Small Ruminant - Renal and Urinary Tract Disease

Question 1

Describe the clinical signs of ulcerative posthitis and vulvitis of small ruminants (‘Pizzle Rot’).

Answer 1

• Begins as a moist ulcer at/near mucocutaneous junction of the prepuce, covered by a scab, focal swelling, painful.
• Spreads along mucosal surface inside the prepuce –> entire prepuce swollen, dysuria, vocalise during urination.
• May progress to fibrous adhesions between penis and prepuce, restriction of urine egress due to swelling of glans penis or impairment of breeding soundness (blood/exudate in ejaculate, penis adhesions, scarring prepucial orifice, suppuratives urethritis.
• Weight loss in chronic cases.
• Ewes/does: ulcerative lesions on vulva and perineum, gross vulvar enlargement, dysuria.
• Ddx: orf, ulcerative dermatosis (poxvirus), urolithiasis, caprine hervesvirus-1.

Question 2

Describe the pathophysiology of ulcerative posthitis and vulvitis in small ruminants.

Answer 2

• Corynebacterium renale: aerobic, gram-positive, pleomorphic, club-shaped bacteria; normal flora of skin and external genitalia.
• Bacteria contains enzyme urease.
• High-protein diet –> inc ammonia in rumen –> urea elim thru kidneys –> C. renale proliferate in alkaline urine and urease hydrolyses urea to ammonia –> chemical irritation and ulceration of prepuce and surrounding skin.

Question 3

Describe the epidemiology of ulcerative posthitis and vulvitis in small ruminants.

Answer 3

• Males > females.
• Risk factors: inc/excessive dietary protein (>16%, as low as 12%) e.g. alfalfa hay or lush legume pastures.
• Inc plane of nutrition in intact males prior to breeding.
• Breeds w dense wool or hair e.g. Merino, Angora.
• Organism persists in wool, hair and scabs for up to 6mo and can survive freezing in scabs/exudative material.
• Can occur in single or multiple animals; venereal transmission reported.
• Causes losses from debilitation caused by pain, incapacitation of breeding animals, loss of breeding soundness, deformation of external genitalia.

Question 4

Outline the treatment of ulcerative posthitis and vulvitis in small ruminants.

Answer 4

• Reduction of protein and non-protein nitrogen intake.
• Isolate affected animals.
• Clip hair around affected region and apply topical ABs.
• Systemic ABs in severe cases e.g. penicillin, oxytet.
• NSAIDs if required for pain/inflammation.
• Sx of severe strictures to allow normal urine flow.

Question 5

Describe the prognosis associated with ulcerative posthitis and vulvitis in small ruminants.

Answer 5

• Response to tx optimal early in infection before deformation of prepuce or vulva as a result of fibrosis.
• Changes for full recovery poor if dietary protein not restricted.
• Complete recovery of breeding soundness unlikely if internal ulcerative posthitis.

Question 6

Describe the common signalment of ruminants with urolithiasis.

Answer 6

• Common metabolic dz in all livestock spp.
• Castrated small ruminants at greatest risk.
• Dx in single animal suggests whole herd is at risk due to important of diet/enviro factors in pathogenesis.
• Can occur as epidemics or indv disorder.

Question 7

Describe the clinical presentation of acute urethral obstruction secondary to urolithiasis in ruminants.

Answer 7

• Impacted calculi –> urethral trauma and bladder distension –> stranguria and abdo pain.
• CSx: restless, swish tail, grind teeth, stranguria, vocalise, tachycardia, tachypnoea, mild bloat sec to rumen stasis.
• Stranguria may result in rectal prolapse.
• Visible dilation or palpable pulse in urethra at midline of perineum proximal to obs may occur.
• Anuria or urine dribbling.
• May see blood or crystals on prepuce.
• Distended bladder on abdo/rectal palpation.
• Most common site of obstruction = sigmoid flexure in cattle and urethral process in sheep and goats.
• NB always ultrasound kidneys as hydronephrosis –> poor Px.

Question 8

Describe the clinical presentation of chronic urethral obstruction secondary to urolithiasis in ruminants.

Answer 8

• Uncommon, but may occur if calculi cause partial obstruction of urethra and still allow for urine flow.
• CSx: slow/intermittent urine flow during voiding, lethargy, dec appetite, thin BCS if renal failure has developed.
• Rectal may reveal small bladder with thick wall.
• DDx for urine dribbling: neuro dz, previous urethral trauma –> stricture formation, congenital anomalies of urogenital tract, infection, neoplasia, internal ulcerative posthitis.

Question 9

Describe the clinical presentation of urethral rupture secondary to urolithiasis in ruminants.

Answer 9

• Common complication of urethral obstruction.
• Wall of urethra undergoes pressure necrosis –> leakage of urine into s/c tissue of perineum and ventral abdo.
• Sequelae: cellulitis, penile adhesions, urethral fistula formation, urethral stricture, erection failure.
• CSx: depression, inappetence, bilaterally symmetric pitting oedema in ventral perineum, inguinal region, prepuce and ventral abdo, may –> gangrenous necrosis.

Question 10

Describe the clinical presentation of urinary bladder rupture secondary to urolithiasis in ruminants.

Answer 10

• Prolonged bladder distension secondary to urethral obs –> pinpoint perforations, tears or necrosis of large areas of bladder wall.
• Most common location for rupture is dorsum of the bladder fundus.
• Rupture –> relief of stranguria.
• CSx 1-2d post-rupture: abdo distension, depression, anorexia, weakness, dehydration, shock; breath may smell of ammonia; may ballot fluid wave in abdo; death.
• U/s –> free fluid w collapsed or partially filled bladder.
• Abdominocentesis: larve vol blood-tinged fluid.

Question 11

Describe the clinical presentation of ureterolithiasis and nephrolithiasis in ruminants.

Answer 11

• Acute ureteral obs may present w severe colic if obs is complete, or absent/milder colic.
• Enlarged ureter/L kidney may be palpated rectally.
• Rectal/transabdo u/s may aid dx.
• May see evidence on u/s of pyelonephritis (necrotic debris/calculi may be released into ureter from infected renal pelvis) or ureteral or renal rupture.
• If no signs of colic may be see non-specific signs of illness –> serum chem/urinalysis/ultrasound for definitive dx.

Question 12

Describe the procedure of examination of the urethral process for stones/sand-like grit in small ruminants.

Answer 12

• Sedation: diazepam or acepromazine +/- butorphanol; recomm to avoid xylazine as inc urine production.
• Can admin epidural instead of/as adjunct to sedation; 1ml/15kg 2% lignocaine, no more than 15ml.
• Prop sheep/goat on rump w spine perpendicular to floor.
• Apply lidocaine jelly to prepuce, exteriorise penis by pushing sigmoid flexure cranially from base of scrotum and pull sheath caudally.
• Inspect/palpate urethral process and amputate w scalpel blade if stones/grit palpated.

Question 13

Describe clinicopathologic findings in ruminants with acute and chronic urethral obstruction.

Answer 13

• CBC/chem may be WNL if acute.
• May see hyperglycaemia and stress leukogram.
• Dec water intake –> haemoconc and azotemia.
• Chronic obst: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.
• Haematuria and proteinuria are consistent abnormalities; crystalluria is variable finding; +/- pyuria.

Question 14

Describe clinicopathologic findings in ruminants with bladder rupture.

Answer 14

• HypoNa, hypoCl, hyperP, uraemia, haemoconc.
• K+ conc is variable, depending on appetite and time prior to dx; bladder rupture usually –> hyperK in animals but in ruminants K is usually low or normal due to anorexia, salivary potassium excretion and aldosterone release.
• Peritoneal fluid:serum creat 2:1 or greater.
• May see leukocytosis and hyperfibrinogenaemia secondary to peritoneal inflammation.

Question 15

Describe clinicopathologic findings in ruminants with ureterolithiasis and nephrolithiasis.

Answer 15

• Azotemia and secondary hydronephrosis most severe if condition is bilateral.
• Chronic: hypoNa, hypoCl, hypoCa, hyperP, severe azotemia w isosthenuria.
• Pyuria present w traumatic urethritis, cystitis or secondary bacterial infection.

Question 16

Describe the pathophysiology of urolithiasis in ruminants.

Answer 16

• Mucopolysaccharides, ions, organic acids in urine act as intrinsic inhibitors of crystallisation of calculogenic ions.
• Calculus formation initiated if supersaturation of urine w crystalloids exceeds capabilites of these inhibitors –> crystalloids rendered insoluble and precipitate out of urine.
• Dietary, enviro, management factors interact to determine degree of supersat of urine w calculogenic minerals.
• pH: struvite (Mg amm phos), Ca phos, Ca carb less soluble in alkaline urine; Ca ox not affected by pH, silica debatable.
• Rare cause and rare consequence of UTIs in ruminants.
• Vit A defic may create nidus for calculi formation through desquamation of epi cells/altered cell surface charac.
• Ad lib feeding may dec calculi formation, as 1-2 feedings/day –> ADH release after feed –> urine conc.
• Water hardness may be sig, partic Mg content.

Question 17

Describe factors influencing development of phosphatic urinary calculi in ruminants.

Answer 17

• High phosphorus (grain-based) diet –> struvite (Mg amm phos) or apatite (Ca phos) calculi.
• Ca:Phos outbreaks of urolithiasis.
• Struvite dev primarily affected by Mg content in diet; Mg > 0.6% DM.
• High dietary K+ alters DCAD –> inc risk uroliths.
• Pelleted rations –> inc risk phosphatic uroliths; dec saliva prod w pellets –> dec GI phos loss –> inc renal excr.
• Struvite uroliths: white or grey, smooth, radiopaque, easily broken; single stone or sand-like debris.

Question 18

Describe factors influencing development of silica urinary calculi in ruminants.

Answer 18

• Ruminants grazing native rangeland grasses of western North America; silica content higher in mature grass.
• Periods of water deprivation –> water and Na resorption by kidneys –> highly conc urine –> silic acid conc and polymerises to polysilicic acid –> binds to urinary mucoproteins and becomes insoluble.
• Incidence may be inc by dietary defic of Cu and Zn and high dietary Ca:PO4 content > 2.8:1 (opp to struvite!).
• Silica uroliths are hard, smooth, white to brown, radiopaque, often layered; 20% mucoprotein, 75% silicon dioxide and variable amounts Ca ox and Ca carb.

Question 19

Describe factors influencing development of calcium-based urinary calculi in ruminants.

Answer 19

• Two main types: Ca oxalate and Ca carbonate.
• Ca carb common in small ruminants grazing lush, rapidly growing clover pastures or fed alfalfa hay, high in Ca, low in PO4 and Mg, high oxalate content.
• Oxalate binds GI Ca –> inc urinary Ca excretion; ruminal bacteria metabolises oxalate to bicarb –> alkaline urine; both factors –> inc Ca carbonate calculogenesis.
• High oxalates, low Ca in diet and dec water intake –> inc risk of Ca oxalate uroliths.
• Ca carb uroliths: round, smooth shape, golden colour.
• Ca oxalate uroliths: dense, hard, white to yellow, smooth or jagged.

Question 20

Describe the epidemiology of urolithiasis in ruminants.

Answer 20

• Gender: obs urolithiasis almost exclusively dz of males; testosterone –> inc urethral diameter, therefore castration (esp prior to puberty) = risk factor.
• Season: inc incidence in late Autumn and Winter: limited water avail, inc silica content, higher number of young, growing male animals; higher risk in arid months of year in warmer climates.
• Age: tendency in younger ruminants, maybe due to management factors e.g. high grain rations.
• Other: inherent indv diff in animals’ mineral metabolism or urinary tract health.
• Breed: higher risk in African Pygmy goats; truley higher risk or management facts due to pet status?

Question 21

List surgical treatment options for management of urolithiasis in ruminants.

Answer 21

• Amputation of obstructed urethral process.
• Perineal urethrostomy.
• Prepubic urethrostomy.
• Urethrotomy.
• Cystotomy.
• Tube cystotomy.
• Bladder marsupialisation.

Question 22

Describe medical management options for treatment of urolithiasis in ruminants.

Answer 22

• Tranquillisers: antispodic effect on urethra and relaxation of retractor penis muscle –> relaxation of sigmoid flexure (NB low success of NSAIDs, IVF, tranquillisers alone).
• Percutaneous drainage of bladder prior to Sx or as adjunct to medical therapy.
• Percutaneous inj of Walpoles soln into the bladder –> dec urine pH to 4-5 to dissolve uroliths in bladder/urethra.
• Pre-operative stabilisation of hypovol and correction of electrolyte abnorm e.g. hypertonic followed by 0.9% NaCl.
• If hyperK can give IV dextrose, sodium bicarb or insulin to move K into cells.
• Slow drainage of urine from abdo cavity to reduce pressure on diaphragm and slow progression of metabolic derangements.
• Peri-operative ABs to prevent UTIs.

Question 23

Describe factors of management which can prevent or decrease the risk of urolithiasis in ruminants.

Answer 23

• Perform ration and urolith analysis to ID dietary factors.
• Goal: dilution of urine to reduce urinary concentration of calculogenic mineral ions.
• Dietary management of phosphotic calculi:
• • Ca:P 2:1 or greater; dec grain (high phos), inc Ca w alfalfa or other legumes.
• • 0 mEq DCAD diet w ammonium Cl –> urine pH 6-6.5.
• • Inc long-stemmed forage –> inc saliva –> inc P excr.
• Dietary management of silica calculi:
• • Cannot change silica content or range grasses.
• • Can only add salt to inc water intake; up to 15% DM NaCl or 1% NH4Cl.
• • Dec Ca:P from 2:1 to 1:1 –> trend towards less calculi.
• Dietary management of Ca carb uroliths:
• • Supplement hay w grass hay instead of alfalfa alone.
• • Salt grass hay to inc water intake.
• • NH4Cl to inc water intake and acidify urine.
• Water management: clean feeders, in shade in Summer, warmed in Winter, multiple sites, check regularly.