Retroviridae part 2 Flashcards
What is the etiology of avian leukosis? how are the viruses classified?
- 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
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.
egg; first few; persistent viremia
t/f - birds that become PI with avian leukosis may grow normally but subsequently develop viremia
true
t/f - birds that are PI with avian leukosis are not a threat to healthy birds.
false; major source of virus that spreads to other birds by contact
describe avian leukosis transmission/outcomes
- 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.
primary target of avian leukosis?
lymphocytes, with b-lymphocyte markers in bursa
what is the difference between exogenous replication competent/defective viruses?
- 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
what are the three major clinical features of exogenous replication competent avian leukosis viruses?
- lymphoid leukosis (visceral lymphomatosis; big liver dz)
- osteopetrosis (thick leg); proliferation of periosteal osteoblasts of long bones
- renal tumors
what are the three clinical features of exogenous replication defective avian leukosis viruses?
- myelocytomatosis
- myeloblastosis
- erythroblastosis
outcome of above: anemia, leukemia
what is the etiology of FIV? what is the grouping?
- feline lentivirus
- 5 subtypes (a-e); variations of env gene
which subtypes of feline lentivirus dominate north america?
a & b
t/f- FIV does not infect wild felids
false; it can infect some wild felids
FIV is mainly shed in ______
saliva
FIV infection lasts _____
whole life
principal mode of FIV transmission is ______
cat bites
the hallmark of FIV is disruption of _______; this is due to progressive loss of ________
immune function; CD4 t-helpers in early stages, as well as CD8’s in later
what are the four causes of CD4 loss in FIV cats?
1- decreased production due to bone marrow or thymic infection
2- cytopathic effect of fiv
3- CTL mediated cytoloysis of cells
4- death by apoptosis
what are the three phases of FIV?
acute
latent
terminal
what is characteristic of the acute phase of FIV?
- asymptomatic; or transient fever, malaise, lymphadenopathy, and diarrhea
- antibodies against virus, but ineffective at eliminating
what is characteristic of the latent phase of FIV?
- follows acute phase
- variable duration; may persist for years before signs of immunodeficiency occur
- persistent lymphadenopathy
what is characteristic of the terminal phase of fiv?
- 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
what is the major tool for diagnosis of FIV? what protein is involved?
detection of p24 core protein by snap test
t/f - FIV can infect humans
false; no evidence of this. highly species-specific virus. felines only
what is the etiology of equine infectious anemia? what else is it called?
equine lentivirus
AKA Swamp Fever
transmission of equine infectious anemia (EIA) occurs by transfer of ________ from infected horse to another.
blood cells
what can aid in the transmission of EIA?
tabanids (horseflies, breeze flies), stable flies (Stomoxys), mosquitos, and probably Culicoides spp
all horses infected with EIA develop a lifelong _____
viremia
in EIA: Persistent __________ results in damage to vascular endothelium (_______), followed by inflammatory changes in parenchymatous organs, especially ______.
antigen-antibody formation [immune complex hypersensitivity]; vasculitis; the liver
what are some potential CNS signs in horses with EIA?
ataxia, spinal leptomeningitis, encephalomyelitis
due to CNS vasculitis
what may result in the kidneys of a horse with EIA?
glomerulonephritis; immune complex mediated
how does anemia happen in horses with EIA?
- 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]
how does the MAC work, and why is it relevant to EIA? (think back to immuno.. :( )
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
in EIA, you will see splenic macrophages doing what?
phagocytosing RBC’s
what are the three stages of EIA? What are their important features?
- Acute: severe anemia, jaundice, blood-stained feces, petechial hemorrhages of mucosae
- subacute: moderate fever –> recovery
- chronic: episodic or persistent fever, cachexia, ventral edema.
how does the spleen appear grossly in EIA?
enlarged, hemorrhagic
bone marrow ______ is common in EIA
hyperplasia
what’s the name of the test for EIA Dx?
Coggins test
what is the coggins test?
- 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
the coggins test detects all infected animals except:
those in the early incubation period, first 2-3 wks after infection
what causes CAE (caprine arthritis-encephalomyelitis)? who is the host?
caprine lentivirus
goats!
the main route of CAE transmission is _______
colostrum and milk from doe to newborn
CAE results in a persistent infection of ______
monocytes and macrophages
what’s the role of immune complexes in CAE?
immune complex hypersensitivity rxns lead to chronic inflammatory response in tissues.
with goats that have CAE, arthritis is seen in goats of what age? how common is it? how does it appear clinically?
goats 12 months and up
seen 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)
in goats with CAE, encephalomyelitis appears at what age? how would you characterize the encephalomyelitis?
- kids 1 to 5 months of age
- progressive leukoencephalomyelitis with ASCENDING paresis and paralysis
in addition to arthritis and encephalomyelitis, what are two clinical signs common to CAE?
- interstitial pneumonia (mostly in adults)
- indurative mastitis (“Hard Bag”); swelling of mammary; firm
methods of controlling CAE?
- 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
what is the etiology of Maedi/Visna dz?
ovine lentivirus
they are caused by the same or very closely related lentiviruses
what;s the host of Maedi/Visna dz?
adult sheep, and some goats
what are the mehtods of transmission of Maedi/Visna dz?
- aerosol
- ingestion of feces/urine contaminated water
- colostrum/milk; intrauterine infection rare
- biting arthropods
- contaminated surgical instruments
Maedi/Visna dz result in a lifelong ______-associated viremia
mononuclear(lymphocyte) cell
clinical signs of Maedi dz include?
- shortness of breath (ovine progressive pneumonia - OPP)
- couhging, progressive weight loss, emaciation, dyspnea
- pregnant ewes may abort or deliver weak lambs.
clincial signs of Visna dz?
- wasting
- slowly progressive ataxia, trembling, paresis or paralysis
- diffuse, demyelinating encephalomyelitis
what two major signs are common to Maedi and Visna dz?
arthritis: polyarthritis, severe lameness
non-inflammatory indurative mastitis
Maedi/Visna persists in the presence of _________
antibodies and cell-mediated immune response
