32 Viral Flashcards
Predictors of bacterial meningitis:
- Low CSF glucose
- High CSF protein
- High CSF WBC count
- High CSF neutrophil count
can present similarly to viral meningitis:
partially treated bacterial meningitis
clinical course of viral meningitis:
self-limited, with complete recovery in 7-10 days
Appearance of a patient with viral meningitis?
does’t appear extremely ill (not encephalopathic)
- Fever & malaise
- HA
- Neck stiffness
- Low back pain (overshadowed by HA)
Outcome for a patient with viral meningitis?
resolves without significant neurologic sequalae
Recurrent viral meningitis can result from:
persistent or latent infections
Viruses causing meningitis:
80% caused by enterovirus (Echo, Coxsackie, Enterovirus 71)
10% attributed to Mumps (without MMR vaccine)
Viruses causing recurrent aseptic meningitis:
HSV-2 (genital herpes), HIV, VZV
Viruses causing Viral encephalitis:
arborviruses
enteroviruses
HSV-1
Transmission of arbovirus?
mosquitos, ticks (**seasonality)
MC affected by arbovirus?
old + young
Cause of enterovirus inf?
family
Types of HSV encephalitis?
acute
reactivated latent
Characteristic site of damage in HSV encephalitis?
Lab/imaging?
temporal lobe
necrosis in temporal lobe, RBC in CSF
Dx of HSV encephalitis?
PCR (false neg happen though)
Prognosis of HSV encephalitis?
Curable if treated early
Devastating if treatment is delayed
Structure of Flaviviridae?
Small, enveloped, nonsegmented, (+) strand RNA
Diseases caused by Flaviviridae?
Flaviviruses: St. Louis encephalitis, West Nile, Japanese encephalitis
Hepatitis C virus
Replication of Flaviviridae?
a) R-mediated endocytosis –> nucleocapsid delivered into cytoplasm following pH- dependent fusion
b) RNA translated by host ribosomes –> polyprotein –> cleaved by a combination of viral (cis-cleavage) and host (trans-cleavage) proteases
c) Viral polymerase replicates genomic RNA
d) Structural proteins (capsid and envelope glycoproteins) assemble genomic RNA into virions –> bud into ER/Golgi –> enveloped viruses released during transport at cell surface
What is notable about genome of Flaviviridae?
contains 5’- cap
Transmission of Flaviviridae?
insect vectors
Initial location of Arbovirus replication?
site of inoculation (endothelium or epithelial cells
surrounding bite site) and establish transient primary viremia
Location of Arbovirus replication 3-7d post-exposure?
macrophages, spleen, or lymph nodes
Progression of arbovirus infection?
- mild systemic disease (most infections do not progress beyond this point)
- If infection not controlled by immune response, secondary viremia ensues and results in severe systemic disease (e.g. encephalitis)
Geographical location of St. Louis encephalitis epidemics?
North, Central, and South America
Colorado, California, Florida, Texas, and Arkansas
Clinical syndromes that occur with St. Louis encephalitis?
1) Febrile headache
2) Aseptic meningitis
3) Encephalitis
Onset of StLE is characterized by:
- generalized malaise, fever, headache, sore throat or cough
- followed in 1 to 4 days by acute or subacute meningeal and neurological signs
The most effective means of control of StLE is:
reduction of the mosquito vector population.
Symptoms of a mild form of West Nile virus?
febrile HA
myalgia
occ. rash + LAD
Symptoms of a severe form of West Nile virus?
- Severe HA with high fever
- Neck stiffness, muscle weakness
- Stupor, disorientation, convulsions, tremors
- Coma, paralysis, and, rarely, death.
Structure of Togaviridae?
Small, enveloped, nonsegmented, (+) strand RNA viruses
Types of Togaviridae?
Rubiviruses (Rubella)
Alphaviruses
Initial site of replication of Togaviridae?
muscle + fibroblasts of numerous organs
Progression of Togaviridae?
infection –> repl in muscle/fibroblasts –> viremia w/ CNS invasion –> neuron destruction
Symptoms of Togaviridae?
- fever x2wks
- Dizziness + Incr LOC
- Encephalitis w/ coma –> death
Structure of Bunyaviridae?
Enveloped, spherical particles with segmented (2-3), single-strand, negative-sense RNA
genomes
Types of Bunyaviridae causeing CNS infections?
a) California encephalitis virus
b) La Crosse encephalitis virus
Location of replication of Bunyaviridae?
exclusively in the cytoplasm
mRNAs are not spliced
MC cause of rboviral-induced pediatric encephalitis in the U.S.?
Symptoms?
LaCrosse virus
seizures and focal neurological signs
Structure of Rhabdoviridae?
Enveloped, nonsegmented, negative-strand RNA viruses
“bullet-shaped”
Human disease-causing genera of Rhabdoviridae?
Vesiculoviruses –> vesicular stomatitis virus
Lyssaviruses –> rabies virus
Replication/dissemination of Rhabdoviridae?
- enters muscle cells (pH-dependent manner following endocytosis)
- transported through periph sensory nerves to spinal ganglia (neuronal cell replication)
- travels up spinal cord, disseminates once reaches brain
During the final stages
of the disease, Rabies Virus is found replicating in high concentrations in:
the salivary glands
Efferent nerves transport virus to the submaxillary salivary glands
Primary mechanism of Rabies spread?
saliva (animal bite)
open wound
Prognosis of untreated Rabies?
death
Once infected, Rabies virus predominates in:
neurons of the limbic system, midbrain, and hypothalamus.
Phases of Rabies symptoms?
- Prodromal (mild, nonspecific symptoms; abn sensation around bite)
- Acute neurologic phase (anxiety, agitation, paralysis, delirium, hydrophobia)
- Coma (up to 30 days, death from resp arrest)
Trx of Rabies?
washing of the wound
instillation of wound with human anti- rabies Ig
administration of multiple doses of inactivated vaccine (thigh or deltoid)
Why is vaccination an effective trx?
long incubation period
Structure of arenaviridae?
- Enveloped
- Contain 2 ambisense RNA segments (encoding 4 proteins)
- Often contain host cell ribosomes
Cell entry of arenaviridae?
pH-dependent pathway following endocytosis
Replication of arenaviridae?
nonconventional “ambi-sense” transcr/transl:
- Either L (long) or S (short) RNA segment used as a template for transcription –> NP and L mRNAs
- polymerase then produces a full-length antigenome for each of the segments
- ”(+)”-sense antigenome used as a template for transcription of the glycoprotein mRNA
- Assembly + release via budding
Transmission of arenaviridae?
inhalation of aerosolized virus from rodent excreta and saliva
Progression of Lymphocytic choriomeningitis virus infection?
- ever, headache, nausea, and vomiting
which coincides with viremia - aseptic meningitis usually begins about 10 days later
Possible side-effect of Lymphocytic choriomeningitis virus infection?
sudden-onset deafness can occur during the meningeal phase
Neurologic complications occur in __% of AIDS patients
40
Direct neuro effects of HIV inf?
- Acute aseptic meningitis (at seroconversion)
- Chronic meningitis
- HIV dementia complex
- Vacuolar myelopathy
- Peripheral neuropathy
- Cranial neuropathy
- Inflammatory myopathy
Indirect neuro effects of HIV inf?
- opportunistic infections (CMV encephalitis, PML, etc)
- Neoplasms (1’ CNS lymphoma, metastatic Karposi’s)
- Nutritional and metabolic disorders (drug toxicity of anti-retrovirals)
