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Flashcards in Common Viral Pathogens Deck (43)
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4 ways to diagnose a viral infection

1. Look for virus grown in tissue culture - distinctive patterns of CPE can be recognized

2. Assay for viral antigens using enzymatic reactions or immunofluorescence (i.e. rapid flu test)

3. PCR - amplifies a portion of viral genome in body tissues

4. Look for host immune response to viral infection - i.e. ELISA


Herpes - Basics + 8 Types

Herpes are ds-DNA viruses that come in 8 varieites:

HHV-1: Herpes Simplex 1 (HSV1)
HHV-2: Herpes Simplex 2 (HSV2)
HHV-3: Varicella Zoster Virus (VZV)
HHV-4: Epstein Barr Virus (EBV)
HHV-5: Cytomegalovirus (CMV)
HHV-8: Kaposi's Sarcoma Virus


HSV-1 / HSV-2 Primary infection

HSV-1 primary infection often occurs durig childhood and is usually asymptomatic; HSV-2 primary infection usually occurs as a result of sexual contact and is often asymptomatic

If symptomatic, painful vesicles usually develop 1-3 days after inoculation and are contained to the area of infection


Manifestations of HSV Infection (4)

Gingivostomatitis - painful mouth ulcers of lips, gums, tongue; i.e. "Cold Sores"

Herpetic whitlow - inoculation of virus from oral secretions onto fingers

Herpes gladitorum - inoculation of virus from oral secretions onto skin

Herpes keratitis - infection of cornea



HSV is the most common cause of encephalitis in the US; HSV infection in the brain has a predilecton for the temporal lobe, often presenting as psychiatric illness


Neonatal HSV

Primary infection of the infant transmitted perinatally via exposure to maternal secretions containing HSV (active lesions or asymptomatic viral shedding)

Often infects the skin, eye, and CNS; may become disseminated, causing hepatitis, DIC

HSV-associated encephalitis in a newborn is associated with 30% mortality; 75% of survivors will have intellectual disability


Prevention & Treatment of neonatal HSV

Pregnant women with HSV are treated prophylactically with anti-virals; if active genital lesions are present at the time of delivery C-section is recommended

Skin vesicles in a neonate < 1 month old are assumed HSV until proven otherwise; treated with acyclovir


HSV Latency & Reactivation

Latency occurs in the sensory ganglia of the areas affected by the primary infection - trigeminal (orofacial infection) and sacral ganglion (genital infection) are most common

Reactivation is provoked by a variety of stress stimuli and may include asymptomatic shedding or symptomatic reactivation infection


HSV Treatment

Oral antiviral therapy - patients with active outbreaks often prevent too late for therapeutic benefit but may be given extra refills to start taking at first sign of next outbreak

IV Acyclovir - for severe infections such as neonatal herpes, encephalitis, or active HSV in immunocompromised hosts


Chickenpox Vaccine

Live, attenuated vaccine, consists of a 2 dose series at 12-15 months and 4-6 years; not recommended for immunocompromised patients

Varizig - VZV immune globulin given within 4 days of exposure can reduce severity of varicella in high risk individuals (passive immunization); consists of pooled antibodies from donors with high VZV titers


Shingles vaccine

Zostavax - one dose recommended for healthy individuals 60+; boosts T-cell immune response to VZV, preventing reactivation


VZV Primary Infection

Chickenpox; highly contagious with incubation period of 10-21 days; disease begins with fever, malaise, headache, and progresses to itchy vesicular rash described as "dew drops on a rose petal"; lesions appear in successive waves and typical course lasts 7 days


VZV Secondary Infection

Shingles; VZV remains dormant in the cranial, dorsal root, or trigeminal ganglia; reactivation is always symptomatic

Occurs as a result of declining T-cell mediated immunity vs. latent VZV with age

Begins as pain at the site where vesicles will erupt; lesions develop over a single dermatome and usually subside within 2 weeks

Post-herpetic neuralgia (PHN) is the most common complication; pain may last weeks to months after lesions resolve


VZV Pathogenesis

Virus gains entry through the respiratory tract then spreads to the lymphatic system; primary viral replication takes place in regional lymph nodes and is followed by primary viremia; secondary replication occurs in the liver, spleen, and other organs and spreads through secondary viremia to the skin


VZV treatment

Chickenpox is usually self-limited and requires no treatment; immunocompromised patients should receive anti-viral treatment

Shingles may be treated with Acyclovir within 48-72 hours of symptoms to decrease number and duration of lesions as well as pain


EBV Primary Infection

Transmitted via saliva - 95% of individuals are infected by 40 years

Primary infection in young children is often asymptomatic; primary infection in teens/adults causes infectious mononucleiosis in 40% characterized by fever, sore throat, lymphadenopathy, fatigue, exudative tonsillitis, and splenomegaly; symptoms resolve in 4-8 weeks


EBV Pathophysiology

EBV infects the nasopharyngeal epithelium, resulting in cell lysis and viral spread to adjacent oropharyngeal lymphoid tissue; viremia occurs with distribution to the liver, spleen, and B lymphocytes

EBV remains latent in nasopharyngeal epithelium and B cells; may contribute to some B cell cancers (Burkitt's and Hodgkin Lymphoma)


EBV Diagnosis

Many patients display >10% atypical lymphocytes in peripheral blood smear

Monospot/heterophile test - detects presence of antibodies that agglutinate horse/sheep/cattle RBCs via cross-reaction with EBV

EBV serology - presence of IgM indicates recent infection (4-6 weeks); IgG indicates past infection


CMV Epidemiology

Transmitted via infected body fluids (saliva, breast milk, sexual contact, blood, tears, urine) or from mother to fetus (in utero, perinatal)

40-80% of people in the US infected by 40 years old


CMV Primary Infection

CMV infects the epithelia of the salivary gland or genital tract; primary infection in healthy persons is almsot always asymptomatic but may be serious in immunocompromised patients and cause retinitis, colinitis, etc.


CMV Secondary Infection

CMV remains latent in monocytes and lymphocytes; reactivation infection is asymptomatic in normal patients but virus is being shed in bodily secretions

Reactivation may be serious in immunocomrpomised patients; often non-focal viral syndrome or organ-specific infection (hepatitis, pneumonitis, etc.)


Diagnosis of CMV


IgM alone is seen in primary CMV infection

IgG alone is seen in previous CMV infection

IgM and IgG together are seen in recent reactivation infection

Tissue histology - infected cells have "owel's eye" appearance (densely staining body surrounded by a halo) due to intranuclear inclusion bodies (viral proteins or particles)


CMV treatment


Passive immunization for pregnant women positive for CMV - pooled CMV antibodies


Risk of CMV transmission during pregnancy

CMV is the most common in-utero infection in the US; risk of transmission is 3-5% for a mother with primary CMV and <1% for a mother with reactivated CMV

10-15% of infected infants will have symptoms at birth


Congenital CMV Syndrome

Low birth weight
Hearing loss - leading cause of congenital hearing loss in the US
Mental Impairment
Skin rash (blueberry muffin spots)

Treated with oral valganciclovir or gancyclovir


RSV Pathogenesis

RSV is an enveloped virus with a ssRNA genome transmitted by contact with respiratory droplets at mucus membranes; localized infection of respiratory tract with cell-cell transfer of virus leads to spread from upper to lower respiratory tract

2 important surface proteins:
G protein mediates viral attachment to host cells; F (fusion) protein mediates fusion of infected cells to neighboring cells to form syncytia, multi-nucleated giant cells


RSV Primary Infection

Usually symptomatic and causes acute respiratory disease in patients of all ages: most often bronchiolitis (children < 1), viral pneumonia (children and the elderly) and URI (children and adults)

Most common cause of bronchiolitis and viral pneumonia in young children; almost all children infected at least once by 2 years

Infection more commonly leads to severe respiratory disease in premature infants <32 weeks


RSV Reinfection

Presents in older children and adults as a severe cold / URI


RSV Diagnosis & Treatment

Diagnosis is usually clinical; rapid test exists but is not very sensitive (false negatives are common)

Treatment is mostly supportive - some children may benefit from a bronchodilator; Ribavirin can be used in high risk patients


Rotavirus - Epidemiology

Leading single cause of severe diarrhea and gastroenteritis in infants and young children worldwide