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Eradication of porcine factor H deficiency in Norway
  1. K. Høgåsen, MD, PhD1,
  2. J. H. Jansen, DVM, PhD2 and
  3. M. Harboe, MD, PhD1
  1. 1 Institute of Immunology and Rheumatology, The National Hospital and University of Oslo, Oslo, Norway
  2. 2 Department of Morphology, Genetics and Aquatic Biology, Division of Pathology, Norwegian College of Veterinary Medicine, Oslo, Norway

Abstract

In pigs a hereditary deficiency of the complement-inhibitory protein factor H consistently leads to the development of lethal membranoproliferative glomerulonephritis type II. This autosoipal recessive disease has been a common cause of early losses of piglets in the Norwegian Yorkshire breed, but has not been reported in the Norwegian Landrace breed. The aim of the present work was to identify carriers of factor H deficiency and to eradicate the disease from commercial pig populations. Factor H in plasma was measured by an enzyme immunoassay. Sixteen known carriers of the disease (parents of factor H-deficient offspring) had half the level of factor H (median 110, range 87 to 156 mg/litre) recorded in 17 homozygous healthy Yorkshire pigs (median 212, range 183 to 293 mg/litre) and 20 Landrace pigs (median 227, range 200 to 255 mg/litre). Factor H analysis in 397 piglets produced by the mating of known carriers revealed an approximately 1:2:1 distribution of individuals with very low, half-normal and normal levels of factor H representing homozygous deficient, heterozygous and homozygous healthy individuals. Thus, carriers could be identified reliably by measuring the plasma concentration of factor H. Most of the population of Norwegian Yorkshire breeding pigs (490 pigs) was therefore examined, and a half-normal factor H level consistent with the carrier state was found in 13.5 per cent. These animals were prevented from breeding and since then no losses of piglets suspected of being due to factor H deficiency have been reported. No carrier was identified among 102 Norwegian Landrace boars, almost excluding the existence of factor H deficiency in this breed.

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