Cow welfare and ‘quarter culling’

The letter from Burgt and colleagues (VR, April 30,2011, vol 168 p465) on behalf of the National Mastitis Group comprising of mastitis experts regarding ' quarter culling' for the welfare of cow, though late but pertinent. We also commented on this subject (VR, August 8, 2009, vol 165 p 183) that the suggestion of David Harwood and colleagues (VR, March 28, 2009,vol 164, p 407) is not only 'unethical but dangerous also at an operational dairy farm'. Now, the present authors of the letter have further identified the lurking fears of the unlicensed chemicals used for 'quarter culling' and suggested that such practice should be 'strongly discouraged'. As per the anecdotal evidence of 'quarter culling' by U.K. farmers, they need to be educated regarding the problem of recurrent mastitis in dairy animals. As far as ceasing of milking and drying off the quarter(s) it was also suggested by Blowey and Deyes (VR, April 4, 2009, vol 164, p 437).

We have also encountered cases of chronically affected mastitic cows and buffaloes. While distilling the causes of this problem disparately we have come to the conclusion that the basic cause appears to be the disturbed homeostasis of citrate perpetually in the quarter(s) at a particular vulnerable site. Most of these cases of recurrent mastitis occur during first quarter of lactation when there is ample supply of milk (a marker of mastitis). Citrate has been dubbed as the 'harbinger of lactogenesis' (Peaker and Linzell 1975) and its concentration is directly proportionate to the volume of milk secreted and its calcium content throughout lactation. The other cardinal function of citrate in udder is to sequester Ca2+ and maintain the equilibrium of Ca2+ and H+ and pH (~6.50) of milk and thus plays the crucial role of most vital buffer system in the udder (Shennan and Peaker 2000). Citrate plays an abiding role in cellular energy metabolism, being an intermediate in the tricarboxylic acid cycle but mammary epithelium is impermeable to citrate in both directions, hence, milk citrate levels reflects the mammary activity only rather than the general metabolism. Therefore, any aberration in the synthesis of citrate in udder i.e., lowered levels of citrate, all the mechanisms involved in the production of milk go haywire.

It is well known that pH of mastitic milk of bovines is higher (7.20 and above) than normal pH (~6.50) whereas in contrast the concentration of citrate in mastitic milk is lower (30-60mg/100ml) than normal milk (120-180 mg/100ml). Thus, when citrate level fall its moderator effect of Ca2+ sequestration is subdued in the system. The free Ca2+ cause injury to the secretory epithelial tissue leading to inflammation with the result intercellular impermeable tight junctions and blood-milk barriers become compromised and leaky (Neville 1995b). Due to leakage there is free exchange of blood and milk constituents e.g., sodium, potassium, chloride, bicarbonate, citrate and proteins bringing the milk pH equivalent to that of blood (7.40 and above). Henceforth, the presence of lesion(s) inflicted by Ca2+ and alkaline pH in the udder provides the most conducive environments for the growth and multiplication of the environmental pathogens present on skin and in udder which manifest as infectious mastitis. These are almost the same organisms which are commonly isolated from mastitic milk. Simultaneously, the phagocytes mainly polymorphonuclear leucocytes (PML) due to diapdesis reach the injured site and set-up explosive inflammatory reaction and immunological response of varying degrees. There is enormous increase in the number of somatic cell count (SCC) a 'marker' for mastitis and quality control of milk. The neutrophils produce free radicals in defense and immunological components like haptoglobin, serum amyloid A with further aggravation of tissue damage, inflammatory signs, fall in milk yield, lactose etc., (Pyorala and others 2011).

We proposed to quench this burst by replenishing the deficiency of citrate with oral administration of tri-Sodium citrate @ 30gm dissolved in water once daily till recovery (which was usually 4-6 days). We also treated recurrent cases of mastitis with I/V injections of tri-Sodium citrate dissolved in sterilized normal saline as 5 % solution, 50ml morning and evening followed by oral dose(s), if needed. These cases were reported to be resistant to the routine antibiotic therapy. The I/V therapy with tri-Sodium citrate appears to be more effective possibly due to the leaky tight junctions so that the drug directly reached the site of injury/infection and restored the normal milieu in the udder.

On the basis of our observations in the field for the treatment of clinical cases of mastitis we recommend this line of treatment to avoid culling of the affected quarters. In fact some pharmaceuticals have come-up with certain formulations with tri-Sodium citrate as its major content for the prevention and treatment of different degrees of mastitis in bovines. The treatment is remarkably effective in controlling different types of mastitis, safe, economical, no discarding of milk, no withdrawal period and moreover no culling of the teat or the animal and replacements. We further propose that pH of milk of the suspected quarter(s) be monitored which can be done on the spot with graded pH papers or pen-pH meter and if required treatment can be initiated immediately with instant results. This procedure can be adopted as a routine on herd basis for control of mastitis on a dairy farm successfully. 

NEVILLE, M.C. Lactogenesis in women: A cascade of events revealed by milk composition. In The composition of milks, ed. Jensen , R.D. 1995b p87-89. San Diego: Academic Press

PEAKER, M & LINZELL J.L (1975) Citrate in milk: a harbinger of lactogenesis. Nature 253, 464

PYORALA, S, HOVINEN, M, SIMOJOKI, H, FITZPATRIC, J, ECKERSALL, P.D, & ORRO, T. (2011) Acute phase proteins in milk in naturally acquired bovine mastitis caused by different pathogens. Veterinary Record 168, 535

SHENNAN, D.B & PEAKER , M (2000) Transport of milk constituents by the mammary gland. Physiological Reviews 80, 925-951