During studies designed to determine the etiology and pathogenesis of a disease known as Idiopathic Cutaneous and Renal Glomerular Vasculopathy of Greyhounds (CRGV), we discovered what appears to be an exceptionally good animal model of the Hemolytic Uremic Syndrome (HUS). The first paper detailing our work has been published recently in Veterinary Pathology. This paper provides evidence of the pathologic similarity between CRGV and HUS. A paper detailing the clinical and treatment aspects of CRGV has been submitted. Finally, a paper proposing CRGV as a spontaneously occurring animal model of human disease is in preparation.

The evidence that CRGV is caused by Shiga-like toxin-producing E. coli is very strong. This is based on the fact that the epidemiology, clinical disease, pathology, and response to therapy of CRGV are similar (in many cases identical) to those of HUS. In addition, Shiga-like toxin-producing E. coli (serotype 0157:H7) and verotoxin activity have been found in samples of the 4D- beef fed to racing Greyhounds (termed 4D because of being from cattle which are diseased, debilitated, dying, or dead). In most case the 4D- beef is fed raw. Interestingly, CRGV only occurs in racing Greyhounds being fed raw 4D-beef. No cases have occurred in pet dogs or in Greyhounds fed cooked 4D-beef. Fecal samples of Greyhounds with CRGV contain E. coli 0157:H7 and virotoxin activity. Thin-layer chromatographic studies of Greyhound kidney demonstrate the presence of globotriaosyl-ceramide (Gb3), the binding site of Vero- and Shiga-like toxins. Finally, lesions similar to CRGV can be experimentally induced in healthy Greyhounds by injecting small amounts of purified verotoxin-1 (VT-1).

CRGV of Greyhounds appears to be the canine equivalent of E. coli food poisoning in humans and an excellent animal model of HUS. However, a number of important questions remain to be answered concerning the utility of CRGV as an in vivo model of HUS.

We are currently looking for collaborators who are interested in working together on an RO1 research proposal under the DK-96-007 program. The scope of our project is not completely defined. Clearly, it is important we continue to evaluate and better define a canine model of HUS. In addition, to expedite the development of a better understanding of the pathophysiology of HUS, more effective treatments, and preventative strategies, we are also looking for other investigators who might be interested in contributing their special expertise to our program. We would appreciate it if you would share our interest in collaborative studies with other investigators in the field. Suggestions as to investigators that we might contact directly would also be appreciated.

If you have any questions or suggestions, please do not hesitate to contact me directly: