UTI in Ruminants

What are the main structures of the ruminant urinary tract?

Renal vessels, kidneys, renal pelvis, ureters, bladder, and urethra

How do bovine kidneys differ from small ruminant kidneys?

Cattle have lobulated kidneys with distinct lobes; sheep and goats have smooth kidneys resembling those of carnivores

What anatomical features of male ruminants are clinically significant?

The sigmoid flexure and urethral process (especially in small ruminants), common sites for urethral obstruction

What are the main physiological roles of the kidneys?

Filtration, secretion, fluid/electrolyte balance, acid-base regulation, waste elimination, and endocrine functions including erythropoietin, renin-angiotensin-aldosterone system, and prostaglandins

What steps are used to diagnose urinary tract disease in ruminants?

• History: individual and herd

• Physical exam: distance & hands-on

• Ancillary tests: catheterization, clinical pathology, ultrasound, radiographs, necropsy

What serum and CBC findings are important for renal assessment?

BUN and creatinine elevations indicate azotemia.

• Extra-renal: dietary (urea)

• Prerenal causes: dehydration, shock

• Renal causes: infection, toxins, hypoxia

• Postrenal causes: obstruction

Causes for Azotemia: Creatinine & Urea

Creatinine: Ingestion, Endogenous 

Urea: Ingestion, dietary protein, catabolism

What can urinalysis reveal?

pH, blood, protein(can have false +), glucose, ketones, bilirubin, urobilinogen, and via microscopy—RBCs, WBCs, crystals, and casts

What factors contribute to urolithiasis in ruminants?

Nidus formation (desquamated cells, infection, estrogens) and precipitation of solutes influenced by urine pH, low water intake, and dietary mineral imbalances

Which animals are most at risk of urolithiasis?

Castrated male small ruminants (goats, sheep) and feedlot cattle

What history and signs are typical of urolithiasis?

• History: diet high in concentrates/pellets, limited water, seasonal changes.

• Signs: stranguria, dysuria, anuria/oliguria, tail swishing, treading, vocalizing (goats), abdominal distension, rectal prolapse

What feed can cause urolithiasis? 

• milk replacer → magnesium

• forage → silica, estrogens, oxalates

• grains/concentrates → phosphates

• pelleted feeds

• pasture to feedlot, meal feeding

• water access, quality, mineral content 

• salt 

What are the main differential diagnoses for urinary obstruction?

Incomplete blockage, infection (cystitis, urethritis), GI or neurologic disease

What ancillary tests confirm diagnosis?

Urinalysis, PCV/TP, biochemistry, ultrasound, and radiographs

How is urolithiasis treated medically?

Symptomatic

• Remove urethral process (small ruminants)

• Retrograde/anterograde flushing (“Bonanno” catheter)

• Urinary acidifiers (ammonium chloride)

• Antispasmodics (acepromazine)

What are surgical options for urolithiasis?

Perineal urethrotomy, urethrostomy, laparocystotomy, tube cystotomy

What happens after rupture of bladder or urethra?

• Bladder rupture: abdominal distension, depression, death.

• Urethral rupture: “water belly,” necrosis, fistula formation, death

What are the major types of urinary calculi in ruminants?

• Magnesium ammonium phosphate (struvite)

• Silicate

• Calcium carbonate

• Calcium oxalate

How can urolithiasis be prevented?

• Diet: Ca:P ≥ 2:1(exam Q), limit Mg, avoid high-P grains/pellets, add salt (3–5%) and ammonium chloride (0.5–1%).

• Water: ensure clean, frequent, accessible supply.

• Management: avoid sudden feed changes.

What causes Struvite formation?

Magnesium ammonium phosphate, high phosphorus diet

What causes Struvite formation?

Grasses of western north america, inc with maturity, inc occurance with dec water intake, high Calcium to Pho ratio

What are the routes and bacteria involved in UTIs in ruminants?

• Ascending (most common): Corynebacterium renale, E. coli, other Enterobacteriaceae.

• Descending (hematogenous): Salmonella, Trueperella pyogenes, C. pseudotuberculosis (sheep/goats)

What are the clinical forms?

Cystitis (pollakiuria, dysuria, thickened bladder) and pyelonephritis (fever, depression, enlarged kidney)

What factors predispose ruminants to UTIs?

Trauma (dystocia, catheterization), reflux from bladder dysfunction, poor vulvar conformation, pneumovagina, and metritis

Describe Corynebacterium renale and its significance

Gram + rod with pili aiding epithelial attachment (enhanced by alkaline urine). Spread is horizontal, venereal, or iatrogenic. Difficult to eradicate once endemic

UTI clinical signs

Cystitis

• pollakiuria, dysuria

• agitation → treading, twitching tail

• thickened bladder

• abnormal urine 

• systemic signs 

Pyelonephritis 

• fever, depression, inappetance, dec milk production

• mild colic

• cystitis

• painful L kidney, loss of lobulation

• enlarged kidney, abnormal shape

How are UTIs treated and what is the prognosis?

• C. renale: high-dose penicillin/ampicillin ≥ 3 weeks.

• E. coli/coliforms: ampicillin, penicillin, ceftiofur, TMS.

• Prognosis depends on extent, duration, bilaterality, and azotemia; fatality/culling ~ 18–33%

What are the causes of Acute Tubular Necrosis in ruminants?

• Ischemic: hypovolemia, DIC, renal vein thrombosis.

• Nephrotoxic: aminoglycosides(neomycin, gentamicin, amikacin), tetracyclines, sulfonamides, metals (As, Hg, Pb, Cd), toxic plants (Quercus, Amaranthus, Rumex), and compounds like monensin, mycotoxins, oxalates, ethylene glycol

• Endogenous compounds: Hemoglobin, Myoglobin, Bile

What signs and lab findings indicate ATN?

• Signs: depression, diarrhea, weakness, bloat, fever, tachycardia.

• Labs: ↑ BUN/creatinine, proteinuria, hematuria, casts, hypochloremia, hyponatremia, hyperphosphatemia, hypocalcemia, metabolic alkalosis

DDx for ATN

• vague signs

• infectious and non-infectious diarrhea

• pregnancy toxemia 

• recumbency 

How is ATN treated?

• Remove cause

• Correct fluids/electrolytes, remove toxin, establish urine flow.

• Furosemide (1 mg/kg IV/IM), mannitol (0.25 g/kg IV), or dopamine infusion if anuric.

• Monitor acid-base, electrolytes, BUN/creatinine.
  Prognosis: variable; poor if ischemic, better if caught early in toxic cases

What causes ulcerative posthitis (“pizzle rot”) in small ruminants?

C. renale overgrowth in alkaline urine from high-protein diets → mucosal ulceration

Signs: painful ulcers, swelling, scabbing, possible obstruction.
Treatment: isolate, shear wool, apply topical + systemic antibiotics (penicillin/tetracycline).
Prevention: reduce dietary nitrogen.
Prognosis: good if treated early

What is amyloidosis and its pathophysiology?

Chronic AA amyloid deposition due to persistent antigenic stimulation (infection/inflammation), causing protein-losing nephropathy → diarrhea, weight loss, edema, enlarged kidney.
Prognosis: poor; no effective treatment

How does glomerulonephritis differ from amyloidosis?

Immune-complex or antibody-mediated inflammation of glomeruli; rare, similar signs; poor prognosis, no treatment

What renal congenital defects occur in ruminants?

Cysts, agenesis, hydronephrosis, renal dysgenesis, oxalosis (in beefmaster calves)

Which Leptospira serovars affect cattle kidneys, and what are the outcomes?

• Hardjo: host-adapted, causes chronic interstitial nephritis, infertility, abortion.

• Pomona and Grippotyphosa: cause hemolytic disease, nephritis, tubular necrosis, abortion.
  Diagnosis: MAT, PCR, urine FA stain, necropsy.
  Treatment: oxytetracycline, penicillin/ampicillin/amoxicillin, tilmicosin