Abstract

The north-western part of South Africa, in particular, is well known for mineral imbalances. Aphosphorosis, resulting in rickets and osteomalacia, received a lot of attention at the turn of the nineteenth century (1882–1912). This was followed in 1997 by research on Vryburg hepatosis, another area-specific mineral imbalance–related disease in young calves reared on manganese-rich soil derived from the weathering of dolomitic (carbonate) rock formations. In 1982, a totally new syndrome (osteochondrosis) manifested in, amongst others, areas in South Africa where aphosphorosis was rife. Osteochondrosis was also identified in the south-western parts of Namibia as well as southern Botswana and other areas in South Africa. Osteochondrosis has a multifactorial aetiology and this study focused on the role of minerals, particularly phosphorus, in the development of the disease. A significant improvement in the clinical signs in experimental animals and a reduction of osteochondrosis occurred on farms where animals received bioavailable trace minerals and phosphorus as part of a balanced lick. An increase in the occurrence of the disease on farms during severe drought conditions in 2012–2013 prompted researchers to investigate the possible role of chronic metabolic acidosis in the pathogenesis of the disease.

Highlights

  • Since the 1800s, the north-western parts of South Africa, the North West and Northern Cape Provinces, have been known as an area characterised by aphosphorosis (‘stiff sickness’) in cattle (Theiler 1912; Theiler et al 1927), caused by a phosphorus deficiency that resulted in osteomalacia

  • The macroscopic and microscopic lesions associated with osteochondrosis are well documented, and the lesions noted in the experimental cattle did not differ from those reported (Hill et al 1998; Reiland 1978; Ytrehus et al 2007)

  • The current study confirmed that failure of endochondral ossification resulting in necrosis of either the physis or the articular–epiphyseal cartilage was central in the pathogenesis of the lesions, as proposed by Ytrehus et al (2004) and Ytrehus et al (2007)

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Summary

Introduction

Since the 1800s, the north-western parts of South Africa, the North West and Northern Cape Provinces, have been known as an area characterised by aphosphorosis (‘stiff sickness’) in cattle (Theiler 1912; Theiler et al 1927), caused by a phosphorus deficiency that resulted in osteomalacia. Affected animals often developed botulism because of the consumption of bones contaminated with Clostridium botulinum (Theiler, Du Toit & Malan 1937; Theiler et al 1927). The bone meal and coarse salt licks introduced to prevent osteomalacia and botulism seemed to have resolved the osteomalacia or rickets syndrome in the north-western parts of the country. In 1982, farmers and local veterinarians started reporting lameness accompanied by swelling of the stifle joint in cattle. The lameness seemed to affect only a small number of show animals and it was seen in Phase D tested bulls, but the incidence steadily increased, and in 2004, farmers reported an incidence that ranged from 2% to 20%. The only factor in common amongst affected animals was the geographical area in which they lived

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