Cattle - Renal and Urinary Tract Disease

Question 1

List the clinical signs associated with renal amyloidosis in cattle.

Answer 1

Mature animals with:

• Chronic diarrhoea.
• Weight loss.
• Poor productivity.
• +/- Generalised or ventral oedema.
• +/- Enlargement of the left kidney on rectal (non-painful).
• +/- stable foam on urine.

Question 2

What clinical pathology abnormalities will be seen in cattle with renal amyloidosis?

Answer 2

• Marked proteinuria.
• Marked hypoalbuminaemia.
• Advanced dz: azotemia.
• Chronic, active dz: hyperfibrinogenaemia, hyperglobulinaemia.

Question 3

What two diseases cause prolonged proteinuria in cattle? How would you differentiate between the two in the live animal?

Answer 3

• Renal amyloidosis and glomerulonephritis.

- Renal biopsy.

Question 4

Describe the pathophysiology of renal amyloidosis in cattle.

Answer 4

• Chronic inflammatory disease e.g. TRP, mastitis –> circulating serum amyloid A; abnormal catabolism of SAA or inherent abnormality in SAA –> misfolding of SAA and deposition of amyloid fibrils which are resistant to proteolysis in glomerulus –> sustained albuminuria.
• Dxa: GIT wall oedema or amyloid deposition in GIT.
• Renal or pulmonary thrombosis: loss of low-molecular weight anticoagulant proteins through the compromised kidney.

Question 5

Described the gross and histopathology of kidneys of cattle with amyloidosis.

Answer 5

• Gross: large, yellow-tan to white kidney, waxy quality of renal parenchyma; generalised oedema.
• Histo: amyloid deposition in glomerulus, interstitium and tubule lumen (congo red –> light pink or bright green under polarised light).

Question 6

What is the prognosis associated with renal amyloidosis?

Answer 6

Hopeless.

Question 7

What is the common common route of infection in cattle with pyelonephritis and what are the two most common aetiologic agents?

Answer 7

• Ascending infection from the lower urinary tract e.g. urogenital trauma during calving, abnormal vulvar conformation, urine retention, catheterisation.
• Corynbacterium renale - contagious; adhere to urinary tract epithelium via pH-mediated pili i.e. adherence enhanced in alkaline urine and dec in acidic urine.
• Escherichia coli - faecal contamination.

Question 8

List bacteria that have been implicated in causing pyelonephritis of haematogenous origin in cattle.

Answer 8

Salmonella, Staphylococcus, Streptococcus, P. aeruginosa and T. pyogenes.
{Corynbacterium pseudotuberculosis (small ruminants)}.

Question 9

List the clinical signs of acute pyelonephritis in cattle.

Answer 9

• Sudden reduction in feed intake.
• Sudden reduction in milk production.
• Fever.
• Tachycardia.
• Tachypnoea.
• Dehydration.
• Rumen stasis, mild colic.
• Scleral injection.
• +/- signs of cystitis: dribbling urine, swishing tail, arched stance after urinating, discharge on distal vulva.
• +/- L kidney large, painful, smooth on rectal palpation.

Question 10

List the clinical signs of chronic pyelonephritis in cattle.

Answer 10

• Vague clinical signs: weight loss, muscle wasting, poor growth, anorexia, diarrhoea, reduced milk production.
• Pale mucous membranes due to anaemia.
• There may be no abnormal behaviour or posturing during urination.
• +/- loss of lobulation in L kidney on rectal (may not be pain or enlargement).

Question 11

Describe ultrasound findings in acute pyelonephritis.

Answer 11

• R kidney in 12th ICS and R paralumbar fossa.
• L kidney: L paralumbar fossa or per rectum.
• Renal enlargement, abnormal kidney shape, dilated renal calyces, flocculent echogenic material in the renal pelvis and ureter.

Question 12

Describe clinicopathologic abnormalities in cattle with pyelonephritis.

Answer 12

• Neutrophilic leukocytosis w hyperfibrinogenaemia.
• If more chronic expect hyperglobulinaemia and hypoalbuminaemia (renal loss).
• Chronic: anaemia (dec EPO and renal loss).
• Bilateral pyelonephritis –> azotemia and isosthenuria = poor Px.
• Haematuria, proteinuria, bacteria; USG 1/005-1.020.

Question 13

Describe the epidemiology of pyelonephritis in cattle.

Answer 13

• Israeli study: prevalence 0.3-2.7%.
• Female predisposed due to short urethra and potential contamination and trauma from breeding/parturition.
• Majority of cases w/in 90d of calving.
• C. renale is difficult to eliminated on a herd level once established.

Question 14

List necropsy findings in cattle that have died from pyelonephritis.

Answer 14

• Bladder has evidence of haemorrhage, ulceration and fibrin deposition of epithelial surfaces; may extend through urethra.
• Polypoid growths may develop with chronicity.
• Ureters may be enlarged and filled w purulent debris.
• Kidney(s) enlarged, may have grey, odourless exudate in renal pelvis, medulla and cortex (acute) or abscess (chronic).

Question 15

Describe the treatment of pyelonephritis in cattle

Answer 15

• Agressive and long-term ABs: penicillin; if coliform infection and no response after 96h gent, ceftiofur, TMPS.
• Diuresis with oral or IV fluids to remove necrotic debris and bacteria from the UT.
• Nephrectomy if unilateral pyelonephritis that is unresponsive to medical therapy.
• Perform urinalysis and urine culture 1wk after stopping therapy to confirm efficacy.

Question 16

What is the prognosis for cattle with pyelonephritis?

Answer 16

• Treatment more efficacious if instituted early.
• Case fatality/cull rates of 18-47% reported.
• Recrudescence rate of 9.4% reported.

Question 17

Describe the pathophysiology of glomerulonephritis in cattle.

Answer 17

• Immune-mediated damage to the glomerulus.
• Reported w acute septic dz, cattle w BVD and fascioliasis, mesangiocapillary GN in landrace lambs, preg tox in ewes.
• Ab may be directed against host or foreign Ag in the vascular endothelium, mesangial cells or BM of the glomerulus or Ag-Ab complexes may deposit –> complement activation, chemotaxis of leukocytes –> glomerular injury –> inc glomerular permeability.

Question 18

List clinical signs displayed by ruminants with glomerulonephritis.

Answer 18

• Weight loss or poor productivity.
• Chronic diarrhoea.
• Lethargy.
• Generalised oedema.
• Kidneys maybe mildly enlarged, non-painful on rectal.
• Signs of concurrent dz: BVD, fascioliasis, preg tox.
• Mesangiocapillary GN of Landrace lambs: 1d-3mo old, dull, ataxic, appear blinds, seizures, fine muscle tremors, colic.

Question 19

Describe clinicopathologic abnormalities in ruminants with glomerulonephritis.

Answer 19

• Heavy proteinuria.
• Mild anaemia.
• Hypoalbuminaemia.

Question 20

Describe prognosis for ruminants with glomerulonephritis.

Answer 20

• Treatment not described.
• Prognosis poor.
• Mesangiocapillary GN of Landrace lambs not invariably lethal; some lambs may survive to adulthood.

Question 21

Describe congenital defects of the kidneys reported in ruminants.

Answer 21

• Renal cysts: common in cattle; no clinical significance unless multiple (polycystic kidney dz).
• Renal agenesis: most common renal defect in lambs.
• Renal oxalosis: inherited in Beefmaster calves –> weakness, lethargy, anorexia, dehydration, dxa, alopecia w/in wks of birth due to accum of Ca oxalate crystals.
• Extopic ureter: rare in ruminants.

Question 22

Describe urinary tract neoplasias (not related to bracken fern ingestion) in ruminants.

Answer 22

• Primary bladder tumours reported in 0.05% cattle in Nth Am abattoirs = adenomas, papillomas, TCCs.
• Fibropapillomas and SCC of genitalia may impinge upon urethra.
• Renal carcinoma has been reported in cattle.
• Nephroblastoma has been reported in a ewe and a lamb.
• Urinary tract involvement occ seen w lymphosarcoma.

Question 23

Haemolytic uraemic syndrome occurs in people following ingestion of E. coli O157:H7. It has been reported in 4 horses and 2 cattle. Describe the pathophysiology and clinical findings in cattle with HUS.

Answer 23

• Thrombotic microangiopathy disorder charac by microangiopathic haemolytic anaemia, thrombocytopaenia and renal failure; normal clotting times.
• Cattle CSx: severe progressive anuric renal failure, acute haemolytic anaemia and consumptive thrombocytopaenia; haemolysis and tendency to bleed.
• Necropsy: renomegaly, renal infarcts, scattered petechial and ecchymotic haemorrhage w/in renal parenchyma, ATN, fibrin thrombi in glomerular capillaries.

Question 24

List aetiologic agents of acute renal failure in ruminants.

Answer 24

• Aminoglycosides.
• Tetracycline.
• Ionophores.
• Ethylene glycol.
• Oxalate-containing plants.
• Vitamin C or D overdose.
• Oak, acorns, pigweed, Easter lily, phildendron, ponderosa pine, cocklebur, jessamine.
• Myoglobin.
• Haemoglobin, methaemoglobin.
• Arsenic, mercury, cadmium, chromium, lead, zinc.

Question 25

List clinical signs of acute renal failure in ruminants.

Answer 25

• Non-specific; freq presented for poor appetite, diarrhoea or epistaxis.
• May be anuric, oliguric or polyuric.
• Depression, nasal discharge, ileus, melena and mild free-gas bloat may be present.
• If concurrent septic dz: fever, scleral inj, tachycardia.
• Acid-base, elec, fluid imbalances –> weakness.
• Uraemia –> saliva w ammonia smell, enceph signs.

Question 26

List clinicopathologic abnormalities in cattle with acute renal failure.

Answer 26

• CBC: if inflammatory condition affecting renal tubules: neutropaenia or left shift.
• Azotemia: elevated BUN (maybe as influenced by rumen physiology); elevated creatinine.
• HypoNa, hypoCl, variable K +/- hyperMg, hyperPO4, hypoCa.
• Metabolic alkalosis (acidosis in calves w concurrent dxa).
• Urinalysis: proteinuria, haematuria, granular casts, FE sodium >4%.

Question 27

Describe the pathophysiology of acute renal failure in ruminants.

Answer 27

1. Reduced blood flow/ischaemia in kidneys: secondary to blood loss, septicaemia, endotoxaemia, severe dehydration from mastitis, metritis, enteritis, rumen acidosis or intestinal accidents, heat stress (lambs) –> infarction of renal cortex, renal v thrombosis, damage to tubular BM.
2. Bacterial infection: bilateral pyelonephritis –> destruction of nephrons by bacterial toxins and host inflam resp.
3. Pigment nephrosis: haemoglobin/myoglobin –> renal vasoconstriction and tubular obstruction from protein coagulation.
4. Toxic nephropathies: various mech e.g. sulphonamides –> deposition of insoluble precipitates in renal tubules, NSAIDs –> dec Pg synth and medullary crest necrosis, aminoglyc –> cell death of tubules thru mitochond inj.

Question 28

Outline the treatment of acute renal failure in ruminants.

Answer 28

• Remove offending toxin or source: rumenotomy, activated charcoal, heavy metal chelators.
• Promote diuresis through IVFT (IV, oral or rumen) and diuretic meds (furosemide or mannitol until urinating).
• Correct acid-base and electrolyte derangements.
• Additional therapy if indicated in specific cases: broad-spectrum ABs, plasma, PPN or transfaunation.

Question 29

Describe leptosira bacterial structure and transmission.

Answer 29

• Motile, gram-negative, obligate aerobic, tightly coiled spirochetes 0.1-0.3um diam and 6-20um length.
• Persist in chronic infections of renal tubules of maint host –> little or no dz.
• Transmitted to incidental host through urine from maint host (directly or contam feed/enviro).
• Causes multi-organ dz in incidental hosts e.g. abortions, repro failure, kidney, liver or CNS dz.
• Survives in warm, moist enviro for 6mo; survives short period if dry and cold; doesn’t survive freezing.
• Seasonal incidence higher in Summer/Autumn in temperature regions or rainy season in warm climates.

Question 30

Describe epidemiology of leptospirosis in cattle.

Answer 30

• Cattle are primary maintenance host reservoir of L. interrogans serovar hardjo type hardjopragitno (UK) and L. borgpetersenii servo hardjo type hardjobovis (worldwide).
• Also maint or incidental host for L. interrogans serovar pomona and L. interrogans serovar grippotyphosa.
• Serovars hardjo, pomona and grypotyphosa most often implicated in renal infection in cattle; renal dz caused by lepto in small ruminants rare but may serve as carriers.
• Urine/renal/seroprev varies in US from 2-47%.
• Infection w host-adapted serovar hardjo –> mild dz; overt losses attrib to effects on reproduction.
• Incidental infection w non-host adapted strains –> acute severe renal dz (particularly in calves).

Question 31

Describe clinical presentation of host-adapted Leptospira serovar hardjo infection in cattle.

Answer 31

• Asymptomatic.
• Chronic interstitial nephritis; renal dys rarely observed.
• Infertility, stillbirth, abortion and birth of weak calves.
• Milk-drop syndrome/flabby udder: fever, agalactia, mastitis, milk yellow/red-tinged and thick; udder soft.

Question 32

Describe clinical presentation of non-host-adapted Leptospira serovars infection in cattle.

Answer 32

• Severe systemic disease in calves > adult cattle.
• Haemolytic anaemia (some L. serovars prod haemolysins), hepatitis, interstitial nephritis, tubular nephrosis, fever, anorexia, lethargy, dec milk prod, petechiation.
• Agalactica and mastitis in lactating cows; +/- abortion.
• Renal lesions result from damage to vascular endothelium, pigement nephropathy, interstitial nephritis –> azotemia, proteinuria, pyuria, granular casts, +/- haemoglobinuria.

Question 33

Describe the pathophysiology of leptospirosis in cattle.

Answer 33

• Leptospires ingested or penetrate external mucosa surfaces and scarified skin, mutliply, enter bloodstream thru lymphatics or direct penetration of blood vessels.
• Bacteraemia 4-7d –> infection multiple organisms.
• Leptospires become localised in mammary gland, kidney or genital tract; appear to be protected from IR.
• Leptospires cleared from body OR chronic infection of renal prox tubules/repro tract occurs –> shedding for wks to months (non-adpated) or years (host-adapted).
• Virulence factors: toxin effect of lipopolysaccharide, adhesion to cells and extracellular matrix, bacterial motility, haemolysins and iron sequestration.

Question 34

How is leptospirosis diagnosed in cattle?

Answer 34

• Microscopic agglutination test (MAT) is most widely-used serologic test: detects ABs to specific serovars, but cross-reactivity occurs b/w related serovars.
• Acute infection: four fold inc b/w acute and convalescent sample or conversion from -ve titre to titre >100.
• Chronic infection: titres may be -ve, inc, dec, static.
• L. shedding in urine or semen can be assessed via culture (often unrewarding), PCR, phase-contrast or dark-field microscopy, FA, nucleic acid hybridisation or immunblot.
• Urine testing: admin furosemide, discard first sample, clean vulva of gross debris, collect and test 2nd sample.
• Histo renal tissue: Warthrin-Starry or Levaditi stains.

Question 35

Outline treatment of leptospirosis in cattle.

Answer 35

• Oxytetracycline for 5-7d (reported clinically effect but not proven); PPG/ampicillin (efficacy in cattle unproven).
• IV or oral fluids, blood transfusions, diuresis if ARF.
• Oxytet, ceftiofur, tilmicosin and tulathromycin have been shown effective in clearing renal shedding in herds.

Question 36

What is the prognosis associated with leptospirosis in cattle?

Answer 36

• Varies w virulence of serovar involved, host immunity, extent of renal lesions.
• Guarded prognosis in azotemic cattle as >75% nephrons affected in such cases, therefore even if acute dz tx, may –> chronic interstitial nephritis and fibrosis.

Question 37

Outline strategies to prevent leptospirosis in cattle herds.

Answer 37

• Draining or fencing off standing water.
• Maintaining a dry, clean environment.
• Limiting rodent and wildlife contact with cattle and their feed and water.
• For host-adapted strains, eliminate renal carrier state.
• Vaccination (pentavalent vacc) is considered effective at preventing losses but may not consistently prevent renal colonisation w host adapted hardjobovis.
• Recommended at a young age followed by annual boosters to prevent initial renal colonisation.

Question 38

Describe the aetiology of enzootic haematuria of ruminants.

Answer 38

• Chronic (1-3 mo) ingestion of bracken fern (Pteridium aquilinum).
• Toxins in plant –> haemorrhagic cystitis –> chronic or intermittent haematuria.
• Chronic ingestion + bladder infection w BPV-2 –> bladder neoplasm of epithelial, mesenchymal or mixed origin.
• NB distinct from acute Bracken Fern toxicity –> acute coagulopathy or fulminant septicaemic crisis assoc w severe bone marrow suppression.

Question 39

Outline clinical signs of enzootic haematuria in ruminants.

Answer 39

• Group of animals grazing same pasture or cutting of hay.
• First CSx is protracted, poss intermittent haematuria +/- blood clots in urine.
• Chronic blood loss –> tachycardia, tachypnoea, exercise intol, pale MM, dec productivity and body condition.
• May palpate bladder wall thickening per rectum.
• +/- dysuria, pollakiuria, obstr of bladder trigone (tumour) or urethra (clot).

Question 40

Describe diagnostic test findings in cattle with enzootic haematuria.

Answer 40

• Ultrasound: bladder thickening, irregularly shaped bladder wall.
• CBC: severe anaemia; may see low platelet, seg neut and lymphocyte counts.
• Urinalysis: haematuria, proteinuria, +/- pyuria.

Question 41

Describe the pathophysiology of enzootic haematuria in ruminants.

Answer 41

• All parts of the plants are toxic to sheep and cattle.
• Several compounds in bracken fern possess irritant, mutagenic, immunosuppressive or carcinogenic activities incl ptaquiloside, quercetin and alpha-ecdysone.
• May cause recrudescence of latent BPV-2 through immunosuppression.
• Mutagenic compounds interact w BPV-2 in bladder to induce local neoplasia.
• Bladder carcinomas from cows w enzootic haematuria express COX-1 and COX-2 at a high level compared to normal controls.

Question 42

Describe the epidemiology of enzootic haematuria in ruminants.

Answer 42

• Described in America, UK, Aus, Europe.
• Occurs most in US in Pacific Northwest and upper Midwest.
• Plant grows best in well-drained, fertile coils and is often localised in open areas of forests; poisoning occurs in ruminants grazing pasture itself or hay w bracken fern.
• Primarily adult sheep and cattle; haematuria seen in cattle 2-3yo, neoplasia 3-7y after grazing commences.
• Up to 90% adult cattle affected in endemic areas.

Question 43

Describe the necropsy findings in ruminants with enzootic haematuria.

Answer 43

• Tissue pallor from anaemia.
• Bladder wall thick and mucosa haemorrhagic and ulcerated.
• Histo bladder wall: capillary engorgement, intramural haemorrhage, metaplasia of bladder epi, several type of bladder tumours.
• Metastasis of epi neoplasms to regional LNs or other organs can occur.

Question 44

Describe the treatment and prevention of enzootic haematuria in ruminants.

Answer 44

• Tx limited to reduction or elim of bracken fern in diet.
• Haematuria will cease if bracken feeding is discontinued before onset of tumour formation.
• Early culling may help prevent low productivity from anaemia and neoplasia.