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Taylor Viro Final > retro 2 > Flashcards

retro 2 Flashcards

1
Q

What is the etiology of avian leukosis? how are the viruses classified?

A

-alpharetrovirus-10 subgroups, based on antigenic differences in viral envelope antigens-subgroup a & b; most field outbreaks of leukosis-subgroups c & d; infrequent-subgroup e; endogenous, non-oncogenic-subgroup j; myeloid leukosis

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2
Q

If avian leukosis virus is transmitted congenitally via the _____ or within the ______ days of life, the chicken develops a _____ because of the induction of immunological tolerance.

A

egg; first few; persistent viremia

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3
Q

t/f - birds that become PI with avian leukosis may grow normally but subsequently develop viremia

A

true

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4
Q

t/f - birds that are PI with avian leukosis are not a threat to healthy birds.

A

false; major source of virus that spreads to other birds by contact

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5
Q

describe avian leukosis transmission/outcomes

A

-if infected horizontally when more than 5 or 6 days of age, they are unlikely to get leukemia. instead they develop transient viremia, and produce a neutralizing antibody-vertical transmission trhough provirus integrated into host germ cells; usually latent, no viremia, no leukemia.

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6
Q

primary target of avian leukosis?

A

lymphocytes, with b-lymphocyte markers in bursa

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7
Q

what is the difference between exogenous replication competent/defective viruses?

A

-competent: proviral DNA is integrated into many different kinds of cells—sometimes, by chance, in a location where the activity of a c-onc gene is disturbed-defective: viruses acquire an oncogene (v-onc) from a cellular onc (conc) gene and then can induce malignant tumors rapidly

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8
Q

what are the three major clinical features of exogenous replication competent avian leukosis viruses?

A

-lymphoid leukosis (visceral lymphomatosis; big liver dz)-osteopetrosis (thick leg); proliferation of periosteal osteoblasts of long bones-renal tumors

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9
Q

what are the three clinical features of exogenous replication defective avian leukosis viruses?

A

-myelocytomatosis-myeloblastosis-erythroblastosisoutcome of above: anemia, leukemia

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10
Q

what is the etiology of FIV? what is the grouping?

A

-feline lentivirus-5 subtypes (a-e); variations of env gene

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11
Q

which subtypes of feline lentivirus dominate north america?

A

a & b

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12
Q

t/f- FIV does not infect wild felids

A

false; it can infect some wild felids

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13
Q

FIV is mainly shed in ______

A

saliva

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14
Q

FIV infection lasts _____

A

whole life

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15
Q

principal mode of FIV transmission is ______

A

cat bites

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16
Q

the hallmark of FIV is disruption of _______; this is due to progressive loss of ________

A

immune function; CD4 t-helpers in early stages, as well as CD8’s in later

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17
Q

what are the four causes of CD4 loss in FIV cats?

A

1- decreased production due to bone marrow or thymic infection2- cytopathic effect of fiv3- CTL mediated cytoloysis of cells4- death by apoptosis

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18
Q

what are the three phases of FIV?

A

acutelatentterminal

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19
Q

what is characteristic of the acute phase of FIV?

A

-asymptomatic; or transient fever, malaise, lymphadenopathy, and diarrhea-antibodies against virus, but ineffective at eliminating

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20
Q

what is characteristic of the latent phase of FIV?

A

-follows acute phase-variable duration; may persist for years before signs of immunodeficiency occur-persistent lymphadenopathy

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21
Q

what is characteristic of the terminal phase of fiv?

A

-immunodeficiency syndrome-predisposed to chronic recurrent, opportunistic infections cause by bact and fung… i.e. chronic stomatitis, gingivits, chronic respiratory dz, chronic diarrhea/wasting, dermatitis, neuro signs, etc

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22
Q

what is the major tool for diagnosis of FIV? what protein is involved?

A

detection of p24 core protein by snap test

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23
Q

t/f - FIV can infect humans

A

false; no evidence of this. highly species-specific virus. felines only

24
Q

what is the etiology of equine infectious anemia? what else is it called?

A

equine lentivirusAKA Swamp Fever

25
Q

transmission of equine infectious anemia (EIA) occurs by transfer of ________ from infected horse to another.

A

blood cells

26
Q

what can aid in the transmission of EIA?

A

tabanids (horseflies, breeze flies), stable flies (Stomoxys), mosquitos, and probably Culicoides spp

27
Q

all horses infected with EIA develop a lifelong _____

A

viremia

28
Q

in EIA: Persistent __________ results in damage to vascular endothelium (_______), followed by inflammatory changes in parenchymatous organs, especially ______.

A

antigen-antibody formation [immune complex hypersensitivity]; vasculitis; the liver

29
Q

what are some potential CNS signs in horses with EIA?

A

ataxia, spinal leptomeningitis, encephalomyelitisdue to CNS vasculitis

30
Q

what may result in the kidneys of a horse with EIA?

A

glomerulonephritis; immune complex mediated

31
Q

how does anemia happen in horses with EIA?

A

-virus antigens adsorb to RBC’s-host antibodies bind the antigens-erythrophagocytosis is triggered by mononuclear phagocytes, and there is complement mediated erythrolysis (hemolysis) [type II hypersensitivity]

32
Q

how does the MAC work, and why is it relevant to EIA? (think back to immuno.. :( )

A

MAC binds to the surface of the RBC, due to activation of complement; allows water, ions, other molecules to move freely in/out of a cell, resulting in cell death. This is one of the mechanisms for anemia in EIA

33
Q

in EIA, you will see splenic macrophages doing what?

A

phagocytosing RBC’s

34
Q

what are the three stages of EIA? What are their important features?

A

-Acute: severe anemia, jaundice, blood-stained feces, petechial hemorrhages of mucosae-subacute: moderate fever –> recovery-chronic: episodic or persistent fever, cachexia, ventral edema.

35
Q

how does the spleen appear grossly in EIA?

A

enlarged, hemorrhagic

36
Q

bone marrow ______ is common in EIA

A

hyperplasia

37
Q

what’s the name of the test for EIA Dx?

A

Coggins test

38
Q

what is the coggins test?

A

-AGID test-detects antibodies to p26 (major group specific antigen of EIA)-results valid for 6 mo to 1 yr from date of blood collection

39
Q

the coggins test detects all infected animals except:

A

those in the early incubation period, first 2-3 wks after infection

40
Q

what causes CAE (caprine arthritis-encephalomyelitis)? who is the host?

A

caprine lentivirusgoats!

41
Q

the main route of CAE transmission is _______

A

colostrum and milk from doe to newborn

42
Q

CAE results in a persistent infection of ______

A

monocytes and macrophages

43
Q

what’s the role of immune complexes in CAE?

A

immune complex hypersensitivity rxns lead to chronic inflammatory response in tissues.

44
Q

with goats that have CAE, arthritis is seen in goats of what age? how common is it? how does it appear clinically?

A

goats 12 months and upseen most often-appears as: unilateral or bilateral swelling of mostly carpal joints (big knee-also appears as pain and thickening of joint capsules (hyperplastic synovitis)

45
Q

in goats with CAE, encephalomyelitis appears at what age? how would you characterize the encephalomyelitis?

A

-kids 1 to 5 months of age-progressive leukoencephalomyelitis with ASCENDING paresis and paralysis

46
Q

in addition to arthritis and encephalomyelitis, what are two clinical signs common to CAE?

A

-interstitial pneumonia (mostly in adults)-indurative mastitis (“Hard Bag”); swelling of mammary; firm

47
Q

methods of controlling CAE?

A

-kids must be removed from dam at birth, and provided colostrum from pregnant free does-colostrum from CAE does can be used if treated at 56C for one hour

48
Q

what is the etiology of Maedi/Visna dz?

A

ovine lentivirusthey are caused by the same or very closely related lentiviruses

49
Q

what;s the host of Maedi/Visna dz?

A

adult sheep, and some goats

50
Q

what are the mehtods of transmission of Maedi/Visna dz?

A

-aerosol-ingestion of feces/urine contaminated water-colostrum/milk; intrauterine infection rare-biting arthropods-contaminated surgical instruments

51
Q

Maedi/Visna dz result in a lifelong ______-associated viremia

A

mononuclear(lymphocyte) cell

52
Q

clinical signs of Maedi dz include?

A

-shortness of breath (ovine progressive pneumonia - OPP)-couhging, progressive weight loss, emaciation, dyspnea-pregnant ewes may abort or deliver weak lambs.

53
Q

clincial signs of Visna dz?

A

-wasting-slowly progressive ataxia, trembling, paresis or paralysis-diffuse, demyelinating encephalomyelitis

54
Q

what two major signs are common to Maedi and Visna dz?

A

arthritis: polyarthritis, severe lamenessnon-inflammatory indurative mastitis

55
Q

Maedi/Visna persists in the presence of _________

A

antibodies and cell-mediated immune response

Taylor Viro Final (12 decks)

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