viral infections of the CNS Flashcards
routes of viral infection of the brain
hematogenous, neuronal
sterile meningitis causes
virus, fungi, TB, infections near the CNS.
80% are enteroviruses, 10% are HSV 1/2, 10% arboviruses,
symptoms of viral meningitis
mental status normal (compare with encephalitis), HA, fever, chills, stiff neck, malaise, sore throat, nausea, vomiting, abdominal pain, photophobia.
diagnose viral meningitis
elevated lymphocytes in the CSF (no bacteria) viruses can be detected in the CSF.
treatment for viral meningitis
supportive care. there are drugs for herpes, and fungal.
prognosis for viral meningitis
usually benign and resolves in 2 weeks, encephalitis is rare complication.
nuchal rigidity sign for meningitis
brudzinski sign. the neck is so stiff that the knees flex when the neck is forcefully flexed.
encephalitis
brain inflammation. rare. mainly in infants and elderly.
causes of encephalitis
virus, influx of immune cells to the brain, cerebral edema, intracerebral hemorrhage distinguishes this from meningitis.
symptoms of viral encephalitis
altered mental status, fever, HA, vomiting, photophobia, stiff neck and back, confusion, sleepiness, irritability, stumbling.
urgent symptoms of encephalitis
unresponsiveness or coma. seizures, muscle weakness or paralysis. memory loss, flat, affect, withdrawal, poor judgment.
diagnosis of viral encephalitis
tap indicates inflammation of the CSF, PCR is gold standard, EEG for seizures, MRI and CT can show foci of inflammation or hemorrhage.
treatment for viral encephalitis
supportive care and symptom relief. can give antivirals (acyclovir) for HSV. anti seizure meds such as dilantin, anti-inflammatory tend to decrease the cerebral edema. sedatives.
prognosis of viral encephalitis
can be benign or severe. some total recovery
permanent damage of systems can results.
pathogenesis of viral encephalitis
cytolytic viruses directly kill neurons/tissues. death of neurons.
host factors that effect viral encephalitis
age and immune status (young and elderly more susceptible), genetics (innate differences in susceptibility).
what affect does activity have on the dissemination of viral infections?
exercise and activity cause further dissemination of viral infections to the CNS
acute disseminated encephalomyelitis
post infectious encephalitis following viral infection 1-2 weeks. associated with measles, mumps, VZV, influenza, parainfuenza virus. this is an autoimmune disorder.
examples of neuronal spread
herpes (alpha-viruses), rabies
fecal-oral spread examples
picornaviruses (enteroviruses)
insect vector virus example
flavivirus, togavirdae viruses (arboviruses)
which herpes virus causes meningitis/encephalitis
HSV-2»HSV-1 to cause meningitis. HSV-1 most common cause of sporadic viral encephalitis.
HSV-1 encephalitis
most common. 10-20% of all cases.
treatment of herpes encephalitis
aggressive treatment with acyclovir.
routes of infection for herpes encephalitis
primary -oropharynx > trigeminal nerve > CNS
recurrent -trigeminal nerve > CNS
also can reactivate in situ (or in the CNS)
signs and symptoms of viral encephalitis
altered mental status, focal cranial nerve deficits, hemiparesis, slurred speech, stumbling, seizures, fever.
diagnosing herpes encephalitis
PCR of CSF, brain imaging shows predominant unilateral temporal lobe abnormalities.
rabies virus transmitted
through the bite of an infected animal or by aerosols in caves populated by infected bats.
what happens after the rabies virus gets into the body through a bite?
it replicates in muscle. incubation period is about weeks to months. it then infects peripheral nerves and uses them to travel to the brain.
what symptoms occur when the rabies virus gets to the brain?
it replicates in the brain causing hydrophobia, seizures, hallucinations, paralysis, coma and death.
how can we prevent rabies?
postexposure vaccination can prevent disease because of its long incubation period.
rabies virulence/transmittance summary
virus inovulated > replicates in muscle > enters peripheral nervous system > replicates in the dorsal root ganglion > rapidly ascend the spinal cord > infects the spinal cord, cerebellum, brain stem
picornavirus examples
poliovirus, coxsackie, echovirus, enterovirus, rhinovirus. many of these cause paralytic disease, meningitis and encephalitis.
transmission of picornaviruses (enterovirus)
fecal-oral route.
populations at risk for enterovirus
poliovirus: young children (asymptomatic to mild disease) older children, adults (mild to paralytic disease).
coxsackie and enterovirus: newborns and neonates at highest risk.
what times of the year are more prevalent for these viruses?
polio is ubiquitous but almost completely irradiated.
enteroviruses are more common in the summer.
are there vaccines for picornaviruses?
poliovirus has a vaccines live oral or inactivated. not vaccines or antivirals for others.
dissemination of the picornaviruses
oral > replicates in oropharynx and intestine > lymph node > blood > skin, muscle, brain, meninges, etc.
when picornavirus reaches the skin what happens?
can cause hand-foot-mouth disease, rash, herpangina. (coxsackie)
when picornavirus reaches the muscle what happens?
(echovirus, coxsackie A/B) reach the heart and thorax can cause pericarditis, myocarditis, and pleurodynia.
when picornavirus reaches the brain what happens?
(polio and coxsackie A/B) cause paralytic disease to encephalitis.
when picornavirus reaches the meninges what happens?
echo, polio and coxsackie all cause meningitis
togavirdae examples
Venezuelan equine virus, eastern and western equine, chikungunya, rubella.
VEE vector and disease
ades and culex mosquitoes. causes mild systemic and severe encephalitis
EEE vector and disease
aedes and culiseta mosquitoes. causes mild systemic and encephalitis
WEE vector and disease,
culex and culiseta mosquitoes. mild systemic and encephalitis.
chikungunya vector and disease
aedes mosquitoes. fever, arthralgia, arthritis.
rubella vector and disease.
no vector causes rubella.
EEE vectors, hosts and dead end hosts
hosts are birds, vectors are the aedes and culiseta mosquitoes. dead end hosts are horses and people.
flavavirdae that cause encephalitis. examples
Japanese encephalitis virus. west nile, st, luis encephalitis virus, russian spring summer, powassan virus.
JE vector and disease
culex mosquitoes, encephalitis
west nile vector and disease
culex mosquitoes, fever, encephalitis, hepatitis
SLE vector and disease
culex mosquitoes, encephalitis
russian spring summer vector and disease
ixodes, dermacenter ticks; encephalitis
powassan vector and disease
ioxdes ticks; encephalitis
where are aedes mosquitoes found?
urban areas.
culex mosquitoes found where?
urban areas and forest areas.
the transmission of falviverdae is more common when?
when the vectors are outside and people are also outside. AKA summer.
which of the flaviverdae have vaccines?
yellow-fever and JE. no antivirals.
how are the flaviviruses disseminated?
mucosal surfaces > lymph > primary bactermia > various tissues (vascular endothelium, macrophages, liver, spleen, etc) > secondary bacteremia > encephalitis, yellow fever hepatitis, hemorrhagic fever.
WNV meningoencephalitis symptoms
occurs in 1% of WNV infections. HA, fever, stiff neck, disorientation, coma, tremors, seizures, paralysis
WNV meningoencephalitis high risk pops.
cancer, diabetes, HTN, kidney disease.
WNV meningoencephalitis prognosis
recovery over weeks to months. some of the neurological effects are permanent. mortality is 10%
summer/fall meningitis virus
enteroviruses: coxsackie, echovirus, polio.
summer/fall encephalitis viruses.
WNV, SLE, EEE, WEE, california encephalitis
winter/spring meningitis viruses
mumps, lymphocytic coriomeningitis virus.
winter/spring encephalitis viruses
measles, mumps.
any season meningitis viruses
HSV-2, HIV infection
any season encephalitis viruses
HSV-1, HIV
