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336 Cards in this Set
- Front
- Back
How many serotypes of rabies are there?
|
one
(but there are many antigenic variants or strains) |
|
rhabdovirus
|
enveloped RNA virus with helical nucleocapsid; bullet shaped
|
|
Which rabies strain is of human origin?
|
Flurry strain
|
|
rhabdovirion consists of envelope with large peplomers called
|
G-glycoproteins
|
|
In regards to rabies, what is a fixed strain?
|
virus that has been passaged (say in rabbits) and has reached a standard incubation time in that host - usually less virulent?
|
|
where does rabies replicate
|
in the cytoplasm
|
|
negri bodies
|
intracytoplasmic inclusions in brain neurons
|
|
genus of rabies virus
|
lyssavirus
|
|
Once rabies virus has been transmitted, how does the rabies virus reach the CNS?
|
The virus replicates locally at bite wound in muscle fibers in the vicinity of the neuromuscular junction. The virus then enters nerve endings and migrates up the nerve by axoplasm flow (3 mm/hour). The virus reaches the CNS and infects neurons in different parts of the brain.
|
|
true or false: rabies virus is very resistant
|
FALSE
|
|
Once in the CNS, how does the rabies virus cause disease?
|
Once the rabies virus has reached the CNS, it then spreads DOWN the nerves to the salivary glands and other organs. Clinical signs result from virus replication in these tissues.
|
|
rabies virus is easily inactivated by:
|
heat, UV light, and common disinfectants
|
|
Is there a viremia with rabies virus?
|
No.
|
|
antigenic variants or strains of rabies
|
street, fixed, flurry
|
|
True or False: Clinical signs of rabies always commence prior to presence of the virus in the saliva.
|
False
|
|
street virus
|
refers to field isolates
|
|
What are the three forms of disease with rabies?
|
prodromal
furious paralytic or dumb |
|
fixed virus-
|
virus that has been passaged and has reached a standard incubation time in that host- usually less virulent?
|
|
What form of rabies is seen more often in dogs, cats, and horses?
|
furious form
|
|
flurry strain
|
strain of human origin
|
|
What signs of rabies are observable in the prodromal form of rabies?
|
(usually overlooked, but...)
change in temperament +/- ulcer due to excessive licking at bite site lameness in horses |
|
what mammal is quite resistant to infection by rabies
|
opossums
|
|
characteristics of the furious form of rabies
|
abnormal aggressive behavior
change in voice salivation abnormal sexual behavior tenesmus in cattle |
|
5 principle reservoirs of rabies in the US
|
skunks, racooons, foxes, bats, coyotes
|
|
characteristics of paralytic form of rabies
|
Progressive ascending paralysis starting with hind legs
Paralysis of the mandible and pharyngeal muscles causes salivation and difficulty in swallowing Death from suffocation |
|
rabies transmission
|
via bites- inoculation of infected material (Saliva) into wounds, scratches
|
|
What is observed on histopath with rabies?
|
Non-suppurative encephalomyelitis, neuronal degeneration, perivascular cuffing, +/- Negri bodies in cytoplasm of CNS neurons
|
|
true or false: sites of infection that occur farther from the CNS are less likely to cause rabies
|
TRUE
|
|
If present, what is pathognomonic for rabies?
|
Negri bodies in CNS neuronal cytoplasm
|
|
incubation period of rabies
|
usually 3 weeks, may be as long as 5 years
|
|
where does the rabies virus replicate?
|
locally at the bite wound, specifically in muscle fibers in the vicinity of the neuromuscular junction
|
|
What percentage of people exposed to a rabid dog will typically develop rabies?
|
20%
|
|
When should animals be vaccinated for rabies?
|
at 3 months of age (other people say 4 months), at one year of age, and then every one or three years thereafter depending on local regulations
|
|
after rabies reaches the CNS, it spreads ______ to salivary glands and other organs
|
centripetally
|
|
Most rabies vaccines are derived from what source?
|
tissue culture cells
|
|
true or false: varus is only present in the saliva after clinical signs of rabies are seen
|
FALSE
|
|
In the case of human exposure to an unvaccinated pet dog, how many days should the animal be quarantined for rabies watch?
|
10 days
|
|
true or false: while rabies has a long incubation period, the duration of clinical signs will last a few days only
|
TRUE
|
|
Once an animal shows clinical signs of rabies, how long will it typically take to die?
|
usually between 2 and 7 days
|
|
in domestic animals in the US and mexico, the disease is:
|
uniformly fatal
|
|
If a vaccinated pet is bitten by a rabid animal, what is the recommended course of action?
|
booster the vaccine within 5 days
|
|
reseroir for rabies in the philippines and africa
|
canines
|
|
three forms of rabies
|
prodromal, furious, dumb
|
|
What first aid should be used by a human bitten by a rabid or rabies-suspect animal?
|
immediately scrub the bite wound with soap and water and rinse with rubbing alcohol
|
|
When and how should rabies immune globulin be administered?
|
to an unvaccinated human bitten by a rabid or rabies-suspect animal; local infusion around the bite wound and an additional IM injection at a distant site
NOT TO VACCINATED INDIVIDUALS! |
|
another term for dumb form
|
paralytic
|
|
In previously vaccinated humans, what should be done following first aid in the event of a bite by a rabies-suspect animal?
|
vaccine booster with the human diploid cell vaccine on days 0 and 3
|
|
most important clinic sign of prodromal for,?
|
change in temperament
|
|
What does prion stand for?
|
proteinaceous infectious particle
|
|
clinical signs of prodromal form?
|
slight fever, diatation of pupiles, change in personality, incessant licking.
|
|
What characteristics are observed on histopath with prion diseases?
|
vacuolation and degeneration of neurons (grey matter), hypertrophy of astrocytes, and complete absence of inflammation
|
|
In what organs is pathology found with prion diseases?
|
the brain only
|
|
Is there a detectable host immune response to prion diseases?
|
No.
|
|
How do prions cause disease?
|
prions aggregate, polymerize, and form helical filamentous rods which eventually form plaques that are characteristically seen in affected neurons
|
|
What prion diseases are observed in animals?
|
1. scrapie
2-4. BSE, FSE, and EUSE (bovine, feline, and exotic ungulate spongiform encephalopathies) 5. transmissible mink encephalopathy 6. chronic wasting disease 7. atypical scrapie and BSE |
|
salivation occurs due to
|
paralysis of the pharyngeal muscles
|
|
What prion diseases are observed in humans?
|
1. Kuru
2. Creutzfeld-Jakob disease 3. vCJD (variant CJD) 4. Gerstmann-Straussler-Scheinker syndrome 5. Fatal Familial Insomnia |
|
change in voice can occur due to
|
laryngeal paralysis
|
|
What species is infected and what is the source of infection for scrapie?
|
sheep (and goats)
Placenta, blood, fetal tissues |
|
cats with rabies are often described as
|
anxious, staring, having a blank look, spooky
|
|
How are FSE (feline spongiform encephalopathy) and EUSE (exotic ungulate spongiform encephalopath) transmitted?
|
ingestion of BSE-contaminated meal
|
|
in the paralytic form, what causes salivation and difficulty swallowing?
|
paralysis of the mandible and pharyngeal muscles
|
|
How do prions propagate?
|
prion proteins PrPSc convert normal cellular proteins PrPC to PrPSc prion proteins
|
|
What are PrPC?
|
PrPC are normal cellular glycoproteins that form part of the cell membranes of neurons and lymphoid cells.
|
|
negri bodies appearance
|
eosinophilic, round inclusions.
|
|
What are the clinical signs of scrapie?
|
pruritis (itching and rubbing) , tremors (trembling), weaving gait and incordination, and eventual hindquarter paralysis
|
|
are negri bodies pathognomonic when present?
|
yes
|
|
What is the incubation period of scrapie?
|
1 to 4 years
|
|
only 20% of people bitten by a rabid dog will
|
develop rabies
|
|
what is thought to play an important role in recovery from rabies?
|
IFN
|
|
Pastures contaminated with scrapie by infected sheep placentas remain contaminated for how long?
|
3 years
|
|
How does scrapie get to the CNS?
|
Following inoculation, Scrapie agent is present in the blood of infected sheep and is associated with the lymphoid tissues. The agent may gain access to the brain via the sympathetic nervous system.
|
|
vaccinated pets bitten by a rabies suspect should
|
receive a booster in 5 days
|
|
What characteristic reflex is associated with scrapie?
|
the "nibbling reflex"
|
|
How long does it take for the full progression of the scrapie disease?
|
6-12 months
|
|
an alternative to euthanasia for rabies is
|
6 mo quarentine plus 3x vaccination
|
|
If a veterinarian suspects scrapie, what should he or she do?
|
contact the USDA
|
|
psot exposure treatment in humans
|
if unvaccinated- rabies immuno globulin + diploid cell vaccine (5 doses)
|
|
If a case of scrapie is confirmed, what will the USDA do?
|
slaughter all infected animals and their genetic “family members,” then quarantine the farm
|
|
why arent prevaccinated individuals given immune globulin?
|
it will interfere with anamnestic response
|
|
How does one confirm a diagnosis of scrapie?
|
Part of the nictitating membrane or tonsils are removed and tested for the prion agent by immunohistochemistry using a monoclonal that recognizes PrPSc protein only
|
|
TSEs are caused by
|
prions
|
|
Where does the scrapie prion accumulate?
|
in infected lymphocytes, which accumulate in lymphoid tissues
|
|
can prions be seen under EM?
|
no
|
|
Is there a genetic susceptibility component to scrapie?
|
Yes.
|
|
are prions viruses?
|
no
|
|
What clinical signs are observed with BSE?
|
an initial period of hyper-excitability during which some animals become aggressive and charge people; followed by Incoordination, ataxia, and slow progressive paralysis
|
|
can prions be destroyed?
|
no, nearly impossible
|
|
How is routine screening of slaughtered cattle for BSE routinely performed?
|
Brain, brain stem, and spinal cord from slaughtered cattle are sectioned, put on slides, and digested with proteinase K which digests PrPC but not the PrPSc protein. The slide is then treated with a monoclonal Ab that recognizes the PrPSc protein, and an immunoperoxidase (IPX) is performed.
|
|
diseases caused by prions have incubation period of
|
months to years
|
|
What are the clinical signs of chronic wasting disease in moose and deer?
|
Clinical signs include teeth grinding, abnormal behavior, excessive water intake, and marked loss of weight
|
|
true or false: diseases caused by prions are always fatal
|
TRUE
|
|
True or false: CWD can be detected in clinically normal wild deer.
|
True
|
|
protracted
|
takes a long time for pathogenesis to occur
|
|
What is "unusual" (in regards to typical prion diseases) about the transmission of chronic wasting disease (CWD)?
|
the prion may be present in the feces
|
|
histopathology of TSEs
|
vacuolation and degeneration of neurons, hypertrophy of astrocytes, and by a complete abscense of inflammation
|
|
in the host, prions:
|
aggregate, polymerize and form helical filamentous rods which eventually form plaques
|
|
What is leukemia?
|
a myeloproliferative tumor of the blood and bone marrow
|
|
What type of virus is feline leukemia virus (FeLV)?
|
a retrovirus belonging to the family Retroviridae
|
|
species/source of infection for scrapie
|
sheep/ placenta, blood, fetal tissues
|
|
What are the subtypes of Feline Leukemia Virus?
|
types A, B, and C
|
|
species/source of infection for BSE
|
cattle/ prion contaminated meat and bone meal
|
|
What is p27?
|
In FeLV, it is a major internal structural protein and is produced in excess during virus replication. It is released into blood. ELISA detects this p27 antigen.
|
|
species/source of infection for transmissible mink encephalopathy
|
mink / prion contaminated meat
|
|
Neutralizing antibodies for FeLV are directed towards this envelope glycoprotein.
|
gp70
|
|
species/source of infection for CWD
|
mule deer, elk/ feces, placenta (?)
|
|
This envelop protein has immunosuppressive properties in FeLV.
|
p15E
|
|
species/source of infection for feline spongiform encephalopathy
|
cats, zoo felids / BSE-contaminated meal
|
|
What does FOCMA stand for?
|
Feline Oncorna Cell Membrane Associated antigen
|
|
species/source of infection for exotic ungulate spongiform encephalopathy?
|
kudu, nyala / BSE contaminated meal
|
|
Where are FOCMA found?
|
protein present on the surface of CELLS transformed by FeLV.
|
|
species/source of infection for atypical scrapie and BSE
|
sheep, cattle / sporadic origine
|
|
Does the IDEXX SNAP test detect antigen or antibody?
|
antigen
(p27 antigen) |
|
species/source of infection for kuru
|
humans / cannibalism
|
|
Can the body's immune system produce antibodies against FOCMA? If so, what happes?
|
Yes.
Ab to FOCMA induces lysis of FeLV transformed cells. |
|
species/source of infection for creutzfeld jakob disease
|
humans / sporadic, familial, iatrogenic
|
|
What protein serves as the basis for subtype differentiation in FeLV?
|
gp70
|
|
species/source of infection for vCJD
|
humans / BSE contaminated meat
|
|
Is FeLV relatively stable or labile in the environment?
|
labile - susceptible to drying and disinfectants
|
|
species/source of infection for gerstmann-straussler-scheinker syndrome
|
humans / familial germ line mutation of PrP
|
|
What is the biggest risk factor associated with FeLV?
|
multi-cat household
|
|
species/source of infection for fatal familial insomnia
|
humans / familial germ line mutation of PrP
|
|
Where are FeLV virus particles found?
|
vast majority is in saliva
(small amount in urine, milk, and feces - but not significant source of infection) |
|
how can CJD be transferred from human to human?
|
dura mater transplant
|
|
What is the usual route of transmission for FeLV?
|
direct contact involving saliva - mutual grooming, sharing of food and water bowls, biting
|
|
PrPc
|
normal cellular glycoproteins that form part of the cell membranes of neurons and lymphoid cells
|
|
What scenario is most likely to result in an FeLV-infected cat?
|
Prolonged exposure of a young cat (especially < 6 weeks old) to a high dose of virus in a multi-cat household is most likely to result in infection and disease
|
|
what is the function of PrPc
|
unknown
|
|
Where does FeLV replicate?
|
in lymphoid tissue of oropharynx
|
|
PrPsc has the same chemical structure as PrPc, but has a
|
different configuration: a-helices --> b-sheets
|
|
Is there a viremia associated with FeLV infection?
|
Yes
(lymphocyte/monocyte associated) |
|
the abnormal PrPsc proteins:
|
accumulate, polymerize and form helical rod like structions that are formed within the the cells and cause lesions in the CNS
|
|
Cats that develop neutralizing antibodies to gp70 in FeLV within what time period will recover from the disease?
|
3 weeks
|
|
scrapie
|
a non febrile, fatal, chronic dz of sheep/goats
|
|
What happens to cats that do not develop neutralizing antibodies (or have a weak NA response)?
|
cat can become persistently viremic and has an 80% chance of dying of FeLV associated disease within 3 years
|
|
Regarding infections with FeLV, what is the incubation period?
|
Following infection, it may take 4 8 weeks before the cat becomes persistently viremic.
|
|
How long does it take to develop leukemia, lymphosarcoma, or other FeLV associated disorders?
|
3-36 weeks following infection
|
|
only sheep older than ____ will show clinical signs of scrapie
|
18 months
|
|
Is it more common to die of FeLV neoplasia or of non-neoplastic complications such as secondary infection?
|
For every cat that dies of FeLV neoplasia, 2.6 die of non neoplastic FeLV complications.
|
|
hereditary predisposition to scrapie
|
suffolk breeds
|
|
FeLV is thought to be responsible for about what percentage of all feline tumors?
|
30%
|
|
where is scrapie widely distributed
|
europe and n- america
|
|
FeLV is thought to induce about what percentage of all feline hematopoietic tumors?
|
90%
|
|
transmission of scrapie
|
natural transmission is by ingestion. Prenatal transmission can occur
|
|
What are the most common presenting clinical signs in cats with FeLV?
|
anorexia & slow progressive weight loss
anemia & pale gums persistent fever gingivitis/stomatitis behavior changes lymphadenopathy dyspnea due to pleural effusion occasional regurgitation (from esophageal pressure) |
|
how does the scrapie agent gain access to the brain?
|
via the sympathetic nervous system
|
|
What are lymphomas (lymphosarcomas)?
|
solid tumors consisting of accumulations of proliferating transformed malignant lymphocytes
|
|
following incoluation, where is scrapie agent present?
|
in blood and is associated with lymphoid tissues
|
|
What are the forms of lymphomas?
|
multicentric
alimentary thymic or mediastinal unclassified |
|
when the prion agent interacts with PrPc it reconfigures it to
|
PrPsc
|
|
In lymphomas, are the T cells normal? What about the B cells?
|
T cells are malignant.
B cells are normal. |
|
clinical signs of scrapie
|
aggression, rubbing, pruritis, nibbling reflex, uncoordination, emaciation, hindquarter paralysis
|
|
how can scrapie be diagnosed
|
at necropsy
|
|
What organs are most commonly affected in multicentric lymphoma of cats?
|
lymph nodes, spleen, liver
|
|
what can be tested in live sheep for scrapie?
|
lymphoid tissues- nictitating membrane or tonsils
|
|
what type of test is done in live sheep to detect scrapie?
|
immunohistochemistry using a monoclonal that recognizes PrPsc protein only
|
|
Where are alimentary lymphoma tumors observed?
|
mesenteric lymph nodes
|
|
What tissue is primarily involved with leukemia?
What cells may be seen circulating in peripheral blood with leukemia? |
bone marrow
lymphoblasts |
|
when was BSE first recognized?
|
1986
|
|
What 5 non-neoplastic diseases are associated with FeLV?
|
1. non-regenerative anemia
2. enterocolitis (panleukopenia-like syndrome) 3. thymus atrophy 4. immunosuppression 5. reproductive failure |
|
what is BSE characterized by
|
period of hyperexcitability (aggression), incoordination, ataxia, slow progressive paralysis.
|
|
Morphologically, what is the appearance of lymphomas?
|
typically cream white in color with some red stippling on the cut surface
|
|
how long will animals survive after the onset of clinical symptoms
|
few weeks to months
|
|
Is virus replication typically attempted with the FeLV diagnostic workup?
|
No. It does not grow well in culture.
|
|
what was fed to cows as a supplement, resulting in BSE
|
meat and bone meal
|
|
What is a good test if the cat is ELISA negative for FeLV antigen, but you still suspect FeLV?
|
PCR
|
|
true or false: almost half of the BSE cases occurred in herds where only one animal was infected
|
TRUE
|
|
Does the ELISA for FeLV detect antigenemia or viremia?
|
Antigenemia
(it detects the p27 antigen in the blood, which is not necessarily the complete virus) |
|
What does the IFA test for FeLV detect?
|
The IFA detects FeLV antigens on virus infected lymphocytes in peripheral blood (submit air dried blood smear).
|
|
an enzyme that digests PrPc but not the PrPsc
|
proteinase k
|
|
transmissible mink encephalopathy is similar to
|
scrapie
|
|
What percentage of patients positive by the FeLV ELISA test (ie are antigenemic) are positive by the IFA test (ie are viremic)?
|
70%
|
|
TME first recognized
|
1947 after infected sheep carcasses were fed to minks
|
|
Will a negative ELISA and IFA rule out FeLV infection?
|
No.
Because of the possibility of non virus producing LSA tumors, a negative ELISA or IFA will not rule out FeLV infection. |
|
minks have developed TME after being fed
|
downer cows
|
|
Interpret the following results for FeLV testing:
negative ELISA |
(1) non viremic, (2) not exposed, (3) immune.
May have sequestered lesions in the bone marrow or salivary glands. |
|
CWD was first noted in
|
1980 - captive mule deer in Fort Collins, Co
|
|
Interpret the following results for FeLV testing:
positive ELISA |
May be viremic susceptible to FeLV disease and may be excreting FeLV
|
|
diagnosis of CWD was first made because of
|
brain lesions that were typical of spongiform encephalopathy
|
|
true or false: all animals affected with CWD have clinical symptoms
|
false- some are clinically normal
|
|
clinical signs of CWD
|
teeth grinding, abnormal behavior, excessive drinking, marked weight loss
|
|
where can the prion for CWD be found?
|
in the feces
|
|
Cats with sequestered lesions are what in regards to FeLV?
|
latently infected
|
|
atypical spongiform encephalopathies are generallly observed in
|
older, clinically normal animals
|
|
Interpret the following results for FeLV testing:
positive ELISA + positive IFA |
Cat is viremic and contagious.
80% chance of eventually developing FeLV disease. 98% will remain IFA(+) for life. |
|
A seropositive cat for FeLV would tell you what?
|
either (1) that the cat has recovered from infection or (2) has been vaccinated
|
|
antibody specific for PrPsc derived from mouse
|
monoclonal
|
|
Interpret the following results for FeLV testing:
positive ELISA + negative IFA |
"the discordant cat"
30% of ELISA(+) cats are discordant. • may be due to faulty ELISA test repeat • may be in early phase of infection retest in 1 mth if ELISA ( ) is OK • may be immune cat with sequestered lesion • Serology virus NA and FOCMA antibodies can be detected not routinely tested |
|
greek word for rod or bullet shaped
|
rhabdos
|
|
In a cat with a sequestered lesion from FeLV, what medication may induce the disease?
|
corticosteroid therapy
|
|
alpha helices change to ____________ during PrPc--> PrPsc conversion
|
beta sheets
|
|
saliva cells in which RV replicate
|
acinar
|
|
type of wound assocated with RV transmission
|
bite
|
|
A seronegative test for FeLV would tell you what?
|
either (1) never have been infected or (2) may actually have FeLV (since diseased cats do not develop Ab)
|
|
acetylcholine receptors are also receptors for this virus:
|
rabies virus
|
|
How are recombinant live FeLV vaccines made?
|
Recombinant (live) canary poxvirus with FeLV gene inserted in poxvirus genome
|
|
procedure used to visualize PrPsc in cattle brain
|
immunoperoxidase
|
|
If cats are to be vaccinated for FeLV, what is the ideal vaccine schedule?
|
Vaccinate at 10 12 weeks of age with 2 doses and boost annually thereafter.
|
|
a frequent clinical sign observed of RV infected animals
|
salivation
|
|
What does the FeLV vaccine accomplish? Are there any risks?
|
will prevent tumor, but cats may become latently infected with FeLV or may induce soft tissue sarcoma at injection sites
|
|
transmissible organ responsible for latrogenic transmission of CJD
|
cornea
|
|
Regarding FeLV and catteries, what should be done to develop an initial FeLV control program?
|
Test all cats. If all test negative, retest after 3 months, after which you can consider the cattery to be FeLV negative. All new cat introductions must test negative before joining the cattery. If FeLV exists in the cattery, all cats that test positive should be removed. You may retest these after 2 months, and allow cats that retest negative at this time to re-join the cattery. Retest every 3 months. Can clean cattery of FeLV within 6 months !!
|
|
never observed during rabies spread throughout body
|
viremia
|
|
What treatment has been successful in causing some cats with FeLV to go into remission?
|
cyclophosphamide + Vincristine + prednisone
|
|
TSE in cats is caused by prions originating from which animals
|
cattle
|
|
tissue tested for prion in live sheep
|
tonsil
|
|
What is feline sarcoma virus (FeSV)?
|
an endogenous highly oncogenic replicative-defective virus associated with tumors, primarily fibrosarcoma of the skin
|
|
routine for non vaccinated pets bitten by rabid animal
|
euthanasia
|
|
What is the relationship of FeSV with FeLV?
|
FeSV carries a v-onc gene that replaces part of the env gene – because they lack the envelope and capsid proteins, infectious particles cannot be formed and the virus cannot leave the infected cells and be transmitted. However, it can hijack the FeLV capsid and leave the cell as FeLV!
|
|
a term denoting intense itchiness
|
pruritis
|
|
one characteristic of sheep and cattle with atypical TSE
|
they are older
|
|
lagos and duvenhage viruses of bats belong to the genus
|
lyssavirus
|
|
another name for rabies in humans
|
hydrophobia, le rage
|
|
paralysis of these muscles results in excessive salivation during RV infection
|
pharyngeal
|
|
the term used to describe structural change from PrPc into PrPsce
|
reconfigure
|
|
mammal that carries most of the known lyssaviruses
|
bat
|
|
most common way by which prions are naturally transmitted
|
ingestion
|
|
type of vaccine used to elimiante rabies in wildlife
|
recombinant
|
|
denotation for normal cellular prion protein
|
PrPc
|
|
paralysis of these muscles results in change in phonation during RV infection
|
laryngeal
|
|
medium RV uses to migrate up the nerves
|
axoplasm
|
|
type of scrapie and bse recently discovered in sheep, cattle and goats
|
atypical
|
|
source of RV for most cases of rabies in cattle in mexico
|
vampire bat
|
|
animal secretion that is most important for RV transmission
|
saliva
|
|
protein situated just below the RV envelope
|
matrix
|
|
a clinical sign frequently observed in rabies infected cattle
|
tenesmus
|
|
vCJD is usually caused by prions originating from which animals?
|
cattle
|
|
RV inclusion body
|
negri body
|
|
name for TSE in sheep
|
scrapie
|
|
animals with CWD ______ excessively
|
drink
|
|
name for TSE in deer
|
CWD
|
|
RV incubation period can be as long as five
|
years
|
|
typical rabies virus incubation period in weeks
|
three
|
|
cell compartment where RV inclusions are situated
|
cytoplasm
|
|
rabies form more frequently observed in canine and feline species
|
furious
|
|
PrPsc replicate in ____ cells after entering the M cells
|
dendritic
|
|
first phase or form recognized during RV infection of animals
|
prodromal
|
|
cause of wool loss in scrapie infected sheep
|
rubbing
|
|
tissue besides brain where PrPsc accumulate
|
lymphoid
|
|
structures resulting from polymerization and aggregation of prions
|
plaques
|
|
BSE is also known as
|
mad cow syndrome
|
|
name for TSE in elk
|
cwd
|
|
TSE propagated by cannibalism
|
kuru
|
|
behavior responsible for kuru
|
cannibalism
|
|
signifcant reservoir of rabies in Carribean islands
|
wild dogs
|
|
food source responsible for BSE outbreak
|
meat meal
|
|
street, fixed, flurry are examples of rabies
|
strains
|
|
most wildey distributed RV reservoir
|
bat
|
|
the only TSE that has resulted in human disease
|
BSE
|
|
CWD is endemic in an area where three states meet:
|
NE, WY and Co
|
|
RV must replicate in this organ before migrated to the saliva
|
CNS
|
|
non inflammatory dz of the brain
|
encephalopathy
|
|
early clinical sign of rabies in horses
|
lameness
|
|
animals infected with RV die of
|
respiratory failure
|
|
organ that is a source of scrapie prion for other sheep
|
placenta
|
|
test for detecting RV RNA and MRNA in tissues
|
PCR
|
|
number of amino acids that change during the conversion from PrPc to PrPsc
|
none
|
|
number of CWD cases in OK in the past ten years
|
none
|
|
cells besides neurons that contain PrPc
|
lymphocytes
|
|
zoo animal species that developed TSE from eating BSE tainted meat
|
felines
|
|
routien for vaccinated pets bitten by rabid animal
|
revaccinate
|
|
commonly observed in neurons of brains affected with TSE
|
vacuoles
|
|
another name for the rabies paralyic form
|
dumb
|
|
species in which CWD was diagnosed in OK in 1998
|
elk
|
|
this is never observed in CNS of animals and humans with TSE
|
inflammation
|
|
ththe progression of terminal paralysis observed in RV infected animals
|
ascending
|
|
RV genome
|
RNA
|
|
conservative estimate of number of human deaths per year world wide
|
50,000
|
|
provides long term protection after Rv vaccination
|
IgM
|
|
a frequent clinical sign observed of RV infected animals
|
aggression
|
|
cell where RV inclusion is observed
|
neuron
|
|
food source responsible for BSE outbreak
|
bone meal
|
|
a differential for Rv clinical sign in cattle
|
chocking
|
|
surveillance program responsible for the discovery of atypical TSE
|
slaughter
|
|
fluid in addition to serum where one can detect RV IgG
|
saliva
|
|
characteristic of the dumb form of rabies
|
paralysis
|
|
you should never ship brain in this state for RV diagnosis
|
frozen
|
|
small proteinaceous infectious particle
|
prion
|
|
RV reservoir on atlantic seaboard
|
raccoons
|
|
test used by state lab to diagnose RV in brain
|
IFA
|
|
FELV virus family
|
retroviridae
|
|
where is FeLV more commonly seen?
|
in cats from multi cat households
|
|
Felv is transmitted primarily via
|
saliva
|
|
young kittens exposed to a large amount of virus over an extended period of time are most likely to
|
become persistently viremic
|
|
what percentage of cats will have an ineffective immune response after exposure
|
40%
|
|
80-90% of _________ cases are associated with felv
|
mediastinal or thymic lymphoma
|
|
what is lymphoma made up of?
|
malignant t-cells
|
|
clinico-pathological conditions of feline leukemia include
|
lymphomas, leukemia, immunosuppresion
|
|
the most important viral disease of cats
|
felv
|
|
felv genus
|
gammaretrovirus
|
|
p27
|
major internal structural protein- produced in excess during virus replication is released into blood. Elisa detects this as p27 antigen
|
|
gp70
|
envelope glycoprotein with a mw of 70000 daltons- neutralizing ab are directed to gp70. this protein serves as the basis for subtype differentiation
|
|
p15E
|
envelope protein- has immunosuppressant properties
|
|
FOCMA
|
feline oncorna cell membrane associated antigen- protein present on the surface of cells transformed by felv. It is a virus encoded tumor specific antigen- ab to this focma induces lysis of felv transformed cells
|
|
felv is a very _____ virus
|
labile
|
|
protein present on the surface of cells transformed by felv
|
FOCMA
|
|
where does felv replicate?
|
lymphoid tissue of oropharynx
|
|
what follows replication?
|
viremia (lymphocyte/monocyte associated)
|
|
what is the felv incubation period
|
4-8 weeks before the cat becomes persistently viremic, 3-36 months to develop leukemia, lymphosarcoma, etc.
|
|
the most common presenting clinical signs include
|
loss of appetite, slow progressive weight loss, anemia, persistent fever, pale gums, gingivitis, stomatitis, behavior changes and lymphadenopathy
|
|
lymphomas
|
solid tumors consisting of accumulations of proliferating transformed malignant lymphocytes
|
|
multicentric lymphomas
|
generalized tumors involving lymph nodes, spleen, liver. Cat is presented with painless peripheral lymphadenopathy and anemia
|
|
alimentary lymphoma
|
tumors affect the mesenteric lymph nodes and cats prsent with vomiting, diarhea or constipation, weight loss.
|
|
form of lymphoma that is more common in older cats
|
alimentary
|
|
cats with which lymphoma will often test negative for felv by elisa
|
alimentary
|
|
thymic/mediastinal lymphoma
|
thymus and/or lymph noes in anterior mediastinum. Tumor can cause pressure on esophagus and large blood vessels resulting in swallowing difficulties and pleural effusion.
|
|
which lymphoma affects younger cats?
|
thymic/mediastinal
|
|
all hematopoietic cell lines are susceptible to ____ by felv
|
transformation
|
|
what is the most common FELV induced leukemia
|
acute lymphocytic leukemia
|
|
what is the most important presenting clinical sign with felv induced leukemias
|
anemia
|
|
non neoplastic diseases associated with felv include
|
nonregenerative anemia, enterocolitis, thymus atrophy, immunosuppresion, reproductive failure
|
|
what is the most common type of anemia in a cat
|
non regenerative, normocytic, normochromic.
|
|
what subtypes is non regenerative anemia most associated with
|
A and C
|
|
immunosuppresion predisposes cats to:
|
hemobartonellosis, infectious peritonitis, fiv, persisten stomatitis and gingivitis
|
|
where is reproductive failure generally seen?
|
catteries
|
|
what is the most important consequence of felv infection
|
immunosuppresion
|
|
refractory anemia
|
a very important clinical presenting sign
|
|
felv can cause abnormal prliferation of ____ and ____ cells
|
erythroid and myeloid
|
|
what color are most lymphomas
|
creamwhite with some red stippling on the cut surface
|
|
is virus isolation usually attempted for routine felv diagnostic workup?
|
no, the virus grows with difficulty
|
|
what will pcr detect?
|
felv proviral dna
|
|
what will rt-pcr detect?
|
the viral rna in blood and secretions
|
|
what is the cheapest method of detecting felv?
|
detection of viral antigen
|
|
when is PCR a good test?
|
if the cat is elisa negative for the felv antigen but you still suspect felv
|
|
what can be tested for virus by rt-pcr to determine if the cat is viremic?
|
bone marrow aspirates
|
|
what does the elisa detect?
|
p27 antigen in blood
|
|
are all elisa positive cats viremic?
|
no
|
|
what will IFA detect?
|
felv antigens on virus infected lymphocytes in peripheral blood
|
|
_____ % of cats positive by the IFA test are viremic
|
98%
|
|
wwhat does a negative elisa mean?
|
nonviremic; not exposted; immuno. May have sequestered lesions in the bone marrow or salivary glands
|
|
what does a positive elisa / positive IFA mean?
|
cat is viremic and contagious- 90% chance of eventually developing Felv dz. 98% will remain IFA postive for life
|
|
sequestered lesions
|
can be seen in latently infected cats- small foci produces antigen but there are no infected cells
|
|
the felv vaccine will prevent ____ but cats may still become latently infected
|
tumor
|
|
____ can decrease the amount of virus shed and the degree of viremia
|
AZT
|
|
feline sarcoma virus
|
endogenous, hihgly oncogenic replicative defective virus associated with tumors, primarily fibrosarcoma of the skin.
|
|
what does feline sarcoma virus carry?
|
a v-onc gene that replaces part of the env gene
|