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opportunistic infections Flashcards

1
Q

how are viruses classified

A

Baltimore classification
(by their replicative life cycle)

all produce positive sense mRNA -> generate proteins for their replication

nature of genomes mean different classes achieve this through different mechanisms -> implications of life cycle, dx and rx

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2
Q

definition of opportunistic infection

A

An infection caused by an organism that does not normally cause disease

…Or symptomatology may be altered in the immunocompromised compared to immunocompetent

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3
Q

what are endogenous opportunistic infections

A

Latent viruses that reactivate in the absence of a normal immune system
Acquired in the past prior to immune suppression – eg Varicella Zoster (VZV) and can get disemminated herpes zoster

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4
Q

what are exogenous opportunistic infections

A

acquired from the environment
Increased severity in the immunocompromised – eg influenza, SARS-CoV-2.. Or even primary acquisition of VZV

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5
Q

AIDs defining illness

A
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6
Q

How do we diagnose viruses

A

indirect detection
* see if ever had infection
* response of immune system to virus

direct detection
* currentlt have infection
* viral proteins - lateral flow/ag test
* viral genetic material
* PCR

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7
Q

summarise indirect detection of virus using serology

A

measure levels of Ab in serum
IgM - active or resolving infection
IgG - indicates past infection >6wks ago

Ab levels are reduced in immunocomp

serological course may differ wih different virus eg hepatitis

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8
Q

hepatitis A serology

A
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9
Q

hepatitis B serology

A
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10
Q

PCR to detect virus

A

detect viral genome via amplification
sensitive and specific
viral load can be used to monitor infection
can remain +ve after infection has resolved.

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11
Q

how are viruses diagnosed in the immunocompromised

A

cant use serology - no immune system

screen for viral infections before give immunosuppression - identify infections that might reactivate, guide antiviral prophylaxis

**monitor with PCR **- means can see viral reactivation promptly -> Rx, detect infection

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12
Q

A 51-year-old with a recent HSCT is unwell. Which is the most appropriate test?
ALT = 800 IU/mL

EBV IgG/IgM
HBV sAb
Parvovirus PCR
HEV PCR
CMV IgG/IgM

A

HEV PCR

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13
Q

scale of immunosuppression and how it relates to risk of getting opportunistic viral infections

A

As go up list – immunosuppression increases – allogenic gives highest risk of opportunistic viral infections

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14
Q

summarise immunosuppression for transplant

A

In Hematopoietic stem-cell transplantation: conditioning regimen, eradicating pre-exisiting disease. Then ongoing immunosuppression to prevent graft versus host.

Solid organ: induction to prevent T cell activation and maintenance therapy to prevent rejection

haematopoietic: Conditioning – wipe out the disease – when conditioned – do the transplant – then wait while ait for transplant to take - neutrophils start to go up – need immunosuppression to prevent graft vs host disease.Can stop immunosuppression

In solid organ – not completely irradiating body but will be on lifelong immunosuppression. Trying to prevent T cell activation

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15
Q

sources of viral infection in transplant recipients

A

virus from graft - eg HBV (serostatus, risk assessment)
virus from host - eg HSV (serostatus, monitoring PCR, prophylaxis, pre-emptive therapy)
novel infection from infected individual eg VZV (isolation-barrier nursing, post exposure prophylaxsis, vaccinating contacts, control of diet)

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16
Q

chronology of HSCT infections

A

day 0 is day of transplant - wait 30 days for neutrophils to start recoving
so in 1st 30 days - most worried about bacterial/fungal
then more concerned of viruses

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17
Q

chronology of solid organ transplant infections

A
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18
Q

things screen for when immunosuppressed become unwell

A

Screen and molecular test according to symptoms
Screen for specific infections knowing that they are immunocompromised
Blood – PCR
Biopsy of gut/PCR

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19
Q

considerations when using anti-virals in people who are immunosuppressed

A

pre-emptive rx
prophylaxis
increased doses
longer duration
combination therapy
increased levels of antiviral resistance
increased toxicity of antivirals - because have to give more for longer

20
Q

how are viral infections different in the immunocompromised

A

present differently
disseminated - multiple systems
different organs
more severe
oncogenic
lack of immune mediated cells

21
Q

difference between HSV in immunocompetent and immunocompromised

A

increased frequency
increased severity/risk of dissemination
more organs involved - pneumonitis, eosophagitis, hepatitis
increased risk of acyclovir resistance

HSV L = immunocompetent R = oesophagitis
22
Q

mx of HSV in immunocompromised

A

HIV - start antiretroviral therapy – as soon as get CD count up – they will stop getting viral infetcions

Prophylaxis:
* Test IgG before give transplant
If they have it – day 5x day acyclovir (until 1mo after bone marrow, 3-6mo after solid organ)

23
Q

varicella in immunosuppressed

A

chicken pox:
* pneumonitis
* encephalitis
* hepatitis
* purpura fulminans in neonate

shingles:
* multi-dermatomal/disseminated
* often late - presenting immunosuppresion

Desemminated varicella R - Purpura fulminans in neonate
24
Q

prevention of varicella in immunocompromised

A

Prophylaxis (prolonged if post-bone marrow) – acyclovir/valicyclovir – if bone marrow transplant >1yr

PEP (post exposure prophylaxis) – incubation can be 20(?) days – gave give IVIG within 10 days of contact

Vaccination

25
treatment of varicella in immunocompromised
Varicella Anti-viral (acyclovir/valicyclovir) for 7-10 days IV until no new lesions; PO until all crusted Zoster Anti-viral (IV if disseminated) + analgesia If Ramsay-Hunt: add steroids If HZO: add topical steroids Bells palsy or ophthalmic we add sterods to redcue inflammation
26
A patient who received a stem cell transplant 2 weeks ago presents with mouth ulcers. Which of the following viruses would you test for on the mouth swab? A. Enterovirus PCR B. Adenovirus PCR C. HSV PCR D. HHV6 PCR E. HHV8 PCR
HSV PCR
27
what is EBV and post-transplant lymphoprolfierative disease
Latently infected B cells – polyclonal activation Predisposes to lymphoma Occurs in solid organ or allogenic haematopoietic cell transplants Related to the level of immunosuppression Suspicion on rising EBV viral load (> 105 c/ml) and CT scan Confirmation with biopsy of lymph nodes
28
issues with EBV and immunosuppression
Onchogenesis * B cell latency, high turn-over * T-cells monitor/control this B-cell lymphomas PTLD (post-transplant lympho-proliferative disorder
29
Mx of EBV in immunosuppressed
**Monitor EBV levels** (proactive monitoring) - reg PCR once or twice wk in stem cell transplant pts **Ix for lymphoma** as needed Rx: **?Rituximab – monoclonal Ab**, small studies have shown benefits Rx: **reduce immunosuppression** – need to decide whether infection of not being immunosuppressed is worse
30
issues with CMV in immunosuppressed
HIV/AIDS: CD4 less than 50 * Ocular (retinitis) * Polyradiculopathy * **Pneumonitis** * GI tract SOT (solid organ transplant) * Allograft disease * GI tract (i.e. renal)
31
mx of cytomegalovirus in
Prophylaxis (i.e. lung transplant) May need to do bronchiolar lavarge Pre-emptive treatment (i.e. renal transplant / HSCT) Treat if disease (HIV/AIDS) Rx: Ganciclovir / Valganciclovir Rx: Reduce immunosuppression
32
difference between CMV in transplant between SOT and BMT
SOT: CMV remains latent in dendritic cells so if some of these are transplanted with organ -> very sick because dont have immune system to fight it Likewise if a bmt is received from a donor who has never seen CMV before and the reciepent reactivates the latent CMV -> greater morbidity and mortality – donor immune system is naive to CMV and finds it hard to clear
33
how do we prevent CMV in transplant patients
BMT patients we monitor and if the virus goes above a certain level we treat Solid organ prophylaxis
34
CMV treatment in transplant patients
Ganciclovir (IV): bone marrow suppression Valganciclovir: oral and less toxic Foscarnet (IV) (nephrotoxicity) Cidofovir (nephrotoxicity) Can give IVIg (with another drug ie antiviral for pneumonitis) *CMV treatment is fairly toxic and resistance is not uncommon*
35
summarise John Cunningham virus
polyomavirus think get in childhood no treatment progressive leukoencephalopathy (PML) effective antiretroviral therapy -> reduced PML in HIV +ve also see PML when immunocomp due to: * humanised monoclonal antibodies * Natalizumab (for treatment of multiple sclerosis) so don’t continue them on the drug for >2yrs
36
what is progressive multifocal leukoencephalopathy
Demyelination of white cells -> neurological deficits Cognitive disturbance, personality change, motor deficits other focal neurological signs dx: MRI and PCR on CSF
37
what is BK virus
polyomavirus double stranded DNA resides in kidney may reactivate in immunosuppressed -> * haemorrhagic cystitis in BMT pts (catheter fills with blood) * nephropathy in renal transplants Rx:cidifovir which is nephrotic itself, so often the level of immunspression is reduced
38
resp viruses in the immunocompromised
increased risk of complications eg pneumonitis esp with: Influenza A and B Parainfluenza 1, 2, 3 and 4 Respiratory Syncytial Virus (RSV) Adenovirus SARS-CoV-2
39
mx of influenza A and B in immunocompromised
**Oseltamivir (oral drug) for 5 days** If resistance/severe/immunosuppressed  → **zanamivir (inhalation or IV)**
40
mx of covid in immunocompromised
Sotrovimab or Casirivimab/imdevimab Discuss with infection/virology team
41
compare the different hepatitis biruses in immunocompromised
Hep A: more severe, vaccinate Hep B: re-activation, vaccinate/prophylaxis Hep C: ?increased fibrosis, Rx direct-acting antiviral Hep E: chronic infection, reduce immunosuppression
42
summarise Hep B in the immunocompromised
either: * carriers have flare * past infection can reactivate - RFs are: cell depleting therapies (i.e Rituximab), IL-6 inhibitors - tocilizumab
43
prevention of hep B in immunocompromised
Nucleoside (lamivudine) nucleotide (tenofovir, entecavir) Prophylaxis
44
serology of hep B
The  **hepatitis B envelope antigen (HBeAg)** is found between the core and lipid envelope within HBV and is present in both **acute and chronic infection.** * indicates **active viral replication** -> higher risk of transmissibility. * used to distinguish active and inactive chronic infection. **HBeAg  seroconversion is the development of antibodies against HBeAg (anti-HBe);** it marks a **transition from active disease to an inactive ‘carrier’** state. **Anti-HBe remains in serum for life** and indicates **acquired, natural immunity (i.e. immunity from a previous infection only)**
45
what is a possible case of monkeypox
46
Mx of monkey pox
prophylaxis - small pox vaccine isolation isolation analgesia tecovirimat if very severe (eg encephalitis) screen for other STIs consider psychosocial impact inform UKSHA

PATHOLOGY (94 decks)

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