Low incidence of bovine leukocyte adhesion deficiency (BLAD) carriers in Indian cattle and buffalo breeds

Abstract

BLAD is an autosomal recessive genetic disease that affects Holstein-Friesian (HF) cattle worldwide. It is a disease characterized by a reduced expression of the adhesion molecules on neutrophils. The disease is caused by a mutation that replaces adenine at 383 with guanine, which causes an amino acid change from aspartic acid to glycine. Blood samples and a few semen samples were collected from 1250 phenotypically normal individuals, including HF (N=377), HF crossbred (N=334), Jersey (105), other breeds of cattle (N=160) and water buffalo Bubalus bubalis (N=274) belonging to various artificial insemination stations, bull mother farms (BMFs) and embryo transfer (ET) centres across the country. PCR-RFLP was performed to detect a point mutation in CD18, surface molecules of neutrophils. The results indicate that out of 1250 cattle and buffaloes tested for BLAD, 13 HF purebreds out of 377 and 10 HF crossbreds out of 334 appear to be BLAD carriers. In the HF and HF crossbred population, the percentage of BLAD carriers was estimated as 3.23%. The condition is alarming as the mutant gene has already entered the HF crossbred cattle population and therefore, the population of HF and its crossbreds needs regular screening to avoid the risk of spreading BLAD in the breeding cattle population of India.

Incidence of bovine leukocyte adhesion deficiency, complex vertebral malformation, and deficiency of uridine-5-monophosphate synthase carriers in Brazilian Girolando cattle

“…However, it was considerably different from the frequency found in bulls by Patel et al (2007) in Indian Holstein Friesian crossbred cattle (2.99%), Norouzy et al (2005) in Iranian Holsteins (3.3%), Powell et al (1996) in American Holsteins (8.2%), Czarnik et al (2007) in the Polish Holstein-Friesian, Polish Red, and Polish Red-and-White breeds (4.3%), and Meydan et al (2010) in Holstein cows in Turkey (4.0%). The allele frequencies estimated for bulls may not fully reflect the allele frequencies for the breed since the tested bulls were derived from the Girolando progeny test and are therefore unlikely to represent a random sample of the population because they were included in the progeny test for their genetic superiority based on parent-average predictions.…”

“…The observed frequency of BLAD carriers among cows (0.76%) may be explained by the fact that this mutation is common in Holstein bulls in different countries (Norouzy et al, 2005;Akyüz and Ertuğrul, 2006;Czarnik et al, 2007;Patel et al, 2007), and carrier bulls were most likely used as founding sires during the establishment of the breed. Three of the 5 affected cows were daughters of the carrier bull evaluated in the study.…”

Factor XI deficiency in Indian Bos taurus, Bos indicus, Bos taurus x Bos indicus crossbreds and Bubalus bubalis

“…At 0.6% the frequency of FXI-deficiency carriers in the Holstein-Friesian population observed in our study is half that of the 1.2% reported in the Holstein sire population of the USA (Marron et al, 2004). The mutant gene for factor XI deficiency in Indian Holstein-Friesian cattle was higher than citrullinaemia (Murleedharan et al, 1999;Patel et al, 2006) and very much lower than BLAD (Patel et al, 2007), other autosomal recessive genetic diseases observed in Indian Holstein population. Because of the paucity of literature regarding the molecular diagnosis of FXI-deficiency, it is difficult to compare the carrierfrequency in the Indian Holstein-Friesian population to that found in other countries.…”

Türkiye’deki holştayn ineklerde üridin monofosfat senteaz eksikliğinin (DUMPS) belirlenmesi

“…Sığırlarda önemli verim kayıplarına neden olan otozomal çekinik kalıtsal hastalıklar çoğunlukla ırka özgüdür (6,7,8). Hem siyah-beyaz alaca hem de kırmızı-beyaz alaca holştaynlarda görülen üridin monofosfat senteaz eksikliği (DUMPS), bu tür kalıtsal bozukluklardan birisidir (8).…”

“…Hem siyah-beyaz alaca hem de kırmızı-beyaz alaca holştaynlarda görülen üridin monofosfat senteaz eksikliği (DUMPS), bu tür kalıtsal bozukluklardan birisidir (8). Pirimidin nükleotid sentezinin son aşamasında ortaya çıkan orotik asit, üridin monofosfat senteaz enzimi (UMPS) tarafından üridin monofosfata (UMP) dönüştürülür (4,9).…”