Sheep Health & Production

Urolithiasis | Posthitis | Enlargement of bulbo-urethral glands in wethers | Diseases of the kidney | Recommended reading

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Urolithiasis

The obstruction of the urethra or, occasionally, the ureter of male sheep by calculi or uroliths produces the disease of urolithiasis or calculosis. The formation of calculi occurs also in ewes but, because of their short, wide urethra, obstruction rarely occurs.

Uroliths are usually mineral concretions formed by the precipitation or crystallization of mineral salts on an organic matrix. Their formation is, therefore, dependent on a number of factors, some dietary and some environmental.

In general terms, the disease causes significant economic losses of wethers and rams as a result of urethral obstruction, rupture of the urethra or bladder and death from uraemia. The morbidity is generally low but can be as high as 10% annually in exceptional circumstances. The disease in valuable rams may occasionally warrant attempts at treatment.

The development of uroliths

The chemistry of their formation is not well understood. The chemical composition depends on the available minerals and the pH of the urine, both of which are determined by the diet.

Phosphates

This group includes magnesium ammonium phosphate (struvite) and calcium phosphate. They occur in alkaline urine, associated often with the feeding of cereal grain.

Silica

These can be pure silica or mixed with calcium oxalate, calcium carbonate or organic materials. They occur most frequently in sheep grazing oat stubbles, eating oaten hay or grass hay.

Carbonates

Calcium carbonate is the most common carbonate in uroliths. These occur in alkaline urine. The excreted products of many herbaceous diets are alkaline carbonates. Plants particularly high in calcium or oxalates predispose sheep to carbonate urolithiasis.

Phyto-oestrogens

Obstructing material is soft and not heavily mineralized. Obstruction due to: (1) desquamated cells and secretions of accessory glands under oestrogen influence, (2) benzcoumarin calculi in the renal pelvis ('clover stone') which cause renal fibrosis in ewes and wethers, (3) calcium carbonate in a white organic paste obstructing the urethra.

Oxalate

Excessive, unaccustomed intake of oxalate can lead to crystallization in the urine and renal tubular nephrosis and urolithiasis.

Cystine, xanthine

These occur uncommonly.

Diagnosis

History

A history of concentrate feeding, cereal stubble grazing, oestrogenic pastures etc

Clinical signs

• partial obstruction; inappetence, stretching, dribbling blood-stained urine and straining
• total obstruction; anorexia, 'stretched out' stance or recumbency, relief when rupture occurs
• rupture of urethra; swelling of subcutaneous tissues of ventral abdominal wall
• rupture of bladder; abdominal distension

Radiography

Diagnostic radiography involves the use of contrast media; medium being introduced after amputation of the urethral process.

Clinical pathology

The presence of uroperitoneum differentiates the uraemia from that of renal failure.

Necropsy

Hydronephrosis, ruptured ureter, bladder or urethra and 'sand' in bladder are diagnostic of urolithiasis.

Treatment

Amputation of the urethral process is often effective. Retrograde flushing, laporotomy, cut-down, perineal urethrostomy are less often useful. Euthanasia is often indicated.

Prevention of further losses

Deaths may continue despite control measures. For phosphate calculi, add calcium carbonate to concentrates, change diet, acidify urine with ammonium chloride, attempt to increase urine flow.

For calcium carbonate, silica and phyto-oestrogenic calculi, changing the diet may be all that can be done.

Posthitis

Also called balanoposthitis, enzootic posthitis or pizzle rot, the disease is an inflammation of the prepuce which extends in some cases to the penis, caused by Corynebacterium renale and, probably, other Corynebacterium spp under particular dietary conditions. The disease affects wethers, particularly mature wethers, and young rams. The lower incidence in mature rams is probably associated with the separation of the penile and preputial epithelial surfaces as rams mature. (A balanitis (knob rot) of unknown aetiology has also been reported in rams.) The organism has also been isolated from vulvitis of ewes and posthitis in goat wethers.

Development of lesions

C renale is capable of hydrolyzing urea and proliferates more rapidly when higher concentrations of urea are present. The tissue necrosis may be caused by ammonia rather than the organism itself. Urinary concentration of urea is raised when sheep graze high protein pastures such as lush, legume dominated pastures. Under conditions favourable for the development of the disease, up to 60% of wethers may be affected with clinically significant posthitis[1].

The disease has two distinct stages. The mild, early stage is an external ulceration of the skin near the preputial orifice. Scabs develop over these ulcers. After a period of weeks or months, extension of the lesion within the prepuce may occur, leading to the second stage of internal ulceration. In animals with internal ulceration, the prepuce swells and the passage of urine may be difficult. Necrotic material and pus accumulate inside the prepuce and discharges accumulate in the belly wool. The area becomes attractive to fly strike. The serious losses of production which make the disease of economic significance are associated with the development of internal lesions.

Clinical signs

Sheep that only have external lesions show no clinical signs other than a mild, superficial necrosis of the skin of the preputial orifice which is usually covered in a brown scab. Clinical signs of the internal lesions include swelling of the sheath, dribbling of urine, restlessness, irritation or pain, hump-backed stance and frequent recumbency. The wool around the prepuce is heavily stained and the sheep may be fly-struck on the belly. In advanced cases, the penis becomes involved (balanitis) and the urethra may become obstructed. The major economic consequences of posthitis are from deaths from severe lesions and from flystrike. Losses of wool production and liveweight gain are probably small except in the most severe cases[2].

Prevention

Testosterone injections are the preferred prophylactic treatment. A number of testosterone products are available. For best effect they should be given immediately before a high risk period. In one experiment, 75mg of testosterone enanthate liquid (Tesgro, MSD Agvet) and 75mg of testosterone cypionate liquid (Banrot, Pitman Moore) produced higher blood levels of a shorter duration than 70mg of testosterone propionate pellets (Ropel, Schering Pty Ltd) implanted subcutaneously which provided adequate preventive levels for at least 10 weeks[3]. Testosterone treatment will only slightly reduce the incidence of external lesions but will markedly reduce the incidence of internal ulceration. There are side-effects to treatment with testosterone. Two doses of 70mg of testosterone propionate (autumn and spring) will increase GFW by up to 7%, decrease yield, increase CFW by up to 4%, FD by about 1% and liveweight by 2kg or more independent of effects on production by controlling pizzle rot[4].

Prophylactic testosterone should be given to wethers grazing clover dominant pastures in spring and possibly in autumn, at the start of the seasonal pasture growth.

The removal of belly wool by shearing is known to reduce the incidence of posthitis but 'ringing' - the shearing of wool just around the preputial orifice which is commonly performed when wethers are crutched to prevent the contamination of wool near the orifice and subsequent fly strike - has little effect on the incidence of pizzle rot[5].

Pizzle dropping - the surgical lowering of the preputial orifice by incising the skin fold between the abdominal skin and the prepuce - has also been claimed to reduce the incidence of pizzle rot. Pizzle dropping, if carried out properly, will dramatically reduce urine staining of wool and the incidence of flystrike of the belly[6]. There appears to be an additional benefit on the incidence of severe pizzle rot[7].

Treatment

Dietary change

For cases of external ulceration, a change to a low protein diet will reduce the prevalence of lesions.

Local treatment

The wool around the prepuce should be removed, the scabs removed, and the prepuce irrigated with antiseptics. The installation of 2 to 3ml of antiseptic solution into the sheath from a plastic squeeze bottle then smearing of the antiseptic around the orifice as it drains has been shown to be effective. Treatment should be repeated every 2 or 3 days until they are resolved. Originally, an alcoholic solution of 20% cetrimide was recommended but this product is no longer readily available. Chlorhexidine digluconate in 0.8% solution (undiluted Hibitane, Coopers) is also effective. It may be less effective than cetrimide but is also less irritant to tissues. Cetrimide should not be used in rams and should not be applied to the vagina of ewes⁽⁶⁾.

Parenteral treatment

The causative organism is sensitive in vitro to penicillin and slightly sensitive to oxytetracycline and nitrofurantoin. It is less sensitive to erythromycin, neomycin and streptomycin[8]. 500mg of oxytetracycline per os daily for 4 days is ineffective in vivo[9]. Procaine penicillin parenterally is reportedly effective in resolving lesions[10] but should be given in conjunction with local therapy, if given at all.

Testosterone, at double the dose recommended for prophylaxis, is recommended for treatment of internal ulceration. Lower doses have shown marginal efficacy when given alone. In one experiment, 90mg of testosterone propionate was 49% effective in treatment and prevention while 90mg testosterone plus local treatment with cetrimide were 88% effective[1].

Surgical drainage

'Slitting' the prepuce to provide drainage is an effective treatment of internal ulceration even in advanced cases. The incision is either a single ventral slit posteriorly from and including the preputial orifice or the removal of a V-shaped section of the ventral prepuce. If the single slit is performed, the incision should extend to the tip of the urethral process but not too far posteriorly to avoid exposing the penis to trauma and drying conditions[10]. Wool adjacent to the incision may become urine-stained and attractive to strike flies[11].

Enlargement of bulbo-urethral glands in wethers

This occurs in wethers, but not rams, grazing oestrogenic pastures. The glands undergo hyperplasia and the wethers suffer a loss in condition and, in some cases, death. Testosterone is protective of the oestrogenic effect[12].

Diseases of the kidney

Renal diseases of the sheep are not common and, with the exception of some plant and chemical intoxications, tend to occur very sporadically. Ovine renal disease can be classified, on the basis of aetiology, into 4 major classifications (Table 18.1).

Congenital malformations

These are uncommon in sheep. The most common urinary tract defect in a Western Australian survey of dead lambs was agenesis of one or both kidneys[13].

Immunologically mediated glomerulonephritides

In sheep, glomerulonephritis is an inflammatory disease resulting from the deposition of antigen-antibody complexes along the basement membrane of the glomerular capillaries. The most common form in sheep is membranous glomerulonephritis[14] or membranoproliferative glomerulonephritis[14]. The disease occurs only sporadically, usually in adult sheep, but has been reported in lambs with coccidiosis[16]. A genetically controlled congenital glomerulonephritis (mesangiocapillary glomerulonephritis or MCGN) has been reported in Finnish Landrace sheep and their crosses. Lambs with MCGN are clinically normal at birth but within a few weeks stop sucking, often demonstrating signs of a secondary encephalopathy. At examination either pre-or post-mortem, the gross renal enlargement is the outstanding sign; the kidneys may be up to 6 times normal size[14].

Table 18.1 : Classification of ovine renal disease (from Angus 1991)[15]

Infectious nephropathies

A number of bacterial species can cause infections, particularly abscessation, of the kidney following haematogenous spread. These include Corynebacterium pseudotuberculosis, Streptococcus spp, Staphylococcus spp and other pyogenic bacteria which may enter the body through wounds or by navel infection and cause simultaneous infections in other organs and joints. Renal lesions may also occur in lambs infected with pestivirus (hairy shaker lambs).

Ascending infections of the kidney are uncommon in sheep but may occur in animals with urolithiasis and in lambs with navel infections.

Toxic nephropathies

Toxins exert their effects on the tissues of the nephron in two ways. Firstly, by inducing ischaemia, as many bacterial endotoxins do as part of a generalised process of capillary endothelial damage and, secondly, by direct effect on the sensitive tissues of the nephron. The proximal tubule is particularly susceptible to this form of damage, possibly because it is highly specialised and it is exposed to toxins which are reabsorbed after glomerular filtration. The primary lesion in most forms of toxic nephrosis is tubular; glomerular dysfunction may follow.

The epsilon toxin of Clostridium perfringens type D is particularly lethal to the renal tubule. The destruction of the renal tubule is an important component of the pathogenesis and post-mortem diagnosis of enterotoxaemia in sheep.

18.2 : Toxic nephropathies of sheep

Isotropis spp poisoning (lamb poisons)

There are 9 recorded species of this plant genus; 6 of them occur in WA where most cases of intoxication have been recorded. Of the 9 species, 5 have been associated with toxicity. Isotropis atropurpurea occurs in all states except Queensland and has caused toxicity in WA, NT and NSW. In WA, poisoning has been recorded in the north-west, desert regions, south-west agricultural and pastoral zones[17]. Poisoning occurs most commonly in spring when green suckers occur. The plants appear to be very palatable[18].

The experimental intoxication of sheep with a bolus dose of 300g of dried plant material of Isotropis forrestii has been described[19]. Clinical signs included weakness, depression, anorexia, diarrhoea and oliguria. Some animals showed clinical signs on day 1, all were anorexic by day 5. At necropsy, the kidneys were pale, surrounded by gelatinous oedema extending into mesenteries; some had ascites and hydrothorax. Histologically there was severe renal tubular damage, mild to moderate gastro-enteritis (possibly through uraemia rather than a direct effect of the toxin). The tubular damage appeared to be a result of a direct effect of the toxin rather than one mediated by ischaemia. Peracute deaths have also been reported from ingestion of Isotropis spp. The toxic principle has not been identified.

Oxalate nephrosis

The following plants often contain high levels of oxalates:

Family Oxalidaceae

Soursob     Oxalis pes-caprae

Family Chenopodiaceae

Soft roly poly     Salsola kali

Black pigweed     Trianthema portulacastrum

Soda bush     Threlkeldia proceriflora

Family Polygonaceae

Sheep sorrel     Acetosella vulgaris

Dock     Rumex spp

Spiny emex     Emex australis

Family Grystomaceae

Pigweeds     Portulaca spp

Family Aizoaceae

Slender iceplant     Mesembryanthemum nodiflorum

A number of cultivated grasses, which generally have only moderate levels of oxalate, include:

Setaria      Setaria sphacelata[20]

Panic     Panicum antidotale, P maximum

Buffel grass     Cenchrus ciliaris

Kikuyu grass     Pennisetum clandestinum

Soursob occurs extensively in southern NSW, northern Victoria, SA and south-west WA. Many of these areas are of medium rainfall (around 480 mm per annum) and contain many sheep. The chenopodiaceous plants are salt bushes and succulents and are prevalent mainly in the inland areas of Australia and are grazed extensively by sheep. The cultivated grasses occur chiefly in Queensland.

[The following pathogenesis of plant oxalate poisoning is derived from Seawright (1982)[21].]

Ruminants are able to graze these plants in most circumstances without oxalate intoxication. Soluble oxalate is rapidly broken down to carbonate and formate in the rumen through microbial action, or else precipitated as insoluble calcium oxalate in the rumen contents. Both processes prevent or reduce the uptake of oxalate into the ruminal mucosa and into the bloodstream. If substantial amounts of oxalate are absorbed, calcium oxalate will precipitate in submucosal arterioles and damage the rumen mucosa. Similar damage may occur in lung capillaries, causing pulmonary oedema. In the kidneys, oxalate is secreted by the tubular epithelial cells, causing them damage, and calcium oxalate crystals are precipitated in the tubular lumina.

Plasma calcium concentration falls in the presence of high plasma oxalate levels and clinical signs of hypocalcaemia may occur. Animals dying from acute oxalate poisoning often have terminal pulmonary oedema, with copious amounts of stable froth in the trachea and bronchi and marked hyperaemia of the mucosa of the forestomachs and of the lower alimentary tract. Kidneys are usually swollen and the cortex pale.

Acute oxalate poisoning usually occurs when hungry stock are placed on pasture dominated by oxalate-containing plants which are, at the time, high in oxalate levels. Fasting, or low calcium diets prior to exposure predispose to intoxication. Fasting reduces the numbers of methanogenic bacteria which utilize formate, and if formate is not metabolised oxalate breakdown itself is inhibited. Damage to the ruminal mucosa can be followed by fungal or bacterial invasion leading to acute rumenitis and intractable indigestion. Animals acutely or subacutely intoxicated with oxalate respond only transiently or not at all to calcium borogluconate therapy and death occurs due to severe metabolic disturbance complicated by renal, pulmonary and gastro-intestinal injury. Three outbreaks of acute oxalate poisoning by buffel grass (Cenchrus ciliaris) have been described in which 5%, 1% and 18% of the mob died within 12 to 120 hours of exposure to the pasture, following 2 days of starvation. Clinical signs included dyspnoea, collapse, loss of consciousness and death without struggling[22]. Slender iceplant (Mesembryanthemum nodiflorum) has also been associated with acute poisoning in WA[23].

Chronic oxalate toxicity usually occurs in animals grazing Oxalis pes-caprae. Animals grazing soursob develop ahigh degree of tolerance to ingested oxalate. There is, however, usually a low level of oxalate absorption with progressive renal injury and deposition in the kidneys of calcium oxalate crystals. Over a period of 2 to 12 months of grazing on such pastures, animals gradually develop renal failure and the occasional death occurs. At necropsy, the kidneys are small, white and fibrotic with large amounts of crystals.

Recommended reading

Chapman HM and Sutherland RJ (1990) Urolithiasis in sheep In Sheep Medicine, University of Sydney Post-graduate Committee in Veterinary Science, Proceedings No 141, p 33

[1] Southcott WH (1962) The prevention and treatment of ovine posthitis with testosterone propionate Aust vet J 38 p 33

[2] Osborne HG, Bentley JB and Pearson IG (1989) Economic aspects of balanoposthitis in Merino wethers Advances 1989, Australian Veterinary Asoociation

[3] Sacket DM, Wright PJ and Darvill FM (1987) Plasma testosterone concentrations in wethers treated with commercial preparations of testosterone Aust Vet J 64 p 386

[4] Osborne WB (1968) The effect of testosterone on the components of fleece weight in Merino wethers Aust Soc Anim Prod 7 p 407

[5] Southcott WH (1965) Epidemiology and control of ovine posthitis and vulvitis Aust vet J 41 p 225

[6] Marchant RS and Burbidge SG (1986) Effect of pizzle dropping and testosterone propionate on production of Merino wethers Aust Soc Anim Prod 16 p 419

[7] Watts TJ (1986) Pizzle dropping Mackinnon Project newsletter, University of Melbourne, May, 1986, p 4

[8] Southcott WH (1965) Etiology of ovine posthitis: Description of a causal organism Aust vet J 41 p 193

[9] Swan RA (1971) Treatment of posthitis in sheep Vet Rec 88 p 304

[10] Dent CHR (1971) Ulcerative vulvitis and posthitis in Australian sheep and cattle Vet Bull 41 p 719

[11] Gardner JJ and Adams NR (1986) The effect of zeranol and testosterone on Merino wethers exposed to highly oestrogenic clover pasture Aust Vet J 63 p 188

[12] Chamley WA, Findlay JK and Nairn ME (1977) The effect of testosterone and an anti-oestrogen on hypertrophy of bulbourethral glands of wethers grazing oestrogenic pastures Aust Vet J 53 p 476

[13] Dennis SM (1979) Urogenital defects in sheep Vet Rec 105 p 344

[14] Majid HN and Winter H (1986) Glomerulonephritis in lambs with coccidiosis Aust Vet J 63 p 314

[15] Angus KW (1991) Renal diseases in Diseases of Sheep 2nd edition ed WB Martin and ID Aitken publ Blackwell Scientific Publications, London

[16] Rothwell JT and Marshall DJ (1986) Suspected poisoning of sheep by Anagallis arvensis (scarlet pimpernel) Aust Vet J 63 p 316

[17] Gardiner MR and Royce RD (1967) Poisoning of sheep and cattle in Western Australia due to species of Isotropis (Papilionaceae) Aust J agric Res 18 p 505

[18] Seawright AA (1982) Isotropis spp in Chemical and Plant Poisons, Animal Health in Australia vol 2, publ Australian Bureau of Animal Health, p 53

[19] Cooper TB, Huxtable CR and Vogel P (1986) The nephrotoxicity of Isotropis forrestii in sheep Aust Vet J 63 p 178

[20] Seawright AA (1970) An outbreak of oxalate poisoning in cattle grazing Setaria sphacelata Aust Vet J 46 p 293

[21] Seawright AA (1982) Oxalates in Chemical and Plant Poisons, Animal Health in Australia vol 2, publ Australian Bureau of Animal Health, p 74

[22] McKenzie RA, Bell AM, Storie GJ, Keenan FJ, Cornack KM and Grant SG (1988) Acute oxalate poisoning of sheep by buffel grass (Cenchrus ciliaris) Aust Vet J 65 p 26

[23] Jacob RH and Peet RL (1989) Acute oxalate toxicity of sheep associated with slender iceplant (Mesembryanthemum nodiflorum) Aust Vet J 66 p 91