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Kat's Pathology > Opportunistic Viral Infections > Flashcards

Opportunistic Viral Infections Flashcards

1
Q

What are the different types of immunodeficiency found in a host? (2)

A

Primary immunodeficiency.

Acquired immunodeficiency.

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2
Q

What is an example of a primary immunodeficiency?

A

UNC93B deficiency and TLR3 deficiency predisposes to herpes simplex encephalitis, epidermodysplasia verruciformis, SCID.

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3
Q

What are some examples of acquired immunodeficiencies? (4)

A

Solid organ transplantation.
Bone marrow transplantation.
Immunosuppressive drugs.
Advanced HIV infection.

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4
Q

In HIV, what can be used to predict the risk of developing specific opportunistic infections?

A

CD4 count.

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5
Q

What are some AIDS-defining illnesses? (8)

A

Invasive cervical carcinoma.
CMV disease (other than liver, spleen, or nodes)
CMV retinitis (with loss of vision)
HIV related encephalitis.
Herpes simplex: chronic ulcers, or bronchitis, pneumonitis or oesophagitis.
Kaposi’s sarcoma.
Burkitt’s lymphoma.
Progressive multifocal leukoencephalopathy.

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6
Q

What are some major classes of immunosuppressive agents (5)

A

Glucocorticoids or steroids.
Calcineurin inhibitors (T-cell function) (cyclosporine, tacrolimus).
Antiproliferative agents (azathioprine, mycophenolate mofetil (MMF) or mycophenolic acid (MPA), sirolimus)
Antibodies (depleting, and non-depleting)
Co-stimulation blockers.

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7
Q

What immunosuppressive state puts you at the greatest risk of acquiring an opportunistic viral infection?

A

Allogeneic stem cell transplant.
Advanced HIV infection.
Solid organ transplant.

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8
Q

What are the three points in time that a transplant patient can catch a viral infection.

A

Viruses acquired from graft e.g. HBV.
Viruses reactivated from host e.g. HSV.
Novel infection from infected individual e.g. VZV

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9
Q

How can you reduce the risk of virus acquisition from grafts? (2)

A

Serostatus.

Risk assessment.

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10
Q

How can you reduce the risk of viral reactivation from host following transplant? (4)

A

Serostatus.
Monitoring.
Prophylaxis.
Pre-emptive therapy.

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11
Q

How can you reduce the risk of novel infection from infected individuals infecting patients with organ transplants (5)

A 
Isolation barrier nursing. 
Advice for family/contacts
Post-exposure prophylaxis. 
Vaccinating contacts. 
Control of diet.
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12
Q

What organisms are screened for in pre-transplant serology (8)

A 
HIV
HBV
HCV
EBV
CMV
HSV
VZV
HTLV
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13
Q

What organisms are continuously monitored for post-transplant until discharge/recovery. (4)

A

CMV monitoring or prophylaxis.
EBV monitoring.
Adenovirus monitoring (paeds bone marrow transfusion - BMT)
HSV prophylaxis if indicated.

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14
Q

What organisms are detected in CSF (8)

A 
HSV
VZV
Enterovirus 
EBV
CMV
Adenovirus
HHV6
JC virus.
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15
Q

What organisms are detectable in the blood (5)

A 
CMV
EBV
Adenovirus
HHV6
Parvovirus
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16
Q

What organisms are detected in sputum (9)

A 
Flu A/B
Paraflu 1-4 
Adenovirus 
Enterovirus
RSV
HMPV
Rhinovirus
Coronaviruses
CMV in BAL
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17
Q

What organisms can be detected from stool samples (3)

A

HSV
CMV
Adenovirus

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18
Q

What is the challenge with treating opportunistic infections

A

They are often more difficult to treat

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19
Q

What is required when treating opportunistic infections (4)

A

Early treatment
Higher doses required
Longer courses of antibiotics required
Sometimes drug combinations are required

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20
Q

What is an increased risk of treating opportunistic viral infections

A

Increased risk of antiviral drug resistance

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21
Q

What viruses form part of the family of human herpes viruses (6)

A 
Herpes simplex virus (HSV) 1 and 2. 
Varicella zoster virus (VZV)
Cytomegalovirus (CMV)
HHV6 (human herpes virus 6)
Epstein Barr Virus (EBV)
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22
Q

What kind of viruses are human herpes viruses

A

DNA viruses

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23
Q

What is the danger of human herpes virus infections.

A

The virus establishes a latent infection that persists for the life of the host.
In the latent state only a small subset of the viral genes are expressed.
Reactivation with expression of viral proteins and production of new virus particles may occur at intervals to produce recurrent infections.

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24
Q

Post allo stem cell transplant, what is the first latent infection to recur

A

HSV

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25
Q

What is the most common presentation for herpes simplex virus (2)

A

Cold sores, stomatitis, mouth ulcers.

Recurrent genital disease (particularly in HIV and adult transplant)

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26
Q

What are the serious complications of herpes simplex infection (4)

A

Cutaneous dissemination
Oesophagitis
Hepatitis
Viraemia

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27
Q

What is the treatment for herpes simplex infection (3)

A

Aciclovir or valaviclovir.
Foscarnet.
(Ganciclovir sensitive also)

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28
Q

When does HSV infection occur post-transplantation

A

Reactivation in the pre-engrafement period (usually less than 1 month post-transplant)

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29
Q

How is HSV reactivation prevented post-transplantation

A

Aciclovir prophylaxis until CD4 count increases above a certain threshold or for a specific time period.

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30
Q

What are the risk of primary varicella zoster infection in the immunocompromised (4)

A

Pneumonitis
Encephalitis
Hepatitis
Purpura fulminans in neonates

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31
Q

What is a late complication of VZV in the immunocompromised

A

Shingles

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32
Q

What can shingles in a young person be indicative of

A

HIV infection

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33
Q

What form of VZV is associated with higher mortality

A

Multidermatomal or disseminated shingles

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34
Q

What are some late complications of shingles in the immunocompromised (3)

A

Acute retinal necrosis (ARN)
Progressive outer retinal necrosis (PORN)
VZV-associated vasculopathy

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35
Q

How can VZV be prevented in the immunocompromised (2)

A

Aciclovir prophylaxis provides some protection.

Post-exposure prophylaxis of varicella with VZIg.

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36
Q

What is the first line treatment for VZV infection

A

Aciclovir

Valciclovir
Foscarnet sensitive
Ganciclovir sensitive

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37
Q

What are the manifestations of CMV infection (4)

A

Brain (encephalitis)
Eye (retinitis)
Lung (pneumonia)
Stomach and intestines (gastroenteritis)

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38
Q

What is risk of CMV infection post-transplant related to

A

Relates to pre-transplant serostatus

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39
Q

In solid organ transplant, what serotype carries the greatest risk of reactivation fo CMV

A

D+/R-

40
Q

In bone marrow transplant (adoptive immunity) what serotype carries the greatest risk of reactivation

A

D-/R+

41
Q

How can CMV be prevented post-transplant (2)

A

CMV viral load twice weekly, treat if virus reactivates until suppressed (pre-emptive therapy)
Valganciclovir prophylaxis for 100 days.

42
Q

What is the treatment of CMV (9)

A 
Ganciclovir (IV) bone marrow suppression. 
Valganciclovir - oral. 
Foscarnet IV (nephrotoxicity) 
Cidofovir (nephrotoxicity). 
IVIg (with another drug for pneumonitis) 
Letermovir 
Maribavir 
Brincidofovir 
Fomiversin
43
Q

What are the clinical phases of EBV infection

A

Acute phase.

After the acute phase.

44
Q

What occurs during the acute phase of EBV infection (3)

A

Febrile illness.
Lymphadenopathy.
Moderate hepatitis.

45
Q

What occurs after the acute phase in EBV infection

A

Lifelong, latent, subclinical infection of B cells.
Intermittent attempts at viral replication kept in check by immunosurveillance.
EBV stimulates host cells to divide - also kept in check.

46
Q

What does EBV cause post-transplant

A

PTLD (post transplant lymphoproliferative disease)

47
Q

What is PTLD?

A

Post transplant lymphoproliferative disease.

Latently infected B cells - polyclonal activation

48
Q

What does PTLD predispose to

A

Lymphoma

49
Q

What increases the suspicion of lymphoma in PTLD

A

Rising EBV viral load (>10^5c/ml) and CT scan

50
Q

What confirms lymphoma in a patient with PTLD

A

Biopsy of lymph nodes

51
Q

How is PTLD managed (2)

A 
Reduce immunosuppression (regression in less than 50%)
Anti-CD20 monoclonal antibody therapy (B cell marker - rituximab)
52
Q

What is kaposi’s sarcoma?

A

A cutaneous or visceral lesion, which presents as a brownish/purplish vascular lesion.

53
Q

What are the characteristics of kaposi’s sarcoma? (3)

A

Spindle cell proliferation.
Neo-angiogenesis.
Inflammation and oedema.

54
Q

How is the diagnosis of kaposi’s sarcoma made?

A

Biopsy.

55
Q

How is kaposi’s sarcoma treated? (2)

A

Chemotherapy.

Initiation of antiretroviral therapy.

56
Q

What is human herpesvirus 8 associated with? (3)

A

Kaposi’s sarcoma.
Primary effusion lymphoma (PEL)
Multicentric Castleman disease.

57
Q

What are the stages in JCV infection? (4)

A

Primary infection.
Sites of latency.
Reactivation.
Neuroinvasion.

58
Q

What is the pathogenesis of JCV infection (4)

A

Primary infection: infection is thought to occur following inhalation of virus – primarily in tonsillar tissue.
Sites of latency: latency is established in the kidneys and bone marrow. JCV gene rearrangements are found in patients with PML.
Reactivation: immunosuppression facilitates reactivation of JCV. Virus detected in blood is predominantly cell-associated.
Neuroinvasion: the JC virus is though to be transported across the BBB within B cells, subsequently, JCV can establish productive infection of oligodendroglia.

59
Q

What is a sequale of JCV infection

A

Progressive multifocal leukoencephalopathy. (PML)

60
Q

What kind of virus is JC

A

Polymavirus

61
Q

What percentage of patients with AIDS would develop PML prior to the introduction of effective antiretroviral therapy

A

5%, with a high mortality.

62
Q

What groups of people are at risk of PML? (2)

A 
AIDS
Multiple Sclerosis (due to natalizumab).
63
Q

What are the clinical signs of PML (4)

A

Cognitive disturbance
Personality change
Motor deficits
Other focal neurological signs

64
Q

What is the main pathological features of PML

A

Demyelination of white matter with neurological deficits corresponding to the areas of the brain affected

65
Q

How is PML diagnosed (2)

A

MRI

PCR on CSF

66
Q

What is the standard monitoring method for patients on natalizumab for JCV

A

Yearly brain MRI (regardless of risk index)

67
Q

What does BK virus cause

A

BK cystitis

68
Q

Who is at risk of BK virus infection

A

Post-transplanation patients (renal transplant)

69
Q

How is BK virus diagnosed

A

PCR/NAAT

70
Q

What are the clinical signs of BK virus (2)

A

Fever

Cystitis

71
Q

How is BK virus treated (2)

A

Bladder irrigation

Modulation of immunosuppressive treatment

72
Q

What group of immunosuppressed patients is adenovirus a particular risk to

A

Post-bone marrow transplant (particularly in children)

73
Q

What are the two pathogeneses of adenovirus infection in immunosuppressed patients

A

Exogenous infection or reactivation of persistent endogenous infection

74
Q

What are the clinical signs of adenovirus infection (4)

A

Fever
Encephalitis
Pneumonitis
Colitis

75
Q

What can cause a high mortality with adenovirus infection

A

Disseminated infection

76
Q

How are post-transplant paediatric patients screened for adenovirus infection

A

Weekly blood monitoring

77
Q

How are post-transplant adult patients screened for adenovirus infection

A

Symptomatic screening only - urine, respiratory, stool and staging for disseminated disease to include blood if any of these are positive

78
Q

How is adenovirus infection treated in immunosuppressed patients

A

Cidofovir + hyperhydration + probenecid 3 times a week until viral load <400cp/mL twice.

Taper off the immunosuppressive drugs if possible

79
Q

What is the largest risk of respiratory viral infections in the immunocompromised

A

Pneumonitis and high mortality

80
Q

What respiratory viruses pose a high mortality risk in the immunocompromised (5)

A 
Influenza A and B 
Parainfluenze 1, 2, 3 and 4 
Respiratory syncitial virus (RSV) infection 
Adenovirus 
Novel coronavirus: MERS coronavirus
81
Q

How are respiratory viruses diagnosed in the immunocompromised (4)

A

Naso-pharyngeal aspirates (paeds)
Bronchio-alveolar lavage
Nose and throat swabs
Multiplex PCR is the investigation of choice

82
Q

How is influenza A and B treated in the immunocompromised (2)

A

Oseltamivir (oral drug) for 5 days.

If severe immunocompromised, risk of oseltamivir resistance so use zanamivir (inhalation or IV) as an alternative.

83
Q

How can influenza infection be prevented in the immunocompromised (4)

A

Influenza vaccination (life-long for organ/BMT recipients)
Influenza vaccination for close contacts.
Oseltamivir prophylaxis if significant contact with a case of influenza.
Infection control: handwashing, protective clothing, limit visitors, isolate immunocompromised patients, cohort nursing.

84
Q

What can human parvovirus B19 cause in the immunocompromised

A

Chronic anaemia

85
Q

How is human parvovirus B19 diagnosed (2)

A

Serology (IgM) not useful in the immunocompromised

PCR on blood

86
Q

How is human parvovirus B19 treated in the immunocompromised (2)

A

Human normal immunoglobulin

May require blood transfusion.

87
Q

What are you considered to have chronic hepatitis B infection

A

After 6 months if the virus has not been cleared

88
Q

What does the following serology indicate:

HBV sAg +
HBV core Ab +
HBV sAb -

A

Current Hepatitis B infection

89
Q

What does the following serology indicate:

HBV sAg -
HBV core Ab +
HBV sAb +

A

Past Hepatitis B infection

90
Q

What does the following serology indicate:

HBV sAg -
HBV core Ab -
HBV sAb +

A

Vaccination against Hepatitis B

91
Q

What are the risks of hepatitis B in the immunocompromised (2)

A

Carriers may have flares of the disease

Those who have had a past infection can reactivate

92
Q

In the immunocompromised, when is the risk of hepatitis B reactivation particularly significant

A

In patients on B-cell depleating therapies (e.g. rituximab)

93
Q

How can hepatitis B infection/reactivation be prevented in the immunocompromosed

A

Nucleoside/nucleotide analogues (lamivudine, tenofovir, entecavir) prophylaxis

94
Q

What is a major cause of enterically transmitted viral hepatitis in the UK and Europe

A

Hepatitis E

95
Q

What is the predominant genotype of Hepatitis E in developed countries

A

A zoonosis caused by genotype 3 virus

96
Q

What is the predominant genotype of hepatitis E in developing countries

A

Mainly genotype 1 virus

97
Q

How is hepatitis E transmitted (3)

A 
Mainly through undercooked pork. 
Blood transfusions (uncommon). 
Possibly through organ donation

Kat's Pathology (105 decks)

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