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Block 1 > Micro 3 > Flashcards

Micro 3 Flashcards

1
Q

what’s tegument and which virus has it?

A

protein b/w capsid and envelope –> virion stabilization, transpxn factors; HSV

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2
Q

general characteristics of HSV

A

cause lytic and latent infxn, cause syncytia and inclusion bodies, initiala binding to heparan sulfate, painful lesions

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3
Q

dzs b/w HSV 1 vs 2

A

above the waist, herpes labialis, gingivostomatitis, temporal lobe encephalitis, keratoconjunctivitis, herpetic whitlow, herpes gladitorium vs herpes genitalis, meningitis (6-60y), neonatal encephalitis

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4
Q

neurotropic spread vs latent infxn vs recurrent dz of HSV

A

retrograde to sensory ganglia vs maintained as episomes, regulation of viral transcpxn by latency-associated transcripts, CMI vs replication = reactivated, anterograde viral spread along nerve to peripheral tissue, manifests at site of primary infxn

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5
Q

diff b/w primary and recurrent dz for HSV depends on?

A

prodrome (length, systemic sxs) and local sxs (length, severity)

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6
Q

why are there lesions for HSV?

A

direct tissue dmg by lytic infxn AND host immune response/CMI (CD8, CD4 Th1)

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7
Q

why does congenital HSV occur?

A

neonate has immature immune system –> lack ab –> screen mom carefully

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8
Q

how to dx HSV?

A

Tzank, pap smear, cowdry type A body, syncytia, ophthalmic staining solutions, PCR

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9
Q

2 phases of dissemination and viremia for VZV

A

1st phase = resp to liver, spleen, organs; 2nd phase = organs to skin

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10
Q

VZV = benign and self limiting dz but what complications occur for immunocompetent vs compromised children?

A

bacterial superinfxn vs protracted varicella, multiorgan involvement, hemorrhagic varicella

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11
Q

explain immune response for VZV

A

viral cytopathicity AND host immune response give rash; ab limits dissemination but little role b/c cell to cell spread by syncytia –> CD8 and IFNy = critical for controlling virus; but high CD8 –> inc cytok prod –> interstitial PNA in adults

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12
Q

how to dx VZV?

A

by sxs or confirmed by CPE (Cowdry type A intranuclear inclusion bodies, syncytia)

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13
Q

vaccines for VZV

A

generally live attenuated vax to make ab; zostavax = live atten vax and shingrix = recombinant protein vax for adults >50y

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14
Q

where is CMV found in?

A

blood, tissue, most body fluids

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15
Q

CMV transmission

A

congenital, sex, oral, vertical (replicating in cervix), organ transplant, blood transfusion

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16
Q

CMV sxs

A

mostly asx, can become carriers

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17
Q

how to dx CMV?

A

cytomegalic cells (enlarged cells w/ intranuclear and intracytoplasmic inclusion bodies; detected in circ)

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18
Q

HHV 6/7 transmission

A

saliva (initial replication in salivary gland)

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19
Q

when is HHV 6/7 reactivated?

A

immunosuppressed and AIDs pts

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20
Q

what causes HHV 6/7 rash? diff b/w HHV 6 and 7?

A

anti viral DTH. 7 = milder dz

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21
Q

dissemination of parvovirus

A

initial site = resp tract –> disseminates to bone marrow then other tissues

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22
Q

can B19 infect other animals?

A

no, it’s an only human pathogen

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23
Q

parvovirus B19 biphasic dz

A

phase 1/febrile stage: infectious stage (7-10d), lytic infxn, non-specific flu like sxs
phase 2/symptomatic stage: noninfectious stage (1-2wk in children, mo in adult), immune mediated rash and arthralgia, slapped cheek rash

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24
Q

child vs adult dz for parvo B19

A

more arthralgia than rash in adults b/c higher ab titers

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25
Q

receptor of parvo B19. primary virulence factor?

A

P ag (globoside) on erythroid precursor cells, integrin = coreceptor on erythroid precursors but not on mature RBCs. lytic infxn on erythroid precursor cells

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26
Q

what happens if pregnant women get infected w/ parvo B19?

A

hydrops fetalis; no evidence parvo B19 causes congenital defects; no inc risk for seropositive pregnant women

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27
Q

what kind of immunity fights parvo B19?

A

strong ab response –> immune mediated rash and arthralgia; little role for CMI b/c it targets RBCs which don’t express MHC

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28
Q

how to dx parvo B19?

A

clinical sxs like the rash, ELISA in pregnant women

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29
Q

virulence factors of AdV

A

lytic infxn, persistence in lymphoid tissue, no envelope

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30
Q

receptor vs tropism for AdV

A

Coxsackie adenovirus receptor vs muco/epith cells, lymphoid cells, target cell depends on fiber and penton proteins (fibers binds to CAR, penton binds to coreceptor); incubation = 4-9d and infectious for wks when shedding in nasal secretions and stools

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31
Q

dz caused by Ad3/7 vs Ad4/7 vs AdV5 vs 40/41/42

A

pharyngoconjuctival fever (pharyngitis + conjunctivitis), from unchlorinated pools vs acute resp dz in mil recruits, atypical PNA vs pharyngitis vs gastroenteritis

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32
Q

at risk ppl for AdV

A

immunocompromised, children <14yo, ppl in crowded areas

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33
Q

how to dx AdV?

A

sx and elim of other pathogens, basophilic intranuclear inclusion bodies on cx

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34
Q

how to prevent vs tx AdV?

A

ab but serotype specific, hygiene, live Ad4/7 vax for mil recruits vs supportive

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35
Q

AdV as biotherapeutic

A

deletion of genes –> vector replication-incompetent, gene therapy –> deliver fxnal copy of mutated genes, vax vector –> give gene encoding ag

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36
Q

epidemiology of polyomavirus

A

primary infxn asx, CD8 control –> latent infxn in kidneys, reactivation in immunocompromised d/t lost CMI

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37
Q

how to tx polyomavirus?

A

supportive, inc immunocompetence

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38
Q

at risk ppl for reactivation of polyomavirus

A

HIV, transplant, immunosuppressed pts

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39
Q

JC vs BK dz of polyomaviruses

A

latency in kid, cross blood brain barrier –> infect oligodendrocytes and astrocytes –> PML –> demyelination –> progressive sxs like clumsiness, weakness, change in vision & speech, fatal 1-4mo post dx vs BKV-associated nephropathy in kidney transplants –> kid dmg d/t lost CD8 response

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40
Q

how does poxvirus replicate entirely in cyto?

A

brings DNA dep RNA pol, encodes DNA dep DNA pol, encodes viral thymidine kinase

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41
Q

human vs zoonotic pathogens of poxvirus

A

smallpox/variola, molluscum vs vaccinia virus, cowpox, monkeypox, orf virus

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42
Q

smallpox dz

A

viremic and lymphatic spread –> rash erupts over entire body at same time

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43
Q

how did Edward Jenner make smallpox vax? impact?

A

thought milkmaids don’t have smallpox due to their
infection with cowpox –> made vaccinia virus vax –> CMI. 1970: global vaccination program; key to eradication = human only pathogen

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44
Q

how to dx molluscum?

A

lesion appearance, molluscum body (eosinophilic intracytoplasmic inclusion body in infected keratinocyte)

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45
Q

can natural infx of smallpox give good immunity?

A

yes can give life long immunity but poxvirus can encode proteins w/ immunosuppressive activity; common ag determinants b/w fam –> cross reactive immunity

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46
Q

how to dx poxvirus infxn?

A

lesions at same stage (chickenpox at diff stages), pt hx, PCR of lesion fluid

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47
Q

how to tx vs prevent poxvirus?

A

quarantine or modified behavior, target VTK vs vaccinia virus live attenuated vax, OSHA recs

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48
Q

can poxviruses be used as viral vectors?

A

yes b/c well-characterized genomes –> modified vaccinia ankara, fowlpox and canarypox

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49
Q

general zoonotic poxvirus dz

A

animal pox viruses; single nodular lesion –> cluster of vesicular lesions

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50
Q

monkeypox vs orf virus

A

from saliva of infected pet vs contagious pustular dermatitis

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51
Q

lytic vs latent vs transformative infxn of EBV

A

stages depend on EBV gene expression. infect epithelium and B cells, shed in saliva, CD8 response vs in mem B cells, viral genes suppress viral protein synthesis, CD8 response, reactivated by immunosuppression vs cell cycle control = overridden by infected cells

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52
Q

how to dx EBV

A

sxs (lymphadenopathy,
splenomegaly, exudative pharyngitis; extreme fatigue), monospot test (heterophile ab to sheep, and horse RBCs (Paul-Bunnell Ag)), hematology (lymphocytosis, downey cells = atypical lymphocytes)

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53
Q

how to tx vs prevent EBV

A

limit activity d/t danger of ruptured spleen vs difficult d/t asx shedding

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54
Q

EBV proteins and transformataion

A

Activation of cellular oncogenes, Translocations of B cell genes, LMP 1/2

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55
Q

burkitt’s lymphoma vs nasopharyngeal carcinoma vs post-transplant lymphoproliferative d/o vs hairy oral leukoplakia

A

monoclonal B cell lymphoma, t(8,14) translocation –> moves c-myc oncogene to highly active promoter; starry sky vs EBV infected epithelial cells in Asia vs T cell suppression –> massive B cell prolif vs EBV infected epithelial cells in immunocompromised

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56
Q

HHV8 transmission. virulence factors?

A

sex. lack of T cells, latent infxn in endothel cells, transformation of endothel cells to spindle cells, prod of virally encoded cytok

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57
Q

what happens if there were no T cells in HHV8?

A

latent becomes lytic, spindle cells survive and grow

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58
Q

how to dx HHV8?

A

lesion appearance, bx, XR and bronchoscopy

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59
Q

HPV transmission

A

surfaces, sex, asx w/ shedding

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60
Q

HPV replication

A

Enter microabrasions in epithelial layer –> migrate to undifferentiated basal
keratinocytes –> infect/replicate in sq epith cells by expressing E1&2 –> inc cell # in basal and prickle layers –> specific cellular keratins made –> late proteins L1&2 made –> progeny virions made and shed –> viral DNA maintained as episomes in warts; viral DNA = integrated into host genome in ca

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61
Q

E5 vs E6 vs E7 oncogenes

A

stabilizes cellular epidermal growth factor (EGFR) –> more sensitive to growth signals vs bind to p53 and degrade it via host ubiquitin proteasome vs bind to Rb and inactivate it

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62
Q

why does HPV persist in basal keratinocytes?

A

keratinocytes = immunoprivileged; low viral ag produced there –> innate/adaptive immunity impt for fighting warts

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63
Q

how to dx vs tx vs prevent HPV?

A

Koiliocytes in ALL HPV serotypes vs imiquimod, aldara vs gardasil (6, 11, 16, 18), cervarix (16, 18), gardasil 9 (the prev 4, 31, 33, 45, 52, 58)

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64
Q

mutation rate, resistance, and VAP of HBV

A

low mutation rate; resistant to detergents, low pH, heat; VAP = HBV surface ag (HBsAg spherical and filamentous particle not infectious; Dane particle)

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65
Q

transmission vs at risk ppl for HBV

A

blood, sex, vertical, parenteral/needle vs healthcare workers, IVDU, babies of chronic HBV moms, blood/organ recipients

66
Q

immune response for HBV

A

Ab = protective early in infxn, spherical and filamentous particles puts high ag in blood –> neutralizes ab; strong CMI can resolve infxn but cause sxs of dz

67
Q

acute vs chronic vs carcinogenic HBV

A

Strong CMI (CD8, NK, ADCC) response –> rapid clearance; in hepatocytes w/ little to no dmg vs weak CMI response w/ delayed or no clearance; low levels of viral prod –> can clear, asx, cirrhosis, HCC vs chronic dz w/ rpted bouts of mild sxs

68
Q

% of individuals that will clear infxn, be a/sx for HBV

A

90% clear, 5-10% become chronic; children = asx for mild dz; 25% symptomatic

69
Q

how to tx vs prevent HBV

A

HBV immunoglobulin, RT inhibitors vs HBsAg vax

70
Q

replication and immune response for HAV

A

replicatess in hepatocytes and Kupffer cells –> little to no dmg; shed in stool; induce CMI (CD8, NK, ADCC) response –> life long immunity

71
Q

how to dx HAV?

A

sx/hx, confirm w/ antiHAV igM in serum

72
Q

HAV vs HEV

A

pos ssRNA, icosahedral, no envelope –> acid stable/resistant, transmitted by contaminated shellfish, Africa vs pos ssRNA, icosahedral, no envelope –> acid stable/resistant, transmitted by contaminated water, Asia, Calici-like, 20% infxn in pregnant women

73
Q

how many major genotypes for HCV?

A

6, in diff geographic locations

74
Q

what cells does HCV infect?

A

hepatocytes, B cells

75
Q

mutation rate of HCV

A

high mutation rate –> produce quasi species –> escape ab and CD8 –> CD8 can still control but cause dmg

76
Q

acute vs chronic HCV

A

similar to HBV vs 70-75% infxn = chronic –> continuous, low level prod of virus; exac by alc or coinfxn w/ HIV or HBV

77
Q

how to dx vs tx HCV?

A

ELISA for HCV ab, then confirm by PCR vs combo therapy (protease/polymerase inhibitor) but DEPENDS ON GENOTYPE

78
Q

why is HDV called “satellite virus” and what does it cause?

A

b/c can’t make own attachment protein –> coinfect w/ HBV –> dz causing cytolysis of hepatocytes; causes 40% of fulminant hepatitis –> fatal

79
Q

hepatocellular carcinoma

A

d/t combo of viral and immunological factors, continued cycles of immune-mediated dmg and repair –> genomic instability

80
Q

HBV X protein

A

oncoprotein to transactivate cellular transcription –> inc cell growth and replication; interfere with p53 activity and mitochondrial function; Integration of HBV into host cell genome –> activation of oncogene –> increases chronic viral production

81
Q

dissemination of polio

A

cytolytic infxn –> tissue dmg –> dz sxs; oropharaynx –> GI enterocytes –> Peyer’s patches M cells –> intestinal wall BM –> nerves to brain –> motor neurons of anterior horn

82
Q

receptor for polio

A

poliovirus receptor (PVR) or CD155

83
Q

can serum ab limit polio spread?

A

yes –> prevent infecting target tissue and major clinical dz

84
Q

how many types of polio?

A

3 types, most dz caused by type 1

85
Q

phases of primary infxn of polio

A
  1. asx for 90% of infxns
  2. abortive poliomyelitis/minor illness: M cells infected
  3. nonparalaytic poliomyelitis/aseptic meningitis: virus infected CNS –> back pain, muscle spasms
  4. paralytic polio/major illness: anterior horn cells an motor cortex of brain
86
Q

coxsackie virus receptor

A

coxsackie adenovirus receptor (CAR), and ICAM-1 for some

87
Q

at risk ppl for enterovirus D68

A

kids w/ asthma

88
Q

clinical pres for enterovirus D68

A

acute: runny nose, sore throat, cough
prolonged: wheezing, fever, vomit, rash
severe: neurological, difficulty breathing

89
Q

acute flaccid myelitis

A

from CSF: coxsackie A16, enterovirus D68 & A71

90
Q

tropism vs dz vs complications for rhinovirus

A

epith cells, fibroblasts vs nasal epith –> release bradykinin and histamine => rhinorrhea; sxs like HA, sneeze, sore throat induced by immune mediators vs mg to resp epith and mucosa, sinusitis

91
Q

why can’t rhinovirus infect beyond URT?

A

b/c grows best >33 degrees C

92
Q

how to tx vs prevent rhinovirus

A

steam, pleconaril vs hygiene, no vax b/c >100 serotypes

93
Q

hallmark of coronavirus

A

envelope w/ club shaped protein peplomers forming a corona –> protect against GI conditions

94
Q

tropism for coronavirus

A

resp or GI epithelium w/ E2 or spike glycoprotein; grows bet <35 degrees C –> mild URT infxn and can lead to LRT infxn

95
Q

are there ab for coronavirus?

A

yes against E2/spike glycoprotein but short lived d–> no sustained protection

96
Q

SARS 1 & 2

A

zoonotic coronaviruses; spread by droplet but also in sweat, urine, stool; causes atypical PNA; causes cytokine storm after infecting pulm mac/DC; mortality rate depends on age

97
Q

transmission, tropism, ADE of flaviviridae

A

by mosquito vector => arbovirus; Aedes (dengue, yellow, zika), Culex (West nile, JEEV); tropism = mono/mac, spread to brain liver, vessels, skin; have ab dependent enhancement for infxn; strong ag cross-reactivity

98
Q

prevention of flaviviridae

A

mosquito control, live atten vax for yellow fever and JEEV

99
Q

pathogenesis of dengue

A

4 ag distinct strains. inc vasc permeability –> plasma leakage, bleeding, dec coag

100
Q

acute vs severe dengue

A

break bone fever, severe HA, retro-orbital pain, mild hemorrhage vs reinfxn of diff strain –> DHF or DSS; bleeding in mult organs, hypovolemic shock in DSS

101
Q

ab dependent enhancement (ADE)

A

ab binding inc infxn –> bypasses VAP; also seen in alphaviruses b/c they co-circ with same vector and cross react

102
Q

acute vs severe yellow fever

A

early stage; flu like vs yellow stage; black vomit

103
Q

acute vs severe zika

A

80% symptomatic; conjunctivitis; no inc risk for woman if infected AND cleared before preg vs microcephaly, deaf/blind, Guillain Barre

104
Q

acute vs severe West Nile

A

seasonal encephalitic arbovirus. 20% symptomatic, west nile fever: body aches, rash, fever, HA vs 1%; meningitis, encephalitis, elderly at risk

105
Q

gen characteristics of chiungunya

A

togaviridae, alphavirus, pos ssRNA, enveloped, icosohedral capsid

106
Q

transmission vs VAP vs tropism vs new vector of chikungunya

A

Aedes mosquito vs E2 vs broad vs aedes albopictus d/t point mutation in E1

107
Q

diff b/w dengue and chikungunya?

A

muscle pain vs joint pain

108
Q

acute vs recurrent chikungunya

A

high fever, HA, myalgia, arthralgia vs crippling arthralgia in small joints, 7-10d/episode, recurrent episodes for mo-yrs

109
Q

gen characteristics of rubella

A

togaviridae

110
Q

is rubella virus an only human pathogen?

A

yes

111
Q

tropism of rubivirus

A

resp epith –> throughout body; extended period of viral shedding

112
Q

how to get congenital rubella?

A

1st trimester: virus crosses placenta –> replicate in fetal tissue –> cataracts, deafness, mental retardation

113
Q

immune responses to rubella

A

ab controls viremic spread –> IC deposition –> rash and arthralgia, CMI clears infxn; maternal ab prevent transplacental spread

114
Q

rubella prevention

A

live atten MMR vax, give to children so they don’t infect preg

115
Q

immune response to rabies

A

natural immunity = slow replication and immunoprivileged tissue; ab can neutralize virus but too slow to make; CMI has little role

116
Q

VAP and receptors for rabies

A

G glycoprotein. AChR, NCAM

117
Q

how to name flu strains

A

formal name, represent time/place/date, common name

118
Q

replication of flu

A

HA binds to sialic acid –> virion = endocytosed –> M2 forms channel in endosome –> uncoat envelope and release capsid –> capsid goes to nucleus and replicates –> viral particles made at membrane surface –> NA claves sialic acid and release viral particles by budding

119
Q

which flu strain infects both animals and humans?

A

A; binds to 2,3 and 2,6 linked sialic acid residues

120
Q

which flu strains do ag drift vs shift?

A

A,B vs A

121
Q

how to tx vs prevent flu

A

inhibit attachment (HA), inhibit uncoating (M2) for A, inhibit release (NA) for A & B vs inactivated or subunit

122
Q

paramyxoviridae members

A

measles, mumps, parainflu

123
Q

tropism for paramyxoviridae

A

epith, URT; cont shedding before sx

124
Q

VAP for paramyxoviridae

A

HN or H –> hemagluttinin; fusion F protein –> fuse viral memb w/ host memb AND infected cell memb w/ uninfected cell memb; syncytia –> cell to cell spread, immune evasion

125
Q

immune response to paramyxoviridae

A

CMI can control but cause dz sxs

126
Q

host cell receptors for measles

A

CD46, SLAM

127
Q

tropism for measles

A

epith –> lymphocytes, mac/DC, neurons

128
Q

how to dx vs tx measles?

A

sxs vs passive immunoglobulin therapy

129
Q

at risk ppl for RSV

A

premature infants, elderly, bone marrow/heart-lung transplants

130
Q

RSV dzs

A

URTI w/ rhinorrhea, bronchiolitis, elderly LRTI w/ PNA; direct cytopathologic effects + host immune response

131
Q

immune response for RSV

A

ab = protective only during initial infxn d/t syncytia; maternal ab = protective but too low; CMI clears infxn (mostly CD4 Th2); natural immunity wears off –> we get reinfected q 2-5y

132
Q

how to prevent RSV?

A

maternal ab an Palivizumab against F protein

133
Q

transmission vs tropism of filovirus (ebola/maraburg)

A

bodily fluids from infected animals vss mono/mac/DC –> myeloid cells –> cytok storm –> tissue necrosis

134
Q

VAP for filovirus

A

G glycoprotein

135
Q

initial pres of filovirus

A

flu like sxs

136
Q

how to tx vs prevent filovirus

A

convalescent sera, monoclonal ab vs recombinant vax, quarantine, minimize contact w/ body fluids

137
Q

early vs late sxs of hantavirus pulm synrome

A

fatigue, fever, muscle aches vs cough, SOB, lungs w/ fluid

138
Q

how is hantavirus transmitted?

A

urine/feces of infected rodents, dry weather

139
Q

arenaviridae

A

seasonal and geographical dz based on rodent reservoir, infect macs but T cells cause tissue destruction

140
Q

VAP vs receptor vs coreceptor for HIV

A

gp160 –> 120 + 41 vs CCR5 (mac/DC, T cells) vs CXCR4 (T cells)

141
Q

HIV replication

A

gp120 binds to CCR5 or CXCR4 –> gp 120/41 undergoes conformational change to expose fusion peptide –> Capsid released and uncoated into cyto –> 2 ssRNA genomes transcribed to 2 dsDNA molecules via RT –> dsDNA transported to nucleus and integrated into host genome by integrase –> Proviral DNA is transcribed –> host and viral mRNA go to cyto –> proteins made near cell memb by protease –> viral proteins released by budding

142
Q

drug targets at HIV replication

A

Attachment – receptor and co-receptor antagonists
Entry – fusion inhibitors
Replication – RT and integrase inhibitors
Assembly/Release – protease inhibitors

143
Q

why is HIV resistant to anti-retroviral therapy (ART)?

A

RT = error prone –> high mutation rate

144
Q

mac vs T cell infxn of HIV

A

M tropic, low viral prod in latent vs lytic and latent –> dec CD4 d/t viral induced AND immune meditated lysis

145
Q

in HIV, dec CD4 cells can lead to inc B cells –>

A

inc nonspecific ab –> hypergammaglobulinemia

146
Q

how to dx vs prevent HIV

A

aba to gag/pol/env vs behavaior, nonoxynol 9, post exposure ART

147
Q

challenges for HIV clearance

A

Destruction of the immune system –>opportunistic infections
Viral replication in immunoprivileged sites
Viral latency
Antigenic variation
Direct cell-to-cell transmission of virus

148
Q

acute vs latent vs AIDS for HIV

A

CD4 > 500, flu like sxs vs CD4 200-500, M tropic R5 virus to T tropic X4 virus vs CD4 count < 200, opportunistic infxn

149
Q

tropism and resistance of rotavirus

A

partial chemical and heat resistance, VP4 = target of neutralizing ab in vaxxed infant

150
Q

why are young children more at risk for rotavirus?

A

b/c older children and adults have protective ab like igA

151
Q

3 pathogenic pathways for rotavirus

A

infxn/dmg of absorptive cells, stimulation of enteric nervous system, prod of viral enterotoxin NSP4

152
Q

viral gastroenteritis

A

extended virus shedding, alteration of intestinal villi

153
Q

at risk ppl for norovirus

A

older children and adult b/c it binds to H blood ag (young children don’t have it)

154
Q

gastroenteritis for rota vs noro

A

leading cause of infant vs leading cause of epidemic

155
Q

HBV ag for transmission vs replication vs resolved vs vax vs healthy carrier vs infective carrier

A

HBV DNA vs HBsAg vs HBsAg igG and HBcAg igG vs HBsAg igG vs HBeAg w/o DNA vs HBeAg w/ DNA

156
Q

nml protein v prion structure

A

PrPC w/ 3 alpha helices vs PrPSC w/ 2 alpha helices and 1 beta sheet

157
Q

does prion have nucleic acid?

A

nope just protein

158
Q

how does prion become bad?

A

spont; external src like food, injection, transplant, contact w/ contamination

159
Q

challenges to elim prions

A

highly resistant to most disinfectants –> autoclave longer; little inflamm –> little to no clearing in body

160
Q

human v animal prion dz

A

very slow progressing. creutzfeld-jakob dz (CJD) v bovine spongiform encephalopathy aka mad cow dz

161
Q

spongiform encephalopathy

A

vacuolation of brain tissue d/e build up of prion fibrils that can’t be degraded. dx: proteinase K-resistant PrP, 14-3-3/tau protein in CSF

Block 1 (20 decks)

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