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Year 5 Path Charis > Micro 11 - Opportunistic viral infections > Flashcards

Micro 11 - Opportunistic viral infections Flashcards

1
Q

Endogenous vs exogenous viruses

A

o Endogenous
 Latent viruses that reactivate in absence of immune system
 Acquired in past prior to immune suppression e.g. VZV

o Exogenous
 Viruses acquired from the environment
 Increased severity in immunosuppressed e.g. Influenza, Sars-cov-2

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2
Q

Detection of viruses in immunocompetent vs immunocompromised

A

Immunocompetent
direct –> PCR
Indirect –> serology (IgM, IgG)

Immunocompromised
serology not helpful if immunocompromised

Serological screening –> serology (screen prior to immunosuppression)
monitoring/prophylaxis –> PCR

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3
Q

Marker of replication for HAV

Marker of replication for HBV

A

Marker of replication for HAV = HAV in stool

Marker of replication for HBV = HbsAg in blood

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4
Q

Monitoring/ prophylaxis during immunosuppression

A

CMV + EBV PCR

BK virus (renal + BMT)
Adenovirus (paeds BMT)
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5
Q

Relative risk of opportunistic infection

A

Allogeneic stem cell transplant

Advanced HIV infection (CD4 dep)

Solid organ transplant

Various monoclonal antibody therapies

Cytotoxic chemotherapy

DMARDs and steroids

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6
Q

List names of calcineurin inhibitors

A

Cyclosporine
Tacrolimus

(sirolimus (rapamycin) is NOT a calcineurin inhibitor)

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7
Q

Give 2 examples of infections that happen in the pre-engraftment interval (<30d from transplant)

A 
HSV
HHV6
HHV7
Candida
Respiratory and enteric viruses
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8
Q

Give 2 examples of infections that happen in the early post-engraftment interval (30-100 from transplant)

A 
CMV
EBV
VZV
Adenovirus
PCP Pneumocystis jirovecii 
Toxoplasma gondii
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9
Q

Immunosuppression in HSCT vs solid organ transplant

A
  • Haematological transplantation (HSCT)  patient immunosuppressed for some time and tapered down
  • Solid organ transplants (SOT)  patients immunosuppressed for life
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10
Q

List the different HHV viruses + the time at which they infect the host after the transplant

A

o HHV-1, HHV-2 (HSV 1 and 2) <1 month

o HHV-3 (VZV) >1 month

o HHV-4 (EBV)
>1 month

o HHV-5 (CMV)
>1 month (~6m)

o HHV-6 (Roseolovirus) <1 month
o HHV-7 (Roseolovirus) <1 month

o HHV-8 (Kaposi’s sarcoma-associated HV)

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11
Q

How does infection with HHV/HSV present

A

Pneumonitis
Hepatitis
Oesophagitis

DOES NOT cause encephalitis
o Q/A  HSV is most likely to cause pain on swallowing after a liver transplant

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12
Q

Prophylaxis for HSV infection

A

Test for HSV IgG in recipient

Solid organ transplant –> give prophylaxis for 3-6m

Bone marrow transplant –> give prophylaxis for 1 month

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13
Q

How does VZV present in immunocompromised

A

Encephalitis
Purpura fulminans in the neonate

Hepatitis
Pneumonitis

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14
Q

VZV mx in immunocompromised

varicella
zoster

A

Varicella
acyclovir 7-10d
IV until no new lesions
PO until all have crusted

Zoster
o Anti-viral (IV if disseminated) + analgesia
o If Ramsay-Hunt – add steroids
o If HZO (herpes zoster ophthalmicus)– add topical steroids

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15
Q

What can EBV cause

A

Post transplant lymphoproliferative disease (latently infected B cells - polyclonal activation)

B cell lymphoma

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16
Q

CMV pathognomic histological feature

A

Owl’s eye lung pneumocytes (inclusion bodies)

17
Q

CMV risk in solid vs HSCT

A

 SOLID (e.. renal) organ transplantation  greatest risk = donor +ve past CMV; recipient -ve  immunosuppressed patient gets given some CMV for the first time

 HSCT / BM transplant  greatest risk = donor -ve past CMV; recipient +ve  patient with CMV has immune system replaced with one that hasn’t seen CMV

18
Q

CMV prevention strategies post transplant

Solid organ transplant
HSCT

A

Solid organ transplant
valganciclovir prophylaxis for 100 days

HSCT
2x weekly CMV PCR
Treat if virus reactivates

19
Q

CMV reactivation mx post transplant

A 
HSCT
Foscarnet IV (nephrotoxic)

SOT
Ganciclovir IV (BM suppression)
Valganciclovir PO

other
Cidofovir (nephrotoxicity)
IVIG with another drug for pneumonitis

20
Q

What is JC virus and how do we ix it

A

John Cunningham virus
Polyomavirus
>12m of transplantation

causes progressive multifocal leukoencephalopathy

MRI
PCR CSF

21
Q

BK virus dx + mx

A

BK dx - PCR/NAAT

modulation/ reduction of immunosuppression

Post HSCT –> BK haemorrhagic cystitis –> intravesical cidofovir (avoids nephrotoxicity) + bladder irrigation

Post renal Tx - BK nephropathy - IVIG

22
Q

Respiratory viruses in the immunocompromised ix

A

Multiplex PCR of NPA, BAL, nose, throat swabs

23
Q

Influenza A+B mx

A

Oseltamivir PO 5/7

Zanamivir (IV or inhalation) if resistance/severe/immunocompromised

24
Q

Covid mx

A

Sotrovimab

or

Casirivimab/ imdevimab

25
Q

Hepatitis virus mx

A
B
C
E

A

• Hep A
o More severe
o Vaccinate

• Hep B
o Re-activation
o Vaccinate/prophylaxis

• Hep C
o Increased fibrosis
o Rx – direct acting antiviral

• Hep E
o Chronic infection
o Reduce immunosuppression

26
Q

Hepatitis B

chronic infection vs full recovery

A

chronic infection - HbsAg persist

Full recovery - loss of HbSAg

27
Q

Patients at risk of HBV reacivation

A

B cell depleting therapies e.g. rituximab

IL-6 inhibitor

Covid

28
Q

HBV sAg +
HBV cAb +
HBV sAb -

A

Current

https://medschool.co/images/detail/hepb.gif

29
Q

HBV sAg -
HBV cAb +
HBV sAb +

A

Past

https://medschool.co/images/detail/hepb.gif

30
Q

HBV sAg -
HBV cAb -
HBV sAb +

A

Vaccination

https://medschool.co/images/detail/hepb.gif

31
Q

HBV prevention

A

o Nucleoside reverse transcriptase inhibitor (lamivudine)

o Nucleotide reverse transcriptase inhibitor (tenofovir, entecavir)

o Prophylaxis

32
Q

“Preemptive therapy”

A

involves directing prophylaxis only toward high-risk transplantation recipients (e.g., patients in whom early replication of CMV occurs) in an attempt to prevent the progression of asymptomatic infection into CMV disease.

33
Q

Biopsy of Kaposis sarcoma + mx

A

• Diagnosis from biopsy  characteristic histological findings:
o Spindle cell proliferation
o Neo-angiogenesis
o Inflammation and oedema

• Treatment
o Chemotherapy
o Antiretroviral therapy

34
Q

see menti qs

A

x

35
Q

HBV sAg -
HBV cAb +
HBV sAb -

A

cAb only produced by resolved infection
post infection can also look like cAb+ and sAb+
sAb wanes after both natural infection + immunisation
in people who have had hep B the core antibody is much longer lasting than the surface antibody (therefore isolate cAb+ but sAg-  have had hep B long time in the past)

36
Q

HBV sAg +
HBV cAb -
HBV sAb -

A

E carrier – ongoing chronic activation of hep B

Year 5 Path Charis (44 decks)

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