Mono causing Herpes Virus Flashcards Preview

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Flashcards in Mono causing Herpes Virus Deck (30):

Most important factor in ability to infect

Cell attachment. Number one requirement


Herpes viruses

All can cause latent infections. 8 main human pathogens. DNA viruses.



cold sores



genital Herpes lesions



chickenpox and shingles



aka EBV. Most common cause of Infectious Mononucleosis (IM). Associated with Burkitt’s lymphoma and nasopharyngeal cancer



aka CMV. congenital disease + disease in immunocompromised


First indications for mono

atypical lymphocytes up! liver enzymes up, throat culture negative (not strep). Symptoms: hoarseness, difficulty swallowing, sore throat, fever, fatigue, myalgia, enlarged tonsils, lymph nodes (cervical), splenomegaly


Atypical lymphocyte description

larger, nucleus looks lacey and spread out. Latent infection in B cells. viral genome does not normally integrate into the cellular DNA but forms circular episomes which reside in the nucleus.


DDX - other possibilities

Infectious mononucleosis due to CMV or EBV (more common than CMV), streptococcal pharyngitis, retropharyngeal abscess, gonococcal pharyngitis, and toxoplasmosis


IM - characteristics

Primary EBV infection: usually subclinical in childhood. Adolescents and adults: 50% symptomatic infection. IM is usually a self-limited disease. Atypical lymphocytes (activated CD8+ T cells). Cytokines cause disease symptoms. Complications occur rarely but may be serious (e.g. splenic rupture, meningoencephalitis). In few, chronic IM can occur (patient dies of lymphoproliferative disease or lymphoma)


Incubation and transmission of IM

30-50 days. Transmitted primarily by saliva. Can be spread by asymptomatic individuals.


Children show symptoms of mono less. Why?

The symptoms are mostly due to the immune system response. Since they have less developed system, they don’t show it as well.


Testing for IM

Heterophile AB (reaction to RBCs from other animal - weird but it works. Show up around 2wks). Negative in 10-15%, so need more specific ones to EBV (IgG and IgM)


Pathogenesis - carrier

Lifelong carrier state: low grade infection kept in check by the immune defenses. EBV is able to immortalize B-lymphocytes in vitro and in vivo. Few EBV-immortalized B-cells can be demonstrated in the circulation -which are continually cleared by immune surveillance mechanisms.



In developed countries, 2 peaks of infection are seen: the first ages 1 - 6 yr and the second 14 – 20 yr. Eventually 80-90% of adults are infected. In developing countries, infection occurs at a much earlier age so that by the age of two, 90% of children are seropositive.


Diseases associated with HSV-4

top 4 most common. 1. Infectious Mononucleosis 2. Burkitt's lymphoma 3. Nasopharyngeal carcinoma 4. Lymphoproliferative disease and lymphoma in the immunosuppressed. 5. X-linked lymphoproliferative syndrome 6. Chronic infectious mononucleosis 7. Oral leukoplakia in AIDS patients 8. Chronic interstitial pneumonitis in AIDS patients.


Burkitt’s lymphoma

B cell malignancy. Common in children in Africa and Papua New Guinea. Found in areas with malaria (causes immunosuppression). Responds well to chemo.


Complications of EBV

Ampicillin rash (like Joc! Test first!). Airway obstruction. Splenic rupture (life threatening but rarer)


Risks of immunosuppressed individuals

Lymphomas. encephalitis, myocarditis, hepatitis, malignant B cell tumors. EBV and AIDS: oral hairy leukoplakia


Tx for IM/EBV

Antivirals ineffective. No vaccine! Just deal with it and wait it out.



CMV most common in immunosuppressed transplant patients. Must differentiate from CMV, HSV, and fungi such as Histoplasma capsulatum, Cryptococcus neoformans, Mucor and Aspergillus. (All of these organisms can cause pneumonia and gastritis)


CMV characteristics

CMV = one of most successful human pathogens. Transmitted vertically or horizontally usually with little effect on normal host. Developed countries: 40% of adolescents infected and ultimately 70% of the population developing countries, over 90% of people are ultimately infected. Transmission may occur in utero, perinatally or postnatally. Once infected, you have a friend for life


CMV congenital infection

Transmission to fetus may occur following primary or recurrent CMV infection. 40% chance of transmission to the fetus following a primary infection. Possible during all stages of pregnancy. Damage to fetus results from destruction of host cells. Can cause problems much later in life of child


CMV infection (not in fetus)

Usually asymptomatic except for a few cases of IM (clinically indistinguishable from EBV). Can cause Infectious Mono: Fever, pharyngitis, lymphadenopathy, splenomegaly (although less common than in EBV). Also self limiting. No run to heterophiles AB, test for specific AB


CMV symptoms in immunosuppressed

Spiking fevers most common symptom. Recipients of bone marrow: Pneumonitis most common. Recipients of solid organ transplants: Hepatitis, Thrombocytopenia, Pneumonitism, Vasculopathy after cardiac transplantation or graft rejection



25% of patients develop disease due to CMV. Disseminated disease common. 90% of infections are retinitis. Esophagitis, Colitis, Encephalitis, Polyradiculopathy: flaccid paralysis result


CMV pathogenesis

Replicates in many types of tissues and cells. Primary infection is followed by latent infection in granulocyte precursors and macrophages. Formation of giant cells (cytomegaly). Postnatal infection mainly occurs through saliva. Sexual transmission may occur as well as through blood and blood products and transplanted organ.


CMV Diagnostic tests

Cell culture; Histological exam of “suspect” tissues; DFA (fluorescent dye-labeled AB); PCR and other molecular methods; Virus in urine; Serology: finding of CMV IgM (ELISA or EIA)


CMV treatment

Gancyclovir (acyclovir variant). Same mode of action as acyclovir. Foscarnet can be used in cases of resistance. No vaccine.