Genetic Association Between Parameters of Innate Immunity and Measures of Mastitis in Periparturient Holstein Cattle

Abstract

Relationships between genetic measures of mastitis (somatic cell score, score for clinical mastitis, and scores for IMI with major or minor pathogens) and immunological parameters (physiological and molecular markers) were examined for periparturient Holstein cows. Physiological markers included 11 in vitro immunological assays. Molecular markers included the second exon of the DRB3 locus of the bovine major histocompatibility complex, the IgG2 isotype genotype, and the CD18 genotype (the locus responsible for bovine leukocyte adhesion deficiency). A gene substitution model was used to estimate the additive genetic effects of alleles of the three molecular markers on estimated breeding value (EBV) for mastitis measures. Pearson correlation coefficients between EBV for immunological assays and EBV for mastitis measures were computed. Molecular markers explained up to 40% of the variation in EBV for measures of mastitis. The presence of allele DRB3.2*16 was associated with higher EBV for SCS. Allele DRB3.2*8 was associated with increased EBV for clinical mastitis, as was the IgG2b allele and the normal CD18 allele. Alleles DRB3.2*11, *23, IgG2a, and the recessive allele for bovine leukocyte adhesion deficiency were associated with decreased clinical mastitis. A positive genetic association was found between allele DRB3.2*24 and EBV for IMI by major pathogens and between DRB3.2*3 and IMI by minor pathogens. Several correlations between EBV for immunological assays and EBV for mastitis measures were significantly different from 0. Cows with low EBV for SCS tended to have neutrophils that had greater functional ability at maximal immunosuppression, low serum IgG1, and high numbers of circulating mononuclear cells. Immunological parameters, including physiological and molecular markers, are useful aids to understand the genetics of resistance to mastitis.

Effect of Holstein–Friesian genetic group on peripartum and early lactation haematological and acute phase proteins profiles, health and fertility

“…Bannerman et al (2008) reported small temporal breed differences (Jersey v. Holstein-Friesian) in the onset, duration and cessation of SAA response. It is difficult to identify whether the presence of an intramammary infection elicits an acute phase response causing the alteration of the immunological parameters, or whether it is the individual cow's immunological capabilities that modify susceptibility to mastitis (Kelm et al, 1997;Bannerman et al, 2004 and. It has been demonstrated that bacteria type (e.g.…”

“…These samples were sent to the laboratory for analysis, which included a semi-quantitative test, the 'California mastitis test' (CMT score: 0 5 negative, 1 5 trace, 2 5 distinct precipitation with no gel, 3 5 mixture thickens immediately, 4 5 gel forms on surface, with CMT score >2 indicating clinical mastitis (CM)) as well as the determination of presence (yes/no), quantity (0, 1-50, 51-100 and .100 cfu/ml) and type of bacteria (i.e. contagious (yes/no: presence/absence of Streptococcus agalactiae, Staphylococcus aureus and Staphylococcus epidermidis, Corynebacterium bovis or Mycoplasma) and/or environmental (yes/no: presence/absence of Escherichia coli, Klebsiella, Serratia, Pseudomonas, Proteus, Enterobacter spp., Streptococcus uberis, Streptococcus dysgalactiae) (Fox andGay, 1993, Smith andHogan, 1993)) in each quarter sample. The existence of CM throughout the study was monitored when cows were fore-stripped prior to morning and evening milking.…”

Severity of E. coli mastitis is mainly determined by cow factors

“…Different characteristics of peripheral PMN, such as stimulated CL activity, cytochrome c reduction, chemotaxis, and stimulated L-selectin and CD11b expression, have also been related to the severity. In addition, other pre-infection metabolic parameters in blood, such as b-hydroxybutyric acid, non-sterified fatty acids, glucose, Mg 2+ , Ca 2+ , cortisol, and cholesterol concentration, as well as in milk, such as SCC, albumin, fat, and casein production, have also been found to be associated with the severity of E. coliinduced mastitis [52,59,93,116,121,126,210,245,259]. Other studies have compared the functionality of PMN between early and later stages of lactation [158][159][160].…”

Genetics of resistance to mastitis in dairy cattle

“…Although specific milking devices have been developed, large-scale recording of conductivity has not yet been implemented and further work on the interpretation and modelling of data is still needed. Finally, recent works [18,19,37,93] show that parameters of the immune response may be promising for studying genetics of mastitis resistance.…”

“…Detilleux et al [19] found moderate heritabilities for migration (0.2 to 0.5) and phagocytosis (0.3-0.7) of neutrophils and for serum complement activity (0.4-0.5), using in vitro assays for 137 cows sampled three times around calving. Using the same data, Kelm et al [37] estimated correlations between breeding values for the different traits and showed that animals with low somatic cell counts, clinical mastitis frequency and intramammary infections tended to exhibit better functionality of neutrophils. These cows were additionally vaccinated with an inert antigen, ovalbumin, and with Escherichia coli [94].…”