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Teat scoring and hyperkeratosis

ISSN 2398-2993

Alexander Corbishley

Introduction
Pathogenesis
Diagnosis
Treatment
Prevention
Outcomes
Further Reading

Synonym(s): Teat-end Hyperkeratosis, Teat Scoring, Mastitis Development, Udder Health, Milking Management, Statistical Sampling, Herd Sampling

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.

Presenting signs

Hyperkeratosis is clinically manifested by the development of raised, smooth or rough rings at the teat ends of lactating cows .
One or more teats can be affected in an individual animal.

Geographic incidence

Worldwide.

Age predisposition

Incidence increases with parity.

Breed/Species predisposition

Although scientific proofs are scarce, it is the author’s opinion that high yielding cows (Holstein Holstein and Holstein -Friesian, Swiss-Brown, Flechvieh, Kostroma and Guernsey Guernsey Dairy Cows) are potentially more prone to develop hyperkeratosis.
This predisposition is likely due to the substantially longer milking times, frequent milking, the higher incidence rates of negative energy balance and lowered immunity after parturition (or until peak lactation) associated with these breeds.

Public health considerations

Hyperkeratosis is not a direct threat to public health but can indirectly contribute to increased rates of subclinical and clinical mastitis and thus affect milk production and the quality of milk.
In the absence of teat disinfection after milking, hyperkeratosis scores two, three and four is associated with increased levels of SCCs and subclinical mastitis and would therefore directly reduce the quality of milk intended for human consumption.
Since it can lead to improper teat sanitation, it can also affect the levels of potentially zoonotic pathogens in the milk (E. Coli Escherichia coli, S. aureus Staphylococcus spp, Actinomyces pyogenes or Streptococcus dysgalactiae Streptococcus spp).

Cost considerations

To the author’s knowledge, no comprehensive studies on the economic impact of hyperkeratosis exist, but the reduction in the rates of hyperkeratosis can also mean reduction in mastitis and consequently reduced treatment and management costs, less labor and less milk dumped.
The costs of treating mastitis include the cost of extra labor, the actual cost of therapy (drugs and vet bills), the cost of lost milk, and cost of disinfectants, losses associated with lower parlor throughput (valuable management time) and the cost of culling or replacing affected cows.

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.

Teat scoring and hyperkeratosis