zoonotics Flashcards

1
Q

examples of BACTERIAL zoonotic dz

A

yersinia pestis - plague
francisella tularensis - tularemia
borrelia burg - lymes

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2
Q

types of plague

A

bubonic
septicemic
pneumoic

**usu progress in that order

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3
Q

bubonic plague

A

lymph gland swelling

  • 2-5 day post flea bite
  • 60-90% mortality if untreated
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4
Q

septicemic plague

A

invasion of organs with no evidence of prior dz

  • death in 12-24 hours
  • NO buboes
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5
Q

pneumonic plague

A

primary or secondary lung infx
100% fatal if untreated
-can now spread via aerosol or hematog

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6
Q

characterisic stain of yersinia pestis

A
  • geisma stain
  • SAFETY PIN
  • g (-)
  • non motile
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7
Q

PLASMA encoded macrophage destruction products of Yersinia pestis

A

VW surface ag
type III secretion system
flea associated virulence factors
coagulase fibrinolysin

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8
Q

CHROMOSOMALLY encoded mac destruction of Yersinia pestis

A

iron aq system
attachment and invasion factors
endotoxin

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9
Q

types of tularemia (5)

A

1) glandular- tick bite, no primary lesion
2) ULCEROGLANDULAR- breach skin, DIRECT contact with infected animal (80%)*****
3) oculoglandular (1%)
4) typhoidal- ingestion of meat, H2O >10^7 orgs
5) pulmonary

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10
Q

morphology of tularemia. how does it evade the immune system?

A

g(-) coccobacillus

  • pleiomorphic
  • faculative intracellular
  • cystein for growth
  • PHASE VARIATION –> varies pilli
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11
Q

Tularemia infx are mostly associated with _____? Vector is ____?

A

rabbits, cats

ticks

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12
Q

tularemia drugs

A

streptomycin/genamicin
levo
doxy

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13
Q

t/f: plague and tularemia are potential bioterrorism weapons?

A

true.

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14
Q

tularemia and the plague both spread by what modes?

A

aerosol

insect vectors

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15
Q

Can the plague be transmitted person to person?

A

YES. tularemia cannot.

Pneumonic plague

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16
Q

what stage (and percentage) of ixodes tick development is associated with lyme?

A

nypmh stage. 98%. Little. Size of the D on dime.

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17
Q

lymes disease bug? percentage of ticks that carry it?

A

borrelia burgdorferi
10-36%
-rate of transmission related to hours attached to skin

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18
Q

morphology of borrelia?

A

spirochetes

hard to culture

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19
Q

most common clinical presentation of Lyme? other maifestations?

A

-erythema migrans –> ONLY 30% of patients
-arthritis
-bells palsy
-radiculopathy
meningities
cardiac

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20
Q

general course of lyme disease? (3 stages)

A
  • incubation: 3-30 days, multiply in skin, move into blood
  • Stage 1: localized, ERYTHEMA MIGRANS, 1-4 wek
  • Stage 2: disseminated infx, 1week- 6 months, sx are intermittent
  • Stage 3: persistent infx, acrodermatitis chronica atrophicans, 6 months - 30 years
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21
Q

explain borrellia borgdorferi’s love for collagen

A
  • spirochetal decorin binding proteins A and B bind decorin GAGs on collagen fibrils
  • see it in EXM in heart, NS, joints
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22
Q

treatment of Lyme?

A

primary/secondary infx (skin, joints, heart block) –> oral doxy

tertiary infx (add nervrous system findings) –> ceftriaxone, cefotaxime IV 14-28 days

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23
Q

frequent co infections of Lyme

A

babesia
ehrlichia
TBE

24
Q

diagnostic tests of lyme’s

A

two tier: elisa/ ifa with western

NOT pcr

25
Q

body lice can carry….

A

rickettsia
bartonella
borrelia

26
Q

rickettsiae characteristics

A
  • obligate intracellular
  • weekly g(-), but stains well with Giemsa
  • replicate in cytoplasm
  • need NAD+/ A-CoA
  • animal reservoirs –> humans are incidental host
  • arthropod transmitted
  • fever, HA, vasculitis/rash
27
Q

clinical presentation of rickettsia infection

A

abrupt fever, HA, petechial rash (vascular invaion and leakage)

complications: lesions in brain, kid, lung, heart

28
Q

rickettsia

  • spotted fever group
  • typhus group
A

spotted fever= rickettsii (rockey mountain spoted fever)

typhus group

  • epidemic typhus= prowazekii
  • brill zinsser dz= prowazeki
  • endemic (murine)
29
Q

difference in rash from spotter group to typhus group?

A

spotted fever= cetripetal, moves from extremeties to trunk
***10% don’t get rash

typhus group: centrifugal, trunk to extremeties (spares hands, feet, head)

30
Q

RMSF epi

A
  • highest incidence in south eaastish
  • spring-fall
  • older people get it more
31
Q

where do you see rickettsia on histology?

A

endothelial cells

32
Q

rickettsia rickettsi is transmited by? prowazekii is trasmitted by?

A

ticks (RMSF)

lice (epidemic typhus)

33
Q

how do ehrlichia and anaplasma present differently than rickettsia?

A

fever, HA, malaise, NO RASH

34
Q

pathogenesis of ehrlichia and anaplasma

A

-obligate intracellular
-infect phagocytic cells –> prevent fusion with lysosomes
-multiply in vacuoles
-Prevent host cell apoptosis
Ehrlichia –> monocyte –> MORULA (cytoplasmic inclusions)***
Anaplasma –> granulocyte

35
Q

treatment of ehrlichiosis and anaplasmosis?

A

eh: tetracycline
anaplas: doxy

36
Q

Viral Zoonotics

A

viruses that normally exist within animals but cause dz when transmitted to humans

37
Q

most EMERGING viruses are zoonotic dz. RNA or DNA?

A

truth. the “zoonotic pool”.

RNA are most common.

38
Q

factors that contribute to emergence/re-emergence of viral diseases

A
  • viral genetic changes –> altered virulence, tropism, transmission
  • human susceptibility
  • international travel/ commerce
  • changes in reservoir host/vector pops –> explosion in deer mouse pop
  • povery
  • climat change
39
Q

break zoonotics into 3 categories in terms of transmission

A

1) animal to humans, but NOT human to human (rabies, west nile)
2) animals to humans, LIMITED human to human cycles (ebola)
3) ORIGINATED in animals, SUSTAINED human to human (SARs, HIV, yellow fever, dengue, zika, influ)

40
Q

rabies

A
  • global distribution
  • 55k-70k/ year (UNDERreported- misdx or peeople don’t seek tx)
  • CANINE (eliminated from US in 70s)
  • affects children living in poverty
  • PREVENTABLE!!! via vax or post exp prophylaxis
41
Q

rabies PEP (post exposure proph)

A

EXPENSIVE

1) treat wound! wash with soap and water
2) includes HRIG (rabies Ig +4 doses of vax)
- inject Ig and vax at different sites
- vax at days 3, 7, 14

-works against ALL strains! even though each host contains a unique virus

42
Q

rhabdoviridae lyssavirus

A

Rabies!

  • bullet shaped virion
  • non-segmented
  • NEG RNA genome
  • lipid envelope
43
Q

clinical manifestations of rabies in humans

A
  • incubation is LONG (2 weeks to 1 year)
  • good for taking advantage of PEP
  • 2 forms of dz
    1) furious- encephalitic (80%)
    2) paralytic (20%)
44
Q

forms of rabies clinical manifestations

A

1) furious (encephalitic)- difficulty swallowing, hydrophobia, hallucination, hypersalivation
2) paralytic- lacks major features of furious form, quad, multiple prgan failure

**both begin with non specific sx

45
Q

rabies path

A

gets into wound –> infects wound –> gets into neurons –> travels retrograde to NS –> replicates in CNS –> makes way to salivary gland where it can then be transmitted

NO viremia

46
Q

Hantavirus (bunyavirus)

A
  • 3 circular segments (BOAR virus)
  • neg sense, ssRNA
  • enveloped –> acq from host golgi

**note most bunyaviruses are arboviruses

47
Q

two major human diseases of hantavirus

A

1) hemorrhagic fever with renal syndrome (HFRS)

2) hantavirus pulm syndrome (HPS)

48
Q

hanta transmission

A

-infects humans via aerosols from rodent urine and feces –> DEAR MICE

horizontal transmission between chronically infected rodent/ aggressive behavior –> aerosols of pee and poop

all have SPECIFIC rodent host

49
Q

hanta virus pulmonary syndrome

A

1) prodrome: fever chills myalgia (3-7 days)
2) progression to RAPID resp failure with crackles and rales –> hyptoension, shock

Distinguishing factors of prodrome: pain in legs/back
CBC with low plt, neutrophilia, elevated LDH, AST

50
Q

viral hemorrhagic fevers

A

all known= zoonotics
-arevnas, filos (ebola), paramyxos

human to human transmission requires CLOSE contact of bodily fluids

51
Q

filoviridae (ebola and marburgvirus)

A
  • FILAMENTOUS morphology (all twisty)
  • nucelocapsid
  • matrix protein
  • ENVELOPED
  • membrane glycoprotein

probably exist in bat reservoirs

52
Q

what different about ebola transmission from something like measles?

A

DROPLET transmission vs aeorosols. Aerosols can travel much further. droplets don’t travel as far and fall to the ground

53
Q

where does ebola virus persist?

A

eye
semen
amniotic fluid
cns

54
Q

HIV strains

A

example of zoonotic origin, spread to humans, PERSISTED in humans –> STRICT human pathogen

HIV1 –> M,N,O,P
group M spread worldwide, human transmission

HIV 2

55
Q

Bunyavirus

A

hanta
arbos