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MICRO - Abbie > 11. Opportunistic viral infections > Flashcards

11. Opportunistic viral infections Flashcards

1
Q

What percentage of fevers following organ transplant are non-infectious?

A

22%

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2
Q

What are causes of immunocompromise?

A

Metabolic/endocrine such as alcohol abuse, diabetes mellitus, uraemia, malnutrition. Impaired barrier to infection such as burns, haemodialysis, IVDU. Pregnancy. Extremes of age.

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3
Q

What are examples of primary immunocomprise?

A

UNC93B deficiency, TLR3 deficiency, epidermodysplasia verruciformis, SCID, hameophagocytic lymphohistiocytosis perforin deficiency, HHV8 associated with STIM1 mutation

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4
Q

What is UNC93B deficiency and TLR3 deficiency associated with?

A

Predisposition to herpes simplex encephalitis

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5
Q

What is perforin deficiency associated with?

A

An increased incidence of EBV

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6
Q

What are examples of acquired immunocompromise?

A

Solid organ transplantation, bone marrow transplantation, immunosuppressive drugs, advanced HIV infection. (NOTE: measles also causes a prolonged immunodeficient state after the infection)

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7
Q

How does HIV infection occur?

A

It is a lentivirus and has a long incubation period. It directly targets CD4+ T cells. Through the loss of CD4+ T cells, you get an increase in the risk of opportunistic infections. Early on in disease you will get a dramatic decline in CD4 count. Then, the CD4+ count will recover but then decline more slowly. As CD4+ count decreases, the risk of opportunistic infection increases

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8
Q

What are major classes of immunosuppressive drugs?

A

Glucocorticoids or steroids, calcineurin inhibitors, antiproliferative agents, antibodies and co-stimulation blockers

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9
Q

What are examples of calcineurin inhibitors (T cell function)?

A

Cyclosporine, tacrolimus

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10
Q

What are examples of antiproliferative agents?

A

Azathioprine, mycophenolate mofetil (MMF) or mycophenolic acid (MPA), sirolimus

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11
Q

What are examples of antibodies immunosuppressive drugs?

A

Depleting, and non depleting (anti CD25 receptor antibodies, costimulation blockers and belatacept)

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12
Q

Relative risk of opportunistic viral infection, from lowest to highest:

A

DMARDs and steroids, cytotoxic chemotherapy, various monoclonal antibody therapies, solid organ transplant, advanced HIV infection (CD4 dep), allogeneic stem cell transplant.

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13
Q

What factors should be considered in immunosuppression?

A

Immunosuppressive treatment (type, timing, intensity), prior treatment (antimicrobial use, chemotherapy), muco-cutaneous integrity (catheters, lines and drains), surgical complications (collections), metabolic conditions (uraemia, alcoholism, DM, age), viral infection (Herpes viruses, HBV, HCV, HIV, RSV, respiratory virus)

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14
Q

When do recipients tend to have reactive viral infections after their transplant?

A

They do NOT tend to reactive viral infections until over a month after their transplant

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15
Q

What doe early infections in the recipient suggest?

A

Early infections (< 1 month) tend to be those that are transmitted from the donor. This can be controlled adequately by testing the donor.

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16
Q

When do viral infections tend to occur in bone marrow transplantation?

A

Early, within 1 month. This is because bone marrow transplant patients will receive intensive immunosuppression

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17
Q

What are sources of infection?

A

Viruses acquired from the graft e.g. HBV, viral reactivation from the host (e.g. HSV), novel infection from infected individual (e.g. VZV).

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18
Q

How can we prevent viruses from the graft?

A

Assessed via serology and risk assessment of the donor

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19
Q

How can we prevent virus reactivation in the host?

A

This can be tackled by looking at the patient’s serostatus, monitoring, prophylaxis and pre-emptive therapy

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20
Q

How can we prevent novel infection from infected individual?

A

Isolation, advice for family and contacts, post-exposure prophylaxis, and vaccinating contacts.

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21
Q

What are diagnostic protocols in transplant?

A

Do a pre-transplant serology. CMV monitoring or prophylaxis, EBV monitoring, adeno monitoring (paeds BMT), HSV prophylaxis if indicated

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22
Q

What can be tested for in CSF?

A

HSV, VZV, enterovirus, EBV, CMV, adenovirus, HHV6, JC virus

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23
Q

What can be tested for in the blood?

A

CMV, EBV, adenovirus, HHV6, parvovirus

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24
Q

What can respiratory viruses can be tested for?

A

Flu A/B, paraflu 1-4, adenovirus, enterovirus, RSV, HMPV, rhinovirus, coronaviruses, CMV in BAL

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25
Q

What can be tested in gut biopsy?

A

HSV, CMV, adenovirus

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26
Q

What does treatment of opportunistic viral infections require?

A

Often difficult to treat and requires: early treatment, higher dose, longer course, sometimes drug combinations. Increased risk of antiviral drug resistance.

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27
Q

What are types of Human Herpes Viruses?

A

HSV1 and 2, VZV, CMV, HHV6, EBV, HHV8

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28
Q

Human Herpes Viruses are latent infections (defining feature). What is the site of latent infection for VZV?

A

Dorsal root ganglion

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29
Q

Human Herpes Viruses are latent infections (defining feature). What is the site of latent infection for CMV?

A

Monocytes

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30
Q

Human Herpes Viruses are latent infections (defining feature). What is the site of latent infection for EBV?

A

B cells

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31
Q

In bone marrow transplants, when do HSV, HHV6 and HHV7 infections tend to occur?

A

Within a month of transplant

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32
Q

Herpes simplex virus symptoms

A

Cold sores, stomatitis, mouth ulcers, recurrent genital disease (HIV and adult transplant)

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33
Q

What are complications of herpes simplex virus?

A

cutaneous dissemination, oesophagitis, hepatitis, viraemia

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34
Q

What is treatment for herpes simplex virus?

A

Aciclovir, valaciclovir, foscarnet

35
Q

What are manifestations of varicella zoster virus?

A

Skin lesions, pneumonitis, encephalitis, hepatitis, purpura fulminans in the neonate, acute retinal necrosis, progressive outer retinal necrosis, VZV-associated vasculopathy

36
Q

What is a late manifestation of VZV post-transplant?

A

Shingles

37
Q

What can shingles be an early manifestation of?

A

HIV

38
Q

What is the mortality in multidermatomal or disseminated zoster?

A

High

39
Q

How can we prevent VZV infection in an immunocompromised person?

A

Aciclovir prophylaxis provides some protection, post-exposure prophylaxis with VZV immunoglobulin

40
Q

What are manifestations of CMV?

A

Retinitis, encephalitis, pneumonia, gastroenteritis

41
Q

What is a pathognomonic histological feature of CMV infection?

A

Owl’s eye appearance of the lung pneumocytes caused by inclusion bodies

42
Q

When does CMV tend to develop after transplantation?

A

Within 6 months of transplantation

43
Q

What is the greatest risk of reactivation of CMV?

A
  • In SOLID organ transplantation: the greatest risk of reactivation is when the donor has had past CMV infection but the recipient is naïve.
  • In BONE MARROW transplantation: the greatest risk of reactivation occurs when the recipient has had past CMV infection but the donor is naïve
  • CMV is a destructive infection that directly threatens the graft and damages endothelial cells
44
Q

What is most concerning about with EBV?

A

Development of malignancy

45
Q

What disease can EBV lead to?

A

Post-transplant lymphoproliferative disease (PTLD)

46
Q

What raises a suspicion of PTLD and what confirms it?

A

Rising EBV viral load associated with widespread lymphadenopathy raises suspicion of PTLD. Confirmed by biopsy of the lymph nodes.

47
Q

What is management for EBV?

A

Reduce immunosuppression, anti-CD20 monoclonal antibodies (Rituximab) - removes the B cells

48
Q

What is Kaposi sarcoma associated with?

A

HHV8

49
Q

What is HHV8 associated with?

A

Kaposi sarcoma, primary effusion lymphoma (PEL), multicentric castleman disease

50
Q

How does Kaposi sarcoma present?

A

Presents with brownish/purplish vascular lesions that can be cutaneous or visceral

51
Q

What are characteristic histological findings?

A

Spindle cell proliferation, neo-angiogenesis, inflammation and oedema

52
Q

How do you diagnose Kaposi sarcoma?

A

Biopsy

53
Q

How do you treat Kaposi sarcoma?

A

Chemotherapy, antiretroviral therapy

54
Q

What type of virus is a JC virus?

A

polyomavirus

55
Q

What is JC virus associated with?

A

Progressive multifocal leukoencephalopathy

56
Q

What is JC virus characterised by?

A

This is a dementing process that is characterised by loss of higher functions (personality change, motor deficits, focal neurological signs)

57
Q

What is the main pathological feature of JC virus?

A

Demyelination of white matter

58
Q

How is JC virus diagnosed?

A

MRI and PCR of CSF

59
Q

Who did progressive multifocal leukoencephalopathy occur in?

A

Before HAART, PML occurred about 5% of AIDS patients and had a high mortality

60
Q

What is an increased risk of PML seen in?

A

Increased risk of PML is associated with the use of Natalizumab (monoclonal antibody used in MS)

61
Q

What type of virus is BK virus?

A

Polyomavirus, dsDNA

62
Q

What can BK virus cause?

A

BK cystitis (post-stem cell transplantation) and BK nephropathy (post-renal transplant)

63
Q

How can we treat BK virus?

A

By reducing immunosuppression

64
Q

When is adenovirus particularly a problem?

A

Particular problem after bone marrow transplant

65
Q

How does adenovirus occur?

A

Can occur as an exogenous infection or reactivation of persistent endogenous infection

66
Q

What are manifestations of adenovirus?

A

Manifestations: Fever (septic appearance), encephalitis, pneumonitis, colitis, HIGH MORTALITY in disseminated infection

67
Q

Adenovirus has a high mortality, therefore what measures should we take in post-transplant patients?

A

Therefore, regular screening of urine, respiratory secretions, blood and stools to check for disseminated disease in post-transplant patients

68
Q

Which respiratory viruses have an increased risk of complications (pneumonitis) and high mortality?

A

Influenza A and B, parainfluenza, RSV, adenovirus, MERS

69
Q

How are respiratory viruses in immunocompromised patients diagnosed?

A

Diagnosed by taking nasopharyngeal aspirates, bronchioalveolar lavage, nose and throat swabs. Multiplex PCR is the investigation of choice

70
Q

What can Human Parvovirus B19 cause in immunocompromised patients?

A

Chronic anaemia

71
Q

How is Human Parvovirus B19 diagnosed?

A

PCR of blood. Serology (IgM) is NOT useful in immunocompromised patients.

72
Q

What is the treatment for Human Parvovirus B19?

A

IVIG - may require blood transfusion

73
Q

What is the serological course of hepatitis B like?

A

If you have been infected, you will develop antibodies against core antigen and surface antigen. If an acute infection progresses to become chronic, the HBsAg will persist.

74
Q

What would HBV serology of someone with current infection look like?

A

HBV sAg +, HBV core Ab +, HBV s Ab -

75
Q

What would HBV serology of someone with a past infection look like?

A

HBV sAg -, HBV core Ab +, HBV sAb +

76
Q

What would HBV serology of someone with a vaccination look like?

A

HBV sAg -, HBV core Ab -, HBV sAb +

77
Q

What are the TWO consequences of HBV in immunocompromised patients?

A

Carriers may have a flare of the disease. Those with a past infection may reactivate.

78
Q

Who is the risk of reactivation of HBV particularly important in?

A

In patients on B-cell depleting therapies (Rituximab)

79
Q

How can we prevent HBV infection?

A

Nucleoside/nucleotide analogue prophylaxis(e.g. lamivudine, tenofovir)

80
Q

How is hepatitis E virus present in the UK?

A

Endemic

81
Q

What is a major cause of enterically transmitted viral hepatitis?

A

Hepatitis E virus

82
Q

In developed countries, what is Hepatitis E caused by?

A

It is a zoonosis caused by genotype 3 virus

83
Q

In developing countries, what is Hepatitis E caused by?

A

Mainly caused by genotype 1 virus

84
Q

Amongst who is hepatitis E associated with a high mortality?

A

Pregnant women

MICRO - Abbie (19 decks)

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