Micro: Viral CNS Infections Flashcards
What are the ways in which viruses can access the CNS?
- Olfactory route
- Neuronal
- Hematogenous
Meningitis definition
Inflammation of the lining of the brain. Aseptic meningitis is NOT caused by bacteria
Encephalitis defitinition
Inflammation of the brain tissues
Meningoencephalitis definition
Widespread infection of the meninges and brain
Cause of aseptic meningitis
Viruses, fungi, TB, infections near the CNS
- 80% enteroviruses, 10% HSV 1 and 2, 10% arboviruses
Symptoms of aseptic meningitis
Mental status is normal, this can distinguish from encephalitis
- Headache, fever, chills, stiff neck, malaise, sore throut, N/V, abd pain, rash, myalgias, photophobia
Diagnosis of aseptic meningitis
Elevated WBC count in spinal fluid, no bacteria
Virus may be detected in CSF
Treatment of aseptic meningitis
Supportive care
Drugs exist for herpesvirus, fungal, and mycobacteria infections
Prognosis of aseptic meningitis
Usually benign, resolves in 2 weeks.
Rare complication: encephalitis
Brudzinski’s sign
Indicative of meningitis
- Neck is so stiff that the knees flex when the neck is flexed
Encephalitis incidence
Rare, ~20,000 cases/year, mainly infants/elderly
Causes of encephalitis
Exposure to virus –> influx in immune cells in brain –> cerebral edema destroys neurons –> intracerebral hemorrhage (distinguishing feature from meningitis)
Symptoms of encephalitis
Altered mental status, fever, headache, vomiting, photophobia, stiff neck, confusion, sleepiness, irritability, stumbling
Urgent: unresponsiveness, coma, seizures, muscle weakness, paralysis, memory loss, flat affect, withdrawal, poor judgment
Diagnosis of encephalitis
Spinal tap indicates inflammation in CSF, may be blood or virus. PCR is gold standard.
- EEG for seizures
- Brain MRI or CT may show foci of inflammation or hemorrhage
Treatment of encephalitis
Supportive care and symptom relief
Antivirals for herpes, antiseizures, anti-inflammatories, sedatives
Prognosis of encephalitis
Ranges from benign with full recovery to severe, fatal
Pathogenesis of viral CNS disease
- Death of neurons – cytolytic viruses can directly kill tissues
- Host factors: age - infants/elderly. Immune status, genetics, activity
- Acute disseminated encephalomyselitis (ADEM) - postinfectious encephalitis follows viral infection by 1-2 weeks. Associated w/ measles, mumps, VZV, influenza, parainfluenza viruses. Autoimmune.
Herpesviruses
HSV2»_space; HSV1
- also VZV, CMV, EMV in immunocompromised
- in weak host, CNS infections progress to severe encephalitis
- treat HSV and VZV aggressively with acyclovir
HSV1 encephalitis prevalence
The most common cause of sporadic viral encephalitis (10-20% of all cases)
HSV1 encephalitis routes of infection
Primary HSV1 in oropharynx –> trigem –> CNS
Recurrent HSV1 –> trigem –> CNS
Reactivation “in situ” HSV1 –> CNS
HSV1 encephalitis symptoms
altered mental status, focal cranial nerve deficits, hemiparesis, slurred speech, stumbling, seizures, fever
HSV1 encephalitis Dx
Gold standard: PCR of CSF for HSV and other viruses
MRI shows predominantly unilateral temporal lobe abnormalities
Pathogenesis of rabies
- Transmitted by saliva via bite from rabid animal or by aerosols in caves populated by infected bats
- Replicates in muscle at bite site
- Incubation weeks-months
- Infects peripheral nerves, travels to brain
- Replication in brain causes hydrophobia, seizures, hallucinations, paralysis, coma, death
- Spreads to salivary glands from where it is transmitted
- Postexposure immunization can prevent disease due to long incubation period
Picornaviruses transmission
enteroviruses are fecal-oral
Picornavirus risk factors
Poliovirus –> young kids asymptomatic/mild disease, older kids + adults asymptomatic to paralytic.
Coxsackievirus and enterovirus–> neonates
Distribution of picornaviruses
- Ubiquitous, poliovirus nearly eradicated
- Enteroviruses more common in SUMMER
Vaccines or antivirals for picornaviruses
Poliovirus: live oral or inactivated polio vaccine
- No vaccines/antivirals for other enteroviruses, rhinoviruses
Picornavirus dissemination
Replication in oropharynx and intestine –> lymph node –> blood –> skin, muscle, brain, meninges
Togavirus examples
VEE, EEE, WEE, Chikungunya, Rubella
Togavirus dissemination
Skin –> blood –> macrophages + spleen, lymphnodes –> brain
Flaviviruses that cause encephalitis
Japanese encephalitis, West Nile, St. Louis encephalitis, Russian spring-summer encephalitis, Powassan virus
Flavivirus dissemination
Mucosal surface –> lymph node –> primary viremia in blood –> vascular endothelium, macrophage, liver, spleen, lymph node –> secondary viremia causing encephalitis, yellow fever hepatitis, hemorrhagic fever
Flavivirus transmission
Mosquitos, ticks
Flavivirus distribution
Determined by habitat of vector: Aedes mosquito is urban, Culex is forest and urban
More common in SUMMER
Flavivirus vaccines/antivirals
- Live attenuated vaccine for yellow fever and Japanese encephalitis
- No antivirals
West Nile meningoencephalitis
-
