L12: BLV And Anaplasma (Donovan) Flashcards
3 forms of “SPORADIC” Bovine LSA**
1) Calf/Juvenile form
- generalized lymphadenopathy in calves and young heifers
2) Thymic/Adolescent form
- thymic involvement in 6-24 mo. Heifers
3) Cutaneous form
- multiple cutaneous lesions in young cattle (
Forms of Bovine LSA
Sporadic Multicentric Cardiac Abomasal Uterine Other (eyes, spinal cord)
Multicentric LSA: CS
- enlarged peripheral LN, esp. Internal iliac and/or subaortic
- dyspnea and/or bloat if thoracic LN involved
- enlarged internal LN
CS of Cardiac LSA
-occasionally see CHF due to lesion in RA/RV
+/- murmur
CS of abomasal LSA
Wt. loss Melena Outflow obstruction "Papple-shaped" abdomen (Abomasum can no longer secrete acid)
CS of uterine LS
Palpable masses in the uterus
+/- abortion
Retrobulbar LSA –>
Exophthalmos
LSA in spinal cord –>
- acute downer cow
- posterior paresis/paralysis
Epidemiology of bovine LSA: animal causes
- genetic susceptibility to viral infection (not well defined)
- genetic susceptibility to develop tumors (BoLA haplotype): many Holsteins carry this!
Epidemiology of bovine LSA: infectious causes
BLV
Epidemiology of bovine LSA: environmental causes
Nutrition?
Concurrent infection?
Other stressors? (Ie. Stress of calving)
T/F: animal MUST have genetic susceptibility for tumor production to occur
T
-LSA occurs in about 2% of BLV+ cattle
Clin path of bovine LSA
Lymphocytosis +/- anemia
Dx of bovine LSA
- AGID to look for Ab
- ELISA to Ag
- Cytology of LN or suspect tissue aspirates
Pathology of LSA
- firm, cream-colored “fish flesh” tumors w/o uniform shape
- LN enlarged up to 0.5 meters in diameter
Ddx of bovine LSA
- Multicentric abscess (abscess won’t be freely moveable)
- Benign LN hyperplasia
- Abomasal ulcers, upper GI obstruction, peritonitis, vagal indigestion
Cardiac: traumatic pericarditis, endocarditis, altitude sickness
Uterine: adhesions, abscess, mummification, other tumors
Spinal: trauma, hypocalcemia, rabies, cattle grubs
Periocular: SCC, retrobulbar abscess
Prevalence of BLV based on geography
More prevalent in the south (most likely due to insect populations)
Is BLV found in semen?
Only if bull has inflammation in reproductive tract
Colostral half life of gp51 Ab?
26 days
Methods of transmission of BLV
- vertical
- colostrum and milk from infected cows
- uterine flush fluids and ova or embryos (unlikely)
- biting/sucking flies (very possible)
- injections
- rectal transmission
- dehorning
- ear tattooing
Testing methodologies for BLV
1) AGID gp51 (industry standard)
- detects Ab induced by infection
- seropositive 4-8 wks post-infection (will be FN during this time)
- sensitive and specific
2) RIA gp51 (same as AGID)
3) ELISA (same as AGID, but positive after only 2-4 wks)
- useful for pooled samples
Effect of BLV on cow health and productivity
- no link b/w BLV infection and mastitis or repro performance (UF study DID find an association)
- increased culling rate in BLV+ cows
1 cause of condemnation of dairy cattle carcasses at slaughter**
BLV infection
BLV may be zoonotic? Found in human breast tissue, and may be associated with breast cancer
:)
Control of BLV
- test and slaughter (requires 3 tests)
- test and segregate (after 2-3 tests)
- corrective management (palpation sleeves, single use needles, house replacements away from herd, dehorning practices)
- no vaccine
CS of anaplasmosis in calf/heifers
- inapparent, asymptomatic
- mild lethargy, partial anorexia for 24-48hrs
CS of anaplasmosis in heifers 1-2 yrs old:
- fever
- dyspnea
- moderate to severe anemia
- anorexia
- decreased rumen motility
- infrequently fatal
CS of anaplasmosis in cows > 2yrs old:
-very high fever (or hypothermia)
-anorexia and agalactia
-dec. rumen motility
-pale mm (anemia)
-constipation w/ dry, bile-stained (dark), mucus-coated feces
-staggering
+/- abortion
-watery blood that fails to clot
-uncommonly death
Geographic distr. of anaplasma
Southeast, West/northwest
Infectious causes of anaplasmosis
Anaplasma marginale
Anaplasma ovis in sheep (asymptomatic)
Environmental causes of Anaplasmosis
Ticks: Dermacentor
Biting flies: Tabanids
Transmission of anaplasma
- predominantly vectors: tick, horsefly (esp. In SE)**
- iatrogenic (common needles, dehorner, etc.)
calves, young heifers have innate resistance
Pathophys. Of Anaplasmosis
~30 day incubation period
# infected RBCs doubles daily for 7-10 days
-erythrophagocytosis of infected RBCs, predominantly in SP and LIV
-immune system coats RBCs w/ autoAb that enhance phagocytosis of infected AND normal RBCs –> severe anemia
-little IV hemolysis, NO hemoglobinuria**
-icterus mild if present
-survivors are chronic carriers
Clin path of anaplasmosis
PCV 12-15% --> CS of severe anemia PCV death Icterus index variable Marginal bodies seen in RBCs with stain -difficult to see if in recovery and infected RBCs destroyed and immature RBCs are prevalent
Dx of anaplasma
Serology:
- complement fixation
- rapid card agglutination
- cELISA
- only verify carrier state, not clinical cows**
- clinical cows won’t have Ab to these tests
Pathology of anaplamsa
- enlarged spleen
- pale mm, musculature, lungs
- distended GB
- variable icterus
- no hemoglobinuria
Ddx of anaplasma
3 and 4 are regional problems and not in SE
1) Lepto
- usually has marked icterus and hemoglobinuria
2) Toxic plants
- bracken fern, Senecia
3) Babesia
4) Bacillary hemoglobinuria
Management of anaplasma
- control ticks/biting flies, iatrogenic blood transmission
- abx: long-acting oxytet or chlortetracycline to eliminate carrier state
- killed vaccine
Vaccination for anaplasma
- killed vax made from erythrocytes of acutely infected cattle
- variable efficacy
- short duration of immunity
- can induce neonatal isoerythrolysis
Tx of anaplasma
Anemia: blood transfusion, reduce stress
Infection: oxytetracycline
Bovine Lymphosarcoma aka Bovine Enzootic Leukemia: signalment
- Adult cattle (>2yrs)
- assoc. with Bovine leukemia virus (BLV)
