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OMS II BECOM Exam 1 > EBV/CMV infections - Stillwell > Flashcards

EBV/CMV infections - Stillwell Flashcards

1
Q

alpha herpes viruses

A
  • HHV-1 (Herpes simplex virus-1/HSV-1) (oral>genital herpes)
    - HHV-2 (Herpes simplex virus-2/HSV-2) (genital>oral herpes)
    - HHV-3 (Varicella zoster virus- VZV) (chickenpox/shingles)
    - HHV-B (Herpes simiae virus- Herpes B virus) (rash/meningoencephalitis/lymphadenitis)
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2
Q

gamma herpes viruses

A
  • HHV-4 (Epstein-Barr virus- EBV) (infectious mononucleosis)

- HHV-8 (Kaposi’s sarcoma herpesvirus- KSHV) (Kaposi’s sarcoma)

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3
Q

beta herpes viruses

A
  • HHV-5 (Cytomegalovirus- CMV) (infectious mononucleosis)
    - HHV-6 (Roseolovirus) (roseola)
    - HHV-7 (Roseolovirus) (roseola)
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4
Q

EBV (HHV-4)

A
  • infectious mononucleosis/”kissing disease”**
  • many infected in childhood and adulthood
  • only infects primates**
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5
Q

EBV transmission

A
  • spread through bodily fluids –> saliva, blood, semen (sexual contact; STI), organ transplants**
  • spread on fomites**
  • once one is primarily infected, can spread to others even after symptoms resolve**
  • virus can reactive asymptomatically to be spread to others**
  • most people are seropositive for EBV**
  • long incubation time 30-50 days (same for CMV)**
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6
Q

EBV viral acquisition

A
  1. tropism- tropism for endothelial cells –> multiple rounds of lytic replication
  2. B cells - EBV tropic to B cells –> antigen infects B cells –> B cells present to T cells
  3. T cells - EBV causes CD8 T cell response –> atypical lymphocytes (downey cells)***
    - cellular immunity better than humoral immunity
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7
Q

EBV latency

A
  1. B cells - serve as reservoir for lifelong infection**
    - shedding of EBV into body fluids upon reactivation is always asymptomatic in healthy people**
  2. EBV-infected B cells transformed into immortalized lymphocytes* –> transform to oncogenic state in immunocompromised
  3. EBV lives in episome in nucleus of B cell
  4. EBV can be malignant with latent infection/gene expression, not acute infection
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8
Q

EBV humoral response

A
  • EBNA (ebstein-barr nuclear antigen) on B cells
  • VCA (viral capsid antigen) with infectious mono
  • Can form cross reactive IgM antibodies (heterophile antibodies) against antigens of certain animals –> used to test for EBV mono* called monospot test
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9
Q

monospot test (heterophile antibody)

A
  • not the best way to test for EBV mono (not always +)

- never + for CMV mono (tests neg)

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10
Q

EBV pathology

A
  • reactive follicular hyperplasia of lymph nodes with lymphadenopathy**
  • splenomegaly –> immunoblasts can resemble Reed-Sternburg cells (in Hodgkin’s) or have hemophagocytosis (RBCs in phagocytic cells as histiocytes)
  • blood abnormalities, but bone marrow biopsy is normal**
  • hepatitis (common) and cholestasis (rare)
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11
Q

follicular hyperplasia vs. follicular lymphoma

A
  • hyperplasia –> mix of lymphocytes, Macs, and plasma cells –> “starry night”*** with immunoblasts
  • lymphoma –> unicellular type appearance**
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12
Q

EBV clinical illness

A
  1. age has influence on expression
  2. children asymptomatic (50% + for heterophile antibody)**
  3. infectious mono syndrome (glandular fever)** occurs in adolescent/adult –> symptomatic (90% + for heterophile antibody)**
  4. infectious mono syndrome –> high prolonged fever* (also in CMV), retro-orbital headache** (seen in HIV or EBV), severe pharyngitis**
  5. rash (uncommon)
  6. rash with EBV infection + amoxicillin/ampicillin*** - hypersensitivity rxn that can involve palms/soles (EBV-induced drug sensitization), more severe
  7. posterior cervical lymphadenopathy*** (also in CMV)
  8. hepatitis - high liver enzymes (ALT, AST)
  9. splenomegaly** - spleen can rupture (refrain from contact sports)
  10. tonsillo-pharyngitis** - “kissing” tonsil obstruction, exudate, petechia on palate
  11. autoimmune hemolytic IgM cold agglutinins (rare)* - more typical is elevated WBC count and atypical lymphocytes** on diff.
  12. neurologic - septic meningitis
  13. cardiac - myocarditis (rare)
  14. pulmonary - pneumonia (rare)
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13
Q

EBV - other associated illnesses

A
  1. X-linked lymphoproliferative syndrome/Duncan’s syndrome** - boys/adolescents, proliferative response of B/T cells to EBV –> life-threatening rxn (hemophagocytic lymphohistiocytosis); pancytopenia from destroying bone marrow, multi organ failure, die at young age, no treatment
  2. chronic, active EBV infection (rare) - multiorgan failure
  3. oral hairy leukoplakia** - in immunosuppressed (ex. AIDS), white lesions on side of tongue (can’t scrape off like candida/thrush infections leading to misdiagnosis)**
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14
Q

EBV - associated malignancies

A
  1. Post-transplant Lymphoproliferative Disorder (PTLD)** - B cells undergo mutations –> malignant lymphoma; immunosuppressive drugs and rituximab kill B cells
  2. Primary central nervous system lymphoma (B-cell)** - seen in AIDS patients –> lymphoma with HIV due to EBV reactivation
  3. Burkitt’s lymphoma** - type of non-Hodgkin lymphoma, in Africa (associated with falciparum malaria), rapidly growing tumor around mandible associated with EBV** (responds well to chemo)**
  4. Hodgkin’s lymphoma - replication of malignant B cells; Reed-sternburg cells*
  5. Nasopharyngeal carcinoma
  6. gastric carcinoma
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15
Q

EBV - diagnosis

A
  1. atypical lymphocytes (downey cells)** - antigen stimulated CD8 cytotoxic T cells, cytoplasm indented by RBCs, also seen in CMV, HIV**
  2. lymphocytosis
  3. leukocytosis - sometime neutropenia/thrombocytopenia
  4. serology - viral capsid antigen (VCA) IgM antibody** in 100% of patients –> gold standard to detect primary EBV; VCA IgG develops shortly after
  5. heterophile antibody/monospot/test - usually pos with EBV and neg with CMV mono** (can have false NEG with EBV) –> false POS seen with autoimmune, lymphoma, viral, or malaria**
  6. EBV DNA PCR - less sensitive with acute infectious mono
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16
Q

EBV treatment

A
  • Acyclovir, ganciclovir and foscarnet - no good antiviral treatment for infectious mono
  • steroids can help with obstructive tonsillo-pharyngitis
  • lymphoproliferative disease treated with reduction in immunosuppressive drugs –> tumor regression** (but can increase risk of graft rejection)
  • oral hairy cell leukoplakia –> EBV usually in lytic phase and responds to acyclovir
17
Q

B symptoms**

A
  • fever for more than 3 days, drenching night sweats, unintentional weight loss over 6 months** –> associated with Hodgkin’s and non-hodgkin’s lymphoma
  • Pel-ebstein fever**
  • other signs with HL, NHL: itching, fatigue, hepatosplenomegaly, anorexia, lymphadenopathy and lymph node pain (if they occur after drinking EtOH, they aren’t B symptoms)***
18
Q

infectious mononucleosis syndrome

A
  • mostly due to EBV, CMV**
  • EBV most common
  • others can cause it (rare) - ex. primary HIV syndrome in 2% cases
19
Q

CMV - epidemiology

A
  • aka HHV-5, cytomegalic inclusion virus or salivary gland virus
  • largest virus to infect humans - large cells
  • passed same way as EBV - also perinatal (birth, breast feeding)
  • usually get in adulthood (rare in newborns) - risk increases with age***
  • long incubation time (20-60 days)**
  • multiple strains –> recurrent infections
  • can be STI –> saliva, urine, semen, vaginal secretions, blood, etc.
20
Q

CMV - viral stages

A
  • tropism for more cell types than EBV –> latent infections after recovering from primary infection
  • usually acquired from person who is asymptomatic and shedding the virus**
  • does not develop into malignancy like EBV**
  • can live latently in non-replicating form in many types of cells –> spontaneous reactivation with body stresses
  • once acquired, you carry it forever (herpes forever!!)**
21
Q

CMV - immune system

A
  • cell mediated immunity (Macs, monocytes, T lymphocytes)** –> most problems with AIDS and transplant patients**
  • humoral immunity for EBV
  • have drugs for treatment
22
Q

atypical lymphocytes

A
  • activated CD8 T lymphocytes

- seen in both CMV, EBV***

23
Q

CMV - pathology

A
  • Owl’s eye inclusion bodies** (nuclear and cytoplasmic inclusions) –> confused with Reed-sternburg cells in HL
  • “starry sky with reed-sternburg cells**
24
Q

CMV - clinical illness

A
  1. most acute infections never diagnosed (asymptomatic)
  2. infectious mono syndrome: even though always heterophile antibody/EBV IgM negative, CMV should be considered a cause if mononucleosis scenario* (CMV IgM to test for mono)
    - less risk of lymphadenopathy, splenomegaly, unlike EBV*
    - high liver enzymes, jaundice rare, typhoidal syndrome (long fever, malaise, headache, myalgias)
    - rash brought on with amoxicillin/ampicillin*
  3. hepatits - after transfusion
  4. myocarditis - most common cause of FATAL myocarditis in immunosuppressed**
  5. thrombocytopenia/hemolytic anemia
  6. CNS infections - can get Guillain-Barre syndrome
25
Q

CMV - other scenarios

A
  1. congenital CMV** - mom is not immune and comes down with acute primary CMV infection while pregnant –> can lead to many morbidities (lethargy, respiratory distress, seizures), even mortality in babies
    - CT with Brain calcifications***
  2. perinatal CMV - passage through birth canal or breast feeding
  3. CMV with AIDS** - worry if CD4 count becomes too low; CMV severe alongside HIV
    - cause retinitis/blindness (starts peripherally –> centrally)
    - CNS involvement (polyradiculopathy, ascending weakness in lower limbs, lose deep tendon reflexes and bowel/bladder control, low back pain)
    - GI involvement (ulcerative esophagitis, colitis)**
    - pancytopenia in certain populations**
  4. CMV reactivation in critically ill - ex. ICU patients, prolonged hospital admissions –> hepatitis and cytopenia after transfusions due to CMV in blood
  5. CMV in renal transplant patients** - usually secondary reactivation; morbidity lower than other transplants
    - “CMV syndrome” in renal transplants with primary infection from transplantation –> fever, leukopenia, atypical lymphocytosis, hepatosplenomegaly
    - secondary infection only associated with fever, hepatitis, interstitial pneumonia
    - CMV increases risk of transplant rejection
  6. CMV in liver transplants** - CMV most common pathogen –> lead to high liver enzymes (AST/ALT) and cholestasis
  7. CMV in HSC transplant patient - most common, life threatening, CMV pneumonitis** (high mortality), increased risk of graft-vs-host disease, respiratory failure
26
Q

HAART therapy

A

-treatment for HIV, helps keep CD4 levels high

27
Q

CMV - diagnosis

A
  • elevated WBCs (not as high as EBV) and atypical lymphocytosis**
  • elevated liver enzymes, anemia, thrombocytopenia
  • CMV IgM antibody for acute CMV - IgG develops weeks after and stays for life**
  • CMV DNA PCR - useful in transplant and HIV+ patients
  • tissue culture - extensive
28
Q

CMV - treatment (drugs)

A
  1. Ganciclovir (IV) and valganciclovir (orally) - myelosuppression
  2. foscarnet - reversible nephrotoxicity**, low Ca2+, Mg2+, phosphate
  3. cidofovir - irreversible acute renal failure**
  4. letermovir
  5. maribavir
  6. Brincidofovir

Acyclovir, Famciclovir, Valacyclovir are inactive against CMV***

29
Q

looks like mono, but is negative for heterophile antibody mono spot test??

A

need to send off VCA and CMV monospot test for mono***

OMS II BECOM Exam 1 (30 decks)

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