Mastitis has a cumulative and lasting effect on milk yield and lactose content in dairy cows.

In dairy cattle, the negative correlation between milk lactose content (LC) and SCC has been reported in various breeds and contexts, and several authors have discussed possible causal relationship and mechanisms responsible for the LC decrease associated with mastitis or high SCC. Genetic and phenotypic correlations between LC and SCC, and between LC and clinical mastitis confirmed the antagonistic relationship of these features. The same applies to milk minerals such as Na and K, whose concentration is usually high in milk with elevated SCC and inversely correlated with LC. Moreover, cows with greater LC in milk seem to have better udder health, fertility, and longevity, and are less likely to be early culled than those with lower LC concentrations.

Lactose content decreases with lactation number and age. The progressive drop in milk LC observed along the cow’s productive life might be attributed to a combination of factors, namely physiological aging, mechanical epithelial stress due to repeated milking, and the cumulative effect of the inflammation events. It can be therefore hypothesized that, to a different extent, the alveolar structure undergoes damage over time, which in turn impairs epithelial functionality and integrity due to leaky tight junctions. Considering that lactose is the major milk constituent, any reduction in LC within the alveolar lumen will alter the blood-milk barrier equilibrium, causing a change in the concentration of other osmotic components, such as Na and K. In the study cited, this hypothesis was tested, i.e. that there is a cumulative and lasting effect of clinical and subclinical mastitis on LC, the major milk constituent, as well as milk yield, possibly due to effects on alveolar permeability and mammary gland secretion ability.

For this purpose, milk test-day records with SCC and gross composition traits were used together with validated clinical mastitis data recorded in Austrian Fleckvieh. In addition, heritability of cumulative mastitis and its genetic correlation with LC and milk yield were estimated. Estimates were obtained using univariate and bivariate linear animal models.

A significant reduction in LC and milk yield was observed in cows that suffered from mastitis compared with those that did not experience udder inflammation. The h² of 0.09 of cumulative mastitis was promising. The genetic correlations between cumulative mastitis with LC and milk yield were negative, suggesting that cows with a great genetic merit for milk yield and LC can be expected to be more resistant to repeated inflammations. When the number of lifetime SCC peaks (≥200,000 or 400,000 cells/mL) to calculate cumulative inflammation events was used, h²was even higher (up to 0.38), implying that subclinical mastitis also has a relevant negative impact on both LC and milk yield.

The findings confirm that there is a lasting and cumulative effect (i.e., cows that experienced several mastitis events produce less and have a significantly lower LC in their milk compared with cows that experienced only one or no events). In addition, LC is negatively phenotypically and genetically correlated with the number of mastitis events experienced. In the case of milk yield, the genetic but not the phenotypic correlation was negative. These results make the cumulative number of cumulative mastitis events a promising phenotype. Quarter-level investigations are advisable to better disclose the development of milk osmolality mechanisms in the presence of mastitis or its permanent alteration after that. Pursuing selection toward cows that are more resistant to recursive inflammations is therefore possible and meaningful, especially if phenotypes available early in life are used.