Bovis ISSN 2398-2993

Teat scoring and hyperkeratosis

Synonym(s): Teat-End Hyperkeratosis, Teat Rings, Teat Erosions, Teat- End Callosity, Teat Flowers, Teat Cornification, Teat-End Roughness

Contributor(s): Daniel Veselinov , Alexander Corbishley

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Introduction

  • Hyperkeratosis means "excessive keratin growth".
  • It is a dynamic, chronic change in the teat end condition, thought to be due to a combination of milking machine faults, milking management issues and environmental factors.
  • Hyperkeratosis could also be a normal physiological response to teat skin abrasions, from various factors such as the milking machine liners, the hand-milker or the calf.
  • Treatment should address the underlying causes.

Pathogenesis

Etiology

  • Various factors can lead to the development of teat-end hyperkeratosis.

Milking machine factors

  • Teat end roughness and callosity are very common in machine-milked animals.
  • Increased pressure applied to teat-ends by the teat cup liners and by the compressed air, during the D-phase of pulsation has been singled out as the most significant contributor to the development of hyperkeratosis.
  • High-tension liners can also cause “wedging” of the teats (teats that look flat or "wedge-shaped" after milking) and thus contribute to the development of hyperkeratosis.
  • An increase in the total milking time per day, with low milk flow rates (less than 1.0 kg/min) can also increase the incidence of hyperkeratosis. 
  • Further information may be found in Teat disorders: classification.

Environmental factors

  • Environmental pathogen load is a significant factor associated with the development of teat end hyperkeratosis and consequently subclinical mastitis.
  • Teats with a highly callused teat ends have an increased microbial load in the teat canal compared with contralateral teats (ie teats that are characterised by lower scores of callosity).
  • Once triggered the process of hyperkeratosis may be exacerbated by chemical irritation to the teat skin (various disinfectants) or improved by the use of skin emollients. Teat-end shape, production level and stage of lactation along with various seasonal and weather conditions may all contribute to the development of teat end roughness (hyperkeratosis), but prolonged expose is necessary.

Host factors

  • There is considerable variation in the levels of hyperkeratosis between herds employing similar milking systems and with comparable levels of yield. This variation suggests a genetic influence.
  • In the absence of scientific literature, there is the pressing need for a further and closer examination of this genetic effect on hyperkeratosis.

Pathogen factors

  • The process of hyperplasia or epithelial erosion is influenced by specific pathogens involved, their virulence and ability to colonize the epidermal and subepidermal skin layers of the teat end. For example the hallmark of Staphylococcus aureus Staphylococcus spp biology is its ability to survive and shelter within bovine epithelial cells, endothelial cells, and even macrophages.  
  • Further details can be found by following this link: Teat: conditions caused by infectious agents.
  • Various trade organisations have produced documents linking different risk factors with speculated reasons for the development of hyperkeratosis. Risk factors are listed in this table: Teat-end hyperkeratosis: risk factors.

Predisposing factors

  • Hyperkeratosis increases progressively with parity.
  • Cows at their 4th and 5th lactation are more frequently diagnosed with hyperkeratosis compared to second and third lactation cows and usually have higher SCCs too.
  • Thickness is increasing from calving to peak lactation and then gradually decreases towards the beginning of the dry period.
  • Thickness once present is not influenced by changes in the milking management.
  • Roughness was thought to be more variable and occurring at any age or lactation number but with higher probability during early to mid-lactation (peak lactation). Recent studies, however, suggest that there is an increase in roughness with age and with parity.

Pathophysiology

  • When exposed to cold, wet and windy conditions, the skin of machine-milked teats often becomes scaly, irritated or chapped (cracked epidermal layer) and the protective film of fatty acids may be removed.
  • Once the protective surface coating is removed, pathogens such as Staphylococcus aureus can colonize the epidermal and subepidermal layers of the teat end tissue.
  • Dry air or mud can further induce hardening or thickening of the teat skin. Drying mud draws moisture from the skin with a consequent loss of elasticity of the teat skin.
  • Chemical irritation due to inappropriate disinfectant, higher concentration, or inappropriate type or concentration of emollients, can exacerbate the effects of harsh weather.
  • The continuous destruction and regeneration of cells from Stratum corneum and Stratum granulosum lead to local hyperplasia and thickening of the tissue and formation of rings.
  • Callous rings and thickness negatively influence the closure of the teat canal, leads to increased microbial load in the teat canal and subsequent colonization of the udder and mastitis .
  • Wide temperature variations between days, low-temperature days with dry air in certain parts of the US (eg Iowa) can be a significant influence on the development of hyperkeratosis.
  • In milder climates (UK or Southern Australia) dry mud and the wind can contribute to winter teat chapping, dryness and roughness.
  • Teat skin changes associated with weather conditions rarely account for herd problems in the UK
  • Smooth “doughnut” shaped rings with thickening usually do not affect milking. However, the smooth hyperkeratotic teat ends would slowly progress into severely hyperkeratotic rings with radial cracks. Severe cracking and ringing makes teat disinfection ahead of milking, especially difficult and is an open door for environmental pathogens .
  • Once the ability to properly sanitize the teat ends is compromised, there is an increased probability of environmental mastitis development.

Timecourse

  • Teat end hyperkeratosis is a medium to long-term change in teat condition and occurs over a period of 2-8 weeks.

Epidemiology

  • Reports of teat-end hyperkeratosis problems are far more prevalent in high-producing herds.
  • There is an increase of reports during the colder periods of the year.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Besier J, Lind O & Bruckmaier R M (2016) Dynamics of teat-end vacuum during machine milking: types, causes and impacts on teat condition and udder health – a literature review. J Appl Anim Res 44(1), 263-272.
  • Sandrucci A, Bava L, Zucali M & Tamburini A (2014) Management factors and cow traits influencing milk somatic cell counts and teat hyperkeratosis during different seasons. Revista Brasileira de Zootecnia 43, 505-511.
  • Paduch J H, Mohr E & Kromker V (2012) The association between teat end hyperkeratosis and teat canal microbial load in lactating dairy cattle. Vet Microbiol 158, 353-359 PubMed.
  • Rasmussen M D (2003) Short-term effect of the transition from conventional to automated milking on teat skin condition. J Dairy Sci 86, 1646-1652.
  • Hillerton J E, Pankey J W & Pankey P (2002) The effect of over milking on teat condition. J Dairy Res 69, 81-84 PubMed.
  • Neijenhuis F, Klungel G H & Hogeveen H (2001) Recovery of cow teats after milking as determined by ultrasonographic scanning. J Dairy Sci 84, 2599-2606 PubMed.
  • Hebert A, Sayasith K, Senechal S, Dubreuil P, Lagace J (2000) Demonstration of intracellular Staphylococcus aureus in bovine mastitis alveolar cells and macrophages isolated from naturally infected cow milk. FEMS Microbiol Lett 193, 57-62 PubMed.
  • Hillerton J E, Ohnstad I, Baines J R & Leach K A (2000) Changes in cow teat tissue created by milking machine action. J Dairy Res 67, 309-317.
  • Neijenhuis F, Barkema H W, Hogeveen H & Noordhuizen J P T M (2000) Classification and longitudinal examination of callused teat ends in dairy cows. J Dairy Sci 83, 2795-2804 PubMed.
  • Neijenhuis F, Barkema H W, Hogeveen H & Noordhuizen J P T M (2000) Classification and longitudinal examination of callused teat ends in dairy cows. J Dairy Sci 83, 2795-2804 PubMed.
  • Rasmussen M D, Frimer E S, Kaartinen L & Jensen N E (1998) Milking performance and udder health of cows milked with two different liners. J Dairy Res 65, 353-363 PubMed.
  • Shearn M F, Hillerton J E (1996) Hyperkeratosis of the teat duct orifice in the dairy cow. J Dairy Res 63, 525-532 PubMed.
  • Rasmussen M D (1993) Influence of switch level of automatic cluster removers on milking performance and udder health. J Dairy Res 60, 287-297 PubMed.
  • Fox L K (1992) Colonisation by Staphylococcus aureus on chapped teat skin. J Dairy Sci 75, 66-71.
  • Agger J F & Willeberg P (1986) Epidemiology of teat lesions in a dairy herd. Associations with sub-clinical mastitis. Nord Vet Med 38, 220-232.
  • Sieber R L & Farnsworth R D (1981) Prevalence of chronic teat-end lesions and their relationship to intramammary infection in 22 herds of dairy cattle. JAVMA 178, 1263-1267 PubMed.

Other sources of information

  • Bade R D, Reinemann D J, Thomson P D (2008) Method for assessing teat and udder hygiene. Written for presentation at the 2008 ASABE Annual International Meeting Sponsored by ASABE Rhode Island Convention Centre, Providence, Rhode Island, USA. June 29 – July 2, 2008.
  • Britten A, Hansen N & Pradraza J (2004) Effect of teat dips on hyperkeratosis. Proceedings of the 43rd NMC Annual Meeting, Charlotte, NC, USA. pp 286-287.
  • Timms L (2004) Winter conditions and teat health. Proceedings of the 43rd NMC Annual Meeting, Charlotte, North Carolina, USA. pp 143-158.
  • Mein G E, Williams D M D, Reinemann D J (2003) Effects of milking on the teat-end hyperkeratosis: 1 Mechanical forces applied by the teat cup liner and responses of the teat. Paper Presented at the 42nd annual meeting of the National Mastitis Council, Fort Worth Texas, USA, January 26-29, 2003.
  • Hemling T C (2002) Teat Condition – prevention and cure through teat dips. Proceedings of the British Mastitis Conference, Institute for Animal Health/Milk Development Council, Brockworth, pp 1-14.
  • Rasmussen M D & Hemling T C (2002) The influence of automatic teat spraying on teat condition. Proceedings of the 41st NMC Annual Meeting, Orlando, Florida, USA. pp 166-167.
  • Mein G A, Neijenhuis F, Morgan W F, Reinemann D J, Hillerton J E, Baines J R, Ohnstad I,  Rasmussen M D, Timms L, Britt J S, Farnsworth R, Cook N & Hemling T (2001) Evaluation of bovine teat condition in commercial dairy herds: 1. Non-infectious factors. Proceedings of the Second International Symposium on Mastitis and Milk Quality. NMC/AABP, Vancouver, BC, Canada pp 347-351.
  • Hillerton J E, Middleton N & Shearn M F H (2001) Evaluation of bovine teat condition in commercial dairy herds: 5 A portfolio of teat conditions. Proceedings of the second International Symposium on Mastitis and Milk Quality, NMC/AABP, Vancouver, Canada. pp 472-473 CD available from www.nmconline.org.
  • Neijenhuis F, Mein G A, Britt J S, Reinemann D J, Hillerton J E, Farnsworth R, Baines J R,  Hemling T, Ohnstad I, Cook N, Morgan W F & Timms L (2001) Evaluation of bovine teat condition in commercial dairy herds: 4. The relationship between teat-end callosity or hyperkeratosis and mastitis. Proceedings of the second International Symposium on Mastitis and Milk Quality. NMC/AABP, Vancouver, BC, Canada. September 2001.
  • Reinemann D J, Rasmussen M D, LeMire S, Neijenhuis F, Mein G A, Hillerton J E, Morgan W F, Timms L, Cook N, Farnsworth R, Baines J R, & Hemling T (2001) Evaluation of bovine teat condition in commercial dairy herds: 3. Getting the numbers right. Proceedings of the second International Symposium on Mastitis and Milk Quality. NMC/AABP, Vancouver, BC, Canada. pp 357-361.
  • Brightling P, Mein G A, Hope A F, Malmo J & Ryan D P (2000) Countdown Downunder: Tech notes for Mastitis Control. Published by Dairy Research and Development Corporation, Australia, ISBN 0642704813 (www.countdown.org.au).
  • LeMire S D, Reinemann D J, Mein G A, Rasmussen M D (1999) Recommendations for Field Tests of Milking Machine Performance. ASAE Paper No. 993020 Written for Presentation at the 1999 ASAE/CSAE International Meeting, Toronto, Ontario, Canada, July 18-21,1999.
  • LeMire S D, Reinemann D J, Mein G A, Rasmussen M D (1999) Recommendations for Field Tests of Milking Machine Performance. ASAE Paper No. 993020 Written for Presentation at the 1999 ASAE/CSAE International Meeting, Toronto, Ontario, Canada, July 18-21,1999.
  • LeMire S D, Reinemann D J, Mein G A, Rasmussen M D (1998) Statistical Considerations for Milking Time Tests. Paper No. 983128, Written for presentation at the 1998 ASAE Annual International Meeting, Orlando Florida July 12-15,1998.
  • Dodd F H & Neave F K (1970) Mastitis control. Bienn. Rev., National Institute for Research in Dairying, Shinfield, UK, pp 21-60.

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