L1 Herpes Flashcards

1
Q

Types of Herpes Viruses?

A

Herpes simplex virus (HSV) 1 and 2
Varicella zoster virus (VZV)
Epstein Barr virus (EBV)
Cytomegalovirus (CMV)
Human herpes virus (HHV) 6, 7 and 8

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2
Q

Pathogenesis of Herpes Virus?

A

Herpes Establish LATENT infection following primary infection.

Sensory nerve ganglia – HSV 1 and 2, VZV
B-lymphocytes – EBV, CMV, HHV8
T-lymphocytes – HHV 6 and 7
Epithelial cells – EBV, CMV

Reactivation may occur at any time – more likely during immunosuppression

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3
Q

Herpes viruses that sequester in the sensory nerve ganglia?

A

HSV 1 and 2
VZV

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4
Q

Herpes viruses that sequester in B-lymphocytes?

A

EBV
CMV
HHV8

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5
Q

Herpes viruses that sequester in T-lymphocytes?

A

HHV 6 and 7

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6
Q

Herpes viruses that sequester in Epithelial cells?

A

EBV
CMV

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7
Q

CMV Routes of transmission?

A
  • Sexual
  • Close contacts (upper respiratory secretions and urine)
  • Blood or tissue exposure
  • Vertical (placenta)
  • Perinatal (breastfeeding)
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8
Q

Pathogenesis of CMV?

A

Virus infects epithelial calls
Asymptomatic (90%)
Establishes latency in mononuclear cells => Mononucleosis (EBV/CMV)
Hepatitis (EBV/CMV)

Primary infection
Reactivation
Recurrent infection

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9
Q

Causes of Mononucelosis?

A

EBV (Most Common)
CMV (lymphadenopathy less common)

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10
Q

Common causes of immunosupression?

A

*HIV
*Transplant recipients
*Immunosuppressive therapy e.g., TNF-alpha antagonists, rituximab

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11
Q

Manifestations of CMV infections in HIV?

A

Retinitis
GI – Esophagitis, colitis, hepatitis
Encephalitis (HSV1)

Highest risk when CD4 < 100
Worsens HIV progression

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12
Q

Manifestations of CMV infections in Solid Organ Transplant?

A

Highest incidence 1-3 months post transplant /cessation of prophylaxis)
Primary infection more severe than reactivation/recurrence

HIGHEST risk in DONOR Positive (IgG +) and RECIPIENT IgG (-)

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13
Q

Diagnosis of CMV in Immunocompromised?

A
  • Infection – detection of CMV in tissue or body fluid
  • Disease – CMV infection plus attributable signs or symptoms (Pneumonitis, hepatitis, colitis)

Viral inclusion bodies (‘owl’s eye’) on H&E stain
Detection of virus/viral antigen in blood, BAL, tissue (PCR for CMV DNA)

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14
Q

Management of CMV diseases in Immunocompromised?

A

Ganciclovir (IV) -thrombocytopenia, neutropenia. (Mutations UL97 and UL54 make resistant against ganciclovir + cidofovir)

Valganciclovir (oral) – good bioavailability

Reduction in immunosuppression

Consider CMV immune globulin – with ganciclovir for pneumonitis

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15
Q

Prophylaxis for CMV in immunocompromised?

A

Valganciclovir x 3-6 months post transplant

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16
Q

What helps control acute EBV Infection?

A

EBV specific cytotoxic T cells produced – control acute infection

Small amount infected B cells remain (latent) – can reactivate later if T cell immunity wanes

17
Q

EBV Pathogenesis

A

Infection of oral epithelial cells
Release into oropharyngeal secretions
Infection of B-lymphocytes
=> Acute infectious mononucleosis (IM)
=> Dissemination of infection

EBV specific cytotoxic T cells produced – control acute infection

Small amount infected B cells remain (latent) – can reactivate later if T cell immunity wanes

18
Q

Classic Triad of acute EBV infection?

A

Fever
Pharyngitis
Lymphandenopathy

19
Q

__________can drive transformation of infected B cells to malignancy

A

EBV (Oncogenic virus): can drive transformation of infected B cells to malignancy

20
Q

Manifestations of EBV in Immunocompromised?

A

Oral hairy leukoplakia
Non-Hodgkin lymphoma in HIV
Post-transplant lymphoproliferative disorder (PTLD)

21
Q

What is Post-transplant lymphoproliferative disorder (PTLD) most often caused by?

A

presence of EBV (>50%)

22
Q

Pathogenesis of Post-transplant lymphoproliferative disorder (PTLD)

A

Absence of normal T cell immunity (immunosuppressive treatment) => Proliferation of EBV-infected B cells =>Development of lymphoma

23
Q

Origin of EBV Infected B Cells?

A

Recipient derived more common in SOT
Donor derived more common in HSCT

24
Q

Diagnosis/Management of CMV

A

Diagnosis
Imaging – evidence of mass lesion
Elevated LDH
Rising EBV viral load in blood (PCR)
Histology

Management
Reduction of immunosuppression
Rituximab (anti-CD20 monoclonal antibody)
Radiotherapy Chemotherapy
Surgical resection

25
Q

Pathogenesis of Varicella Zoster Virus (VZV)

A

Virus infects lymphoid tissue of nasopharynx (airborne viral droplets)

Spreads to regional lymphoid tissue (preferentially infecting memory T-cells)

Migrates to cutaneous epithelia => Infects nerve endings in the skin

Migrates along sensory axons to neurons in regional ganglia (Latency- Shingles/chickenpox)

26
Q

Manifestation of Varicella Zoster Virus (VZV) infection?

A

Primary infection - chicken pox

Reactivation – shingles
Pain, paresthesia, rash
Usually dermatomal pattern (UNILATERAL as Dermatomes don’t cross the midline)
Maybe disseminated (immunocompromised)

Zoster sine herpete – pain, parasthesia, no rash

27
Q

VZV in Immunocompromised

A

Disseminated rash
Visceral involvement common
* Pneumonitis
* Hepatitis
* Encephalitis

High mortality

28
Q

Diagnosis of VZV

A

Often clinical

29
Q

Treatment of VZV?

A

Acyclovir or prodrugs (valaciclovir, famciclovir)

Primary VZV (chicken pox)
* Children – supportive; antiviral if immunocompromised
* Adults – antiviral

Reactivation
* Shingles – oral antiviral
*Disseminated/encephalitis/pneumonitis – IV aciclovir

30
Q

Prevention of VZV

A

VZV vaccine in childhood – not part of routine schedule in Ireland

Shingles vaccine in older adults

VZIG for non-immune (VZV IgG negative) high-risk individuals exposed to VZV

31
Q

Manifestations of HSV in immunocompromised?

A
  • HIV (CD4 <200)
  • Transplant (HSV IgG positive)

Skin or genital lesions
Oesophagitis
Pneumonitis
Encephalitis
Ocular infection

32
Q

Diagnosis/Treatment/Prophylaxis of Herpes Simplex Virus in Immunocompromised?

A

Diagnosis: PCR for HSV-1 or HSV-2 DNA – vesicle fluid, BAL, CSF

Treatment: Oral/IV aciclovir, Oral famciclovir, Oral valaciclovir

Prophylaxis: Aciclovir or valaciclovir

33
Q

Conditions associated with Human Herpes Virus 8?

A

Kaposi’s sarcoma
Primary effusion lymphoma
Castleman’s disease

33
Q

Conditions associated with Human Herpes Virus 8?

A

Kaposi’s sarcoma
Primary effusion lymphoma
Castleman’s disease