Thirty Two Flashcards
What are 3 types of acute CNS infection?
• Meningitis: inflammation/infection of the
meninges, ependyma, or subarachnoid
space
• Encephalitis: inflammation/infection of the
brain parenchyma with clinical evidence of
neurologic impairment
• Meningoencephalitis: combination of the
above
What is viral meningitis like? What is its epidemiology? What is its entry and spread? What are its symptoms? What is its outcome? What kinds of viruses normally cause it?
Viral Meningitis
Viral meningitis is also known as “aseptic meningitis” because cultures of CSF on
bacteriologic medium are negative. Thus, these infections cannot be treated with
antibiotics. Usually a low inflammatory response (lymphocytes) is present.
Epidemiology: Viral meningitis is common, with >36,000 cases/yr in the U.S.
The actual incidence is probably double that amount because mild cases often go
unreported. Note that the etiology of a large proportion of viral meningitis is unassigned.
Entry and Spread: Entry via fecal-oral route, aerosols, or insect vectors. The
level of viremia is often important. Viruses causing meningitis typically infect
endothelial cells, then the choroid plexus epithelium, then are released into the CSF and
spread to the meninges.
Symptoms: include headache, stiff neck, and nausea due to the inflammatory
response. A low to moderate, mostly lymphocytic infiltration may be noted in the CSF.
Outcome: usually benign and self-limiting, resolving in 10 days or less.
Enteroviruses (Coxsackie, Echo, Polio) cause 3/4 of aseptic meningitis in which
an organism is identified. Encephalitis is rare. Infections tend to be seasonal. Virus
spreads via the blood from a primary site of infection, such as the lungs or intestinal tract.
What are two pathogeneses of encephalitis? What happens in each? What signs occur in each?
• Pathogenesis – intraaxonal - organism replicates in peripheral tissue
- ascends peripheral nerves to the CNS
- follows neural tracts in the CNS, causing focal signs
• Pathogenesis – blood-borne
- organism replicates in blood cells or peripheral tissue
- spreads into parenchyma through capillary endothelia,
causing more diffuse signs
What are the symptoms of acute encephalitis? What is the outcome?
Symptoms: In milder cases, these include headache, irritability and/or lethargy.
Severe cases often present with sudden and severe headache and fever and rapidly
progress to confusion, disorientation, drowsiness, seizures, and/or altered behavior and
consciousness. Symptoms are due to destruction of neurons and inflammation.
Drowsiness, weak muscles, a clumsy and unsteady gait may occur with certain viruses.
Meningitis may also be present, and thus symptoms may include vomiting, photophobia,
stiff neck and back. Loss of consciousness or sudden dementia can also occur.
Outcome: In severe cases mortality can be high if untreated or not promptly diagnosed. Long-term neurological deficits may result.
What is the most common causative agent of intraaxonal viral encephalitis? How severe is it? What subtype are most adult cases? How does it usually happen? What occurs in neonatal infections?
Herpes simplex virus (HSV) – is the most common causative agent (0.2 cases/100,000 persons per year or ~1,200 cases) and the most severe. (Mortality rate from encephalitis is 70% if untreated, with serious neurologic sequellae in survivors.) Most adult cases are with HSV-1, occurring during primary infection or during reactivation from its latent state within the trigeminal ganglia. Neonatal infections with more generalized encephalitis can be due to HSV-2 acquired during birth (~800 cases per year).
What are some ways in which VZV can present in the CNS?
Varicella-Zoster virus (VZV) – can reactivate from latency in dorsal root ganglia to cause
shingles. The most common CNS syndrome is hemorrhagic necrosis and inflammation
of the dorsal root ganglion associated with shingles, with mild to severe neuropathy.
VZV encephalitis may present as stroke and is usually delayed relative to the appearance
of shingles. VZV also may disseminate during primary infection of immunosuppressed
individuals to cause fatal encephalitis.
What is an example of blood borne virus that can cause severe meningoencephalitis? What is the most common presentation? What are the symptoms? How does it present in AIDS patients?
Cytomegalovirus (CMV) is another herpesvirus infection can cause severe
meningoencephalitis when virus spreads transplacentally to the fetus (occurs in 1/10
symptomatic infections). Intracranial calcifications resulting in retardation are common,
as is sensorineural deafness. Hydrocephalus and microcephaly are frequent. jaundice, hepatosplenomegaly, petechial rash
- cytomegalic inclusion body disease (CID)
CMV encephalitis in AIDS patients is highly associated with retinitis, and often shows abrupt
onset and rapidly progressive confusion and lethargy.
Waht are 3 microbes that cause post infection encephalitis? How does it work? What are the signs?
- EBV, CMV and measles
- Immune-mediated
- Causes diffuse, multifocal demyelination
How does an arthropod borne virus reach the CNS? What are the initial symptoms like? Later symptoms? What is the CNS attack rate? When do infections occur? How is it age dependent?
Virus is injected directly into the bloodstream from the bite of an infected
arthropod. Virus replicates in peripheral sites and seeds the bloodstream. High titer
viremia assists virus in crossing the blood-brain barrier through ependyma made leaky by
cytokine release. Most infections are subclinical. Symptomatic infections often begin
with flu-like symptoms. The CNS attack rate is low to moderate.
Infections are seasonal due to the lifecycle of the insect vector
Patients develop fever, headache, stiff neck, and sometimes nausea and vomiting,
followed by altered consciousness and seizures. Disease is typically age-dependent;
young children and elderly more commonly develop encephalitis with worse prognosis
and greater neurologic residua than older children and adults. Mortality and severity of
long-term neurologic dysfunction in survivors varies greatly among the viruses.
These may sometimes cause meningitis without encephalitis
What is the epidemiology of Japanese encephalitis? What is the prodromal period like? What are the symptoms? Prognosis? Is there a way to prevent it?
Japanese encephalitis (JE) is the most significant arbovirus encephalitis world-wide,
causing nearly 70,000 infections (30-50,000 neuroinvasive infections) yearly. JEV is
common in rural SE Asia and is spreading. Encephalitis is most common in children and
follows a 2 to 3 day prodrome of fever, chills, and malaise. Symptoms include headache,
sustained fever, photophobia, confusion, delirium, and focal or diffuse weakness. Tremor
is present in almost all patients. Seizures are common in children. Mortality rate is up to
1/3 of patients, with paralysis or permanent neurological sequellae occurs in up to half of
survivors. A vaccine is available but expensive, requires multiple doses, and 5-10% of
vaccinees experience adverse reactions.
What occurs in 20% o f those infected with West nile virus? In only 1%? What is the mortality rate of both groups? Who is at the greatest risk? When is the peak onset?
• West Nile Fever – 20% of those infected
fever, headache, fatigue, myalgia, nausea, occasional rash
• West Nile Encephalitis – 1% of those infected
high fever, headache, stiff neck, muscle weakness, disorientation,
tremors, convulsions, paralysis, stupor, coma
Mortality (U.S.) ~4% of those with fever (10% of encephalitis cases)
> 50 yrs old and immunocompromised at greatest risk
Symptom onset peaks in late summer
