What are the common viral CNS pathogens which give rise to meningitis?
enteroviruses*
herpesviruses*
HIV-1
What are the common viral CNS pathogens which give rise to encephalitis?
herpesviruses* arboviruses* influenza virus HIV-1 rabies
What is the difference in symptoms between viral meningitis and viral encephalitis?
viral encephalitis usually associated with more profound
1) mental status abnormalities
2) neurologic findings
3) seizures
What rae the common symptoms of viral encephalitis?
fever
headache
nuchal rigidity
What are the CSF findings of aspetic meningitis?
Normal/No:
- opening pressure
- clarity
- glucose
- gram stain/culture
Elevated:
- protein
- lymphocytes (WBC)
What are the enterovirus characteristics?
-picornaviridae
(small, ss linear RNA, virus)
-naked/non-enveloped
-replicate in cytoplasm
How does picornavirus replication occur?
- endocytosis (naked)
- release RNA in cytoplasm
- viral protein cap (5’) and poly-A tail (3’)
- polymerase with its own polymerase [big polyprotein cleaved into smaller proteins]
Where does picornavirus infect the body?
oropharynx
lymphoid
blood stream (meninges, brain, spinal cord)
What are the living conditions and seasonality of the enteroviruses genus?
GI
- low pH, 37o
- fecal-oral
summer and early fall
Which population is at-risk for enteroviruses?
children
How is enterovirus infection diagnosed?
RT-PCR using CSF or throat swab
What is the treatment for enteroviruses?
supportive, no treatment
What are the herpesviridae characteristics?
- enveloped
- large
- ds linear DNA
- replicates in nucleus
What is the prevention for enteroviruses?
hand washing
disinfection
hand sanitizer with alcohol >70%
What is the primary infection site and latent infection site of alpha herpesviridae (HHV 1-3)?
primary:
mucoepithelial cells
latent:
nerve ganglia
What are the main differences between HSV-1 and HSV-2?
HSV-1:
- “above the waist”
- latent in trigeminal gaglia
- orally transmitted
- children often infected
- 70% adults infected
HSV-2:
- “below the waist”
- latent in sacral ganglia
- sexually transmitted
- sexually active people often infected
- 25% adults infected
How do herpesviruses produce latent infections?
- after initial infection, infect nerves and “rests” as circular extrachromosomal unit in nucleus
- latency-associated transcripts (LATs) & noncoding regulatory RNAs which maintain latency
- reactivated and dislodges from nucleus
- meningeal branches to reach the brain
How is a herpesvirus infection diagnosed?
- Cowdry type A inclusions
- Tzanck smear (giant cells)
- PCR using CSF [rapid diagnosis for encephalitis or meningitis]
What is the most important anti-viral herpesvirus treatment?
IV acyclovir added to cell and becomes phosphorylated with herpes thymidine kinase (from virus)
- triple-phosphorylated with cell’s own kinases
- enters nucleus and prevents DNA from being extended
- *NOT A CURE**
What is the prevention for herpesviruses?
- safe sex
- gloves
- cesarean delivery if mother is symptomatic
- acyclovir for reoccurrances
What is the clinical presentaiton of varicella-zoster virus?
“chicken pox”
- infection (day 0)
- incubation
- contagious at 11 days
- fever begins at 13 days
- infection of skin/rash at 14 days
What is the at-risk population for varicella-zoster virus?
- children (varicella)
- elderly/immuno-compromised (zoster)
What is the pathogenesis of varicella-zoster virus?
highly contagious
respiratory secretions
What is it unsafe to contract a varicella infection as an adult?
- risk for pneumonia
- progressive infection leads to encephalitis
