Blue-Ebv, Cmv, Yellow Fever, Dengue

Front 1

Describe the clinical presentation of Epstein-Barr virus associated with infectious mononucleosis

Back 1

lymphadenopathy (cervical chains)
pharyngitis (often mistaken for strep throat)
fever (up to 104F) which may last 2 weeks

malaise
splenomegaly
rash (due to immune complex w/virus)
transient ampicillin rash (no normal allergy to it)

Front 2

Describe the pathogenesis of Epstein-Barr virus associated with infectious mononucleosis

Back 2

infection via transfer of saliva. virus enters thru oral epithelial cells -> non-productive proliferative phase -> infects B cells, blocking apoptosis & allowing the virus to replicate w/in the cells to infect more B cells.
- causes a transient B-cell leukemia
- response by body is CD8+ mediated B-cell lysis of infected cells. the activated T cells become huge "downey cells" (atypical lymphocytosis)

Front 3

Describe the epidemiology of Epstein-Barr virus associated with infectious mononucleosis

Back 3

90-95% of world adult population infected (retained latency, normal function of B cells)
Infection is most common in 1-5 y/o's (asymptomatic)
symptomatic Dz occurs when 1st infection is in adolescence (10-19 y/o), esp high in colleges
-rare recurrent/chronic symptoms (prolonged fatigue, but NOT related to chronic fatigue syndrome)

Front 4

Describe EBV-associated oncogenic diseases

Back 4

it is a co-factor or cause of Burkitt's lymphoma (cancer of lymph node), Hodgkin's lymphoma, nasopharyngeal carcinoma (risk if pt is in an immunodepressed state, ie AIDS, post-transplantation)
- EBV proteins can deregulate B cell replication, causing proliferation & transformation (via supression of p53/Rb, activation of c-myc oncogene)

Front 5

Describe the clinical presentation of cytomegalic inclusion disease

Back 5

symptoms at birth:
jaundice
splenomegaly
seizures
purple skin rash (blueberry muffin)
pneumonia
small size of child

permanent: hearing loss, vision loss, mental disability, microcephaly, uncoordination, seizures, ADHD, Death

-initial symptoms can also be late onset (months-> yrs later)

Front 6

Describe the pathogesis of cytomegalic inclusion disease (opportunistic cytomegalovirus infection)

Back 6

prenatal, neonatal or postnatal (mother -> child)
- common infection. persistent, but most often benign.
- multiorgan system

Front 7

Describe the epidemiology of cytomegalic inclusion disease (opportunistic cytomegalovirus infection)

Back 7

- 10% of monocases (heterophile (-))
- reactivation can occur in immunosuppressed pt's causing retinitis, esophagitis, pneumonia, etc
- most infections are asymptomatic; universal virus
- transmitted by saliva, fecal-oral, transplacental, breastmilk, STD

Front 8

Describe the pathogenesis of yellow fever

Back 8

viral infection of endothelium after transmission by mosquito. causes:
intracellular viral antigen inclusions in hepatocytes (councilman bodies)

Front 9

Describe the pathogenesis of dengue fever

Back 9

virus is transmitted by mosquito (aedes aegypti) bite. virus is taken up by dendritic cell, evades destruction & replicates w/in dendritic cell primarily. immune complex deposition is seen as well.

Front 10

describe the following for yellow fever:
1. vector
2. vaccine(s)

Back 10

1. mosquito
2. stamaril vaccine is recommended prior to travel to endemic area

Front 11

describe the following for dengue:
1. vector
2. vaccine(s)

Back 11

1. mosquito (sylvan cycle [infects monkeys] & urban cycle [humans] makes it impossible to competely wipe out virus
2. none, but vector control

Front 12

describe the lab findings for EBV

Back 12

atypical, large lymphocytes
heterophile antibodies (pt blood will react w/sheep RBC's

Front 13

describe transmission of EBV

Back 13

via saliva, esp kissing
incubation period of 30-50 days
infectious for many months afterwards

Front 14

describe the laboratory testing for EBV when a pt has mono-like symptoms

Back 14

monospot (heterophile Ab), if (-) then check CBC, if lymphocytosis or atypical lymphocytes -> EBV IgM test, if (-) then CMV IgM test

Front 15

Describe the treatment for EBV mononucleosis

Back 15

self-limited, treat symptoms (NSAIDS, etc)

Front 16

Describe the laboratory diagnosis for cytomegalovirus

Back 16

IgM Ab (TORCH panel)
- histological sample shows *owl's-eye cells (owl-body, cytomegaly)

Front 17

describe the treatment for cytomegalic inclusion disease

Back 17

gancyclovir, valgancyclovir, foscarnet

Front 18

What class of virus are yellow fever & dengue virus under?

Back 18

arboviruses (arthropod borne)
= ambisense +/- material, ss RNA

Front 19

describe the clinical findings for Yellow fever

Back 19

mild fever/headache, rash -> jaundice/hepatitis, nephritis, encephalitis
- possible coagulation defects
- hemorrhage into stomach due to virus destroying gastric mucosa causing black vomit
- travel history to south america or Africa

Front 20

Describe the clinical findings for Dengue fever

Back 20

fever, headache, anorexia, N/V, retro-orbital pain, back pain, skin rash due to immune complex deposition
deep bone pain breakbone fever
- onset is < 1 week after mosquito bite. disease course is 3-9 days
= severity is proportional to viral load

Front 21

Describe the pathogenesis of dengue hemorrhagic fever

Back 21

this follows a second exposure, where antibodies against the viral antigens are present, however it is a different strain (with a different attachment antigen) & therefore the antibodies do NOT neutralize the virus. Instead they increase the rate of uptake by DC's & macrophages (virus evades lysosome fusion) & increases the rate of viral replication & destruction of phagocytes.
- aka antibody-dependent enhancement, enhanced virus growth in monocytes/macrophages. antibodies act as attachment protein.
- lysis of macro causes a cytokine storm -> increased vascular permeability & plasma loss
= this causes spontaneous hemorrhage all over body & can lead to dengue shock syndrome