Common Viral Pathogens Flashcards
4 ways to diagnose a viral infection
- Look for virus grown in tissue culture - distinctive patterns of CPE can be recognized
- Assay for viral antigens using enzymatic reactions or immunofluorescence (i.e. rapid flu test)
- PCR - amplifies a portion of viral genome in body tissues
- 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-6 HHV-7 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
Encephalitis
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)