Observations On Teat Lesions
Ralph J. Farnsworth, DVM, MS
University of Minnesota
St. Paul, Minnesota
Veterinarians and dairy producers have been required to deal with teat
lesions for many years. Teats traumatized by being stepped on, barbed wire
cuts, etc., have always been a problem. Virus lesions from pseudo cow pox
have also been present for many years. The advent of machine milking added
another possible source of teat trauma, due to the mechanical effects of
the milking machine. In about the last twenty-five years, virus lesions
due to herpes viruses have also come into play as a major problem. The
widespread use of teat dipping opened another area -- the possibility of
chemical burns and injuries when products were improperly compounded, mixed
or applied.
Lesions involving the teat barrel do not generally directly cause mastitis,
but do interfere with the milking process and may cause secondary problems.
Lesions which affect the teat end and orifice frequently result in increased
mastitis problems because of interference with the protective effect of
the teat orifice, which is a major barrier preventing bacteria from entering
the gland.
Significance
The type and extent of lesion that is necessary to produce an increased
intrammary infection is an important consideration. For many years, cows'
teats were described as having "pulled-out ends" or prolapsed sphincters.
It was generally considered that these lesions were due to milking machine
trauma, primarily high vacuum, and progressed to ulcers and scab formation.
This phenomenon was researched by Sieber and Farnsworth in the late '70s.
An important aspect of this phenomenon was discovered almost by accident.
Sieber was collecting teats at a local packing plant for histological section
when they began to process beef cows. Out of curiosity, he began to examine
teat ends on beef cows and discovered that beef cows had the same everted,
pulled-out, prolapsed teat ends that were being attributed to the milking
machine in the dairy cows. Subsequently, cows in hand-milked herds with
no chemical use were examined and also shown to have this same type of
lesion. Histopathology of these teat ends showed these rings to be excess
keratin (one medical school pathologist referred to them as callouses).
This finding raises a fundamental question. A callous may not be normal,
but does it increase bacterial infection rates in quarters where it is
present? It can be theorized that this may have some effect on teat closure,
or that some form of callouses (particularly on pointed teats) are quite
rough and may have spiculite projections that make it hard to clean the
teat orifices at milking time resulting in greater bacterial contamination.
A system of classification of different types of teat end lesions was developed.
A study5 was conducted to examine the correlation of various types of teat
lesions with the prevalence of intramammary infections, as well as the
milking machine and milking practice factors, in about 5,000 cows. Findings
of this study showed no statistical difference in the prevalence of infection
among normal teats the various hyperkeratatic lesions, regardless of type
(rough or smooth) or degree. Teats with erosions or scabs on the teat end
did show a significantly higher prevalence of infection. It was also observed
that the callous-type lesions did not progress from mild to severe to erosions
or scabs as a natural process. Heifers seem to develop a degree of callous
within the first 6-8 weeks of lactation, which then persisted at that level,
regressed to some degree during the dry period, and returned to about the
same level the next lactation.2
A more recent study at the University of Wisconsin2 also failed to show
a correlation between hyperkeratosis and infection.
The correlation of lesions with other factors was also examined. Milking
machine factors such as vacuum level and pulsation ratio, that were varying
but within what are considered the normal ranges, did not appear to affect
the degree of lesions. Milking practices that resulted in extended milking
time -- such as no preparation, no pre-milking stimulation or over-milking
-- did increase the degree of lesions. One of the most significant correlations
was with milk production, which also tends to extend milking time. Later
work conducted by Graeme Mein at Wisconsin showed an increase in what he
termed hyper-keratosis related to the compressive load of the milking machine
liner.
There has been for many years a general assumption that any changes in
teat end condition result in an increase in infection. However, there does
not appear to be any significant data that callouses or hyper-keratosis
of teat ends alone (without erosions or additional lesions) results in
increased intramammary infection.
Milking Equipment
Milking equipment malfunction has traditionally been considered a cause
of teat lesions. There is some evidence that hyper-keratosis and transient
edema may result from this source, however severe lesions such as abrasions
and scabbing of the teat orifice do not appear to be easily produced by
milking machines unless the malfunctions are extremely severe, such as
extremely high vacuum or nearly total pulsation malfunction.
Teat Dipping
The widespread adaptation of the practice of post-milking teat dipping
has also resulted in a significant additional source of teat irritation.
A variety of problems can exist. The incorrect use of concentrated products
such as udder washes or cleaners for teat dip can result in severe lesions
within one or two applications. Improper mixing, freezing or simply production
accidents with these products can also produce a variety of lesions. More
frequently, however, problems with teat dips are associated with drying
of the teat skin rather than ulcers and erosions. When a teat dip is a
source of a problem, changing dips will result in rapid resolution of the
situation. However, many situations involving lesions, particularly in
viral infections, tend to resolve themselves with time -- so an improvement
resulting from using a new teat dip may be coincidental. Unless the dip
can be shown to have chemical or pH abnormality or shown to produce lesions
when it is used again at a later time, it is difficult to be sure of a
cause-and-effect relationship.
Climactic Factors
Teat lesions can also be produced by weather factors. Teat ends or entire
teats can be affected by freezing or frostbite. Animals with edema of the
teats and udder are more subject to this effect and need more protection
than normal animals. Teats and teat ends are also more subject to freezing
when wet with such things as teat dip or a drop of milk remaining on the
teat end after milking. Problems occur primarily when animals are exposed
to both wind and cold temperatures right after milking, such as in milking
parlors where cows exit directly outside and must travel to other housing.
The practice of eliminating post-milking teat dipping during cold weather
is often used to avoid cold damage. But if this practice continues for
any length of time, an increase in infections of contagious pathogens such
as Staph aureus can result. Numerous methods are used for managing teat
dipping in cold weather, but dipping the teats and then blotting off the
excess dip about 15 or 20 seconds before the animals are turned outside
appears to be a practical solution to this problem.
Pseudo Cow Pox
Viral infections have also been a source of teat lesions. Pseudo cow pox
virus, recognized for many years, typically produces vesicles that rupture
and form circular lesions which heal in a week or two. Lesions of the teat
barrel are most common, resulting in difficulty in milking due to discomfort
of the cow. They may also affect milk let-down. Lesions may also affect
the teat end, sometimes causing secondary intramammary infections. Herds
that experience an outbreak of this virus usually exhibit a significant
portion of the herd showing lesions over a short period of time and the
problem is rather rapidly eliminated. In some instances the lesions may
not be typical and may affect only teat ends, making diagnosis somewhat
more difficult. An occasional herd also experiences a slow spread of the
virus. There have been instances in large herds where this virus has resulted
in a continuous problems, with a few animals infected at all times over
a long period of time as animals begin to lose immunity after the initial
infection. However most herds which experience an outbreak one year do
not have a problem again the following year.
Diagnosis of pseudo cow pox can be made by examining fresh scab material
from lesions with electronmicroscopy or looking for inclusion bodies. Serology
has also recently become available and may be a more practical method of
making a diagnosis when adequate lesions for examination are not available.
Herpes Virus Lesions
There are two herpes viruses which have been involved in teat lesions.
The herpes mammalitis virus, or herpes II, has been recognized in Minnesota
since the early '60s. The fact that the herpes IV or DN599 virus also produces
similar lesions was recognized in the mid '70s.3 These viruses appear to
have similar epidemiology and produce clinically similar lesions, although
they are serologically distinct. These viruses have the reputation of producing
very severe erosive lesions. Some cases may result in severe ulceration
of most of the skin of the teat. Lesions are very slow to heal, frequently
resulting in secondary intramammary infections. A syndrome is also seen,
primarily in heifers, where the skin of the much of the teat becomes hard
and is sloughed. This is usually associated with edema around the time
of parturition. Normally these heifers cannot be successfully milked, develop
secondary mastitis and end up being eliminated from the herd very quickly.
The range of lesions due to these viruses, however, is quite wide -- from
animals that simply seroconvert with no lesions, to cows that become hard
milkers but show no physical lesions, to animals that show mild lesions
that eventually heal, to animals which show the very severe lesions. Recent
histological studies have discovered the virus inclusion bodies in areas
near the teat canals in cows that have simply become hard milkers with
no evidence of lesions.
In most herds when a problem is first noticed, a substantial number of
animals particularly heifers may be involved. But in subsequent years the
number of animals involved and the severity tends to decrease to the point
where only an occasional animal is involved. However, a few herds experience
an ongoing problem with heifers and may also have cows involved year after
year. Some of these herds may have 5-10% of the animals with lesions most
of the time. There have never been any factors identified which appear
to be responsible for these differences in herd response.
There appears to be a seasonal relationship to the lesions in the herpes
herds. Problems with lesions are primarily seen between November and April
in the Minnesota and Wisconsin area. Some herds have experienced animals
with problems in warm weather. But in most cases the seasonal pattern is
rather distinct. There has been speculation that due to the better skin
condition in the warm months, the virus is less able to infect. There is
also some evidence that herpes has an affinity to body parts with a lower
temperature, such as the teat. It can be noted that in general, fewer teat
lesions from most causes appear to be seen during the warm weather period.
The method of viral transmission has not been established. When one considers
the general biology of herpes virus along with the epidemiology of the
disease in herds, it appears likely that carrier animals exist. The method
of cow-to-cow spread is also not clear. British literature suggests insect
transmission, but the evidence that the problems are seen primarily during
the times of insect absence in the upper Midwest suggests that other methods
may be more important in this area. The fact that a heifer usually shows
a problem one to two weeks after calving suggests spread during the milking
process. However, blood samples taken at breeding time have shown rather
high titers in heifers at that age.4 Whether the recrudescence that occurs
with the human herpes simplex occurs with these viruses also has not been
determined. As previously noted, titers in heifers at breeding time suggests
early exposure. Instances have been observed when heifers showed titers
at an early age that then decreased or disappeared, but the animal later
showed lesions with a high titer present at the time of calving. This could
simply be early exposure from which the animal did not develop lasting
immunity, or it could be a latent herpes infection that was reactivated
with the stress of calving.
Diagnosis of herpes infection was first attempted by virus isolation. However,
these attempts are usually unsuccessful (although isolation from experimental
infections appears to be quite successful). The use of serum neutralization
titers appears to be more successful and practical. There is no solid data
to determine significance of titer levels, but based on herd epidemiology,
herpes II titers of 1:16 or higher and herpes IV titers if 1:20 or higher
are an indication of exposure to the virus. Herpes II titers of greater
than 1:256 are seldom seen. The herpes IV titers often exceed 1:750 and
may reach 1:1250. Classically, viral diseases are diagnosed by demonstrating
an increase in titers from paired serum samples, one taken early in the
course of the disease and the other one to two months later. However, the
most practical way to use serum titers for diagnostic purposes in this
area appears to be to obtain samples from several (four or five) animals
showing lesions of various durations, being sure that some cases are at
least two weeks or more in duration. At this time it does not appear practical
to make specific animal diagnoses with this method, but the fact that the
virus is in the herd can be established.3 The two herpes viruses do not
appear to cross-react to any extent, so serology testing for both should
be done for diagnostic purposes.
The prevention and treatment of these lesions has been an area of major
frustration for veterinarians and producers. It is difficult to determine
the effectiveness of various procedures without the use of controlled studies
because of the variability in numbers and severity of animals infected
from year to year. The use of serum obtained from animals that had shown
lesions was at one time thought to be effective, however, experience over
a period of time suggests that it is not particularly effective in prevention
-- plus it is somewhat impractical because of the timing necessary. The
use of various teat dips has often been suggested for prevention, however
observations suggest that there is no significant difference in the ability
of products to prevent infections, since lesions occur in herds using most
different types of teat dips.
Milking heifers first has also been suggested. This also may be a good
practice for other reasons such as mastitis control, but again in general
does not appear to prevent problems. If recrudescence or reactivation is
occuring in some herds,1 this would explain the lack of efficacy of either
teat dips or milking order.
There is some evidence that reducing pre-parturient edema in heifers may
help reduce the severity of the problem in these animals. The use of diuretics
to control edema has met with some success in reducing the skin sloughing
and necrosis which occurs in some animals. A rather drastic prevention
measure that appears to be meeting with some success is the use of seasonal
calving. Since problems are normally not seen from May to October, calving
heifers during this time reduces the chances considerably. The poor economics
of this approach, however, make it a rather drastic step since heifers
have to be maintained longer and calved, in most instances, at an older
age than desirable. However, if the alternative is losing the heifer to
skin sloughing and mastitis, it may be economically feasible.
Treatment and healing of lesions is another area where many different approaches
have been attempted. Again, it is difficult to evaluate the effectiveness
of products. The use of products which result in drying has been successful
in some instances. The methaline blue dye type horse wound products have
been helpful in some instances. Some producers prefer to bandage teat ends
with protective ointments. The use of film forming-type teat dips has also
been somewhat successful. The use of anti-viral drugs is often considered.
This is usually not attempted because of expense and milk residue issues.
There is also some suggestion that in humans these drugs need to be used
before lesions appear. In humans with various herpes infections, the patient
knows that the disease is coming on and can start the drugs ahead of time,
a practice which appears to be more effective in prevention of lesions.
There have been some instances of use that appear to be beneficial, however,
there is no controlled data in this area.
The use of vaccines for prevention appear to be a reasonable possibility.
There has been some limited experimental success but there has also been
a failure of some simple experimental products in this area. Currently
there is no product available which has shown consistent success in cows.
Development of a successful vaccine will require considerable research
and development.
One of the biggest problems with teat end lesions is the incidence of secondary
mastitis. The continuation of teat dipping can be of some help in preventing
secondary infections as well as preventing exposure to environmental organisms.
This is an area where bandaging or sealer-type teat dips may have some
use.
The presence of herpes virus in a herd can be determined by observing classical
lesions where they occur and by serology where lesion type is not definitive.
Since there is presently no good control or treatment system, the valve
of a definitive diagnosis may be questioned. However, if a producer knows
the problem is of viral origin, he is more likely to accept that he has
to "live with it" and not continue to search futilely for solutions such
as milking equipment changes that result in unecessary expense.
References
1. Drolet, R., R.E. Werdin and S.M. Goyal. 1986. The role of herpes virus
type 4 (DN-599) infection in Minnesota cattle. Am Assn Vet Lab Diag, 29th
Proceedings, 335-346.
2. Nordland, K. Unpublished data.
3. O’Connor, M., C. Tully, and E.P. Power. 1994. Serological investigation
of nineteen outbreaks of herpes mammalitis. Irish Vet J, 47:168.
4. Scott, F.M.J. and A. Holiman. 1984. Serum antibodies to bovine mammalitis
virus in pregnant heifers, Vet Rec 114:19.
5. Sieber, R.L. and R.D. Farnsworth. 1981. Prevalence of chronic teat-end
lesions and their relationship to intramammary infection in 22 herds of
dairy cattle. JAVMA 178:12, 1269.
Published in the 1996 National Mastitis Council Annual Meeting Proceedings,
pg. 93.
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