zoonotics Flashcards
examples of BACTERIAL zoonotic dz
yersinia pestis - plague
francisella tularensis - tularemia
borrelia burg - lymes
types of plague
bubonic
septicemic
pneumoic
**usu progress in that order
bubonic plague
lymph gland swelling
- 2-5 day post flea bite
- 60-90% mortality if untreated
septicemic plague
invasion of organs with no evidence of prior dz
- death in 12-24 hours
- NO buboes
pneumonic plague
primary or secondary lung infx
100% fatal if untreated
-can now spread via aerosol or hematog
characterisic stain of yersinia pestis
- geisma stain
- SAFETY PIN
- g (-)
- non motile
PLASMA encoded macrophage destruction products of Yersinia pestis
VW surface ag
type III secretion system
flea associated virulence factors
coagulase fibrinolysin
CHROMOSOMALLY encoded mac destruction of Yersinia pestis
iron aq system
attachment and invasion factors
endotoxin
types of tularemia (5)
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
morphology of tularemia. how does it evade the immune system?
g(-) coccobacillus
- pleiomorphic
- faculative intracellular
- cystein for growth
- PHASE VARIATION –> varies pilli
Tularemia infx are mostly associated with _____? Vector is ____?
rabbits, cats
ticks
tularemia drugs
streptomycin/genamicin
levo
doxy
t/f: plague and tularemia are potential bioterrorism weapons?
true.
tularemia and the plague both spread by what modes?
aerosol
insect vectors
Can the plague be transmitted person to person?
YES. tularemia cannot.
Pneumonic plague
what stage (and percentage) of ixodes tick development is associated with lyme?
nypmh stage. 98%. Little. Size of the D on dime.
lymes disease bug? percentage of ticks that carry it?
borrelia burgdorferi
10-36%
-rate of transmission related to hours attached to skin
morphology of borrelia?
spirochetes
hard to culture
most common clinical presentation of Lyme? other maifestations?
-erythema migrans –> ONLY 30% of patients
-arthritis
-bells palsy
-radiculopathy
meningities
cardiac
general course of lyme disease? (3 stages)
- 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
explain borrellia borgdorferi’s love for collagen
- spirochetal decorin binding proteins A and B bind decorin GAGs on collagen fibrils
- see it in EXM in heart, NS, joints
treatment of Lyme?
primary/secondary infx (skin, joints, heart block) –> oral doxy
tertiary infx (add nervrous system findings) –> ceftriaxone, cefotaxime IV 14-28 days
frequent co infections of Lyme
babesia
ehrlichia
TBE
diagnostic tests of lyme’s
two tier: elisa/ ifa with western
NOT pcr
body lice can carry….
rickettsia
bartonella
borrelia
rickettsiae characteristics
- 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
clinical presentation of rickettsia infection
abrupt fever, HA, petechial rash (vascular invaion and leakage)
complications: lesions in brain, kid, lung, heart
rickettsia
- spotted fever group
- typhus group
spotted fever= rickettsii (rockey mountain spoted fever)
typhus group
- epidemic typhus= prowazekii
- brill zinsser dz= prowazeki
- endemic (murine)
difference in rash from spotter group to typhus group?
spotted fever= cetripetal, moves from extremeties to trunk
***10% don’t get rash
typhus group: centrifugal, trunk to extremeties (spares hands, feet, head)
RMSF epi
- highest incidence in south eaastish
- spring-fall
- older people get it more
where do you see rickettsia on histology?
endothelial cells
rickettsia rickettsi is transmited by? prowazekii is trasmitted by?
ticks (RMSF)
lice (epidemic typhus)
how do ehrlichia and anaplasma present differently than rickettsia?
fever, HA, malaise, NO RASH
pathogenesis of ehrlichia and anaplasma
-obligate intracellular
-infect phagocytic cells –> prevent fusion with lysosomes
-multiply in vacuoles
-Prevent host cell apoptosis
Ehrlichia –> monocyte –> MORULA (cytoplasmic inclusions)***
Anaplasma –> granulocyte
treatment of ehrlichiosis and anaplasmosis?
eh: tetracycline
anaplas: doxy
Viral Zoonotics
viruses that normally exist within animals but cause dz when transmitted to humans
most EMERGING viruses are zoonotic dz. RNA or DNA?
truth. the “zoonotic pool”.
RNA are most common.
factors that contribute to emergence/re-emergence of viral diseases
- 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
break zoonotics into 3 categories in terms of transmission
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)
rabies
- 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
rabies PEP (post exposure proph)
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
rhabdoviridae lyssavirus
Rabies!
- bullet shaped virion
- non-segmented
- NEG RNA genome
- lipid envelope
clinical manifestations of rabies in humans
- 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%)
forms of rabies clinical manifestations
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
rabies path
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
Hantavirus (bunyavirus)
- 3 circular segments (BOAR virus)
- neg sense, ssRNA
- enveloped –> acq from host golgi
**note most bunyaviruses are arboviruses
two major human diseases of hantavirus
1) hemorrhagic fever with renal syndrome (HFRS)
2) hantavirus pulm syndrome (HPS)
hanta transmission
-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
hanta virus pulmonary syndrome
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
viral hemorrhagic fevers
all known= zoonotics
-arevnas, filos (ebola), paramyxos
human to human transmission requires CLOSE contact of bodily fluids
filoviridae (ebola and marburgvirus)
- FILAMENTOUS morphology (all twisty)
- nucelocapsid
- matrix protein
- ENVELOPED
- membrane glycoprotein
probably exist in bat reservoirs
what different about ebola transmission from something like measles?
DROPLET transmission vs aeorosols. Aerosols can travel much further. droplets don’t travel as far and fall to the ground
where does ebola virus persist?
eye
semen
amniotic fluid
cns
HIV strains
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
Bunyavirus
hanta
arbos
