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Urolithiasis is an economically significant disease of ruminants. In cattle, fatal urolithiasis is reported anywhere from 3 to 10% [1, 2]. Treatment and prevention of urolithiasis is a continual challenge for bovine practitioners and producers. The morbidity and mortality is devastating for not only steers in feedlots, but also breeding soundness for bulls.

Urolithiasis is a multifactorial disease involving diet, urine pH, and body water balance. Contributing factors include ruminant anatomy, factors favoring nidus development, factors precipitating solutes, and factors favoring cementing of stones. Uroliths occur when minerals precipitate from the urine and bind to an organic matrix or nidus [3]. The organic matrix is a mixture of urinary peptides, proteins, and mucopolysaccharides [3]. The proteinaceous aspect of the matrix can consist of desquamated epithelial cells, casts, or other urinary tract debris for infection or inflammation; however, this is uncommon in ruminants [3].

In cattle, urolithiasis typically falls into two categories: animals consuming high concentrate rations and pastured animals consuming grasses high in silica [4]. High concentrate rations usually fed with feedlot and show animals contain a low calcium to phosphorus ratio. High phosphorus rations typically create phosphate calculi (calcium, ammonium, and magnesium), with struvite being the most common [4, 5]. Ruminants afflicted with phosphate urolithiasis typically have multiple offending calculi that are smooth, soft, and sandy in appearance. These are the uroliths typically associated with calculi on the preputial hairs. Cattle grazing pastures in the western USA high in silica are most at risk of developing silicate uroliths. Silicate uroliths can even occur after removal of the offending forage [4]. Oat grain and oat straw are also high in silica and can be the etiology of silica urolith in the absence of grazing a pasture high in silica [4]. Cattle afflicted with silica urolithiasis typically obstruct with a single urolith that is rough, hard, and white measuring approximately 4–7 mm in diameter. One retrospective study reported 6.6% of cases afflicted with two distinct calculi [5]. Carbonate and oxalate uroliths are uncommonly encountered in cattle [4]. Carbonate uroliths are associated with consumption of legumes and oxalate uroliths are associated with consumption of oxalate‐containing plants such as clover, halogeton, greasewood, soursob, and sorrel [6].

Uroliths tend to form in alkaline urine in ruminants with normal pH ranging from 7 to 9.5. Increasing urine pH results in increasing likelihood that urinary colloids will precipitate [7]. Uroliths that precipitate in alkaline urine include struvite, calcium phosphate, and calcium carbonate [4]. Urine pH has no effect on the calculogenesis of silica uroliths [3, 4].

Inadequate body water balance is a significant risk factor in the occurrence of urolithiasis. Dehydration results in increased solute concentration in the urine, providing more scaffold and calculogenesis opportunities. Seasonality can occur, with an increase of cases seen when decreased water consumption occurs. During the summer, palatable water sources and drought can result in decreased water intake. During times of extreme cold, voluntary decreased intake may occur. Herd outbreaks of urolithiasis can even occur if available palatable water sources are extreme.

The narrow, long, and tortuous male ruminant urethral anatomy contributes to the occurrence of urinary obstruction in cattle. The most common site for urethral obstruction in bulls and steers is the distal sigmoid flexure. Occurrence at the ischial arch is less commonly reported [8]. While urolithiasis is seen in castrated and intact males, obstruction tends to be most common in steers due to the narrower urethral diameter from the absence of testosterone. Early castration has been shown to result in decreased urethral diameter and increased incidence of urolithiasis [9, 10]. Steers greater than eight months of age are the most commonly presented for disease [9]. Because of the effect of castration on urethral diameter, some authors suggest delaying castration until six months of age [1]; however, ethical considerations and castration complications at this weight should be considered before implementation of this recommendation.

Other commonly cited implications for urolith formation include hypovitaminosis A, hypervitaminosis D, and estrogenic intake [1, 4, 8]. However, true evidentiary support in the literature is lacking. Hypovitaminosis A occurs when cattle are fed poor quality hay and silage stored for prolonged periods. Hypervitaminosis D is commonly a result of feeding error during ration mixing. Diethylstilbestrol implantation and estrogen intake are hypothesized to result in hypertrophic effect on seminal vesicles, urethras, and bulbourethral glands, thus increasing the risk for urolithiasis [1, 8, 10].