Bovine Leukocyte Adhesion Deficiency and Complex Vertebral Malformation

Livestock species can be affected by different types of genetic defects. Recently, we are faced with genetic defects in dairy cattle such as bovine leukocyte adhesion deficiency (BLAD) and complex vertebral malformation (CVM) both are autosomal recessive defects leads to an inherited lethal disease in Holstein breed. BLAD is caused by a deficiency in leukocyte surface glycoproteins known as integrin which is a sticky protein generally found on the surface of leukocytes and it is reduced in animals carrying recessive alleles. These proteins are responsible for the cell-cell interactions necessary for neutrophils to adhere to vascular endothelium and enter the tissue for destroying pathogens. It can be found on all T-cells, B-cells, macrophages and neutrophils. Two point mutations have been identified in the gene that In the present research, molecular detection of bovine leukocyte adhesion deficiency (BLAD) and complex vertebral malformation (CVM) in a population of Iranian Holstein cows has been carried outusing milk somatic cells by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The BLAD and CVM are monogenic and autosomal recessive heredity lethal syndrome in Holstein-Friesian cattle. BLAD characterized by affecting the haematopoietic system via reduced expression of the adhesion molecules on neutrophils. CVM characterized by intra-uterine mortality with disorders such as short neck, curved legs, abnormality of ribs and some certain heart abnormalities. In the first step of our research program, tank milk samples from 50 herds were collected. PCR-RFLP was performed to detect a point mutation of both CVM and BLAD genes. After DNA extraction, PCR was amplified using specific primers for 136 bp DNA (CD18 gene) and 233 bp DNA (SLC35A3 gene). TaqI and EcoT22I enzymes were used to identify both BLAD and CVM alleles of both genes by digestion of PCR products. In these herds, we did not find any affected herd with the mutant allele of BLAD comparing with a positive evidence but the mutation of SLC35A3 gene found in 17 different herds. In the next step of our study a herd with 120 cows was randomly selected for individual test using blood samples. We showed two cows out of 120 were identified as carriers of this gene. In this herd, the total number of dominant homozygote (AA), heterozygote (Aa) and recessive homozygote (aa) genotypes for CVM were 118, 2 and 0, respectively and the frequency of A and a alleles were 0.992 and 0.008, respectively. The other affected herds will be tested in the next step of our research program.