CattleII1- Urinary Dz of Cattle

  1. What are the most common organisms causing ascending urinary tract infection in cattle? (2)
    E. coli and Corynebacterium renale
  2. In what conditions does C. renale cause UTI?
    alkaline pH urine--> adheres to urinary epithelium by pilli
  3. Pyelonephritis has ___________ clinical signs.
  4. What are clinical signs of cystitis? (6)
    dysuria, pollakiuria, hematuria, pyuria, painful bladder, blood/pus/crystal precipitate on vulva
  5. What are clinical signs of pyelonephritis? (6)
    fever/depression, colic, decreased feed intake, down on milk, renal pain/loss of lobulations, renal enlargement on rectal
  6. What laboratory changes will occur with urinary tract infection? (9)
    [CBC/Chem] Neutrophilia, increased fibrinogen, increased globulins, hypoalbuminemia, azotemia (pyelonephritis), [UA] proteinuria, low SG, culture, leukocyte casts
  7. What are predisposing factors for UTI? (7)
    female, urogenital trauma, abnormal vulvar conformation, bladder catheterization, urine retention, alkaline urine (C. renale), natural service (venereal transmission)
  8. What antibiotics can you use to treat UTI in cattle, and for how long should treatment last? (4)
    procaine penicillin, ampicillin, K-penicillin, ceftiofur; for 3 weeks then reculture
  9. What is the pathogenesis of enzootic hematuria?
    chronic, intermittent hematuria in animals grazing on bracken fern--> hemorrhagic cystitis--> bladder walls thicken with tumors--> blood loss anemia with little to no regenerative response
  10. What is amyloid?
    beta-pleated sheet of insoluble fibrillar protein, which can be produced in overabundance in response to chronic infection or neoplasia
  11. How can amyloidosis present? (9)
    pericarditis, metritis, chronic lung disease, massive proteinuria, hypoalbuminemia, edema, diarrhea, renal enlargement, chronic wasting disease
  12. Describe the pathogenesis of amyloidosis.
    liver produces serum amyloid A in response to inflammation--> deposition of SAA on filtration barrier in kidneys--> decrease efficiency of filtration, loss of protein, decreased oncotic pressure--> edema
  13. Describe the pathogenesis of glomerulonephritis.
    [immune-mediated] Ag-Ab complex deposition in glomerular basement membrane--> protein losing nephropathy--> albumin loss--> edema
  14. What are clinical signs of glomerulonephritis? (9)
    weight loss, poor productivity, chronic diarrhea, lethargy, generalized edema, enlarged kidney, hypoalbuminemia, mild anemia, proteinuria
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CattleII1- Urinary Dz of Cattle
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