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Volume 13, Number 9—September 2007

Dispatch

Equine Rhinosporidiosis in United Kingdom

Gail Leeming*Comments to Author , Ken C. Smith†1, Mark E. Bestbier†2, Annalisa Barrelet‡, and Anja Kipar*
Author affiliations: *University of Liverpool, Liverpool, United Kingdom; †Animal Health Trust, Newmarket, Suffolk, United Kingdom; ‡Beaufort Cottage Laboratories, Newmarket, Suffolk, United Kingdom;

Main Article

Figure 2

Agarose gel electrophoresis of PCR products from Rhinosporidium seeberi–specific primers (A) and β-actin primers (B). The left lane contains a 100-bp ladder. Samples 1–4, from horses with histologic diagnoses of rhinosporidiosis; sample 5, from the skin of a noninfected horse; sample 6, negative control (water).

Figure 2. Agarose gel electrophoresis of PCR products from Rhinosporidium seeberi–specific primers (A) and β-actin primers (B). The left lane contains a 100-bp ladder. Samples 1–4, from horses with histologic diagnoses of rhinosporidiosis; sample 5, from the skin of a noninfected horse; sample 6, negative control (water).

Main Article

1Current affiliation: The Royal Veterinary College, Hatfield, United Kingdom

2Current affiliation: Rest Associates, Swaffham Prior, Cambridge, United Kingdom

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