Infectious mononucleosis

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Infectious mononucleosis

"kissing disease"
signs/symptoms: Burkitt's lymphoma
EBV and Cytomegalovirus

EBV Family

Herpes viridae

EBV Subfamily

Gammaherpersivinae

EBV Genus

Lymphocryptovirus

EBV Species

Human herpes virus 4 (Epstein Barr Virus)

EBV Structure

Capsid: Icosahedral
Genome: dsDNA, linear
Enveloped: yes

What's EBV cause?

Heterophile positive infectious mononucleosis (mono or kissing disease)

EBV/Mono

may be asymptomatic or vary in severity;
common: 70% of US population will be infected by age 30; 90% of world has been infected by EBV;
35-50% during adolescence or young adulthood;
lifelong latent infection in some immune cells;
Burkitt's lymphoma and nasopharyngeal carcinoma can occur (not common in US) tho not sole cause

Burkitt's lymphoma

aka B cell lymphoma
seen in equatorial Africa; related to EBV infection in 95% cases;
disease has a high chance of involving the jawbone

How to know if you have infectious mononucleosis

milder in children (normally asymptomatic) than adults
typically seen in 15-17 year olds; symptoms include:
traid of lymphadenopathy, fever and exudative pharyngitis lasting for 1-4 weeks
can be accompanied by malaise, splenomegaly, and often hepatosplenomegaly
ampicillin-induced rash
most ppl get better in 2-4 weeks; may feel tired for a few months

What happens with EBV?

EBV can cause recurring disease in some ppl;
EBV infects B cells & epithelial cells of the oropharynx promoting virus shedding into saliva to transmit to others;
Cytotoxic T cells attack these infected B cells and kill them; This attack gives the symptoms of mono (sore throat, fever, fatigue, splenomegaly, ect)
EBV can cause mono, latency or cancer.

Consequence of EBV infection

1. replicate in B cells/epithelial cells
2. cause latent infections of B cells
3. stimulate and immortalize B cells

Lymphoproliferative diseases

generally seen in immunocompromised hosts;
Burkitt's lymphoma is seen in malaria endemic regions of equatorial Africa and accounts for 1/2 of all childhood cancers.
- related to EBV ~100% cases (all tumor cells + for EBV DNA)
- disease has high chance of involving jawbone

Burkitt's lymphoma symptoms

lymph node swelling (neck, arms, groin)
fever
night sweats
fatigue
abdominal pain
unexplained weight loss
itchy skin

Diagnosis of Burkitt's lymphoma

by symptoms
presence of neutropenia (decrease in neutrophils)
histology (large, lobed B lymphocytes w/atypical nuclei)
lymph node biopsy

Burkitt's lymphoma

multi-step process involving environmental, genetic, other factors and promoted by EBV

Hodgkin's lymphoma

accounts for 1/3rd of all lymphomas in the western world;
one of the 1st cancers cured by radiation
one of the 1st cured by combination chemotherapy
one of the most curable cancers

Hodgkin's Symptoms

painless, swollen lymph nodes in the neck, underarm or groin
fever
night sweats
weight loss
fatigue
itchy/sensitive skin

Diagnosis of Hodgkin's lymphoma

presence of Reed-Sternberg cells;
EBV can be found in Reed-Sternberg cells in 1/2 of all Hodgkin's lymphomas

Nasopharyngeal carcinoma

rare in US (2% of all head and neck cancers)
more frequently in SE Asia & N Africa
Men are most likely to develop NC than women

Nasopharyngeal carcinoma symptoms

lump in the neck
bloody discharge from nose
nasal congestion on one side of nose
hearing loss in one ear
frequen ear infections
headaches
double vision
face/neck pain
feeling of fullness in throat and sinus areas

Diagnosis of NC

screenings may look for EBV and/or exam w/endoscope

Oral Hairy Leukoplakia (OHL)

manifestation of EBV infection in an immunocompromised host;
primarily a result of virus multiplication and lysis in host cells;
responds well to antiviral therapy (systemic Acyclovir and Valacyclovir effective in ~90% of cases)

Mono vs OHL/BL

Mono = vigorous cell immunity waging war on EBV
OHL and Burkitt's lymphoma = lack of effective cell immunity

EBV pathogenesis

infects B cells & epithelial cells of the oropharynx which promotes shedding into saliva for transmission;
if infected cells permit transcription of the ZEBRA protein (Transcriptional activator protein), genes are transcribed and virus goes into lytic cycle; virions enter blood, cause viremia and infect additional B cells. Cytotoxic T cells attack and kill infected B cells causing the symptoms

Virus can evade host cell immunity by splicing its DNA into host cell

EBV lab diagnosis

blood work reveals hyperplasia
atypical lymphocytes (more basophilic and vacuolated cytoplasm than normal lymphocytes; nucleus may be oval, kidney-shaped or lobulated)
lymphocytosis (60-70% WBCs are mononuclear w/30% atypical lymphocytes)
heterophile antibody & antibody to viral antigens

Heterophile Ab

detected by end of 1st week of illness;
excellent indicator of EBV infection in adults, not kids

Paul Bunnell antigen (PB Ag)

found on sheep, horse and bovine RBC but NOT guinea pig kidney cells.
Used to test for IgM Ab produced by EBV activated B cells.
Sheep, horse, bovine but not guinea pig kidney cells = heterophile positive

If heterophile test is negative

IgM Ab to VCA, to EBNA etc
EBV Abs are used to diagnose mono if symptomatic with negative Mono test.
Recommended tests: Viral capsid antigen (VCA)-IgM, VCA-IgG and D early antigen (EA-D) tests to detect a current or recent infection.
VCA-IgG and Epstein Barr nuclear antigen (EBNA) tests detect previous infection

EBV complications

(rare)
rupture of the enlarged spleen
hemolytic anemia
pericarditis
myocarditis
encephalitis
Guillain-Barre syndrome

Guillain-Barre syndrome

rare nervous system disorder resulting from nerve damage caused by the body's immune system in response to infection

EBV transmission

saliva
blood transfusions
organ transplants
sex

Treatment of EBV

self-limiting and resolves on its own; treat symptoms
Cortisone for severly swollen tonsils or throat tissues which threaten to obstruct breathing
Penicillin/erythromycin for possible strep (not ampicillin or amoxicillin due to potential rash)
Plasma exchange or intravenous immune globulin (IVIG) for Guillain-Barre syndrome

EBV extra facts

1st virus found to contain micro RNAs (miRNAs; found in B cell latency)

CMV Family

Herpesviridae

CMV Subfamily

Betaherpesvirinae

CMV Genus

Cytomegalovirus

CMV Species

Human herpesvirus 5 (Cytomegalovirus)

CMV structure

Capsid: icosahedral
Genome: dsDNA, linear
Enveloped: Yes

CMV info

largest genome of the human herpesviruses;
encodes largest # of glycoproteins among herpesviruses;
most prevalent viral cause of congenital infections;
issue particularly with AIDS patients and solid-organ transplant recipients
can cause birth defects if woman seroconverts during pregnancy

What does CMV cause?

Heterophile negative infectious mononucleosis
infections of multiple organs in AIDS patients
organ rejections
50% of adults in US have CMV;
most cases, shedding of virus is symptomatic
symptoms are milder version of mono

Histologic landmark for CMV infected cells

cytomegalic cell (enlarged cell that contains dense, central, "owl's eye" basophilic intranuclear inclusion body.

CMV diagnosis

cytomegalic cell
viral culture (takes 2 weeks to 1 month for cultivation)
serology: indirect ELISAs detect anti-CMV Abs
Direct detection of CMV antigens (early antigen p72 and late antigen p65) in blood, CSF or bronchioalveolar lavage through immunofluorescence
PCR, DNA hybridization assays

early p72 and late p65 antigens

detected in blood, CSF or bronchioalveolar lavage through immunofluorescence to detect active CMV infection

CMV complications

Primary infection usually self limited;
rare complications: pneumonitis, aseptic meningitis, Guillain-Barre syndrome

CMV transmission

saliva, urine, blood, throat washings, tears, breast milk, semen, stool, vaginal and cervical secretions, and transplant tissues

orally, sexually, blood transfusions, transplants, in utero, at burth and by nursing

Groups at risk of CMV infection

babies (prior to birth or within 1st month of life)
sexually active ppl
blood and organ recipients
burn victims
immunocompromised individuals

(responsible for the failure of many transplants)

Risks of contracting CMV

if seronegative and exposed to CMV;
worldwide and non-seasonal in occurrence;
seroprevalence from 30-100% depending on age, geographic location, and ethnic/socioeconomic background.
US seroprevalence is around 40-50%;
congenital CMV prevalence in US 0.5-1.5%

CMV Treatment

- Acyclovir (less potent than others)
- Ganciclovir
- Valganciclovir
- Cidofovir
- Foscarnet

Passive administration of CMV serum immunoglobulins is commonly used for prevention or treatment of CMV disease following organ transplantation

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