Pelger–Huët Anomaly in Australian Shepherds: 87 Cases (1991–1997)

Abstract:

Blood smears from 892 Australian shepherds were evaluated for the presence of Pelger–Hue¨t (P-H) anomaly over a 6-year period. During the study, 87 dogs were diagnosed with P-H anomaly (9.8% incidence) following microscopic examination of Wright–Leishman–stained blood smears. Granulocytes from dogs with P-H anomaly had nuclear hyposegmentation resembling bands and metamyelocytes; however, the chromatin pattern was more aggregated than that observed 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 females 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, suggestive of the homozygous form of the anomaly. Because this phenotype was not 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 normal 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 transmitted as an autosomal dominant trait with incomplete or decreased penetrance 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.