L40- Nervous System and Special Senses Infections III Flashcards
(35 cards)
Encephalitis:
- (1) definition
- (2) are the most common causes of primary form
- (3) = secondary cause
1- inflammation of brain parenchyma
2- Viral: HSV-1/2, Arbovirus, Enterovirus
3- ADEM (acute disseminated encephalomyelitis) occurs post-infection and results from an autoimmune attack on myelin
Encephalitis:
- (1) is the major criterion for Dx
- (2) are the other minor criterion
1- Altered Mental Status: impairment of consciousness, memory, mental status
2:
- fever w/in 72hrs of presentation
- seizure
- CSF w/ pleocytosis
- imaging with evidence of parenchymal inflammation
name the associated pathogen with the following unique sign seen in each encephalitis:
- (1) grouped vesicles in dermatomal pattern on skin
- (2) parotitis
- (3) flaccid paralysis
- (4) hydrophobia, aerophobia, pharyngeal spasms, hyperactivity
- (5) tremors in eyelids, tongue, lips, extremities
1- VZV 2- mumps 3- WNV 4- rabies 5- WNV, SLV (st. louis)
Meningitis, indicate if present or absent:
- (1) fever
- (2) HA, lethargy, n/v
- (3) photophobia, neck stiffness
- (4) seizures
- (5) CN palsies
- (6) altered mental status
1- yes 2- yes 3- yes 4- minimal 5- no 6- minimal
Encephalitis, indicate if present or absent:
- (1) fever
- (2) HA, lethargy, n/v
- (3) photophobia, neck stiffness
- (4) seizures
- (5) CN palsies
- (6) altered mental status
1- yes 2- yes 3- no 4- yes 5- yes 6- yes
name the associated pathogen with the following imaging seen in each encephalitis:
- hydrocephalus suggest encephalitis caused by (1)
- (2) involvement of temporal lobe
- (3) involvement of basal ganglia
1- non-viral cause (bacteria, fungal, parasite)
2- HSV
3- respiratory virus infection, Creutzfeldt-Jakob disease, arbovirus, Tb
(1) is the most common cause of encephalitis, ~10% of all cases:
- (2) describe mortality
- commonly affects (3) age group
1- HSV: 1 > 2
2- >50% if untreated
3- any age
describe the clinical presentation of HSV encephalitis- include affected brain regions
-HA, fever for up to 5 days
- personality / behavioral changes –> frontal lobe damage
- memory, speech problems –> temporal lobe damage
-seizures, hallucinations, altered levels of conciousness
Powassan encephalitis:
- (1) describe microbe
- (2) incubation period
- (3) Sxs
1- (rare- US, Canada) Arbovirus transmitted via ticks
2- 7-10 days after bite
3- HA, fever, nausea, confusion, partial paralysis, coma, seizures
describe the progression of infections that cause Brain Abscess — include affected area of brain parenchyma
Hematogenous Seeding
Contiguous Spread:
- subacute/chronic otitis media –> inferior temporal lobe, cerebellum
- frontal / ethmoid sinuses –> frontal lobe
- dental infections –> frontal lobe
Note- most are polymicrobial
brain abscess Sxs
- HA, 90%
- mental status changes, 67%
- hemiparesis, 61%
- fever, 57%
- papilledema, 56%
describe brain abscess Dx (importantly indicate what procedure is contraindicated) and Tx
Dx: CT / MRI
NO LUMBAR PUNCTURE => herniation
Tx: drainage
______ is the most common cause of acute viral myelitis
- Enterovirus: poliovirus
- Flavivirus
- some others
Poliovirus: family, genus, genome, structure
picornaviridae- enterovirus
- (+)ssRNA
- non-enveloped
list the different diseases caused by Poliovirus
1) abortive poliomyelitis: non-specific Sxs: fever, HA, sore throat, anorexia, vomiting, abdominal pain
2) non-paralytic poliomyelitis – aseptic meningitis
3) paralytic poliomyelitis (abortive –> paralysis), <2% of cases
describe progression of paralytic poliomyelitis
<2% cases, Biphasic:
1) Minor Illness / Abortive Poliomyelitis: (non-specific Sxs)
- fever, HA, sore throat
- anorexia, vomiting, abdominal pain
2) Major Illness:
- Meningitis –> Myalgia –> weakness and asymmetric flaccid paralysis
- some groups more involved than others
- respiratory compromise is primary complication
describe Polio prevention
1) inactivated polio vaccine / Salk vaccine:
- IPV given IM, in countries w/o WT-virus
2) live oral attenuated polio vaccine / Sabin vaccine
- OPV is live virus
- given orally –> replicates in GI –> Ab production –> virus is evacuated in BM
- **small risk of associated paralytic disease — VAPP = vaccine associated paralytic polio (WT reversion)
Clostridium botulism microbial features, sources, toxin MOA
anaerobic **spore-forming Gram+ rod, β-hemolytic
Sources:
- Food: poorly canned vegetables OR contaminated honey given <1y/o
- wound contamination
- infection from organism / toxin
Botulinum –> binds presynaptically in NMJ –> prevent ACh release => flaccid paralysis
Clostridium botulism clinical presentation, Tx, and laboratory studies
(ingestion of toxin) —> flaccid paralysis OR death –> Tx with anti-toxin + supportive care
- isolation via wound, stool // toxin detection in blood, stool, food
- Note- may not seen as infection travels fast
- β-hemolytic
Clostridium tetani microbial features
anerobic Gram+ rod
motile, spore forming
catalase-
describe pathogenesis and MOA of C. tetani toxin
1) C. tetani acquired via injury with infected device (eg. rusty nail)
2) anaerobic environment => spore germination
3) Tetanospasmin (neurotoxin is released)
4) binds presynaptic membrane in NMJ
5) internalized –> transported to spinal cord
6) blocks release of glycine / GABA => no inhibition of NMJ
7) spastic / rigid paralysis
list the forms of Prion disease and indicate most common diseases
Sporadic:
- **sporadic Creutzfeldt-Jakob disease (sCJD, *85-95% of all cases)
- sporadic familial insomnia (sFI)
Familial:
- **familial CJD (*5-15% of all cases)
- fatal familial insomnia (fFI)
Acquired: eg. Kuru
list the common neuropathological features of TSEs
- neural loss
- proliferation of glial cells
- absence of an inflammatory response
- presence of small vacuoles w/in neuropil => spongiform appearance
describe the protein changes in TSEs
PrP(Sc) scrapie prion protein — originally PrP(c)
-α-helix –> β-sheets, indigestible
