - multi-dermatomal; often late presenting immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the mangement of VZV in immunocompromise? (prevention + treatment)

A

Prevention:

  • Prophylaxis medication
  • PEP
  • Vaccination

Treatment:

  • Chickenpox (varicella) - antiviral for 10 days IV until no new lesions AND PO until all crusted
  • Shinges (zoster) - antiviral (IV if disseminated) + analgesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What complications of Zoster may require addition of steroids to the treatment?

A

Ramsay-Hunt - add steroids

HZO - add topical steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the biggest concern with EBV infection in immunocompromise? When should you suspect it?

A

Post-transplant lymphoproliferative disease (PTLD) - latently infected B cells (polyclonal activation) which predisposes to lymphoma

Suspect in rising EBV load (>105c/ml) and CT scan. Confirmed with biopsy of lymph nodes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you confirm EBV PTLD?

A

Rising EBV viral load

CT

Confirmed with biopsy of lymph nodes.

22
Q

What is the management of EBV in immunocompromise?

A
  1. Monitor EBV levels
  2. Ix for lymphoma as needed
  3. ? rituximab
  4. Reduce immunosuppression
23
Q

What are the issues with CMV infection in immunocompromised?

A

In HIV/AIDS with CD4 <50 can cause:

  • Retinitis
  • Polyradiculopathy
  • Pneumonititis
  • GI tract e.g. gastroenteritis

Solid organ transplant can cause:

  • Allograft disease
  • GI tract (i.e. renal)
24
Q

What is the management of CMV in immunocompromise? When would you give it prophylactically vs treating disease?

A
  1. Prophylaxis (in lung transplantation)
  2. Pre-emptive treatment (in renal transplant/HSCT)
  3. Treat if disease (in HIV/AIDS)

Management:

  • Ganciclovir/valganciclovir
  • Reduce immunosuppression
25
Q

What pathognomonic feature of CMV infection is shown below?

A

Owl’s eye lung pneumocytes (inclusion bodies)

26
Q

What are the manifestations of CMV in the immunosuppressed?

A

In HIV/AIDS it causes:

  • Retinitis
  • Encephalitis
  • Pneumointis
  • Gastroenteritis

In SOT it can cause allograft disease and affect the GI tract (i.e. renal)

27
Q

What are the CMV prevention strategies post-transplant (solid organ vs HSCT)?

A

HSCT: CMV viral load twice weekly - treat if virus reactivates, until suppressed (pre-emptive therapy)

Solid organ transplant: Valganciclovir prophylaxis for 100 days

28
Q

What are the treatment options for CMV? What are the differences between them?

A

Ganciclovir (IV): bone marrow suppression

Valganciclovir: oral

Foscarnet (IV) (nephrotoxicity)

Cidofovir (nephrotoxicity)

IVIg (with another drug for pneumonitis)

29
Q

What type of virus is JC virus? What disease does it cause?

A

JC virus is a polyomavirus

–> Progressive multifocal leukoencephalopathy (PML)

30
Q

Apart from HIV, what other condition has PML been found in?

A

Effective antiretroviral therapy has drastically reduced PML incidence in HIV+ve patients

PML can also be seen in:

  • Humanised monoclonal antibody use
  • Natalizumab use (for treatment of multiple sclerosis)
31
Q

What are the clinical features of PML? How is it diagnosed?

A

Clinical features:

  • Cognitive disturbance
  • Personality change
  • Motor deficits
  • Other focal neurological signs

Diagnosis:

  • MRI (Demyelination of white matter → neurological deficits)
  • PCR on CSF
32
Q

What is another example of a polyoma virus? Is it DNA/RNA double/single stranded?

A

BK virus

Double stranded DNA

33
Q

What types of transplant is BK infection most common in? What manifestations does it cause?

A
  • BK cystitis post SCT
  • BK nephropathy post renal Tx

(renal and SCT)

34
Q

What is the management of BK virus?

A
  1. Bladder irrigation
  2. Modulation of immunosuppression
  3. Cidofovir - this is nephrotoxic itself though
35
Q

Which opportunistic viral respiratory infections occur in the immunocompromised?

A
  • Influenza A and B
  • Parainfluenza 1, 2, 3 and 4
  • Respiratory Syncytial Virus (RSV) Adenovirus
  • SARS-CoV-2
36
Q

What is the management of Influenza A/B in oseltamavir?

A

Oseltamivir (oral drug) for 5 days

If resistance/severe/immunosuppressed → zanamivir (inhalation or IV)

37
Q

What medication can be used for the treatment of SARS-CoV-2 in the immunosuppressed?

A

Sotrovimab

or Casirivimab/imdevimab

38
Q

How does the course of HAV present in immunosuppression compared to normal?

A

More severe infection

39
Q

How does HBV present in immunosuppression compared to normal?

A
  1. Carriers may have flare of disease.
  2. Those who have had past infection can reactivate
40
Q

What drug is HBV reactivation more common in in the immunosuppressed?

A

Reactivation ↑ B-cell depleting therapies (i.e Rituximab)

IL-6 inhibitor use in COVID also a risk

41
Q

What is the preventative treatment for HBV?

A

Nucleoside (lamivudine) or nucleotide (tenofovir, entecavir) reverse transcriptase inhibitors

42
Q

What do these markers in HBV tell us?

sAg+, cAb+, eAg+

A
  • sAg+ - circulating virus
  • cAb+ - acute immune response
  • eAg+ - circulating virus, infectivity marker
43
Q

What do these markers of immunity tell us in HBV?

sAb, cAb, eAb

A

sAb+ -either generated from virus or vaccine

cAb+ (IgG/total)- generated from cAg (virus) meaning prior infection

eAb+ - generated from eAg (virus)

44
Q

Risk of HBV reactivation:

A

In presence of HBsAg: highest with chemotherapy, anti-CD20 or anti-CD56 treatment and combination of these with steroids

45
Q

How does the course of HCV present in immunosuppression compared to normal?

A
  • Increased fibrosis
  • Treat with direct-acting antiviral
46
Q

How does the course of HEV present in immunosuppression compared to normal?

A

Chornic infection, needs reduction in immunosuppression

47
Q

Menti:

A

D

Antibody tests are not good for infection now.

48
Q

Menti:

A

Allogeneic stem cell transplant

49
Q

Menti:

A

HSV (type 1 is probably most common)

50
Q

Menti

A

Answer is D (mAb)

  • A - targets COVID*
  • B - CMV*
  • C - HSV*
  • E - HBV*
51
Q

Menti:

A

Answer - C

  • A - acute active*
  • B - vaccinated*
  • D - never seen HBV*
  • E - only SAg so carrier with chronic infection*
  • F -unreliable serology*

Year 5 -krish finess (55 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions