Immune complex glomerulonephritis of suspected iatrogenic origin in five Japanese Black calves

BERNIER GOSSELIN, Véronique; KIM, Dae Y.; NAGY, Dusty W.; SHOEMAKE, Brian M.; SHAW, Daniel P.; ROYAL, Angela B.; EVANS, Tim J.; MIDDLETON, John R.

The most consistent and important pathologic finding on all 4 necropsies was immune complex glomerulonephritis. Immune complex glomerulonephritis in cattle is uncommon [2, 3, 8, 12, 14, 15] . Deposition of circulating immune complexes in the glomeruli is usually caused by persistent antigenemia and production of antibodies by the host in response to the infection [2, 3] , although in some cases no infectious cause is identified [8] . Persistent BVDV infection is reported [2, 12] as a cause of immune complex glomerulonephritis, but was ruled out in the four calves that were tested in this report. Production of antibodies in response to vaccination, followed by experimental challenge to Mycoplasma mycoides subsp. mycoides has also been reported to cause glomerulonephritis [7] . Most previously reported cases of immune complex glomerulonephritis were at least 18 months old with the youngest case being 2 months old [12] . Moreover, previous reports of glomerulonephritis in cattle are usually described as single cases, whereas over 50% (7/13) of this group of calves showed clinical signs and were euthanized or died, suggesting a common denominator related to management or environmental exposure. Embryos of the same genetic lineage raised in recipient cattle on other farms under different management did not exhibit clinical signs similar to these calves, suggesting this was not an inherited disorder. While a familial nephropathy has been reported in Japanese Black cattle [6] , only some of the previously reported histologic lesions, including thickening of the glomerular basement membrane and mesangial proliferation, were consistent with findings of the cases reported herein. In contrast to the cases reported here, the familial nephropathy cases had reduced numbers of glomeruli, interstitial fibrosis with inflammatory cell infiltration, clusters of atrophic and cystic tubules, and thickening of the tubular basement membrane [6] . Additionally, immunohistochemistry in familial nephropathy cases was reported to be negative for bovine IgG in the areas of mesangial proliferation [6] .