Influence of Pulsationless Milking on Teat Canal Keratin and Mastitis

Abstract

Twenty-four Holstein cows, producing at least 21 kg of milk/d, were used in two replicate experiments to determine the effect of presence or absence of pulsation on loss of teat canal keratin during machine milking. Left quarters were milked without pulsation and right quarters were milked with pulsation. On d 0 and 10, keratin was collected from one left and from one right teat canal of each cow prior to milking and from the remaining two teat canals after milking. Milk was collected for assessment of SCC and bacteriological status on d 0 and approximately every 3 d until d 18. Quantity of keratin recovered before milking on d 10 did not differ between teats milked with or without pulsation, but loss of keratin because of milking was greater from teats milked with pulsation. By d 7, 30% (12 of 43) of quarters milked without pulsation had become infected, but no (0 of 47) quarters milked with pulsation were infected. By d 14 to 16, new infections had increased to 68% (28 of 41) of quarters milked without pulsation and 2% (1 of 43) in quarters milked with pulsation; mean SCC in pulsationless quarters increased sevenfold relative to pulsation quarters. Protein and water content of keratin did not differ because of treatment, and changes in lipid composition were minor. Histological analysis of the teats of 4 cows indicated that the mean diameter of the teat canal, within 2 h after milking, was greater without pulsation than with pulsation (680 vs. 483 microns).

Innate immune response of bovine mammary gland to pathogenic bacteria responsible for mastitis

“…29 The teat canal is lined with keratin, which provides an additional physical barrier, preventing bacterial migration towards the MG cistern. 28,30 Esterified and non-esterified fatty acids (myristic, palmitoleic, and linoleic) function as bacteriostatics and are associated with keratin. Moreover, certain cationic proteins associated with keratin can bind to pathogenic mastitis microorganisms, increasing their susceptibility to osmolarity changes.…”

Dispositivo fotobiomodulador para prevenção e tratamento de hiperqueratose de teto em vacas leiteiras

“…A ação mecânica exercida durante a ordenha é o principal fator desencadeador desta alteração (Capuco et al 1998). Uma pequena quantidade de hiperqueratose não parece aumentar o risco de uma infecção intra-mamária na vaca em lactação, podendo ser considerada como um benefício fisiológico na resposta do teto à ordenha.…”

Dynamics of teat-end vacuum during machine milking: types, causes and impacts on teat condition and udder health – a literature review

“…If the massage effect of the liner is insufficient, the fluid stays in the teat tissue, and changes of the pliability of the teat tissue cause a decrease in the resistance of the teat canal to bacterial invasion (O'Shea 1987;Neijenhuis 2004). Furthermore, there is a decrease of muscle contractions at the teat end, which facilitates penetration of bacteria and microorganisms into the teat canal (Bramley & Schultze 1991;Capuco et al 1994). So, the main purpose of the adequate vacuum level is to guarantee the massage effect applied by the liner on the teat tissue in order to release the teat from congestion, blood and lymph which accumulated during the liner open (b-) phase of pulsation.…”

“…If the load applied on the teat end during milking is very high (average claw vacuum >42 kPa at very short intervals between milkings), the teat orifice is increasingly surrounded by a ring of keratin and consequently hyperkeratosis develops to a pathological degree (Mein et al 1987Neijenhuis 2004). Higher scores of hyperkeratosis and increasing cell counts within a dairy herd are either an indicator of bad herd management or the malfunction of one or all elements of the milking system and irregularities during milking process (Capuco et al 1994;Shearn & Hillerton 1996).…”

“…This is built by blood-derived immunological factors such as leucocytes, immunoglobulins and other soluble factors in the milk. The main mechanisms for physical defence are binding of bacteria to keratin, desquamation of bacteriacoated keratin by the shearing forces associated with milk flow through the teat canal (Williams & Mein 1986) and desiccation of the canal lumen by evaporation from the external teat orifice (Capuco et al 1992(Capuco et al , 1994Myllys et al 1994;Neijenhuis 2004). Through an excessive removal of keratin from the teat canal, the teat loses its ability of inhibiting pathogens to enter.…”