• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/192

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

192 Cards in this Set

  • Front
  • Back
Viral encephalitis 90% of the tiem is
West nile virus
EEE locale
Swamps
EEE outcome
High case fatality disease
WEE locale
Pastures and flooded areas
Wee age
<10
WEE reservoir
Birds/Horse and small mammall
SLE locale
Flava-Flave, duh, it's in the urban areas
SLE age
>40 or infant
SLE reservoir
only in people?
SLE locale
Midwest Urban
WNV reservoir
BIrds
WNV keywords
Kills birds, draught, viral encephalitis
MAC-ELisa test
Egm test for WNV
WNV cross reacts w/ what viruses
yellow, dengue, StLE
Causes flacid paralysis syundrome
WNV/Botulism in infants
unilateral polio
major sx of WNV
Flacid paralysis
WNV age
>50
Increases with draught
WNV
CAE reservoir
Small mammal
Day feeding mosquito
CAE
La Crosse serogroup
CAE
Squirrel/chipmunk
Colorado Tick Fever
CTF (possibly WEE)
Saddle back fever pattern
CTF
REOvirus
CTF
CTF fever temporal pattern
2-3 days fever
2-3days no fever
2-3 days fever
Flaccid asymmetric paralysis
Poliovirus
Polivirus pahtogeneisis
enters via M cells in Gi to CNS
5'IRE gets into cells, kills host cells
no latent period
5' IRE
poliovirus
Polio latency period
none
5 polio states
1- inapparent infection
2- Abortive illness
3- Non paralytic polio
4- Paralytic poli
5- post- polio syndrome 30-40yrs post infection
Noparalytic polio sx
stiff=neck and back
2-10 days w/ spontaneous resolution
Abortive polio sx
Fever and maiaise, spontaneous recovery
Paralytic poli
Flacid paralysis, LMN damage, bulbar form\
Respiratory failure (iron lung)
Post polio syndrome
30-40 yrs post infection
gradual clinical course of the bulbar form poliovirus
Resp faiilure
Polio pathogenesis
Kills neuron -bulbar form leads to respiratory failure/paralysis
Early polio vaccine associations
SV40- cancer causing virus found in polio vaccine
PML
SV40, or PML post shot
Poliovirus vaccine
Salk vaccine
inactivated polio
Enhanced potency vacine IPV
Trivalent- need Ab for all 3 to givve immunity
Sabin vaccine
Live polio vaccine
Rhabdovirus
Rabies- bullet-shaped
ssRNA
REabies prodrome
fever reffered to the area of the bite
Excitatory phase of rabies
anxiety, hydrophobia, coma, HTN and death
negri bodies
Rabies
Rabies Tx
Human Rabies immunoglobulin (HRIG)
Human diploid cell vaccine (HDCV)
Sporatid fatal encephalitis
HSV1,2
Neonates, <20, >40
Neonate Sporadic fatal encephalitis Sx general
Lethargy, Irritablity, tremors, poor feeding, 4-11d post delivery
neonate sporadic fatal encephalitis Sx specific
Skin lesions- conjunctivits
focal encepalopathy
Frontal and temproal head deformities
Tzanck smear
Fluorescent Ab test for HSV1/2 encephalitis
HSV encephalitis ages/agents
HSV1- adult reactivation
HSV2 (sexual) neonates
HSV tx
Acyclovir
Sheep Prions
Scrapie and Visna- give animals chronic pneumonia and they scrape their butts on rocks
PRPsc
prion responsible for progressive neruological diseases
Mad cow
oral consumption
CJD sx
Dimetnia w/ataxia and seizures
CJD demographic
Incubation ~15 months
Pt 60-70yrs
CJD transmission
Corneal trasnplant, neurosurgery equip, pituitary derived GH
papua New Guinea
CJD/KUru
Pt presents with dimentia/ ataxia/ seizures
CJD mediated
Sporadic CJD
Horizontal transfer from infected individual
direct innoculation
New Variant CJD
Human mad cow disease
Amyloid and halospongiform degeneration
First starts at tonsils
Young Pt
BSE
Amyloid plaque
NVCJD and KURU
Cannibalistic feeding
KURU
Prion transmission (infectous protein)
Blood
Prion pathogenesis
enter through M cells of GI and course to Lymphatics
Prion identification
western blot
Lysis of oligodendrocytes
PML
JC virus infected
PML pathogensis
Immuno system compromised individuals with JC virus
(MS on immune depression drugs)
MS histology characterisitc
Patchy lesions of white matter
young adults
PML sx
mental/ neurological sx
MS tx
Natalizumab
for the slow relapsing form of MS
MS sx
Relapsing, intermiitent course, chronic progression
neurological Sx of burning, pain, photophobia
HIV neurological charactgeristics
With meatter disease, indirect destruction of nerve cells, viral proteins provoke the host response
HIV CNS affects
cognitive and motor issues
Two causes of cyrptococcul meningio-encephalitis
Neoformans and Gatti
where is C Neoformans found?
Bird poo
Produce Laccase
C Neoformans and Gatti
C neoformans Course
Start with skin move to lungs progress to CNS
C. Neoformans identifiers
Bird seed agaer
CBG- Yellow
C Neofrormans Trasmx
inhale yeast cells
C Gatti identifiers
Bird seed agar
CBG- BlueI
Form melanin
Gatti and neoformans
Infects iummuno competent
Crytptococcal meningoencephalitis- C Gatti
C Gatti, Neoformans Cryptococcal meningioencephalitis Sx
Pulmonary infection
flu then fever
headache
Stiff neck
Tigondii Morphology 3-
Bradyzote- chronic disease
Tachyzote- acute and proliferative disease
Zotocyst
Toxoplasmosis Sx
Triad
1- Chorioretinism
2. Hydrocephalius
3. Intracranial calcifications
Toxoplasmosis infectious stage
Cyst form
Zotocyst
Cats while pregnant will give you friggin
toxoplasmosis
Toxoplasmosis Tx
Pyrmine-Thyamine
Sulfadizine
PAM agent
primary acute miniingioencephalitis
Naegleria Fowleri
Naegleria fowleri morph
1-cyst
2- Trophozite (flagellate)
3- Ameboid- sex form
PAM sx
Sever brian infection
-fever, stiff neck
seizure with necrosis
Headache, CNS inflammation
Confusion, Hallucinations
PAM course
infect w/ flagellate trophozite
Sx in 1-14 days,
rapidly fatal
PAM pahtogenesis
enters nasal passage (Can change smell) transforms to ameboid form
travels up olfactory nerve to brian
has sucker apparatus
Lobopodia
Naegeleria Fowleri sucker apparatus
PAM
Naegleria Fowleri lab
Wet mount
clearing on Eccoli Agar (eats bacteria)
PAM transmission
Warm water- neti pots
can't get from drinking contaminated water
Granulomatous Ameoebic Meningitis
GAM
Acanth Ameboe
A. Castellain, A. Culbertsoni
Acanthamoebae morphology
Trophoxite (infectous form, spike pseudomembrane)
Cyst (wl layered wavy wall- resistant)
GAE sx
Facial paralysis, Trouble swallowing, Seizures, paralysis, double vision
Rapid progression
GAM sx
mental/neurological
Flu-like w/edema
GAM course
inhale cyst
travels in blood to CNS
Incubation is weeks
Death in 7-12 days post manifestation
GAM transmission
Resp tract or broken skin
GAM mortality
100%
infects chronically ill and immunosuppressed
Corneal Scrapings
Acanth Amoebiasis
Contact lenses with corneal damage
Acanth Amoebiasis
often misdiagnosed as ocular herpes
DO eye labs
GAE agent
Balamuthia Mandrillaris
Culture with primate hepatic cells or human brain
GAE balmuthia mandarillaris
GAE transmission
Resp tract or broken skin
GAE infectous forms
Both tgrophoziete and Cyst are infectous,
Increased legionella infection w/ disease
E. Rostratum
Tree fungus that grows at body temeperature
contaminated steroid injection from New England compounding center
Two causes of neonatal meningitis
Strep agalactidae
Ecoli
meningits: maternal OB complications
Strep Agalactidae
First five days (EARLY)
sx: bacteremia, pneumonia, meningitis
Meningitis: no maternal OB complications
Strep Agalctidae
7d-3mo (LATE)
bone joint infection
Group B strep Virulence factors
(normal vaginal flora) Neonatal meningitis
Capsular polysaccharide
Hyaluronidase, collagenase
Leading cause of bacterimia w/ meningitis during delivery
Strep Agalacticae Group B strep
E coli neonatal meningitis
Gram neg bacillis- K1 strain from moms rectum
Leading cause of neonatal meningitis
K1 strain of E Coli Gram neg bacillus
Gram neg non motile pleiomorphic coccobacillus
vs
Gram + motile coccobacillus
HIB
vs
Listeria (facultative)
Listeria virulence factor
Listeosin O
Coronary Artery Transplant
Renal Transplant
Brain stem inflammation
Listeria Monocytogenes
Uncooked/undercooked/ raw food
w/ meningitis sx
listeria
Listeria pathogenesis
T-cell mediated
undercooked food
compromised host
Macrophates and parenchymal cells
In-utero acquired inection
listeria
Lipopolysaccharide vs lipooligosaccharide
LPS- Listerosin O
LOS- HIB cell envelope for attachment
Meningitis w/ epiglotitis and bacterimia
HIB meningitis
non-typable strains
Post URI, Otitis media
HIB meningitis
Capsular antigen in CSF, Serum, Urine
HIB meningitis
Gram + lancet shaped
Strep pneumoniae
Strep pneumoniae VF
anti phagocytic capsule
Purulent meningits ofen phemonia or another infection
Strep pneumoniae
alpha hemolytic
strep pneumoniae
Recurrent meningitis
strep pneumoniae
Mot common cause of meningitis in the elderly
Strep pneumoniae
Strep pneumoniae meningites Prophylaxis
23 valent vaccine (65+0
13 valent vaccine (children)
Fastidious gram negative diplococcus
kidney bean shaped
Nisseria meningiditis
Mild Nisseria Meningitis
Trasnient bacterimia 1-2 days
Sever Nisseria meningitis
Acute meningiococcemia
Rash w/ DIC
Waterhoasu Fredreson
Waterhaus
Nisseria meningiditis- hemmorhagic adrenal infarction in children
from DIC of infection
"nonrewarding" CSF gram stain
Nisseria Meningiditis
Nisseria infection requirements
b/c in nasopharynx has to be patient that is fatigued or has open wound (immunocompromised?)
Brain Abscesses
Bac Fragilis Parameningial infection
NEVER meningitis
obligate anaerobe
Bac Faragilis
Bac Fragilis VF
Neuraminidase, hyaluronidase
LPS: hageman factor
Bac Frag days 1-14 events
1-3: early cerebritis
4-9: late cerebritis
10-13: early capsule formation
14> late capsule formation- abscess
Bac frag parameningitis 3 phases
1: Systemic infection- low grade fever
2: increased intracranial pressure- headache
3: Brain damage- ataxia, aplasia, LOC
Bac Frag Dx
Lumbar puncture
What causes the clinical manifestations of Bac Frag?
Bran Abscess- never from bacterial meningitis
Subdural empyema definition
Pus B/t inner surface fo the dura and outer arachnoidl ayer
Subdural empyema
Polymicrobial parameningial infection
Parameningeal infection
polymicrobial infectiou nn cause
usually from paranasal sinusitis
or otitis media
paranasal sinusits/ bone erosion/ otitis media
Polymicrobial parameningial infection
Polymicrobial parameningeal infection symptoms
All acute
HA
fever
impaired conscousness
Epidural Abscss definition
Pus outsid eth dura w/in the spinal cord
Epidural Abscess
Staph A. Parameningieal infection
Acute S. Aureaus parameningial infection
Purulent necrosis of epidural fat
Chronic S. Aureus parameningeal infection
Dura is grey and thick, fat is replaced by granulation (fibrous?) tissue
Pseudomonas A. parameiningeal infection pathology
Malignant external otitis
infects adjacent tissues including the bone- spreads to parameninges
Staph Aureus prameningeal infection method
Direct extension- perforatory wound
Metastasis through blood
S.A. paramenigeal infection Sx
4 phases
1- back pain
2- nerve rood infection
3- progression of lesion
4- paralysis
malignant external otitis
Swollen parotid
CN VI- XIIparalyis
Psuedomonas A parameningeal infection
Acid fast bacillus, obligate intracellular pathogen
Leprosy mycobacterium
Early leprosy
Asymptomatic- poorly defined hypopigmented macule
anesthesia
TT leprosy
Tuberculate: skin lesion granulomatous and hypopigmented
anestheisa of lesion
BB leprosy
Borderlike skin lesions (looks like ringwork)
LL leprosy
Lepramatous- trauma causes infection hand/food deformities from necrosis
rasied skin lesion with marked anesthesia
Why leprosy affect extermitys?
b/c grows at slightly colder temp than body temp, hence extremities
3yr incubation, tropics
leprosy
G+ terminal spores vs
G+ sub-terminal spores
Terminal- Tetani Tennis Racquet
Sub- Botulism
tetani VF
Toxin
Plasmid mediated
Tetani Sx
Spasms, Cramp, Lockjaw, Trismus (trigeminal N affected)
arms flexed
respiratory and cardiac complications
Patients at risk of tetanus
newborn- umbilical
IVDU- injections
Localized tetanus
disease of extrematies
Cephalic tetanus
head wound only
Tetanus death
Resp or ccardiac failure
Botulism VF
Botulinum toxin- neurotoxic
bacteriophage produced
GI- nausea, dry mouth, Diarrhea
Botulism, may lead to respiratory paralysis
Infant w/ flaccid paralysis
Botulism
Symmetric neurological manifestations w/vomiting
Botulism
Botulism cardinal signs
No fever, Symmetric n effects
Responsive pt
no hypotension, no sensory deficit
Botulism diagnosis
stool
Home-canned food
botulims
12-36 incubation (post meal)
botulism
Botulism Tx
Antitoxin- destroy the food.
When do you give Tetanus IG?
To a person with a wound that possibly hasn't been immunized. It is expensive and only provides proteciton for a few months
When do you give tetanus toxoid
to a person that has been immunized but not in a while, and just received a wound. the memory B cells will shout out Abs faster than the bacteria can proliferate.
Also, give to a person that hasn't been immunized so they can start building immunity (even when received a wound)
Non immunized pt with wound: Tetanus, what do youdo?
Ig and Toxoid
Block immediate rxn and build immunity for after Ig wears off
Tetanus shot serum sickness
with equine
Active immunization after the exposure to an infectous disease should be done to prevent the disease only if
the incubation period fo the disease excededs the time required to produce immunity
Toxoids are inducers of active immunty because they:
are immunogenic and antigenic
Immunity induced by tetanus toxoid injection is
antobody mediated and active
passive antibody has the advantage over active immunization in that it
provides immunity (Ab) more quickly
immediate vs few days