L1 Herpes Flashcards
(34 cards)
Types of Herpes Viruses?
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
Pathogenesis of Herpes Virus?
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
Herpes viruses that sequester in the sensory nerve ganglia?
HSV 1 and 2
VZV
Herpes viruses that sequester in B-lymphocytes?
EBV
CMV
HHV8
Herpes viruses that sequester in T-lymphocytes?
HHV 6 and 7
Herpes viruses that sequester in Epithelial cells?
EBV
CMV
CMV Routes of transmission?
- Sexual
- Close contacts (upper respiratory secretions and urine)
- Blood or tissue exposure
- Vertical (placenta)
- Perinatal (breastfeeding)
Pathogenesis of CMV?
Virus infects epithelial calls
Asymptomatic (90%)
Establishes latency in mononuclear cells => Mononucleosis (EBV/CMV)
Hepatitis (EBV/CMV)
Primary infection
Reactivation
Recurrent infection
Causes of Mononucelosis?
EBV (Most Common)
CMV (lymphadenopathy less common)
Common causes of immunosupression?
*HIV
*Transplant recipients
*Immunosuppressive therapy e.g., TNF-alpha antagonists, rituximab
Manifestations of CMV infections in HIV?
Retinitis
GI – Esophagitis, colitis, hepatitis
Encephalitis (HSV1)
Highest risk when CD4 < 100
Worsens HIV progression
Manifestations of CMV infections in Solid Organ Transplant?
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 (-)
Diagnosis of CMV in Immunocompromised?
- 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)
Management of CMV diseases in Immunocompromised?
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
Prophylaxis for CMV in immunocompromised?
Valganciclovir x 3-6 months post transplant
What helps control acute EBV 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
EBV Pathogenesis
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
Classic Triad of acute EBV infection?
Fever
Pharyngitis
Lymphandenopathy
__________can drive transformation of infected B cells to malignancy
EBV (Oncogenic virus): can drive transformation of infected B cells to malignancy
Manifestations of EBV in Immunocompromised?
Oral hairy leukoplakia
Non-Hodgkin lymphoma in HIV
Post-transplant lymphoproliferative disorder (PTLD)
What is Post-transplant lymphoproliferative disorder (PTLD) most often caused by?
presence of EBV (>50%)
Pathogenesis of Post-transplant lymphoproliferative disorder (PTLD)
Absence of normal T cell immunity (immunosuppressive treatment) => Proliferation of EBV-infected B cells =>Development of lymphoma
Origin of EBV Infected B Cells?
Recipient derived more common in SOT
Donor derived more common in HSCT
Diagnosis/Management of CMV
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
