Pelger-Huet anomaly in Australian shepherds: 87 cases (1991-1997)

Blood smears from 892 Australian shepherds were evaluated for the presence of Pelger-Huet (P-H) anomaly over a 6-year period. During the study, 87 dog s were diagnosed with P-H anomaly (9.8% incidence) following microscopic ex amination of Wright-Leishman-stained blood smears. Granulocytes from dogs w ith P-H anomaly had nuclear hyposegmentation resembling bands and metamyelo cytes; however, the chromatin pattern was more aggregated than that observe d in mature segmenters. The granulocyte morphology of dogs with P-H anomaly was similar to that described for humans and rabbits with the heterozygous form of P-H anomaly. Where gender was known, 9.4% of males and 8.8% of fem ales had P-H anomaly, indicating autosomal transmittance of the trait. None of the dogs with P-H anomaly had a predominance of granulocytes with round to oval nuclei (myelocytes) and an extremely coarse chromatin pattern, sug gestive of the homozygous form of the anomaly. Because this phenotype was n ot observed in Australian shepherds, the homozygous form of P-H anomaly may be a lethal trait in utero. Six dogs with P-H anomaly had parents with a n ormal leucocyte phenotype. In addition, the incidence of P-H anomaly in F1 puppies from matings of individuals with normal and P-H phenotypes was less than expected. These observations strongly suggest that P-H anomaly is tra nsmitted as an autosomal dominant trait with incomplete or decreased penetr ance in Australian shepherds. Transmittance of P-H anomaly in this breed of dogs may be governed by more than one allele or expression of the anomaly may modified by genes at a different locus or loci.