Fleckvieh Calves Research Articles

A Missense Mutation in the Collagen Triple Helix of EDA Is Associated with X-Linked Recessive Hypohidrotic Ectodermal Dysplasia in Fleckvieh Cattle.

Mutations within the ectodysplasin A (EDA) gene have been associated with congenital hypotrichosis and anodontia (HAD/XHED) in humans, mice, dogs and cattle. We identified a three-generation family of Fleckvieh cattle with male calves exhibiting clinical and histopathological signs consistent with an X-linked recessive HAD (XHED). Whole genome and Sanger sequencing of cDNA showed a perfect association of the missense mutation g.85716041G>A (ss2019497443, rs1114816375) within the EDA gene with all three cases following an X-linked recessive inheritance, but normal EDAR and EDARADD. This mutation causes an exchange of glycine (G) with arginine (R) at amino acid position 227 (p.227G>R) in the second collagen triple helix repeat domain of EDA. The EDA variant was associated with a significant reduction and underdevelopment of hair follicles along with a reduced outgrowth of hairs, a complete loss of seromucous nasolabial and mucous tracheal and bronchial glands and a malformation of and reduction in number of teeth. Thermostability of EDA G227R was reduced, consistent with a relatively mild hair and tooth phenotype. However, incisors and canines were more severely affected in one of the calves, which correlated with the presence of a homozygous missense mutation of RNF111 (g.51306765T>G), a putative candidate gene possibly associated with tooth number in EDA-deficient Fleckvieh calves.

Macrophages in dermal disease progression of phospholipase D4-deficient Fleckvieh calves.

A new gene defect in Fleckvieh calves leads to a syndrome with partial phenotype overlap with bovine hereditary zinc deficiency. A mutation in a gene encoding phospholipase D4 (PLD4), an endosomal exonuclease, causes the disorder. In mice, PLD4 activity indirectly regulates the Toll-like receptor 9 (TLR9) pathway via degradation of microbial DNA. PLD4 absence thus results in visceral macrophage activation comparable to human macrophage activation syndrome. In this study, disease progression and the role of macrophages in affected calves were monitored clinically, clinicopathologically, and histologically over time. Breeding data identified 73 risk matings of heterozygous carriers resulting in 54 potentially PLD4-deficient calves born on farms. PLD4 status was examined via 5'-exonuclease assay, detecting 6 calves carrying the defect. These were purchased and monitored daily until final necropsy. The calves developed progressive skin lesions starting with small scaling areas terminating in severe crusting dermatitis, especially in areas with mechanical exposure. Histological and immunohistochemical analyses indicated that macrophages with cytoplasmic vacuolation increased considerably in skin sections obtained weekly during the disease course. Macrophage increase correlated with increased dermal lesion severity. Macrophage activation was confirmed by prominent phagocytic activity in the superficial dermis using electron microscopy. Dermal mRNA abundance of CCL2 and CCL3 measured by quantitative polymerase chain reaction verified macrophage activation. Further increase in mRNA of downstream molecule MyD88 and cytokine IL12b connected bovine PLD4 deficiency to increased TLR9 pathway activation. In contrast to human macrophage activation syndrome, the main feature of bovine PLD4 deficiency was local disease in organs with contact to microbial DNA (skin, intestine, lungs).

Zinc Deficiency-Like Syndrome in Fleckvieh Calves: Clinical and Pathological Findings and Differentiation from Bovine Hereditary Zinc Deficiency.

BackgroundZinc deficiency‐like (ZDL) syndrome is an inherited defect of Fleckvieh calves, with striking similarity to bovine hereditary zinc deficiency (BHZD). However, the causative mutation in a phospholipase D4 encoding gene (PLD4) shows no connection to zinc metabolism.ObjectivesTo describe clinical signs, laboratory variables, and pathological findings of ZDL syndrome and their utility to differentiate ZDL from BHZD and infectious diseases with similar phenotype.AnimalsNine hospitalized calves with crusting dermatitis and confirmed mutation in PLD4 and medical records from 25 calves with crusting dermatitis or suspected zinc deficiency.MethodsProspective and retrospective case series.ResultsThe 9 calves (age: 5–53 weeks) displayed a moderate to severe crusting dermatitis mainly on the head, ventrum, and joints. Respiratory and digestive tract inflammations were frequently observed. Zinc supplementation did not lead to remission of clinical signs in 4 calves. Laboratory variables revealed slight anemia in 8 calves, hypoalbuminemia in 6 calves, but reduced serum zinc concentrations in only 3 calves. Mucosal erosions/ulcerations were present in 7 calves and thymus atrophy or reduced thymic weights in 8 calves. Histologically, skin lesions were indistinguishable from BHZD. Retrospective analysis of medical records revealed the presence of this phenotype since 1988 and pedigree analysis revealed a common ancestor of several affected calves.Conclusions and Clinical ImportanceZDL syndrome should be suspected in Fleckvieh calves with crusting dermatitis together with diarrhea or respiratory tract inflammations without response to oral zinc supplementation. Definite diagnosis requires molecular genetic confirmation of the PLD4 mutation.

Survey of disbudding practice on Czech dairy farms

Disbudding is a routine practice in many dairy herds due to the effort to decrease the risk of injuries. Although the disbudding practice is regulated, it can vary among farms. The variation may be caused by many factors, such as herd size or type of breed, but also by farmers' perception of pain caused by disbudding. Hence, the aim of this study was to specify the disbudding practice on dairy farms in the Czech Republic and to assess these practices, including the use of pain mitigation medication, by breed, herd size, and sex of the disbudded calves. We analyzed data from 106 Czech dairy farms, which were collected by a trained interviewer at dairy meetings in 2014-2015. The farmers answered questions regarding the farm's basic characteristics, disbudding practice, and his/her attitude to the pain caused by disbudding. To test the influence of breed, herd size, and sex of disbudded calves on different variables, logistic regression models were used. Disbudding was performed in 92.5% of the surveyed farms; 63.3% of dairy calves were disbudded before 4 wk of age, and Czech Fleckvieh calves were 2.8 times more likely to be disbudded before 4 wk of age than Holstein calves. The hot-iron method was the most used method (69.4%). Calves were 4.5 times more likely to be disbudded by hot iron in herds where both heifers and bulls were disbudded than in herds where only heifers were disbudded. Most (>90%) surveyed farms did not use any pre- or post-procedure medication to mitigate the pain caused by disbudding. The disbudding procedure was performed mainly by farm personnel (94.9%), who were trained by a veterinarian or veterinary technician (46.9%) or by other farm personnel (37.8%) or were not trained (15.3%). Two-thirds of farmers observed behavioral changes in calves after disbudding. Most farmers estimated the pain caused by disbudding to be mild or moderate (20.4 or 45.9%, respectively) and 15.3% of farmers estimated it to be severe. Almost a quarter of interviewed farmers were unable to assess the duration of pain, 39.8% farmers estimated that the pain lasts only several minutes, and 20.4% estimated that the pain lasts up to 6 h. We detected a tendency that farmers of larger herds estimated pain duration to be shorter (odds ratio = 1.2). To improve calves' welfare, training is needed in disbudding practice, focusing on the advantage of pain mitigation.

The effect of different physical forms of starter feed on rumen fermentation indicators and weight gain in calves after weaning

The aim of the study was to determine the effect of different physical forms of starter feed on rumen fermentation indicators of calves after weaning and their weight gain. The experiment was performed with Czech Fleckvieh calves after weaning. The calves were fed ad libitum completely pelleted starter feed or texturized starter feed with chopped straw. The rumen fluid samples were collected after a month of feeding the starter feeds. The calves were weighed monthly. The pH, total acidity, total volatile fatty acids, acetate, propionate, butyrate, lactic acid, ammonia and the number of rumen ciliate protozoa were determined in the rumen fluid samples. The calves receiving the starter feed with straw showed significantly higher rumen pH (6.24 ± 0.51 vs. 5.58 ± 0.30), total volatile fatty acids (98.02 ± 20.46 vs. 61.40 ± 26.51 mmol/l), molar proportion of acetate (61.20 ± 4.87 vs. 50.53 ± 4.66%), and the acetate:propionate ratio (2.38 ± 0.53 vs. 1.34 ± 0.18) and lower molar proportion of propionate (26.55 ± 4.48 vs. 37.92 ± 3.58%) compared with the calves receiving pelleted starter feed. Average daily gain of the calves did not differ significantly. The feeding of starter feed with chopped straw compared with the pelleted starter feed led to better development of the rumen fermentation evaluated by rumen pH, by total volatile fatty acids production, and by the proportion and ratio of acetic and propionic acids. The feeding of starter feed with chopped straw reduced the occurrence of subacute ruminal acidosis in the weaned calves.

A nonsense mutation in PLD4 is associated with a zinc deficiency-like syndrome in Fleckvieh cattle.

BackgroundBovine hereditary zinc deficiency (BHZD) is an autosomal recessive disorder of cattle, first described in Holstein-Friesian animals. Affected calves suffer from severe skin lesions and show a poor general health status. Recently, eight calves with the phenotypic appearance of BHZD have been reported in the Fleckvieh cattle population.ResultsIn spite of the similar disease phenotypes, SLC39A4, the gene responsible for BHZD in Holstein-Friesian was excluded as underlying gene for the disorder in the affected Fleckvieh calves. In order to identify the disease-associated region, genotypes of eight affected calves obtained with the Illumina BovineHD BeadChip comprising 777,962 SNPs were contrasted with the genotypes of 1,339 unaffected animals. A strong association signal was observed on chromosome 21 (P = 5.87 × 10-89). Autozygosity mapping in the eight affected animals revealed a common segment of extended homozygosity encompassing 1,023 kb (BTA 21: 70,550,045 - 71,573,501). This region contains 17 genes/transcripts, among them two genes encoding gastro-intestinal zinc transporters (CRIP1, CRIP2). However, no mutation that was compatible with recessive inheritance could be detected in these candidate genes. One of the affected calves was re-sequenced together with 42 unaffected Fleckvieh animals. Analysis of the sequencing data revealed a nonsense mutation (p.W215X) in a phospholipase encoding gene (PLD4) as candidate causal polymorphism. To confirm the causality, genotypes of the p.W215X-mutation were obtained from 3,650 animals representing three different breeds. None of the unaffected animals was homozygous for the defect allele, while all eight affected calves were homozygous. The deleterious effect of the mutation is manifested in a significantly lower survival rate of descendants from risk matings when compared with the survival rate of descendants from non-risk matings. The deleterious allele has an estimated frequency of 1.1% in the Fleckvieh population.ConclusionOur results provide strong evidence that a newly identified recessive disorder in the Fleckvieh population is caused by a nonsense mutation in PLD4, most likely resulting in an impaired function of the encoded protein. Although the phenotype of affected calves strongly resembles BHZD, a zinc deficiency resulting from malabsorption is unlikely to be responsible for the diseased Fleckvieh calves.Electronic supplementary materialThe online version of this article (doi:10.1186/1471-2164-15-623) contains supplementary material, which is available to authorized users.

Weaning performance of beef Hungarian Fleckvieh calves: 3. Genotype × environment interaction

Abstract. The interaction of sire and population in Hungarian Fleckvieh beef cattle breed were examined in this study on data from the Hungarian Fleckvieh Breeders Association. Data of 2 345 progeny (1 260 male and 1 085 female), born between 1992 and 2003, of 35 sires from two populations were evaluated. Preweaning daily gain (PDG) and 205-day weight (205-dw) were analysed. Population, age of cows, year of birth, season of birth and sex of calves as fixed, sire and sire × population were treated as a random effect. Among the same performance data in the two populations (A, B) genetic correlation (rg), while by the gradiation of sires rank correlation (rrank), were evaluated. Data were analysed with HARVEY’S (1990) Least Square Maximum Likelihood Computer Program and SPSS 9.0 for Windows. Results were as follows: rg=PDGA−PDGB: 0.31(P<0.01); 205-dwA−205-dwB: 0.22(P<0.01) and rrank=PDG: −0.04(P>0.05); 205-dw: 0.078(P>0.05). According to the result of examination important and significant (P<0.001) sire × population interaction were found in case of the two traits in Hungarian Fleckvieh breed.

Weaning results of beef Hungarian Fleckvieh calves 1. Environmental factors

Abstract. Weaning performance of 7 032 purebred Hungarian Fleckvieh calves (3 650 male and 3 382 female) born between 1981 and 2003 from 1 452 cows mated with 113 sires were analysed in two farms. The aim of the study was to evaluate the effect of environmental factors on weaning traits. Farm, age of cows, year of birth, season of birth and sex of calves as fixed, while sire as a random effect was treated. Data were analysed with HARVEY’s (1990) Least Square Maximum Likelihood Computer Program. The overall mean value and standard error of weaning weight, preweaning daily gain and 205-day weight were 214 ± 3.01 kg, 980 ± 17.31 g/day and 236 ± 3.40 kg, respectively. The mean age of the analysed calves was 181 ± 33 days. The results of the examination show that weaning weight, preweaning daily gain and 205-day weight increased as far as the 6 year age cows (the maximum were 226 ± 3.13 kg, 1 049 ± 17.89 g/day, 251 ± 3.54 kg). As for the season effect the calves born in summer were smaller (208 ± 3.12 kg, 946 ± 17.84 g/day and 230 ± 3.52 kg) than that of born in the other seasons (P<0.001). The male calves were heavier than females, the difference was 12 kg, 50 g/day, 16 kg, respectively (P<0.001). The best year was 1985, the worst 2000.

Weaning results of beef Hungarian Fleckvieh calves 2. Genetic parameters, breeding values

Abstract. Weaning weight, preweaning daily gain and 205-day weight of Hungarian Fleckvieh calves (n=8 929, bulls =4 539, heifers =4 390) born from 232 sires between 1980 and 2003 were examined. Variance, covariance components and heritability values and correlation coefficients were estimated. The effect of the maternal permanent environment on genetic parameters and breeding values were examined. Two animal models were used for breeding value estimation. The direct heritability (hd2) of weaning weight, preweaning daily gain and 205-day weight was between 0.37 and 0.42. The maternal heritability (hm2) of these traits was 0.06 and 0.07. The direct-maternal correlations (rdm) were medium and negative −0.52 and −0.74. Contribution of the maternal heritability and maternal permanent environment to phenotype is smaller than that of direct heritabilities (hm2+c2< hd2). The ratio of the variance of maternal permanent environment in the phenotypic variance (c2) changed from 3 to 6 %. Estimated breeding values changed whether the permanent environmental effect of dam wasn’t taken into consideration but the rank of the animals was not modified. The genetic value for weaning results of Hungarian Fleckvieh population has increased since 1997.

Mortality in Austrian dual purpose Fleckvieh calves and heifers

Most countries worldwide already include functional traits in the breeding goals for cattle. Among those are e.g. reproductive traits or longevity while traits regarding calves or heifers are hardly considered. Mortality, but also culling of heifers before first calving may result in higher replacement costs but also in reduced possibility for selection and is thus of importance in cattle breeding. Thus, the aim of this investigation was to explore the genetic background of postnatal mortality and involuntary culling in Austrian Fleckvieh (dual purpose Simmental) calves and replacement heifers. The following periods were defined for analyses: P1 = 48 h to 30 days, P2 = 31 to 180 days, P3 = 181 to 365 days, P4 = 366 days to first calving or a maximum age of 1200 days if no calving was reported, P5 = birth to age at first calving or a maximum age of 1200 days if no calving was reported, P4S = heifers having at least one insemination slaughtered in P4, defined as involuntarily culled. After data editing records of more than 86,000 calves and heifers were investigated. Mortality rates were 1.85, 1.39, 0.36, 0.70, and 5.61% for the defined periods P1–P5, respectively; 7.78% of heifers were involuntarily culled (P4S). For the estimation of genetic parameters a linear and threshold sire model and a linear animal model with the random effects herd ⁎ year and sire as well as the fixed effects year ⁎ month, number of dam's parity, and calving ease were applied. In total, the pedigree consisted of 11,609 animals (sire model, sire–dam relationship) and 237,113 animals (animal model). For mortality traits, heritabilities ranged from < 0.0001 (P3) to 0.018 (P5) for the linear models, and 0.001 (P3) to 0.072 (P1) for the threshold model, respectively. Heritabilities for involuntary culling (P4S) were 0.024, 0.021 and 0.067 for the linear animal, linear sire and threshold sire model, respectively. The rank correlations were > 0.99 between random effects of sires obtained with linear sire and threshold sire models and were lower ( r = 0.77 to 0.90) for animal and sire models, respectively. Total calf and heifer mortality is higher than stillbirth. Consequently, its economic impact on cattle breeding should not be neglected. Based on the results obtained in this study selection against higher postnatal mortality and involuntary culling of heifers should be possible. Furthermore, monitoring of the population and of extreme bulls might be very useful for breeding organisations to avoid deterioration in these traits.

Inheritance of congenital umbilical hernia in German Fleckvieh

SummaryThe frequency of congenital umbilical hernia and its distribution by sires was investigated in German Fleckvieh calves being sold at livestock markets in Miesbach and Traunstein. Data included 53 105 calves from 77 livestock auctions in the years 1996 and 1997. The overall incidence for congenital umbilical hernia was 1.8%. Significant influences were the sex of the calf, the occurrence of multiple births, age of the calf at examination, the market place/market date, the herdmate incidence of congenital umbilical hernia, the sire and the sire line. The inheritance of congenital umbilical hernia could not be explained either by an autosomal recessive or by an autosomal dominant single gene. Testing for oligogenic models revealed that at least three gene loci may be involved. It also seemed likely that dominant alleles can play a role in the mode of inheritance. Congenital umbilical hernias have genetic implications, and thus they should be regarded in the selection of young sires.

Risk Factors for Congenital Umbilical Hernia in German Fleckvieh

Risk factors for congenital umbilical hernias were investigated in German Fleckvieh calves up for sale at livestock markets. Data from 53 105 calves were collected from 77 livestock auctions in 1996 and 1997. The overall incidence of congenital umbilical hernia was 1.8%. A significant influence on incidence was exerted by the sex of the calf, the occurrence of multiple births, the market place/market date, the sire and the sire line. The proportion of Red Holstein blood in the calf, the dam's lactation number, gestation length, 305 day milk performance and the herd milk level were not significant factors. Herdmate averages for calves differed significantly in their incidence. Heritability estimates on the liability scale for congenital umbilical hernia were about 0.4 and progeny groups of sires at risk for congenital umbilical hernia were in the range 0.1% to 14.2%. The segregation pattern could not be explained either by an autosomal recessive or by an autosomal dominant monogenic model. It seems likely that more than one gene locus is involved in the underlying genetic mechanism. Breeders should be aware of the genetic implications of congenital umbilical hernias.