Virology Exam 2

Front 1

what kind of virus is parvovirus

Back 1

small, non enveloped, ss linear DNA, 25nm In diameter

Front 2

what kind of capsid does parvovirus have?

Back 2

icosahedral capsid

Front 3

parvovirus inclusions

Back 3

large, IN, eosinophlic

Front 4

how can parvovirus remain viable in the feces for yaers?

Back 4

when protected by protein

Front 5

what does parvovirus require to replicate?

Back 5

cellular proteins and other components produced during the S phase of cellular replication

Front 6

what do most parvoviruses do/what can be used to charazterize isolates?

Back 6

most hemagglutinate/ HI used to characterize isolates

Front 7

two common ways parvo can be transmitted

Back 7

transplacental and fetal

Front 8

what is parvovirus often referred to as?

Back 8

a radiomimetic virus

Front 9

parvo is ____ _____ dependent

Back 9

cell cycle

Front 10

what cells does parvo replicate in

Back 10

fast dividing- especially leukocytes and enterocytes lining the intestinal mucosa

Front 11

parvo can be transmitted

Back 11

directly from animal to animal, and indirectly via fomites

Front 12

how is parvo excreted

Back 12

via the GI tract

Front 13

feline parvovirus

Back 13

feline panleukipenia virus

Front 14

what does CPV2 cause

Back 14

enteritis in dogs

Front 15

adenovirus inclusions

Back 15

intranuclear, Type B basophilic

Front 16

how can type specific Ag be determined

Back 16

virus neutralization and hemagglutination inhibition

Front 17

functions of the viral capsid

Back 17

to protect the viral genome, to provide structure symmetry, to allow virus to enter cells, aid in virus replication.

Front 18

what is hemagglutination associated with

Back 18

the fiber component of the virus

Front 19

true or false: capsid proteins are not immunogenic

Back 19

false- they are

Front 20

EIA is a ____virus

Back 20

lentivirus

Front 21

Functions of the viral envelope:

Back 21

sometimes provide structural symmetry, allow virus to enter cells, contain enzymes for virus replication,

Front 22

FIV is a _____virus

Back 22

lentivirus

Front 23

rhabdovirus has envelope with

Back 23

g-glycoproteins

Front 24

rhabdovirus- the protein below the envelope

Back 24

matrix

Front 25

where does rhabdovirus replicate

Back 25

in the cytoplasm

Front 26

all animal viruses with helical nucleocapsid are______

Back 26

enveloped

Front 27

rabies virus inclusions

Back 27

negri bodies- intracytoplasmic inclusions in brain neurons

Front 28

____ proteins surrond the nucleic acid

Back 28

nucleoocapsid

Front 29

How many serotypes of rabies are there?

Back 29

one
(but there are many antigenic variants or strains)

Front 30

rhabdovirus

Back 30

enveloped RNA virus with helical nucleocapsid; bullet shaped

Front 31

Which rabies strain is of human origin?

Back 31

Flurry strain

Front 32

rhabdovirion consists of envelope with large peplomers called

Back 32

G-glycoproteins

Front 33

In regards to rabies, what is a fixed strain?

Back 33

virus that has been passaged (say in rabbits) and has reached a standard incubation time in that host - usually less virulent?

Front 34

Which of the following has a nucleocapsid that is infectious? Parvo, herpes, Pox, Retro or Rhabdo

Back 34

Parvovirus

Front 35

where does rabies replicate

Back 35

in the cytoplasm

Front 36

negri bodies

Back 36

intracytoplasmic inclusions in brain neurons

Front 37

genus of rabies virus

Back 37

lyssavirus

Front 38

Once rabies virus has been transmitted, how does the rabies virus reach the CNS?

Back 38

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.

Front 39

true or false: rabies virus is very resistant

Back 39

FALSE

Front 40

Once in the CNS, how does the rabies virus cause disease?

Back 40

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.

Front 41

rabies virus is easily inactivated by:

Back 41

heat, UV light, and common disinfectants

Front 42

Is there a viremia with rabies virus?

Back 42

No.

Front 43

antigenic variants or strains of rabies

Back 43

street, fixed, flurry

Front 44

True or False: Clinical signs of rabies always commence prior to presence of the virus in the saliva.

Back 44

FALSE

Front 45

acyclovir (ACV is considered a pro drug because it is only activated in cells infected with herpesvirus. In a herpesvirus infected cell, ACV is phosphorylated into ACVTP by the herpesvirus enzyme ________-________ in a normal infected cell, this same virus enzyme will phosphorylate _______ (a pyrimidine. once phosphorylated, ACVTP becomes incorporated into the viral genome by the viral enzyme _________

Back 45

thymidine kinase
thymidine
DNA dependent DNA polymerase

Front 46

street virus

Back 46

refers to field isolates

Front 47

describe the two mechanisms by which ACV inhibits herpesvirus replication in infected cells?

Back 47

1 inhibits DNA polymerase- DNA is not made
2 serves as an obligate chain terminator- terminates protein synthesis

Front 48

What are the three forms of disease with rabies?

Back 48

prodromal
furious
paralytic or dumb

Front 49

Both persistently and latently infected cells show no cytopathology despite being infected and harboring the viral genome intracellularly. Please explain the main differences between persistently infected cells and latently infected cells

Back 49

Latently infected cells do not replicate until stimulated. However, persistently infected cells replicate but do not cause cytopathology

Front 50

fixed virus-

Back 50

virus that has been passaged and has reached a standard incubation time in that host- usually less virulent?

Front 51

What form of rabies is seen more often in dogs, cats, and horses?

Back 51

furious form

Front 52

flurry strain

Back 52

strain of human origin

Front 53

What signs of rabies are observable in the prodromal form of rabies?

Back 53

(usually overlooked, but...)
change in temperament
+/- ulcer due to excessive licking at bite site
lameness in horses

Front 54

what mammal is quite resistant to infection by rabies

Back 54

opossums

Front 55

which will you expect to observe in cells latently infected with a herpesvirus?
A herpes viral genome in the cell
b herpes viruses buddding from the cell surface
c herpes viral capsid proteins in the cytoplasm
d herpes viral glycoprotein on infected cell surfaces
e all of the above

Back 55

a herpes viral genome in the cell

Front 56

characteristics of the furious form of rabies

Back 56

abnormal aggressive behavior
change in voice
salivation
abnormal sexual behavior
tenesmus in cattle

Front 57

5 principle reservoirs of rabies in the US

Back 57

skunks, racooons, foxes, bats, coyotes

Front 58

characteristics of paralytic form of rabies

Back 58

Progressive ascending paralysis starting with hind legs
Paralysis of the mandible and pharyngeal muscles causes salivation and difficulty in swallowing
Death from suffocation

Front 59

which of the following are false regarind the replication of retroviruses?
A RV enter the cell by fusion
b Rv uncoat in the cytoplasm of the cell
c the RV DNA genome is transcribed from the parental RNA genome
d RV exit the cell by budding from the plsama membrane of the infected cell
e in order to replicate successfully, the RV DNA genome must be inserted or ligated into the cellular chromosome
f none- all of the above are true

Back 59

f none-- all of the above are true

Front 60

rabies transmission

Back 60

via bites- inoculation of infected material (Saliva) into wounds, scratches

Front 61

What is observed on histopath with rabies?

Back 61

Non-suppurative encephalomyelitis, neuronal degeneration, perivascular cuffing, +/- Negri bodies in cytoplasm of CNS neurons

Front 62

true or false: sites of infection that occur farther from the CNS are less likely to cause rabies

Back 62

TRUE

Front 63

If present, what is pathognomonic for rabies?

Back 63

Negri bodies in CNS neuronal cytoplasm

Front 64

incubation period of rabies

Back 64

usually 3 weeks, may be as long as 5 years

Front 65

which of the following is false regarding the replication of herpesvirus (HV
a HV enter the cell by fusion with the plasma membrane
b HV replicate their genome in the nucleus of the infected cell
c HV proteins are tranlated in the nucleus of the infected cell
d encapsidation of the HV genome takes place in the nucleus of the infected cell
e the icosahedral HV nucleocapsid is assembled in the nucleus of the infected cell

Back 65

c HV proteins are translated in the nucleus of the infected cell

Front 66

where does the rabies virus replicate?

Back 66

locally at the bite wound, specifically in muscle fibers in the vicinity of the neuromuscular junction

Front 67

What percentage of people exposed to a rabid dog will typically develop rabies?

Back 67

20%

Front 68

When should animals be vaccinated for rabies?

Back 68

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

Front 69

after rabies reaches the CNS, it spreads ______ to salivary glands and other organs

Back 69

centripetally

Front 70

which of the following antiviral drugs inhibits the viral enzyme neuramidase?
A 5-iodo-2-deoxyuridine or Idoxuridine
b azidothymidine or AZT
c acyclovir guanosine or Zovirax
d oseltamivir or Tamiflu
e protease inhibitor Ritonavir or Norvir

Back 70

d oseltamivir or Tamiflu

Front 71

Most rabies vaccines are derived from what source?

Back 71

tissue culture cells

Front 72

which of the following is true regarding the replication of picornaviruses?
A picornaviruses enter the cell by fusion
b picornaviruses replicate their genome in the nucleus
c picornaviruses insert their viral peplomers in the plasma membrane
d picornaviruses leave the cell by budding from the plasma membrane
e picronavirsues derive their different viral proteins by chopping up one long viral polypeptide
f all of the above are true

Back 72

e picronavirsues derive their different viral proteins by chopping up one long viral polypeptide

Front 73

true or false: varus is only present in the saliva after clinical signs of rabies are seen

Back 73

FALSE

Front 74

Which of the following false regarding the mde of action of interferons in general. IFNs are antivral proteins that are:
a directly antiviral- IFN bind to viruses intracellularly and prevent uncoating
b indirectly antiviral- IFN activate NK cells that recognize and kill viral infected cells
c indirectly antiviral- IFN induce intracellular enzymes that degrade the viral genome
d indirectly antiviral- IFN induce intracellular enzymes that prevent translation of viral proteins

Back 74

a directly antiviral- IFN bind to virsues intraculluarly and prevent uncoating

Front 75

In the case of human exposure to an unvaccinated pet dog, how many days should the animal be quarantined for rabies watch?

Back 75

10 days

Front 76

true or false: while rabies has a long incubation period, the duration of clinical signs will last a few days only

Back 76

TRUE

Front 77

Once an animal shows clinical signs of rabies, how long will it typically take to die?

Back 77

usually between 2 and 7 days

Front 78

in domestic animals in the US and mexico, the disease is:

Back 78

uniformly fatal

Front 79

If a vaccinated pet is bitten by a rabid animal, what is the recommended course of action?

Back 79

booster the vaccine within 5 days

Front 80

reseroir for rabies in the philippines and africa

Back 80

canines

Front 81

three forms of rabies

Back 81

prodromal, furious, dumb

Front 82

Explain the mechanisms by which a retrovirus, that does not possess an oncogene in its genome, can transform a cell it infects into a cancerous cell

Back 82

it depends on where in the cell genome the virus gets inserted-- inserted in front of cell's own oncogene

Front 83

What first aid should be used by a human bitten by a rabid or rabies-suspect animal?

Back 83

immediately scrub the bite wound with soap and water and rinse with rubbing alcohol

Front 84

When and how should rabies immune globulin be administered?

Back 84

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!

Front 85

another term for dumb form

Back 85

paralytic

Front 86

In previously vaccinated humans, what should be done following first aid in the event of a bite by a rabies-suspect animal?

Back 86

vaccine booster with the human diploid cell vaccine on days 0 and 3

Front 87

most important clinic sign of prodromal for,?

Back 87

change in temperament

Front 88

What does prion stand for?

Back 88

proteinaceous infectious particle

Front 89

clinical signs of prodromal form?

Back 89

slight fever, diatation of pupiles, change in personality, incessant licking.

Front 90

What characteristics are observed on histopath with prion diseases?

Back 90

vacuolation and degeneration of neurons (grey matter), hypertrophy of astrocytes, and complete absence of inflammation

Front 91

In what organs is pathology found with prion diseases?

Back 91

the brain only

Front 92

Is there a detectable host immune response to prion diseases?

Back 92

No.

Front 93

How do prions cause disease?

Back 93

prions aggregate, polymerize, and form helical filamentous rods which eventually form plaques that are characteristically seen in affected neurons

Front 94

What prion diseases are observed in animals?

Back 94

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

Front 95

salivation occurs due to

Back 95

paralysis of the pharyngeal muscles

Front 96

What prion diseases are observed in humans?

Back 96

1. Kuru
2. Creutzfeld-Jakob disease
3. vCJD (variant CJD)
4. Gerstmann-Straussler-Scheinker syndrome
5. Fatal Familial Insomnia

Front 97

change in voice can occur due to

Back 97

laryngeal paralysis

Front 98

What species is infected and what is the source of infection for scrapie?

Back 98

sheep (and goats)
Placenta, blood, fetal tissues

Front 99

cats with rabies are often described as

Back 99

anxious, staring, having a blank look, spooky

Front 100

How are FSE (feline spongiform encephalopathy) and EUSE (exotic ungulate spongiform encephalopath) transmitted?

Back 100

ingestion of BSE-contaminated meal

Front 101

in the paralytic form, what causes salivation and difficulty swallowing?

Back 101

paralysis of the mandible and pharyngeal muscles

Front 102

How do prions propagate?

Back 102

prion proteins PrPSc convert normal cellular proteins PrPC to PrPSc prion proteins

Front 103

What are PrPC?

Back 103

PrPC are normal cellular glycoproteins that form part of the cell membranes of neurons and lymphoid cells.

Front 104

negri bodies appearance

Back 104

eosinophilic, round inclusions.

Front 105

What are the clinical signs of scrapie?

Back 105

pruritis (itching and rubbing) , tremors (trembling), weaving gait and incordination, and eventual hindquarter paralysis

Front 106

are negri bodies pathognomonic when present?

Back 106

yes

Front 107

What is the incubation period of scrapie?

Back 107

1 to 4 years

Front 108

only 20% of people bitten by a rabid dog will

Back 108

develop rabies

Front 109

what is thought to play an important role in recovery from rabies?

Back 109

IFN

Front 110

Pastures contaminated with scrapie by infected sheep placentas remain contaminated for how long?

Back 110

3 years

Front 111

How does scrapie get to the CNS?

Back 111

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.

Front 112

vaccinated pets bitten by a rabies suspect should

Back 112

receive a booster in 5 days

Front 113

What characteristic reflex is associated with scrapie?

Back 113

the "nibbling reflex"

Front 114

How long does it take for the full progression of the scrapie disease?

Back 114

6-12 months

Front 115

an alternative to euthanasia for rabies is

Back 115

6 mo quarentine plus 3x vaccination

Front 116

If a veterinarian suspects scrapie, what should he or she do?

Back 116

contact the USDA

Front 117

psot exposure treatment in humans

Back 117

if unvaccinated- rabies immuno globulin + diploid cell vaccine (5 doses)

Front 118

If a case of scrapie is confirmed, what will the USDA do?

Back 118

slaughter all infected animals and their genetic “family members,” then quarantine the farm

Front 119

why arent prevaccinated individuals given immune globulin?

Back 119

it will interfere with anamnestic response

Front 120

retroviruses bring a ______ into the cell for transcritpion of the parental genome into progeny genomes

Back 120

ss RNA molecule

Front 121

How does one confirm a diagnosis of scrapie?

Back 121

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

Front 122

TSEs are caused by

Back 122

prions

Front 123

Where does the scrapie prion accumulate?

Back 123

in infected lymphocytes, which accumulate in lymphoid tissues

Front 124

can prions be seen under EM?

Back 124

no

Front 125

Is there a genetic susceptibility component to scrapie?

Back 125

Yes.

Front 126

are prions viruses?

Back 126

no

Front 127

What clinical signs are observed with BSE?

Back 127

an initial period of hyper-excitability during which some animals become aggressive and charge people; followed by Incoordination, ataxia, and slow progressive paralysis

Front 128

can prions be destroyed?

Back 128

no, nearly impossible

Front 129

How is routine screening of slaughtered cattle for BSE routinely performed?

Back 129

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.

Front 130

diseases caused by prions have incubation period of

Back 130

months to years

Front 131

What are the clinical signs of chronic wasting disease in moose and deer?

Back 131

Clinical signs include teeth grinding, abnormal behavior, excessive water intake, and marked loss of weight

Front 132

true or false: diseases caused by prions are always fatal

Back 132

TRUE

Front 133

True or false: CWD can be detected in clinically normal wild deer.

Back 133

TRUE

Front 134

protracted

Back 134

takes a long time for pathogenesis to occur

Front 135

What is "unusual" (in regards to typical prion diseases) about the transmission of chronic wasting disease (CWD)?

Back 135

the prion may be present in the feces

Front 136

histopathology of TSEs

Back 136

vacuolation and degeneration of neurons, hypertrophy of astrocytes, and by a complete abscense of inflammation

Front 137

in the host, prions:

Back 137

aggregate, polymerize and form helical filamentous rods which eventually form plaques

Front 138

antivral that inhibits viral specific enzymes essential for replication

Back 138

idoxuridine, AZT

Front 139

What is leukemia?

Back 139

a myeloproliferative tumor of the blood and bone marrow

Front 140

antiviral that inhibits viral polymerases that transcribe the viral nucleic acid

Back 140

acyclovir, AZT

Front 141

What type of virus is feline leukemia virus (FeLV)?

Back 141

a retrovirus belonging to the family Retroviridae

Front 142

species/source of infection for scrapie

Back 142

sheep/ placenta, blood, fetal tissues

Front 143

What are the subtypes of Feline Leukemia Virus?

Back 143

types A, B, and C

Front 144

species/source of infection for BSE

Back 144

cattle/ prion contaminated meat and bone meal

Front 145

What is p27?

Back 145

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.

Front 146

species/source of infection for transmissible mink encephalopathy

Back 146

mink / prion contaminated meat

Front 147

Neutralizing antibodies for FeLV are directed towards this envelope glycoprotein.

Back 147

gp70

Front 148

species/source of infection for CWD

Back 148

mule deer, elk/ feces, placenta (?)

Front 149

acyclovir guanosine, ganciclovir

Back 149

herpesvirus treatment. Only phosphorylated in herpesvirus infected cells. Once P'lated it aborts the synthesis of viral DNA
Obligate chain terminator- terminates DNA synthesis

Front 150

This envelop protein has immunosuppressive properties in FeLV.

Back 150

p15E

Front 151

species/source of infection for feline spongiform encephalopathy

Back 151

cats, zoo felids / BSE-contaminated meal

Front 152

azidothymidine

Back 152

used against HIV, FELV, FIV. Inhibits reverse transcriptase.

Front 153

What does FOCMA stand for?

Back 153

Feline Oncorna Cell Membrane Associated antigen

Front 154

species/source of infection for exotic ungulate spongiform encephalopathy?

Back 154

kudu, nyala / BSE contaminated meal

Front 155

oseltamivir (tamiflu)

Back 155

neuramidase inhibitor. Treatment/preven influenza A and B. orally active. Prodrug.

Front 156

Where are FOCMA found?

Back 156

protein present on the surface of CELLS transformed by FeLV.

Front 157

Cytopathic effects

Back 157

microscopically visible morphological changes in cell cultures induced by viruses

Front 158

species/source of infection for atypical scrapie and BSE

Back 158

sheep, cattle / sporadic origine

Front 159

Does the IDEXX SNAP test detect antigen or antibody?

Back 159

antigen
(p27 antigen)

Front 160

species/source of infection for kuru

Back 160

humans / cannibalism

Front 161

Can the body's immune system produce antibodies against FOCMA? If so, what happes?

Back 161

Yes.
Ab to FOCMA induces lysis of FeLV transformed cells.

Front 162

species/source of infection for creutzfeld jakob disease

Back 162

humans / sporadic, familial, iatrogenic

Front 163

What protein serves as the basis for subtype differentiation in FeLV?

Back 163

gp70

Front 164

species/source of infection for vCJD

Back 164

humans / BSE contaminated meat

Front 165

Is FeLV relatively stable or labile in the environment?

Back 165

labile - susceptible to drying and disinfectants

Front 166

species/source of infection for gerstmann-straussler-scheinker syndrome

Back 166

humans / familial germ line mutation of PrP

Front 167

What is the biggest risk factor associated with FeLV?

Back 167

multi-cat household

Front 168

species/source of infection for fatal familial insomnia

Back 168

humans / familial germ line mutation of PrP

Front 169

Where are FeLV virus particles found?

Back 169

vast majority is in saliva
(small amount in urine, milk, and feces - but not significant source of infection)

Front 170

how can CJD be transferred from human to human?

Back 170

dura mater transplant

Front 171

What is the usual route of transmission for FeLV?

Back 171

direct contact involving saliva - mutual grooming, sharing of food and water bowls, biting

Front 172

PrPc

Back 172

normal cellular glycoproteins that form part of the cell membranes of neurons and lymphoid cells

Front 173

What scenario is most likely to result in an FeLV-infected cat?

Back 173

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

Front 174

what is the function of PrPc

Back 174

unknown

Front 175

Where does FeLV replicate?

Back 175

in lymphoid tissue of oropharynx

Front 176

PrPsc has the same chemical structure as PrPc, but has a

Back 176

different configuration: a-helices --> b-sheets

Front 177

Is there a viremia associated with FeLV infection?

Back 177

Yes
(lymphocyte/monocyte associated)

Front 178

the abnormal PrPsc proteins:

Back 178

accumulate, polymerize and form helical rod like structions that are formed within the the cells and cause lesions in the CNS

Front 179

Cats that develop neutralizing antibodies to gp70 in FeLV within what time period will recover from the disease?

Back 179

3 weeks

Front 180

scrapie

Back 180

a non febrile, fatal, chronic dz of sheep/goats

Front 181

What happens to cats that do not develop neutralizing antibodies (or have a weak NA response)?

Back 181

cat can become persistently viremic and has an 80% chance of dying of FeLV associated disease within 3 years

Front 182

Regarding infections with FeLV, what is the incubation period?

Back 182

Following infection, it may take 4 8 weeks before the cat becomes persistently viremic.

Front 183

How long does it take to develop leukemia, lymphosarcoma, or other FeLV associated disorders?

Back 183

3-36 weeks following infection

Front 184

only sheep older than ____ will show clinical signs of scrapie

Back 184

18 months

Front 185

Is it more common to die of FeLV neoplasia or of non-neoplastic complications such as secondary infection?

Back 185

For every cat that dies of FeLV neoplasia, 2.6 die of non neoplastic FeLV complications.

Front 186

hereditary predisposition to scrapie

Back 186

suffolk breeds

Front 187

FeLV is thought to be responsible for about what percentage of all feline tumors?

Back 187

30%

Front 188

where is scrapie widely distributed

Back 188

europe and n- america

Front 189

FeLV is thought to induce about what percentage of all feline hematopoietic tumors?

Back 189

90%

Front 190

transmission of scrapie

Back 190

natural transmission is by ingestion. Prenatal transmission can occur

Front 191

the cell that produes IFN a and b usually ____ from the viral infection

Back 191

dies

Front 192

What are the most common presenting clinical signs in cats with FeLV?

Back 192

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)

Front 193

IFN a and b (Are/are not) active in the induced cell

Back 193

are not-- they are exported out

Front 194

how does the scrapie agent gain access to the brain?

Back 194

via the sympathetic nervous system

Front 195

IFNs are ____ _____ and extremely______

Back 195

broad spectrum; potent

Front 196

What are lymphomas (lymphosarcomas)?

Back 196

solid tumors consisting of accumulations of proliferating transformed malignant lymphocytes

Front 197

NK cells

Back 197

large granular lymphocytes that exhibit spontaneous cytotoxicity against tumor and viral infected cells

Front 198

following incoluation, where is scrapie agent present?

Back 198

in blood and is associated with lymphoid tissues

Front 199

NK cells (do/do not) need to be senesitized to a particular virus before they attack and kill the viral infected cell

Back 199

do not

Front 200

What are the forms of lymphomas?

Back 200

multicentric
alimentary
thymic or mediastinal
unclassified

Front 201

what activates NK cells?

Back 201

IFN a and b, TNFa, and IL12

Front 202

when the prion agent interacts with PrPc it reconfigures it to

Back 202

PrPsc

Front 203

NK cells have 3 receptors that pay a role in viral immune response:

Back 203

1) natural cytotoxic receptors 2) inhibitory MHC1 rc 3) FC receptors

Front 204

In lymphomas, are the T cells normal? What about the B cells?

Back 204

T cells are malignant.
B cells are normal.

Front 205

when does NK cell activity peak?

Back 205

3 days post infection

Front 206

clinical signs of scrapie

Back 206

aggression, rubbing, pruritis, nibbling reflex, uncoordination, emaciation, hindquarter paralysis

Front 207

when do CTLs apper, post infection?

Back 207

7 days

Front 208

how can scrapie be diagnosed

Back 208

at necropsy

Front 209

when are interferons produced? When does the level peak?

Back 209

as early as a few hours post infection; 3-5 days

Front 210

What organs are most commonly affected in multicentric lymphoma of cats?

Back 210

lymph nodes, spleen, liver

Front 211

what can be tested in live sheep for scrapie?

Back 211

lymphoid tissues- nictitating membrane or tonsils

Front 212

IgM is important in _____, _____ and _____ of virus particles

Back 212

opsonization, neutralizstion and agglutination

Front 213

what type of test is done in live sheep to detect scrapie?

Back 213

immunohistochemistry using a monoclonal that recognizes PrPsc protein only

Front 214

presence of serum IgM to a particular virus indicates

Back 214

tht the animal is undergoing an acute active infection with that virus

Front 215

Where are alimentary lymphoma tumors observed?

Back 215

mesenteric lymph nodes

Front 216

IgA agglutinates and neutralizes viruses-- prevents _____ ____

Back 216

viral adherence

Front 217

What tissue is primarily involved with leukemia?

What cells may be seen circulating in peripheral blood with leukemia?

Back 217

bone marrow

lymphoblasts

Front 218

when was BSE first recognized?

Back 218

1986

Front 219

What 5 non-neoplastic diseases are associated with FeLV?

Back 219

1. non-regenerative anemia
2. enterocolitis (panleukopenia-like syndrome)
3. thymus atrophy
4. immunosuppression
5. reproductive failure

Front 220

when are CTLs detected?

Back 220

4-10 days post viral infection

Front 221

what is BSE characterized by

Back 221

period of hyperexcitability (aggression), incoordination, ataxia, slow progressive paralysis.

Front 222

antigens to which CTLs respond are _____ antigens

Back 222

endogenous

Front 223

Morphologically, what is the appearance of lymphomas?

Back 223

typically cream white in color with some red stippling on the cut surface

Front 224

how long will animals survive after the onset of clinical symptoms

Back 224

few weeks to months

Front 225

Is virus replication typically attempted with the FeLV diagnostic workup?

Back 225

No. It does not grow well in culture.

Front 226

what was fed to cows as a supplement, resulting in BSE

Back 226

meat and bone meal

Front 227

What is a good test if the cat is ELISA negative for FeLV antigen, but you still suspect FeLV?

Back 227

PCR

Front 228

A recombinant canary poxvirus (CPV)/Feline Leukemia virus (FeLV) vaccine is currently available to veterinarians for vaccinating cats against FeLV infection. Like the poxvirus/rabies virus recombinant vaccine, a component of FeLV was “inserted” into the CPV to make the recombinant vaccine. What component of the FeLV was “inserted” into the CPV in order to manufacture this recombinant virus vaccine?
a. Part of the FeLV genome
b. One of the FeLV glycoprotein
c. One of the FeLV capsid protein
d. The FeLV RNA dependent RNA polymerase enzyme
e. The FeLV RNA dependent DNA polymerase enzyme

Back 228

a) part of the FELV genome

Front 229

true or false: almost half of the BSE cases occurred in herds where only one animal was infected

Back 229

TRUE

Front 230

Does the ELISA for FeLV detect antigenemia or viremia?

Back 230

Antigenemia

(it detects the p27 antigen in the blood, which is not necessarily the complete virus)

Front 231

What does the IFA test for FeLV detect?

Back 231

The IFA detects FeLV antigens on virus infected lymphocytes in peripheral blood (submit air dried blood smear).

Front 232

an enzyme that digests PrPc but not the PrPsc

Back 232

proteinase k

Front 233

Which of the following is incorrect regarding the replication of Herpesviruses?

A. Herpesviruses enter the cell by fusion
B. The herpesvirus genome uncoats in the cytoplasm
C. All herpesvirus proteins are translated in the cell cytoplasm
D. Herpesvirus genome transcription takes place in the cytoplasm
E. Herpesvirus morphogenesis occurs in the cell
nucleus

Back 233

Herpesvirus genome transcription takes place
in the cytoplasm

Front 234

transmissible mink encephalopathy is similar to

Back 234

scrapie

Front 235

Which of the following
is correct regarding the
replication of Retroviruses?

A. Retroviruses enter cell by viropexis
B. Retroviruses uncoat in the cell nucleus
C. The first event after uncoating is the translation of reverse transcriptase (RT) from the viral genome
D. The retrovirus genome is transcribed into double stranded RNA molecule by RT
E. Retroviruses bud from the nuclear membrane
F. None—all of the above statements regarding retrovirus replication are incorrect

Back 235

None—all of the above statements regarding
retrovirus replication are incorrect

Front 236

What percentage of patients positive by the FeLV ELISA test (ie are antigenemic) are positive by the IFA test (ie are viremic)?

Back 236

70%

Front 237

Most vaccines fall into which two categories

Back 237

inactivated (killed)
attenuated (live)

Front 238

TME first recognized

Back 238

1947 after infected sheep carcasses were fed to minks

Front 239

how does a killed vaccine work?

Back 239

the killed virus proteins are processed and presented by APCs, which stimulate a humoral Ab response dominated by Th2 helper cells.

Front 240

Will a negative ELISA and IFA rule out FeLV infection?

Back 240

No.
Because of the possibility of non virus producing LSA tumors, a negative ELISA or IFA will not rule out FeLV infection.

Front 241

with killed vaccines, is there a cell mediated immune response?

Back 241

no

Front 242

minks have developed TME after being fed

Back 242

downer cows

Front 243

Interpret the following results for FeLV testing:

negative ELISA

Back 243

(1) non viremic, (2) not exposed, (3) immune.
May have sequestered lesions in the bone marrow or salivary glands.

Front 244

CWD was first noted in

Back 244

1980 - captive mule deer in Fort Collins, Co

Front 245

Interpret the following results for FeLV testing:

positive ELISA

Back 245

May be viremic susceptible to FeLV disease and may be excreting FeLV

Front 246

diagnosis of CWD was first made because of

Back 246

brain lesions that were typical of spongiform encephalopathy

Front 247

true or false: all animals affected with CWD have clinical symptoms

Back 247

false- some are clinically normal

Front 248

in MLV vaccines, how are the live viruses stabilized?

Back 248

by lyophilization

Front 249

clinical signs of CWD

Back 249

teeth grinding, abnormal behavior, excessive drinking, marked weight loss

Front 250

where can the prion for CWD be found?

Back 250

in the feces

Front 251

Cats with sequestered lesions are what in regards to FeLV?

Back 251

latently infected

Front 252

atypical spongiform encephalopathies are generallly observed in

Back 252

older, clinically normal animals

Front 253

Interpret the following results for FeLV testing:

positive ELISA + positive IFA

Back 253

Cat is viremic and contagious.
80% chance of eventually developing FeLV disease.
98% will remain IFA(+) for life.

Front 254

A seropositive cat for FeLV would tell you what?

Back 254

either (1) that the cat has recovered from infection or (2) has been vaccinated

Front 255

which of the following is true regarding virus entry and replication?
a) picorna enter the cell by fusion, uncoat in the cytoplasm and replicate in the nucleus
b) retroviruses enter the cell by viropexis, uncoat in the cytoplasm and replicate in the cytoplasm
c) herpes enter the cell by viropeis, uncoat in the cytoplasm and replicate in the nucleus
d) picorn enter the cell by virpexis, uncoat in the cytoplasm and replicate in the nucleus
e) retro enter the cell by fusion, uncoat in the cytoplasm, and replicate in the cytoplasm
f) herpes enter the cell by fusion, uncoat in the nucleus and replicate in the nucleus

Back 255

e) retro enter the cell by fusion, uncoat in the cytoplasm and replicate in the cytoplasm

Front 256

antibody specific for PrPsc derived from mouse

Back 256

monoclonal

Front 257

Interpret the following results for FeLV testing:

positive ELISA + negative IFA

Back 257

"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

Front 258

greek word for rod or bullet shaped

Back 258

rhabdos

Front 259

In a cat with a sequestered lesion from FeLV, what medication may induce the disease?

Back 259

corticosteroid therapy

Front 260

alpha helices change to ____________ during PrPc--> PrPsc conversion

Back 260

beta sheets

Front 261

saliva cells in which RV replicate

Back 261

acinar

Front 262

type of wound assocated with RV transmission

Back 262

bite

Front 263

A seronegative test for FeLV would tell you what?

Back 263

either (1) never have been infected or (2) may actually have FeLV (since diseased cats do not develop Ab)

Front 264

acetylcholine receptors are also receptors for this virus:

Back 264

rabies virus

Front 265

How are recombinant live FeLV vaccines made?

Back 265

Recombinant (live) canary poxvirus with FeLV gene inserted in poxvirus genome

Front 266

procedure used to visualize PrPsc in cattle brain

Back 266

immunoperoxidase

Front 267

If cats are to be vaccinated for FeLV, what is the ideal vaccine schedule?

Back 267

Vaccinate at 10 12 weeks of age with 2 doses and boost annually thereafter.

Front 268

a frequent clinical sign observed of RV infected animals

Back 268

salivation

Front 269

What does the FeLV vaccine accomplish? Are there any risks?

Back 269

will prevent tumor, but cats may become latently infected with FeLV or may induce soft tissue sarcoma at injection sites

Front 270

transmissible organ responsible for latrogenic transmission of CJD

Back 270

cornea

Front 271

Regarding FeLV and catteries, what should be done to develop an initial FeLV control program?

Back 271

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 !!

Front 272

never observed during rabies spread throughout body

Back 272

viremia

Front 273

What treatment has been successful in causing some cats with FeLV to go into remission?

Back 273

cyclophosphamide + Vincristine + prednisone

Front 274

TSE in cats is caused by prions originating from which animals

Back 274

cattle

Front 275

tissue tested for prion in live sheep

Back 275

tonsil

Front 276

What is feline sarcoma virus (FeSV)?

Back 276

an endogenous highly oncogenic replicative-defective virus associated with tumors, primarily fibrosarcoma of the skin

Front 277

routine for non vaccinated pets bitten by rabid animal

Back 277

euthanasia

Front 278

What is the relationship of FeSV with FeLV?

Back 278

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!

Front 279

test used by state lab to diagnose RV in brain

Back 279

IFA

Front 280

FELV virus family

Back 280

retroviridae

Front 281

where is FeLV more commonly seen?

Back 281

in cats from multi cat households

Front 282

Felv is transmitted primarily via

Back 282

saliva

Front 283

young kittens exposed to a large amount of virus over an extended period of time are most likely to

Back 283

become persistently viremic

Front 284

what percentage of cats will have an ineffective immune response after exposure

Back 284

40%

Front 285

80-90% of _________ cases are associated with felv

Back 285

mediastinal or thymic lymphoma

Front 286

what is lymphoma made up of?

Back 286

malignant t-cells

Front 287

clinico-pathological conditions of feline leukemia include

Back 287

lymphomas, leukemia, immunosuppresion

Front 288

the most important viral disease of cats

Back 288

felv

Front 289

felv genus

Back 289

gammaretrovirus

Front 290

p27

Back 290

major internal structural protein- produced in excess during virus replication is released into blood. Elisa detects this as p27 antigen

Front 291

gp70

Back 291

envelope glycoprotein with a mw of 70000 daltons- neutralizing ab are directed to gp70. this protein serves as the basis for subtype differentiation

Front 292

p15E

Back 292

envelope protein- has immunosuppressant properties

Front 293

FOCMA

Back 293

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

Front 294

felv is a very _____ virus

Back 294

labile

Front 295

protein present on the surface of cells transformed by felv

Back 295

FOCMA

Front 296

where does felv replicate?

Back 296

lymphoid tissue of oropharynx

Front 297

what follows replication?

Back 297

viremia (lymphocyte/monocyte associated)

Front 298

what is the felv incubation period

Back 298

4-8 weeks before the cat becomes persistently viremic, 3-36 months to develop leukemia, lymphosarcoma, etc.

Front 299

the most common presenting clinical signs include

Back 299

loss of appetite, slow progressive weight loss, anemia, persistent fever, pale gums, gingivitis, stomatitis, behavior changes and lymphadenopathy

Front 300

lymphomas

Back 300

solid tumors consisting of accumulations of proliferating transformed malignant lymphocytes

Front 301

multicentric lymphomas

Back 301

generalized tumors involving lymph nodes, spleen, liver. Cat is presented with painless peripheral lymphadenopathy and anemia

Front 302

alimentary lymphoma

Back 302

tumors affect the mesenteric lymph nodes and cats prsent with vomiting, diarhea or constipation, weight loss.

Front 303

form of lymphoma that is more common in older cats

Back 303

alimentary

Front 304

cats with which lymphoma will often test negative for felv by elisa

Back 304

alimentary

Front 305

thymic/mediastinal lymphoma

Back 305

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.

Front 306

which lymphoma affects younger cats?

Back 306

thymic/mediastinal

Front 307

all hematopoietic cell lines are susceptible to ____ by felv

Back 307

transformation

Front 308

what is the most common FELV induced leukemia

Back 308

acute lymphocytic leukemia

Front 309

what is the most important presenting clinical sign with felv induced leukemias

Back 309

anemia

Front 310

non neoplastic diseases associated with felv include

Back 310

nonregenerative anemia, enterocolitis, thymus atrophy, immunosuppresion, reproductive failure

Front 311

what is the most common type of anemia in a cat

Back 311

non regenerative, normocytic, normochromic.

Front 312

what subtypes is non regenerative anemia most associated with

Back 312

A and C

Front 313

immunosuppresion predisposes cats to:

Back 313

hemobartonellosis, infectious peritonitis, fiv, persisten stomatitis and gingivitis

Front 314

where is reproductive failure generally seen?

Back 314

catteries

Front 315

what is the most important consequence of felv infection

Back 315

immunosuppresion

Front 316

refractory anemia

Back 316

a very important clinical presenting sign

Front 317

felv can cause abnormal prliferation of ____ and ____ cells

Back 317

erythroid and myeloid

Front 318

what color are most lymphomas

Back 318

creamwhite with some red stippling on the cut surface

Front 319

is virus isolation usually attempted for routine felv diagnostic workup?

Back 319

no, the virus grows with difficulty

Front 320

what will pcr detect?

Back 320

felv proviral dna

Front 321

what will rt-pcr detect?

Back 321

the viral rna in blood and secretions

Front 322

what is the cheapest method of detecting felv?

Back 322

detection of viral antigen

Front 323

when is PCR a good test?

Back 323

if the cat is elisa negative for the felv antigen but you still suspect felv

Front 324

what can be tested for virus by rt-pcr to determine if the cat is viremic?

Back 324

bone marrow aspirates

Front 325

what does the elisa detect?

Back 325

p27 antigen in blood

Front 326

are all elisa positive cats viremic?

Back 326

no

Front 327

what will IFA detect?

Back 327

felv antigens on virus infected lymphocytes in peripheral blood

Front 328

_____ % of cats positive by the IFA test are viremic

Back 328

98%

Front 329

wwhat does a negative elisa mean?

Back 329

nonviremic; not exposted; immuno. May have sequestered lesions in the bone marrow or salivary glands

Front 330

what does a positive elisa / positive IFA mean?

Back 330

cat is viremic and contagious- 90% chance of eventually developing Felv dz. 98% will remain IFA postive for life

Front 331

sequestered lesions

Back 331

can be seen in latently infected cats- small foci produces antigen but there are no infected cells

Front 332

the felv vaccine will prevent ____ but cats may still become latently infected

Back 332

tumor

Front 333

____ can decrease the amount of virus shed and the degree of viremia

Back 333

AZT

Front 334

feline sarcoma virus

Back 334

endogenous, hihgly oncogenic replicative defective virus associated with tumors, primarily fibrosarcoma of the skin.

Front 335

what does feline sarcoma virus carry?

Back 335

a v-onc gene that replaces part of the env gene

Front 336

FIV

Back 336

retrovirus, genus lentivirus

Front 337

how many subtypes of FIV are there? How can they be differentiated

Back 337

three, by their envelope glycoproteins

Front 338

can cats be infected with more than one subtype?

Back 338

yes

Front 339

FIV glycoproteins play an important role in

Back 339

cell tropism and pathogenicity

Front 340

FIV was discovered in

Back 340

1987

Front 341

FIV transmission

Back 341

primarily by biting during cat fights. Also parenteral route, blood transfusions, in utero, lactogenic, etc

Front 342

what cells does the virus infect

Back 342

CD4 T helped lympthocytes

Front 343

provirus

Back 343

integrated into the chromosome

Front 344

are males or females more likely to have fiv?

Back 344

males

Front 345

after primary infection, virus replicates in

Back 345

lymphocytes within lymphoid tissue

Front 346

___ is the primary site of replciation resulting in ____

Back 346

thymus, T-cell depletion

Front 347

FIV infects t cells to start but will eventually infect

Back 347

mononuclear cells and B-cells

Front 348

what does viremia occur as a result of? How long will it last

Back 348

primary infection; several weeks

Front 349

what happens if the host mounts a solid immune response with circulating antibodies as soon as 2-4 weeks after infection?

Back 349

viremia decreases and virus eventually goes latent

Front 350

chronic infection

Back 350

latent period that may last for years

Front 351

during the latent chronic period, cats are clinically healthy BUT

Back 351

FIV still replciates in lymphocytes and can be isolated from lymphocytes and serum

Front 352

what can stimulate higher levels of FIV replciation

Back 352

stress and illness

Front 353

what can enhance the severeity of clinical FIV illness

Back 353

cats infected at a young age, cats that are also FELV positive

Front 354

congenitally infected kittens are _____ but are not

Back 354

PCR positive, but not viremic

Front 355

three clinical stages of FIV

Back 355

acute, asymptomatic, terminal

Front 356

acute phase-

Back 356

fever with malaise, generalized lymphadenopathy, diarrhea, stomatitis, conjunctivitis, and respiratory dz. Several days to a few weeks,.

Front 357

asymptomatic phase

Back 357

may last a few weeks to 6+ years.

Front 358

terminal phase

Back 358

wasting syndrome. Stomatitis and gingivitis are common.

Front 359

most consistent neurological sign in cats during the terminal stage of infection

Back 359

changes in behavior

Front 360

diagnosing FIV: clinical pathology symptoms

Back 360

anemia, neutropenia, and lymphopenia frequently seen

Front 361

detection of virus/viral nucleic acid

Back 361

RT-PCR to test for presence of provirus.

Front 362

if an adult cat tests seropositive, always assume that it is also

Back 362

RT-PCR positive

Front 363

most important test for diagnosing FIV infection

Back 363

serology- look for Ab in the blood

Front 364

most cats will develop a detectable IgG antibody response by __ weeks post infection

Back 364

8

Front 365

most common test used to diagnose FIV

Back 365

ELISA snap

Front 366

detection of antibody in serum is synonymous with infection in _____ cats

Back 366

unvaccinated

Front 367

once seropostive, does the cat remain seropositive forever?

Back 367

yes

Front 368

what test can confirm a positive elisa?

Back 368

western blot

Front 369

durin what stage will some cats become seronegative?

Back 369

terminal stage

Front 370

what is a disadvantage of using the SNAP test?

Back 370

cant differentiate infected from vaccinated cats

Front 371

what type of vaccine is availablE?

Back 371

inactivated dual subtype

Front 372

what drug can be used to treat?

Back 372

AZT

Front 373

should healthy FIV positive cats be routinely vaccinated?

Back 373

yes - with inactivated vaccines

Front 374

FIP

Back 374

feline infectious peritonitis

Front 375

FIP is caused by a

Back 375

feline enteric coronavirus (FeCoV)

Front 376

FIPV

Back 376

feline infectious peritontis virus

Front 377

how do FIPV and FeCoV differ?

Back 377

genetically, but not antigenically

Front 378

how can FIPV arise naturally in vivo?

Back 378

by mutating and acquiring an enhanged ability to replicate in tissue macrophages and circulating macrophages

Front 379

what age group is most prone to FIP

Back 379

cats <2 years old. Sometimes in very old cats

Front 380

FIP transmission

Back 380

ingestion primarily, inhalation possible

Front 381

how is FCoV shed?

Back 381

in the feces in large numbers during active infection. Can also be excreted in saliva and by respiratory tract

Front 382

where is there a constant source of FCoV infection

Back 382

areas of high cat density (shelters, pet stores, catteries)

Front 383

FcoV is antigenically related to the ____ of pigs, dogs and humans

Back 383

coronaviruses

Front 384

what is very important in the pathogenesis of FIP?

Back 384

repeated exposure to large quantitues of FeCoV and stress

Front 385

incubation period of FeCov

Back 385

short, few days

Front 386

incubation period of FIP

Back 386

> 4 months (5-10 days parenterally)

Front 387

where does feCoV replicate

Back 387

in intestinal epithelial cells

Front 388

what cell types will FeCoV infect

Back 388

circulating macrophages and tissue macrophages

Front 389

FIP is an ______-______ disease nvoling virus, antiviral antibodies and omplement

Back 389

immune-complex

Front 390

true or false: cats that have no antibodies to FeCoV will develop FIP

Back 390

FALSE

Front 391

true or false, de-complemented cats do not develop lesions of FIP

Back 391

TRUE

Front 392

in many cats, infection with FecoV results in a ____ cat with a _____ infection

Back 392

seropositive, persistent

Front 393

how does stress affect FIP?

Back 393

stress suppresses the immune system and depresses the CMI response. This allows the latent FeCoV to replicate and acquire mutations that allows it to replicate even better

Front 394

virus replication in macrophages in the vicinity of blood vessels attracts more Ab and these Ab fix more complement, resulting in

Back 394

inflammation, attraction of neutrophils and formation of pyogranulomas around the blood vessels

Front 395

complement fixation leads to release of

Back 395

vasoactive amines, which increase vascular permeability

Front 396

the clinical and pathological pictures seen are a direct result of

Back 396

vasculitis

Front 397

ADE

Back 397

antibody dependant enhancement- term used to describe pathogenessis of FIP

Front 398

three forms of FIP

Back 398

effusive/wet, granulomatous/dry, mixed.

Front 399

effusive form

Back 399

excessive amounts of fluid develop in chest or abdomen. Anorexia, weight loss, depression, dehydration, anemia. Unresponsive fever, icterus.

Front 400

non effusive / dry form

Back 400

characterized by granulomatous lesions or pyogranulomas in many body areas. Ocular lesions, behavioral changes.

Front 401

FIP infected cats typically came from a ____ in the past yaer

Back 401

multicat environment

Front 402

characteristics of the effusive fluid from the wet form of FIP

Back 402

clear, straw colored, clots on standing, feels slimy. Low cellularity- mostly macrophages and some neutrophils. A:G ratio <.45, TP > 3.5

Front 403

clinical pathology of FIP

Back 403

non regenerative anema, neutrophilia with left shift, hypergammaglobulinemia. Increase acute phase proteins

Front 404

true or false: if the A;G ratio is >,8, the cat does not have FIP

Back 404

TRUE

Front 405

in the wet form, what can appear on the serosal surfaces of abdome and thorax?

Back 405

rough, white deposite. Fibrinous exudate. May also see small pyogranulomas

Front 406

what is the only definitive way to make a positive diagnosis

Back 406

via histopathology (biopsy/necropsy)

Front 407

what is commonly observed in kidneys and liver? (and other organs)

Back 407

necrotic vasculitis

Front 408

how can FeCoV be detected in tissues

Back 408

IHC

Front 409

coronavirus Abs in sera are detected by Ab assay using

Back 409

immunofluorescence

Front 410

feline panleukopenia is characterized by

Back 410

vomiting, severe dehydration, neutropenia

Front 411

panleuk is caused by a _____ virus

Back 411

parvo

Front 412

in the natural population, ___% of cats are seropositve for panleuk

Back 412

70

Front 413

how many serotypes of panleuk exist?

Back 413

one

Front 414

how is panleuk transmitted?

Back 414

orally by contact with infected cats, or with contaminated fomites. Virus is excreted in large quantities in feces of acutely ill cats and is shed for 6 weeks after initial infection. Environmental contamination

Front 415

who is primarily affected by panleuk?

Back 415

unvaccinated young 2-6mo old kittens

Front 416

incubation period of panleuk?

Back 416

1 week

Front 417

primary site of replication for panleuk

Back 417

oropharynx, 18-24hrs post infection

Front 418

virus will replicate only in

Back 418

fast dividing cells/those with high mitotic indexes: lymphocytes, undifferenetiated epithelial cells at base of crypts, myeloid cell precursors including neutrophils, etc

Front 419

when will viremia be observed?

Back 419

2-7days post infection

Front 420

fetal infection can occur as a result of

Back 420

transplacental infection

Front 421

if a pregnant queen is infected early in gestation, the restul is

Back 421

fetal death, reabsorption, infertility

Front 422

if a pregnant queen is ifnected mid gestation,

Back 422

it results in abortion and/or birth of mummified fetuses

Front 423

if a pregnant queen is infected late in gestation or soon after birth,

Back 423

it results in cerebellar hypoplasia and optic nerve atrophy in the kitten. Granular cells of cerebellum are affected

Front 424

if the dam is immune to panleuk, how long will passive immunity protect kittens?

Back 424

2-3 months

Front 425

what plays an important role in the pathogenesis of disease?

Back 425

secondary bacterial infection

Front 426

peracute panleuk

Back 426

seen in young kittens, overwhelming infection with no clinical signs and death within 24hr onset of dz

Front 427

acute panleuk

Back 427

cats present with high fever, depression, anorexia, vomiting. Extreme dehydration. Kittens often hunched over water bowl with head between paws. Tender abdomens with excessive gas and liquid. Fatality anywhere from 25-90%- better prognosis if survive the first few days

Front 428

cerebellar hypoplasia

Back 428

kittens show incoordination, hypermetria and ataxia

Front 429

main clin path sign of panleuk

Back 429

leukopenia- neutropenia, sometimes anemia

Front 430

signs of panleuk at necropsy

Back 430

dehydration, dilated SI, edematous, petechial hemorrhage, edematous lymph nodes

Front 431

histopath of panleuk

Back 431

ballooned crpts, shortened villi, IN inclusions in ileum and jejunum

Front 432

FPV is easily isolated on

Back 432

feline TC cells

Front 433

is virus isolation of FPV frequenly done?

Back 433

no, because FA test is quicker

Front 434

two ways of detecting FPV antigen in infected tissue

Back 434

FA, IHC using viral specific antibodies

Front 435

FPV can be IDd in feces by

Back 435

ELISA

Front 436

PCR will ID the ___ ___ in infected tissue and in feces

Back 436

viral dNA

Front 437

cats that recover from infection develop

Back 437

lifelong immunity

Front 438

when will all kittens respond successfully to vaccination?

Back 438

by 12 weeks of age

Front 439

what can interfere with vaccination

Back 439

maternal antibodies

Front 440

when should kittens be vaccinated for FPV?

Back 440

kittens at 9-10 weeks, and again 2-4 weeks later

Front 441

two types of vaccines available

Back 441

MLV and inactivated

Front 442

which vaccine can be used in young kittens and pregnant queens?

Back 442

inactivated. 2 doses, 2-3 weeks apart

Front 443

panleuk treatment

Back 443

withold food/milk, give fluids, Abs, Disinfect premises

Front 444

CPV-2 causes

Back 444

severe enteritis

Front 445

CPV-2 virus family/genus

Back 445

parvoviridae / parvovirus

Front 446

how many strains of CPV-2 are recognized?

Back 446

four

Front 447

CPV2 transmission

Back 447

oro-fecal route.

Front 448

how long will sick dogs excrete the virus for?

Back 448

10 days

Front 449

____ infections occur in >75% of infected dogs

Back 449

subclinical

Front 450

breeds that are most susceptible to CPV2?

Back 450

rottweilers, dobermans, german shepherds, golden retrievers, alaskan sled dogs

Front 451

breed that is quite resistant to CPV2

Back 451

beagle

Front 452

incubation period of CPV2

Back 452

about 1 week

Front 453

CPV2 is antigenically _____ from CPV1. It is (more/less) related to FPV than to CPV1

Back 453

different; more

Front 454

two syndroms that can be encourated from CPV2

Back 454

enteritis or myocarditis

Front 455

enteritis clinical signs

Back 455

sudden onset diarrhea, grey/foul smelling feces, bloody, watery. Vomiting. Fever/anorexia/dehydration.

Front 456

bloodwork of dogs infected with CPV2 enteritis usually shows

Back 456

leukopenia

Front 457

primary site of replication

Back 457

oropharynx and associated lymphoid tissues

Front 458

when is viremia seen

Back 458

2-3 days after infection

Front 459

what cells does CPV2 infect

Back 459

fast growing cells, including intestinal epithelium, lymphocytes, myocytes

Front 460

what cells in the intestine does CPV infect? What does this cause

Back 460

crypt cells of ileum and jejunum, causing necrosis and necrosis of the peyers patches

Front 461

where is myocardial infection with heart failure seen?

Back 461

in young pups (less than 6 weeks of age)

Front 462

clinical pathology of CPV2

Back 462

leukopenia, neutropenia

Front 463

why is anemia rarely seen with CPV2?

Back 463

because the bone marrow is not affected

Front 464

what is seen at necropsy with CPV2?

Back 464

dehydration, hemorrhagic enteritis with turgid edematous SI, mucosal petechial hemorrhages, hemorrhages within the lumen. Necrotic peyers patches

Front 465

how is CPV2 antigen in infected tissue visualized?

Back 465

FA and IHC using viral specific MAb

Front 466

what is the most important diagnostic test for diagnosing CPV2 ifnection in dogs?

Back 466

the CITE test (IDEXX)

Front 467

what is the CITE test?

Back 467

a solid phase ELISA test that uses a CPV2 MaB to capture the virus on a membrane. Performed in ten minutes.

Front 468

what sample is the CITE test performed on

Back 468

fecal material or intestinal contents.

Front 469

when can circulating Ab be detected to CPV2?

Back 469

7-10 days after infection

Front 470

which pups cannot respond to vaccination?

Back 470

puppies with high levels of maternal antibodies

Front 471

define window period

Back 471

the period during which a pup can become infected but cannot be successfully immunized.

Front 472

when should puppies be vaccinated

Back 472

starting at 6-8 weeks and repeat every 2-3 weeks until the age of 18 weeks

Front 473

how can you protect a puppy from CPV

Back 473

isolate pups from areas where dogs congregation and from other dogs at shelters/boarding facilities

Front 474

CPV1 is an _____ virus

Back 474

avirulent

Front 475

where is CPV1 found?

Back 475

in the feces of clinically normal dogs

Front 476

canine distemper is also known as

Back 476

hard pad disease

Front 477

CDV virus family/genus

Back 477

paramyxoviridae, morbillivirus

Front 478

CDV

Back 478

large enveloped virus, ssRNA, helical nucleocapsid.

Front 479

the envelope has which 2 proteins

Back 479

Fusion (F) and hemagglutination (H)

Front 480

CDV is antigenically related to which two viruses

Back 480

measles and rinderpest

Front 481

how many serotypes of CDV are there? How many strains?

Back 481

1 serotype, several strains (~7)

Front 482

CDV transmission

Back 482

primarily by respiratory droplet. Also contact with mucous membranes, or with urine and feces of infected dogs

Front 483

are covered dogs carries of the virus?

Back 483

NO

Front 484

CDV incubation period

Back 484

4-6 days

Front 485

mild CDV infections

Back 485

ocular nasal discharge (mucopurulent), fever, cough. Indistinguishable from other respiratory infections

Front 486

clin path sign that is common early in the disease

Back 486

leukopenia/lymphopenia

Front 487

clin path sign that may occur later in the disease and mask the leukopenia

Back 487

neutrophilia

Front 488

severe CDV infection

Back 488

respiratory signs, nasal/ocular discharge, mois productive cough often leading to pneumonia (secondary bacterial infection), death

Front 489

what type of nasal discharge is seen with prolonged illness?

Back 489

mucopurulent

Front 490

when will CNS signs appear?

Back 490

1-3 weeks after infection, or 2-4 weeks after the dog seemingly recovers from a mild respiratory dz

Front 491

CNS signs include

Back 491

seizures (chewing gum fits), ataxia, myoclonus, chorea

Front 492

what kind of paralysis may occur?

Back 492

ascending

Front 493

why is CDV known as hard pad disease?

Back 493

dogs can develop hyperkeratosis after they recover from the disease

Front 494

what dogs are most likely to develop CNS signs

Back 494

those with hyperkeratosis

Front 495

chronic progressive distemper encephalitis

Back 495

a rare condition in odler dogs marked by ataxia, head pressing, pacing, uncoordinated high stepping gate.

Front 496

what test can detect the CDV in old dog encephalitis?

Back 496

FA on CNS tissue

Front 497

pathogenesis of CDV

Back 497

virus enters oropharynx, replicates in tissue macrophages. Carried to tonsils and bronchial lymph nodes.

Front 498

what cell types does CDV replicate in?

Back 498

macrophages, dendritic cells, lymphocytes

Front 499

what does viremia follow?

Back 499

virus repcliation in the luekocytes

Front 500

pantropic virus

Back 500

a virus that will infect cells in many different organs

Front 501

disease outcome is dependant upon _____

Back 501

immune response

Front 502

what is necessary for a dog to recover? (must be developed by 9 days)

Back 502

neutralizing antibodies

Front 503

_________ ___________ infection is very important in the pathogenesis of canine distemper

Back 503

secondary bacterial ifnection

Front 504

clin path of CDV

Back 504

leukopenia with absolute lymphopenia

Front 505

what test will reveal CDV antigen in the neutrophils?

Back 505

FA test

Front 506

what test is commonly done on dogs with neuro signs?

Back 506

CSF tap - will show increased intracranial pressure with increased protein and lymphocytes

Front 507

how can CDV virus/viral nucleic acid be detected?

Back 507

by RT-PCR to detect RNA in cells or CSF fluid

Front 508

two most important tests for diagnosis of CDV ag in tissues submitted

Back 508

FA/IHC

Front 509

what will detect the presence of viral Ag in leukocytes during the first five days post infection?

Back 509

FA test on air dried smears

Front 510

high titers of ____ is expected during acute infection

Back 510

anti-CDV IgM Ab

Front 511

what can serum anti CDV igG ab be due to?

Back 511

maternal Ab, vaccination, previous infection, or recent infection

Front 512

what confirms a CDV diagnosis?

Back 512

presence of high concentration of anti CDV IgG ab in CSF

Front 513

CDV treatment

Back 513

supportive. Vitamin A/C supplements? Anticonvulsants, antibiotics

Front 514

best vaccine for protection

Back 514

MLV-CDV

Front 515

pups that consume colostrum can be successfully vaccinated at

Back 515

12-14 weeks of age

Front 516

ICH stands for

Back 516

infectious canine hepatitis

Front 517

ICH is due to

Back 517

CAV-1

Front 518

CAV1 virus family

Back 518

adenoviridae

Front 519

CAV1 is also known as

Back 519

rubarth's disease, fox encephalitis

Front 520

most CAV1 infections are

Back 520

subclinical

Front 521

what type of inclusions does CAV1 cause?

Back 521

basophilic, IN in hepatocytes

Front 522

most CAV1 infections are

Back 522

subclinical, in dogs less than 6 mo of age

Front 523

source of CAV1 virus

Back 523

infected and recovered dogs

Front 524

how is virus excereted by recovered dogs?

Back 524

in urine from infected renal tubule cells

Front 525

transmission of CAV1

Back 525

direct contact- mucosal contact with urine, fomites

Front 526

incubation period of CAV1

Back 526

1 week

Front 527

different syndroms of CAV1

Back 527

inapparent/mild respiratory, acute/hepatitis, ocular, encephalitis

Front 528

what form is very common and important in foxes

Back 528

encephalitic form

Front 529

where does the virus first replicate

Back 529

in the oropharynx/tonsils

Front 530

CAV1 infects ________ cells

Back 530

vascular endothelial cells

Front 531

vascular endothelial cell injury leads to

Back 531

consumptive coagulopathy - DIC, generalized bleeding tendencies

Front 532

damage to hepatocytes results in

Back 532

acute hepatic necrosis with typical inclusions

Front 533

when do antibodies appear?

Back 533

~7 days post infection

Front 534

where are immune complexes deposited?

Back 534

in the kidneys and the eye (ciliary body, resulting in kerato uveitis = blue eye)

Front 535

clin path of CAV1

Back 535

marked neutropenia and lymphopenia in early stages, TCP with prolonged bleeding time, elevated liver enzymes

Front 536

pathological lesion at necropsy

Back 536

swollen, mottled liver with a markedly swollen, sometimes hemorrhagic gallbladder wall. Petechial hemorrhages

Front 537

most important tests for diagnosis? What do they detect?

Back 537

FA and IHC; presence of viral Ag

Front 538

dogs that survive infection develop

Back 538

lifelong immunity

Front 539

what is the vaccine of choice?

Back 539

CAV2-MLV, because it will also protect against CAV1 and is not associated with blue eye

Front 540

CHV causes ___________ in puppies less than 2 weeks old

Back 540

acute, highly lethal generalized infection of young puppies

Front 541

CHV1 is an ________ and there is _____ serotype(s)

Back 541

alphaherpesvirus; one

Front 542

how is CHV transmitted in adult dogs

Back 542

venereally

Front 543

incubation period of CHV?

Back 543

3-7 days

Front 544

does CHV present with fever?

Back 544

no

Front 545

clinical signs of affected puppies?

Back 545

crying, whining, soft green stool, labored breathing, abdominal pain, death within 24-48 hours

Front 546

where is CHV latent?

Back 546

in the sacral ganglia

Front 547

where does CHV1 replicate?

Back 547

on the genital mucosal surface

Front 548

how can newborn pups become infected?

Back 548

during passage through the vagina

Front 549

if the bitch is ____ at whelping, she will pass the anti-CHV1 Ab to the pups via _____ and the pups will be protected against the disease but not the ____

Back 549

seropositive; colostrum; infection

Front 550

if the bitch is _____ at whelping the pups will have _____ and some will develop the ____ form of CHV disease

Back 550

seronegative; no protection; fatal

Front 551

the fatal disseminated form of of the disease is only observed in

Back 551

bitches whelping for the first time

Front 552

what type of lesions may be seen in adults

Back 552

genital

Front 553

bad bitches

Back 553

those with poor mothering ability

Front 554

can you make a diagnosis in puppies based on gross lesions?

Back 554

yes

Front 555

histopath of CHV

Back 555

widespread foci of necrosis and hemorrhage in liver, kidneys, and lungs, with IN inclusions observed in the occasional infected cells in necrotic lesions

Front 556

CHV1 grows well in

Back 556

TC

Front 557

what will PCR ID

Back 557

viral DNA from mucosal samples and from infected tissues

Front 558

dogs that become infected with develop ____

Back 558

NAb

Front 559

NAb will not prevent ____ of the virus from the nerve cells to the mucosa

Back 559

recrudescence

Front 560

if a pup is infected at birth and is protected from dz by maternal Ab, it is possible for the virus to latently infect the nerve cells of the pup without the pup actually mounting an ______. When this pup becomes an adult it can ______ the virus

Back 560

immune response; recrudescence

Front 561

what will increase survival of the infected puppies?

Back 561

increasing body temperature from 101 to 103F treatment

Front 562

temperature sensitive mutants

Back 562

viruses that have been selected for their inability to grow at normal body temperature

Front 563

advantage of temperature sensitive viruses in vaccines?

Back 563

availble for respiratory viruses, they can overcome the protection provided by passive transfer of Abs and can therefore be given to young animals

Front 564

gene deleted viruses

Back 564

can infect animals but cannot cause disease

Front 565

importance of gene deleted virus vaccines

Back 565

infection allows the animal to mount a good response to the virulent virus

Front 566

genetically enginnered vaccines in test in slaughter programs

Back 566

a serological test to detect circulating Ab to the TK protein (for example) can easily ID and take out/slaughter animals that have become infected despite vaccination

Front 567

recombinanct vaccines

Back 567

the recombinant vaccina virus vaccine carries an extra gene that is inserted into the genome. When in the body, the immune response mounts against the vaccina virus proteins and the virus protein. Circulating neutralizing Ab to the virus protein will protect vaccinated animals against later infection with the virulent virus.

Front 568

EIA is also known as

Back 568

swamp fever

Front 569

how is EIA transmitted?

Back 569

arthropod vectors; transfer of viral infected blood cells

Front 570

can EIA be cured?

Back 570

no, horses remain persistent carriers

Front 571

eIA virus can be detected in the ______ of all infected horses (as a provirus)

Back 571

macrophages/monocytes

Front 572

where is the virus during acute illness?

Back 572

blood and secretions

Front 573

why is the blood of healthy carriers infectious when injected into healthy horses?

Back 573

due to the presence of the provirus in circulating monocytes and macrophages

Front 574

clinical signs of acute disease

Back 574

high fever, severe anemia, anorexia, ataxoai, weakness, TCP with petechial hemorrhages on mucosal surfaces. Rapid weight loss, ventral edema.

Front 575

EIA incubation period

Back 575

7-21 days

Front 576

how long will acute signs of EIA last?

Back 576

about a week

Front 577

when will signs of chronic disease be seen?

Back 577

weeks to months after initial acute attack

Front 578

what characterizes EIA?

Back 578

the recurrent attacks of fever

Front 579

characteristics of recurrenct attacks

Back 579

fever, anemia, weakness, emaciation, ventral edema, TCP, hypergammaglobulinemia

Front 580

where does EIA replicate

Back 580

in resident macrophages

Front 581

when does EIA stop replicating and go into latency?

Back 581

when circulating Ab to GP90 appear

Front 582

in between recurrent attacks, where is the EIA virus?

Back 582

in resident macrophages as a provirus

Front 583

EIA constantly undergoes ____ in the ___ as the latent virus replicates at low levels

Back 583

antigenic drift; gp90

Front 584

during a recurrent attack the ____ released by the infected macrophages that undergo lysis attach to circulating RBC

Back 584

hemagglutinins

Front 585

circulating Ab attach to the HA and ___ _____ on the RBC resulting in RBC damage

Back 585

fix complement

Front 586

how are damaged RBC removed from circulation?

Back 586

by erythrophagocytisis via the mononuclear phagocytic system of the liver and spleen

Front 587

what is the anemia of EIA due to?

Back 587

hemolosys and erythrophagocytosis of complement coated RBC

Front 588

what is the only EIA protein to change antigenically?

Back 588

gp90

Front 589

immune-complex mediated glomerulonephritis

Back 589

Ag/ab complexes that are formed in the blood are deposited in kidney and small blood vessels

Front 590

why is hypergammaglobulinemia seen during each recurrent episode?

Back 590

due to ab production during clonal expansion of memory/plasma cells brought on by the high degree of virus replciation and viremia

Front 591

platelets from EIA virus infected hroses have significant levels of bound

Back 591

IgM or IgG

Front 592

many of the clinical signs associated with EIA virus infection are caused by

Back 592

pro inflammatory mediatiors (TNFa, IL1, IL6) released in respsonse to infection of the macrophages

Front 593

chronic disease necropsy lesions

Back 593

hematopoiesis- yellow marrow of long bone is replaced by red marrow

Front 594

acute disease necropsy lesions

Back 594

widespread hemorhage, splenomagaly, emaciation, anemia, enlarged reddish-brown liver (necrosis//hemosiderin deposit)

Front 595

how can the provirus in the macrophage chromosome be detected

Back 595

by PCR

Front 596

can PCR different mecrophages producing infectious particles form those that are latently infected?

Back 596

no, horses remain persistent carriers

Front 597

RTPCR will ID macrophages with

Back 597

replicating virus

Front 598

two tests recognized by the state for the diagnosis of EIA infected horses

Back 598

C-ELISA, AGID

Front 599

what do C-ELISA and AGID dectect?

Back 599

circulating serum Ab to the core p26 protein

Front 600

which test is used for final determination of positivity

Back 600

Coggins/AGID

Front 601

animals in the acute phase of infection may be sero____

Back 601

negative

Front 602

what is the sero test result of a foal born to infected dam?

Back 602

will test seropos until 6 months of age. If truly negative will then test seronegative

Front 603

most animals will develop persistent circulating Ab within ___d of infection

Back 603

45

Front 604

infected animals will generally test positive by ELISA ____d after infection and AGID positive by ___d after infection

Back 604

12, 24

Front 605

most important cause of abortion in mares

Back 605

EHV1

Front 606

equine rhinopneumonitis virus

Back 606

EHV4

Front 607

transmission of EHV1

Back 607

inhalation of infected droplets during respiratory diseases or by ingestion/mucosal contact with infected material such as aborted fetuses

Front 608

major cause of EHV virus recrudescence?

Back 608

stress

Front 609

when is myeloencephalopathy seen with EVH1

Back 609

older horses, predominantly where horses congregate

Front 610

when will EHV abortion occur?

Back 610

after the 6th month of pregnancy

Front 611

abortion storms

Back 611

up to 90% of pregnant mares on a farm can abort

Front 612

most EHV1 infections are

Back 612

subclinical

Front 613

what is the only evidence of infection?

Back 613

seroconversion

Front 614

when will EHV1 myeloencephalopathy be observed?

Back 614

in adult mares during/following abortion storms; 1-3 months after foaling, a few weeks after a respiratory dz outbreak

Front 615

signs of myeloencephalopathy

Back 615

incoordination, ataxia, posterior paresis, paraplegia leading to quadriplegia, recumbancy, death

Front 616

what is advocated in most cases of EHV1 myeloencephalopathy

Back 616

euthanasia

Front 617

what is the paralytic or myeloencephalitic form of EHV1 infection caused by

Back 617

the neuropathogenic EHV1

Front 618

how does the neuropathogenic EHV1 differ from the respiratory virus

Back 618

a mutation in the DNA polymerase virus

Front 619

where will EHV1 replicate

Back 619

upper respiratory tract and lungs (often with no resultant dz)

Front 620

how does the virus spread throughout the body?

Back 620

picked up by alveolar macrophages in the lung, brought to lymph nodes, infect lymphocytes, and carried throughout body

Front 621

how is virus carried to the placenta?

Back 621

by infected lymphocytes

Front 622

how does the virus kill the fetus?

Back 622

invades, destroys lymphocytes, causes focal hepatic necrosis, widespread hemorrhate and death

Front 623

fetuses are aborted as a result of placental infection- the placenta _________

Back 623

separates from the endometrium

Front 624

____ has been associated with vasculitis and thrombosis of blood vessels (Arterioles) in the spinal cord and CNS

Back 624

myeloencephalopathy

Front 625

unless proven otherwise, all abortion in mares

Back 625

should be considered as caused by EHV1

Front 626

aborted fetus lesions

Back 626

icterus, petechial hemorrhages and hepatic necrosis

Front 627

what lesions are charactersistic enough to make a presumptive diagnosis of EHV1 abortion?

Back 627

aborted fetal liver and spinal cord

Front 628

PCR can diagnose EHV1 by detecting

Back 628

viral DNA in blood leukocytes and in nucleic acid extracted from necrotic lesions

Front 629

most consistent lesions in aborted fetuses

Back 629

multiple focal areas of necrosis in the liver with IN inclusions in ifnected cells

Front 630

predominant lesion of myeloencephalopathy?

Back 630

vasculitis

Front 631

a specific PCR is available for

Back 631

differentiating neuropath EHV1 from respiratory EVH1 (SNP in the dna polymerase gene)

Front 632

tests to detect viral Ag in infected cells within necrotic lesions and nervous tissues?

Back 632

FA, IHC

Front 633

can VNT distinguish between EHV1 and EHV4?

Back 633

no

Front 634

what can distinguish between EHV1 and EHV3?

Back 634

C-ELISA

Front 635

is seroconversion a diagnostic test?

Back 635

no

Front 636

_____ is thought to occur only in the presence of circulating Ab

Back 636

myeloencephalopathy

Front 637

what drug can be used to treat EHV1?

Back 637

acyclovir

Front 638

when should pregnant mares be vaccinated and with what vaccine type?

Back 638

5,7,9 months with inactivated virus

Front 639

equine viral arteritis

Back 639

a respiratory and reproductive disease that occurs worldwide. Primarily sublicnical in standarbreds

Front 640

equine viral arteritis family and genus

Back 640

arteriviridae, arterivirus

Front 641

EVA is an ___ virus

Back 641

small, enveloped, RNA

Front 642

transmission of EVA

Back 642

aerosol transmission during outbraks of respiratory dz and venereally through infected semen. Also mucosal contact with aborted foals/palcents

Front 643

most important means of transmission

Back 643

venereally

Front 644

EVA incubation period

Back 644

7 days

Front 645

disease characteristics

Back 645

fever lasting 1 week, URI, severe conjunctivitis with photophobial, supraorbital/periorbital edema, edema of loer legs, genitalia, abdomen, and change in gait (ataxia.stiffness)

Front 646

abortion in mares Is associated with

Back 646

respiratory disease

Front 647

most infected animals will _____

Back 647

recover

Front 648

where does EVA primarily replication?

Back 648

in macrophages and endothelial cells of blood vessles

Front 649

severe necrotizing panvasculitis and thrombosis of arterial wall results in

Back 649

widespread hemorrhages and edema

Front 650

abortion is a result of severe

Back 650

necrotizing myometritis

Front 651

in the stallion, where will the virus establish infection?

Back 651

in the ampulla

Front 652

in the stallion, the persistent infection is

Back 652

inapparent and testosterone dependent

Front 653

what in the history wll allow for a provisional dx of EVA?

Back 653

severe conjunctivitis, edema of limbs, abortions following clinical illness

Front 654

clin path of EVA

Back 654

leukopenia, TCP may be present, no characteristic findings

Front 655

where can EVA be isolated?

Back 655

on TC from blood and infected fetus

Front 656

what can confirm EAV on an isolated virus?

Back 656

FA test

Front 657

what test will detect EVA in nucleic acid extracted from samples

Back 657

RT-PCR

Front 658

good tests for the detection of EVA viral proteins in infected cells within necrotic lesions in the feuts

Back 658

FA, IHC

Front 659

can seroconversion be used to make a diagnosis

Back 659

yes

Front 660

what type of EVA vaccine is available?

Back 660

MLV

Front 661

will vaccinated stallions still carry the virus?

Back 661

yes

Front 662

IBR is primarily a disease of ____ cattle while IPV affects ____ Cattle primarility

Back 662

beef; dairy

Front 663

what has led to an increase of BHV1 infections?

Back 663

intensive farming

Front 664

BHV1 is characterized by ____ rates but low _______

Back 664

high morbidity, low fatality

Front 665

IBR and IPV are the same ____ but can be _____genetically

Back 665

serotype; differentiated

Front 666

transmission of IBRV

Back 666

aerosol

Front 667

IPV transmission

Back 667

coitus

Front 668

characteristic of respiratory disease

Back 668

can be subclinica, mild of severe. Sudden onset of high fever accompanied by profuse naso-ocular discharges

Front 669

progression of nasal discharge

Back 669

serous ---> mucopuruluent with crusting of the discharge around nares. Accompanied by coughing, increased RR, increased lung soundss, and open mouth breathing

Front 670

red nose

Back 670

severe inflammation of nasal turbinates/nasal mucosa; necrosis, ulceration and plaques noted

Front 671

most mortality of BHV1 is due to

Back 671

secondary bacterial infections

Front 672

shipping fever

Back 672

BHV1 predisposes to infection with mannhemia hemolytica

Front 673

genital form of BHV1

Back 673

lesions on the repro tract develop 2-3 d following coitus. Cows- frequent urination, tail switching, vaginal discharge, small pustules/white necrotic areas and ulcerso n vulva/vaginal mucosa. Bulls- lesions on prepuceand penis

Front 674

do BHV1 lesions cause repro problems?

Back 674

no

Front 675

when can BHV abortion occur?

Back 675

usually in last trimester as a sequel to respiratory infection

Front 676

ocular form of BHV

Back 676

conjunctivitis, winter pink eye

Front 677

ocular form characteristics

Back 677

conjunctivitis, profuse lacrimation, often in absence of respiratory dz.

Front 678

who is affected by the systemic form of BHV

Back 678

new born calves less than 2 weeks of ages that were affected in utero or soon after birth (calves that have no ab to BVH1).

Front 679

systemic BHV

Back 679

acute dz, high fever, anorexia, respiratory distress and diarrhea with very high (100%) mortality

Front 680

DNS form of BHV

Back 680

rarely seen in yearlings and older cattle, characterized by incoordination, tremor, convulsion, and high case fatality rate

Front 681

bovine herpes encephalitis caused by

Back 681

BHV5

Front 682

BHV incubation period

Back 682

1 week

Front 683

BHV1 infects

Back 683

moist mucous membranes. Lesions typically erosive, ulcerative, inflammatory and necrotic

Front 684

where does BHV replicate?

Back 684

locally in mucosal cells and spreadds to submucos

Front 685

virus infects the ____ ____ in the mucosa and is taken up by macrophages

Back 685

sensory nerves

Front 686

where does BHV become latent

Back 686

in the nuclei of the neurons of the sensory nerve

Front 687

infected macrophages carry the virus to lymphnodes where they infect and

Back 687

go latent in t-lymphocytes

Front 688

infected lymphocytes can cause ____ and ___ infections

Back 688

placental and fetal

Front 689

viral recrudescnce allows the virus to

Back 689

reinfect the mucosa, replicate and spread (to other animals/to palcenta)

Front 690

BHV1 infected lung macrophages

Back 690

cannot function properly allowing bacteria to replciate and causing secondary infections

Front 691

BHV1 recrudesence can occur in the presence of

Back 691

circulating antibodies

Front 692

____ animals can still become infected with BHV1 but may not become clinically ill

Back 692

seropositive

Front 693

what is very important at preventing BHV1 infection

Back 693

mucosal immunity

Front 694

how should BHV1 vaccines be administered

Back 694

intranasally

Front 695

CMI is more important in _______ while humoral immunity is more important in ____

Back 695

recovery from infection; preventing reinfection

Front 696

BHV1 treatment

Back 696

symptomatic

Front 697

MLV vacciness can be

Back 697

abortogenic

Front 698

vaccine that is safe for pregnant cows

Back 698

MLV with temerature sensitive IBR virus

Front 699

BLV is a

Back 699

deltaretrovirus

Front 700

what is the BLV source of infection

Back 700

seropositive PI cattle

Front 701

is there a genetic predisposition to BLV?

Back 701

yes

Front 702

how is BLV introduced to a herd

Back 702

by acquiring new PI cattle

Front 703

which cattle have the highest evidence of BLV lymphosarcoma

Back 703

cattle between 4-8 years old

Front 704

primary transmission of BLV

Back 704

blood inoculation (insect vectors)

Front 705

where is BLV in seropsitive cattle?

Back 705

in the leukocytes

Front 706

what procedure is very important in transmitting the virus

Back 706

dehorning

Front 707

what is essential for successful transmission

Back 707

prolonged close physical contact

Front 708

two forms of BLV

Back 708

lymphosarcoma, persistent lymphocytosis

Front 709

BLV induced lymphosarcoma

Back 709

highly fatal system malignant neoplasia of the reticuloendothelial system. Characterized by developments of BLV infected neoplastic lymphocytes.

Front 710

Cattle with BLV induced LSA are both

Back 710

seropositive and PCR positive

Front 711

multicentric LSA

Back 711

tumors in most lymph nodes/lymphoid tissues.

Front 712

all cases of LSA are characterized by

Back 712

decreased appetite, decrased milk production, wEIGHT LOSS, and anemia

Front 713

abomasal LSA results in

Back 713

diarrhea, melena

Front 714

cardiac LSA results in

Back 714

hydropericard, hydrothorax, brisket edema

Front 715

_______ may be seen with most cases of LSA

Back 715

enlarged superficial lymph nodes

Front 716

persistent lymphocytosis

Back 716

benign lymphoproliferative condition seen in healthy BLV infected cattle. Cattle show no clinical symptoms, but have marked increase in (Abnormal) circulating lymphocyte number (as high as 150Kcells/ml).

Front 717

animals with persistant lymphocytosis will rarely

Back 717

develop LSA

Front 718

all BLV infected cattle are both

Back 718

seropostive and pcr positive

Front 719

sporadic bovine leukosis

Back 719

lymphosarcomas seen in cattle less than 3 years of age.

Front 720

juvenile LSA

Back 720

calves 1-6mo old

Front 721

thymic LSA and/or cutaneous LSA

Back 721

cattle 1-2 years

Front 722

animals with sporadic bovine leukosis are BLV sero_____

Back 722

negative

Front 723

incubation period for LSA or PL

Back 723

2-4 years

Front 724

BLV infects and transforms b lymphocytes and itnegrates in dna forming a

Back 724

provirus

Front 725

BLV viremia

Back 725

does not occur

Front 726

transmission is via

Back 726

infected lymphocytes

Front 727

60% of animals exposed to BLV will

Back 727

fail to become infected, remain PCR neg and seroneg

Front 728

30% of animals exposed to BLV will become

Back 728

PCR positive and seropositive persistent carriers

Front 729

PCR

Back 729

very sensitive, detect presence of BLV provirus in infected lymphocytes in individual animals and in bulk milk

Front 730

what test is used in test/slaughter programs?

Back 730

ELISA