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EFFECT OF LAMENESS ON OVARIAN ACTIVITY IN POST-PARTUM HOLSTEIN
EDUARDO JOSE GARBARINO
A THESIS PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
MASTER OF SCIENCE
UNIVERSITY OF FLORIDA
Eduardo J Garbarino
In memory of my father, Eduardo Jose Garbarino
I would like to express my sincere gratitude to Dr Jorge Hernandez, Associate
Professor of Veterinary Medicine, for his advice and guidance during my 3 years of hard
work. I also thank him for his help, support, and friendship, which allowed me to
successfully complete my masters program.
I thank Dr. Carlos Risco Professor of Veterinary Medicine for his contributions to
the proj ect. I thank Dr. Jan P. Shearer, Dairy Extension Veterinarian, for his availability
for consultation and interest on the proj ect and Dr. William W. Thatcher, Graduate
Research Professor at the Department of Animal Science for his ideas, his contribution in
the design and interpretation of the study.
I would like to thank Mrs. Coni and Mr. Dale Sauls and the personnel of Condale
Dairy Farm for their support and hard work to make this study possible. I also would like
to acknowledge Shawn Ward for his hard work and friendship.
I thank Julie Oakley and Marie Joelle Thatcher for their help with assay and data
handling and analysis. I also need to thank Sally O,Connel, secretary at the Graduate
School, for her continuous concern and help for graduate students. I would also thank
faculty, residents and staff of the Food Animal Service for their help and patience.
I need to acknowledge my friends in Gainesville, Jackie and Mandy, Elisa and
Charly for being our hotel, mechanics, electricians, baby sitters, painters and for their
constant support and concern but most importantly for their sincere friendship. Thanks to
my friends in Argentina, Gerva, Bebe and Paula, Carlitos and Ceci, Chaca, Carlitos,
Luchito and Rosario, Gonzalo and Sole for their support and for more than 15 years of
I would like to thank my mother and sister, for their love and constant support for
the past 34 years, and my father, who from heaven, looks after every step I take. Finally I
thank my wife Martita, our daughter Sofl and our son Santi, for whom I don't have words
to express my gratitude but I am sure that without them this would not be possible.
TABLE OF CONTENTS
ACKNOWLEDGMENT S .............. .................... iv
LI ST OF T ABLE S ................. ................. viii............
LIST OF FIGURES .............. .................... ix
AB S TRAC T ......_ ................. ............_........x
1 INTRODUCTION ................. ...............1.......... ......
2 LITERATURE REVIEW .............. ...............4.....
Anatomy of the Bovine Foot ................. ...............9........... ...
Foot ................. ...............10.................
Claws ................. ..... ... ...... ......... .... .... ... .... .... .......1
Suspensory Apparatus and Supporting Structure of the Bovine Digit ................ 12
Horn Formation and Growth ................ ........... ..... ....... ....... ........ 1
Microanatomy of the Claw: Structure of the Wall ................ ................. ... 14
Etiology of Lameness ................... ......_._ ...............15......
Infectious Diseases of the Digits .................. ...... ....._ ... ....... ...........1
Interdigital phlegmon (F oot-rot, Interdigital necrob acill osi s) ........._.._..........15
Interdigital dermatitis ........._...... .... .... ._.. ... ......._..... .............1
Digital dermatitis (DD) (Footwarts, Hairy heel warts, Heel warts)............. 19
Metabolic Hoof Horn Disease: Claw Horn Disruption .........._.... ......._.......25
Laminiti s........._._ ......_ _. ...............26...
Forms of laminitis .............. .... ...............29.
Claw Lesions Associated with Laminitis .................... ............... 3
Hemorrhages of the sole and sole ulcer. .........._.._. ......_. .................30
Softening of the horn of the sole ................. ...............30......__ ..
White line disease............... ...............31
Heel erosion............... ...............3 1
Diagnosis of Lameness ................. .............. 1......... ....
Lameness and Animal Welfare............... ...............34
Lameness and Milk Production .............. ...............35....
Lameness and Reproductive Performance............... ..............3
Resumption of Ovarian Activity Postpartum .............. ...............39....
Physiological Factors Involved in Ovarian Activity Potentially Affected by
Energy Balance ................. .... ........ ..... ........ .............4
Effects of negative energy balance in LH secretion ................. .................4 8
Metabolic hormones ................. ...............49.................
Other factors ................. ...............53.................
Lameness and Ovarian Activity............... ...............57
3 MATERIALS AND METHODS............... ...............59
Cows and Herd Management............... ...............5
Study Design............... ...............59.
Data Collection .............. ...............60....
Diagnosis of Lameness ................. ............ ..... ... ...... ....... ...... .........6
Collection of Blood Samples and Detection of Plasma P4 COncentrations ................61
Resumption of Ovarian Cyclicity .............. ...............63....
Reproductive and Health Management .............. ...............63....
Statistical Analyses ................. ...............65.................
4 RE SULT S .............. ...............69....
5 DI SCUS SSION ................. ...............74................
6 CONCLU SION ................. ...............8.. 0..............
LI ST OF REFERENCE S ................. ...............8.. 1......... ....
BIOGRAPHICAL SKETCH .............. ...............97....
LIST OF TABLES
2-1. Studies reporting incidence of lameness in dairy cows ................. ............ .........7
2-2. International terminology of digital diseases............... ...............9
2-3. Incidence of Digital Dermatitis in US dairy herds by herd size and region ........._....22
2-4. Days from calving to 1st ovulation reported in the literature ............... ................. 43
2-5. Incidence rates of delayed cyclicity reported in the literature. ................. ...............44
3-1. Protocol for examination of cows postpartum ................. ...............64.............
3-2. Definitions of metritis done by farm personnel based on discharge and palpation
findings ................. ...............64.................
3-3. Definition of calving outcomes. ............. ...............65.....
3-4. Criteria for monitoring production health and mastitis using Afimilk@ system........65
4-1. Frequency distribution of cows classified as lame or non-lame using a modification
of the locomotion scoring system developed by Sprecher, 1997. ............................71
4-2. Descriptive statistics and unadjusted odds ratios for risk of delayed ovarian cyclicity
in post partum Holstein cows ................ ...............72......_... ...
4-3. Final logistic regression model for risk of delayed ovarian cyclicity in post partum
Hol stein cows .............. ...............73....
4-4. Attributable proportion of cows that experienced delayed resumption of ovarian
cy clicity. ............. ...............73.....
LIST OF FIGURES
1. Normal ovarian cyclicity............... ...............6
2. Normal ovarian cyclicity for cows treated with PGF2 .............. .....................6
3. Delayed resumption of ovarian cyclicity .............. ...............67....
4. Extended luteal phase .............. ...............68....
Abstract of Thesis Presented to the Graduate School
of the University of Florida in Partial Fulfillment of the
Requirements for the Degree of Master of Science
EFFECT OF LAMENESS ON OVARIAN ACTIVITY INT POSTPARTUM HOLSTEIN
Eduardo Jose Garbarino
Chair: Jorge Hernandez
Major Department: Veterinary Medical Sciences
An observational cohort study was conducted to examine the relationship between
lameness and delayed ovarian cyclicity in post partum Holstein cows. We used 253 cows
from a 600-cow dairy herd that calved during a 12-month period. Cows were classified
into one of six categories of lameness during the first 35 days post partum using a
locomotion scoring system. Cows were blood sampled weekly for detection of plasma P4
concentrations during the first 60 days post partum. Cows with a delayed resumption of
ovarian cyclicity were those with consistent P4 COncentrations < 1 ng/mL during the first
60 days post partum. The null hypothesis that risk of delayed cyclicity is the same in
cows classified as non-lame, moderately lame, or lame (after adjusting for potential
modifying or confounding effects of loss of body condition and other variables related
with delayed cyclicity) was tested using logistic regression. Results of the study support
the hypothesis that lameness has a detrimental effect on ovarian activity in Holstein cows
during the early post partum period. Cows classified as lame were 3.5 times at higher risk
of delayed cyclicity, compared to cows classified as non-lame
(OR = 3.5; 95% CI = 1.0 12.2; P = 0.04). Attributable proportion analysis indicated that
delayed ovarian cyclicity in lame cows would be reduced by 71% if lameness had been
prevented. In addition, cows classified as moderately lame were 2.1 times at higher risk
of delayed cyclicity, compared to non-lame cows
(OR = 2. 1; 95% CI = 0.7 6. 1; P = 0. 15).
Lameness is one of the top three health problems that cause premature culling of
dairy cows in the United States. The National Animal Health Monitoring System Dairy
2002 Study (NAHMS 2002) reported that lameness was the reason for culling 16% of
dairy cows sent to slaughter. Overall, 10% of cows were reported affected with lameness
in the previous 12 months. The economic importance of lameness is attributed to cost of
treatment and control methods (Shearer and Elliot, 1998; Shearer et al., 1998; Hernandez
et al., 1999, 2000; Moore et al., 2001), impaired reproductive performance (Lucey et al.,
1986; Lee et al., 1989; Sprecher et al., 1997; Hernandez et al., 2001; Melendez et al.,
2003), decreased milk yield (Warnick et al., 2001; Green et al., 2002; Hernandez et al.,
2002), increased risk of culling (Sprecher et al., 1997; Collick et al., 1989), and decreased
carcass value of culled cows (Van Arendonk et al., 1984). In addition, because of the
pain, discomfort, and high incidence of lameness in dairy cows, this disorder should be
considered an animal welfare issue.
Delayed ovarian cyclicity in the preservice postpartum period is a common
ovarian dysfunction in dairy cows (Opsomer et al., 1998). Late resumption of ovarian
activity post partum has a detrimental effect on reproductive performance in dairy cows
(Thatcher and Wilcox, 1973; Stevenson and Call, 1983; Lucy et al., 1992). Cows
ovulating earlier post partum have fewer services per conception and a shorter
calving-to-conception interval (Lucy et al., 1992). Minimizing the interval from calving
to first ovulation provides ample time for completion of multiple ovarian cycles before to
insemination, which in turn improves conception rates (Butler and Smith, 1989). Losses
in body condition, puerperal disturbances, and ketosis have been identified as risk factors
significantly associated with delayed ovarian cyclicity in dairy cows (Opsomer et al.,
While previous studies have shown that lameness has a detrimental effect on
reproductive performance (i.e., a prolonged calving-to-conception interval) (Lucey et al.,
1986; Collick et al., 1989; Sprecher et al., 1997; Hernandez et al., 2001), the relationship
between lameness and ovarian activity in dairy cows has not been investigated using
objective research methods. Results of previous studies in Florida suggest that as cows
experience increasing positive energy status, there is increased ovarian follicular activity
leading to return to ovulation (Staples et al., 1990; Lucy et al., 1992). As energy status
becomes more positive for cows early post partum, diameter of the largest follicle
increases, the number of double ovulations increases, and time for detection of the first
corpus luteum decreases (Lucy et al., 1991). These changes in follicle size and numbers
and the number of ovulations, are thought to be caused by increases in luteinizing
hormone, follicle-stimulating hormone, insulin, BST, insulin-like growth factor-1, and
possibly other yet-to-be determined compounds that are activated by an improved energy
status (Beam and Butler, 1998).
Clinical observations by veterinarians and dairy farmers in Florida suggest that
lameness has a detrimental effect on ovarian activity in lactating dairy cows. We
hypothesized that as lame cows experience a more pronounced loss in body condition
(hence a prolonged state of negative energy balance) during the early postpartum period,
lame cows are at higher risk of delayed ovarian cyclicity than non-lame cows. Under
field conditions, evidence of corpus luteum function can be determined by monitoring
plasma P4 COncentrations weekly during lactation, before and after diagnosis of lameness
in dairy cows. The obj ective of this study was to examine the relationship between
lameness and delayed resumption of ovarian cyclicity in Holstein cows during the first 60
days post partum.
Knowledge of the epidemiologic aspects of diseases and lesions that cause
lameness is essential to further develop control and prevention methods for lameness in
dairy cows. Risk of lameness during lactation, severity and duration of lameness, and the
relationship between lameness and ovarian activity in lame cows have not been
investigated under US dairy farming conditions. Our prospective research study will
allow us to better characterize lameness in dairy cows under commercial farming
conditions, and examine the relationship between lameness and ovarian activity. An
understanding of the reasons for individual-cow differences in lost revenues will aid
producers in making management decisions at the cow and herd levels to manage
lameness, reproductive performance, and animal welfare.
Lameness is one of the top three health problems that cause premature culling of
dairy cows in the United States. Several studies have reported that the incidence of
lameness in dairy cattle operations varies from 7% to 54.6% (Harris et al., 1988;
Clarkson et al., 1996; Collick et al., 1989; Barkema et al., 1994; Green et al., 2002;
Deluyker et al., 1991), with the highest proportion of cases occurring in the first 100 days
in milk (Collick et al., 1989; Barkema et al., 1994; Green et al., 2002).
The economic importance of lameness is reportedly attributable to cost of
treatment and control methods (Moore et al., 2001; Hernandez et al., 1999, 2000; Shearer
et al., 1998), impaired reproductive performance (Lee et al., 1989; Tranter and Morris,
1991; Sprecher et al., 1997; Hernandez et al., 2001; Melendez et al., 2003), decreased
milk yield (Tranter and Morris, 1991; Coulon et al., 1996; Warnick et al., 2001;
Hernandez et al., 2002), increased risk of culling (Sprecher et al., 1997; Collick et al.,
1989), and decreased carcass value of culled cows (Van Arendonk et al., 1984). In
addition, because of the pain, discomfort, and high incidence of lameness in dairy cows,
this disorder should be considered an animal-welfare issue.
It is difficult to describe the incidence and prevalence of the problem of lameness
in dairy cows, because of the wide variation that exists in published reports. This
variation is due to differences in geographic locations and production systems
(pasture-based vs. confinement) of study herds, that may alter the frequency distribution
of lameness. In addition, the method of gathering data varies among studies (some
collecting data from veterinary practices, and others gathering data directly from the
farmer, or by researchers). Whitaker (1983) reported an average incidence of lameness of
25% (range = 2% to 55%) in 21,000 dairy cows in 185 herds in England and Wales. In
the study by Whitaker (1983), data were collected by a survey of the number of
treatments for lameness either by the farmer or veterinary surgeon. Another study
conducted in 37 dairy farms in the United Kingdom and Wales, Clarkson (1996) reported
an annual incidence of lameness of 54.6% (new cases/100 cows) with a range from
10.7% to 170.1%. This same study (Clarkson et al., 1996) reported the prevalence of
lameness to be 20.6%. Diagnosis of lameness was performed either by the farmer,
student, hoof trimmer, or a veterinarian. All treatments were recorded and were used to
calculate the prevalence and incidence of lameness. Collick (1989) performed a study in
17 dairies in the UK, and reported an incidence of lameness of 17% during a 6- month
period, with a range of 8% to 28%, with 65% of cases occurring in the first 100 days in
milk. In this case, diagnosis of lameness was made by the attending veterinarian.
A study conducted in 80 dairies in France (Faye and Lescourret, 1989), the
reported annual incidence of lameness was 29.5%. They stated that incidence of lameness
was higher than reported incidence rates of mastitis, and that lameness was the most
common disease reported in dairies. A study conducted in 101 dairy farms in Sweden
(Manske et al., 2002a), found a prevalence of lameness of 5%. In this study (Manske et
al., 2002a) lameness examination of cows was done by researchers who looked at every
cow on each farm, with the purpose of identifying claw lesions in lame and non-lame
cows. In other parts of the world with more extensive production system such as New
Zealand, Australia, and Argentina, the incidence/prevalence of lameness differs from
those reported in Europe. Dewes (1978) reported an incidence of lameness of 14%, and
more than 85% of the cases of lameness were detected before 90 days in milk. This study
(Dewes, 1978) was conducted using data provided by four dairy producers from Waikato,
New Zealand. In another study in New Zealand by Tranter and Morris (1991) in three
dairy herds, the annual incidence of lameness was 16% with a range from 2% to 38%. In
this study the mean days to onset of lameness was 92154 (mean +SD). Harris (1988)
conducted a study in 73 dairies in Southern Australia and reported and annual incidence
of lameness of 7% with a range of 0% to 31%. In this study, diagnosis of lameness was
done by the farmer. In a study done in Argentina (Rutter, 1994) involving 4580 dairy
cows from 25 farms, the incidence of lameness was 23.4% with the highest incidence
occurring in first lactation heifers (45%). In most of these studies, sole ulcers and white
line disease were the most predominant lesions observed.
When we examined the incidence and prevalence of lameness studies in the
United States, we also found important variations. Reported incidences of lameness were
4.4%, 5.1% and 9.5% (Bartlett et al., 1987; Weigler et al., 1990; Kaneene et al., 1990). In
these studies, lameness was diagnosed by the farmers. This motivated Wells (1993a), to
design a study on prevalence of lameness, and to compare the diagnosis of lameness
performed by researchers and farmers. In both seasons spring and summer, the observed
prevalence reported by researchers were 3 times higher than that by the farmers. This
study (Wells et al., 1993a) involved 17 dairy farms from Minnesota and Wisconsin and
reported a prevalence of lameness of 14% in the summer and 17% in the spring. In
another study conducted in 13 dairy farms in Ohio, researchers observed that the
incidence of hemorrhages and discoloration of the sole in first calf heifers (from 60 days
pre partum until 100 days post partum) was 62% during this period. In another study by
Sprecher (1997) using a locomotion scoring system, the incidence of lame cows
(Locomotion Score > 4) was 24.5%, the incidence of moderately lame plus lame cows
(LS > 3) was 49. 1% at the time of the first service.
Table 2-1. Studies reporting incidence of lameness in dairy cows
Author, year Country Incidence of lameness (%)
Rutter, 1994 Argentina 23
Harris et al., 1988 Australia 7 (0 to 31)
Faye and Lescourret, 1989 France 29
Dewes, 1978 New Zealand 14
Tranter et al., 1991 New Zealand 16 (2 to 38)
Manske et al., 2002a Sweden 5
Whitaker et al., 1983 United Kingdom 25 (2 to 55)
Collick et al., 1989 United Kingdom 17 (8 to 28)
Clarkson et al., 1996 United Kingdom 54
Bartlett et al., 1987 United States 4
Weigler et al., 1990 United States 5
Kaneene et al., 1990 United States 9
Wells et al., 1993 United States 13.7 summer & 16.7 winter
Sprecher et al., 1997 United States 49
Warnick et al., 2001 United States 46
Almost all reports describing lameness in dairy cows considered claw diseases as
the most common causes of lameness. Some of the papers listed above (Tranter and
Morris, 1991; Deluyker et al., 1991; Murray, 1996) reported claw diseases as responsible
for more than 90% of the cases of lameness. When we examined the most common claw
disorder, reports are not so much in agreement. Differences maybe due to, different
housing types, feeding strategies, environmental challenges and managements systems.
Studies from the United Kingdom (Clarkson et al., 1996; Murray et al., 1996) agreed that
sole ulcers, white line disease, laminitis and subsolar abscess are the most common
diseases affecting the bovine claw. In another study conducted on 101 dairy farms in
Sweden (Manske et al., 2002), sole ulcers and white line lesions were the most common
lesions found in lame cows. In New Zealand and Australia (Tranter and Morris, 1991;
Dewes, 1978; Harris et al., 1988) where cows are kept in pasture all year around,
traumatic pododermatitis (sole bruising), worn soles and interdigital dermatitis the most
common diseases of the claw affecting dairy cows. In a study conducted in Argentina
(Rutter, 1994), digital dermatitis (39.4%) and interdigital dermatitis (26.3%) were the
most common diseases affecting the bovine foot. In the United States, all studies
identified claw lesions as the most common lesions affecting dairy cows (Deluyker et al.,
1991; Smilie et al., 1996; Hernandez, 2002). These studies, however, were not designed
to establish the prevalence of the different diseases of the bovine foot.
With an average incidence of 30 cases per 100 cows per year, a case fatality rate
of 2%, involuntary culling of 20% of cases; an average increase of 28 days open,
treatment costs including veterinary fees, drugs and farmer labor of $23 per case. The
total cost of lameness per 100 cows per year is estimated to be about $9000 (Guard,
1996). This paper is probably underestimating the cost of lameness as it is not taking into
account other factors that are affected by lameness. Lameness has been shown to affect
milk production and this was not included in the estimation, as well as the decrease of the
carcass value of cows sent to slaughter and the increased probability of a cow being
culled if experiencing lameness. In another report from the UK, Kossaibati and
Esslemont (1997) reported that the average total cost per affected cow of a case of sole
ulcer was 424 (approx $600). This estimation included the cost of treatment, herdsman' s
time, discarded milk, reduced milk yield, veterinarian's time, increased risk of culling
and longer calving interval. Increased risk of culling and a longer calving interval
accounted for more than 60% of the cost. Unfortunately, the authors did not explain how
they estimated milk loss and increased risk of culling.
Table 2-2. International terminology of digital diseases
International terminology English Common terms
Dermatitis interdigitalis Interdigital dermatitis Superficial Foot-Rot
Phlegmona interdigitalis Interdigital phlegmon Foot-Rot, Foul in the foot
Erosio ungulae Heel erosion Underrun heel, Slurry heel
Hyperplasia interdigitalis Interdigital hyperplasia Corn, Interdigital fibroma
.Hairy foot warts, Hairy
Dermatitis digitalis Digital dermatitis el
Pododermatitis aseptica difusa Laminitis
Pododermatitis circumscripta Sole ulcer
Pododermatitis septica Traumatic septic Subsolar, toe and white
traumatica pododermatitis line abscesses
Sand cracks: longitudinal
Fissura ungulae Hoof wall cracks
Pododermatitis locale Localizedpododermatiti s Bruises
Ungulae deformans Overgrown hooves Long toes
To compare results from different studies it is important to standardize the
terminology regarding claw lesions. In order to clarify the rest of this manuscript we will
follow the terminology proposed by Weaver (1994) (Table 2-2).
Anatomy of the Bovine Foot
Before we start describing the different pathologies affecting the bovine foot, it is
important to review it' s anatomy and microanatomy.
The foot includes the entire limb below the fetlock j oint. It is comprised of two
digits each of which has a horn-covered claw. It should be noted that in cattle the term
"claw" is preferable to hoof. The front aspect of the foot is referred to as the dorsal side.
The back side of the front foot is referred to as the palmar aspect whereas in the rear foot
is referred to as plantar aspect. When referring to an area nearest the longitudinal axis
(i.e., toward the center) it is designated as axial, whereas items farther away (away from
the center) are designated as abaxial.
Each digit of the foot has 4 bones: phalange 1 (Pl), phalange 2 (P2), phalange 3
(P3), and navicular bone; and 2 joints: proximal interphalangeal (PIP) and distal
interphalangeal (DIP). The proximal end of Pl articulates with the metacarpus (in the
front leg) or metatarsus (in the rear leg) in the fetlock j oint, whereas the distal (away from
the center of the body) end of Pl articulates with the proximal end of P2. This
articulation between Pl and P2 is referred to as the proximal interphalangeal joint (PIP).
The distal end of P2 articulates with the proximal end of P3. This j oint is referred to as
the distal interphalangeal joint (DIP).
P3 is completely enclosed within the claw horn capsule. Its solar surface is
concave or arch shaped and marked on the back edge by a bump known as flexor
tuberosity. The flexor tuberosity is the site of attachment of the deep flexor tendon. This
tuberosity has an important role in the pathogenesis of sole ulcers as it becomes involved
in the process of compression of the corium subsequent to laminitis and the displacement
of P3 (Toussaint Raven, 1989).
The navicular bone (also referred to as the distal sesamoid bone) is attached to P3
by three small ligaments and also to P2 by collateral ligaments. Between the navicular
bone and the deep flexor tendon is the navicular bursa. The navicular bursa contains
j oint-fluid which permits movement of the deep flexor tendon over the surface of the
navicular bone during extension and flexion of the claw. P3, the DIP j oint, navicular bone
and navicular bursa all lie within the claw capsule.
The purpose of the claw hom capsule is to protect the underlying sensitive tissues
of the corium and dissipate the concussion forces that occur when the digits impact the
ground. It consists of the wall which can be divided into the axial (inside) and the abaxial
(outside). The abaxial wall is further subdivided into the dorsal (or front) and lateral
abaxiall side) aspects. The wall is demarcated from the heel on the abaxial side of the
claw by the abaxial groove. The wall consists of two types of horn: perioplic and
coronary. Perioplic hom is the softer horn lying just below the coronet at the skin-hom
junction (corresponding to the human cuticule). At the back of the foot the periople
gradually widens and eventually becomes the horn of the heel. Coronary horn, the hardest
horn within the claw capsule makes up the bulk of the horn of the wall. The wall has faint
ridges or rugae, which run horizontally and parallel to each other. Toward the heel these
ridges diverge reflecting a more rapid rate of growth in the heel region due to faster rates
of wear. In mature Holstein cattle the length of the dorsal wall should be a minimum of 3
inches in length from just below the top of the hairless portion of the wall to the
weight-bearing surface. Ideal heel height is 1.5 inches (Toussaint Raven, 1989; Blowey,
The sole is produced by the solar corium and merges imperceptibly with the hom
of the heel at the heel-sole junction. The sole is connected to the wall by means of the
white line. White line horn is produced by laminar corium. It courses forward from the
area of the heel on the abaxial side of the claw, around the tip of the toe and about 1/3 of
the way back on the axial side of the claw' s weight bearing surface. Where the white line
leaves the weight bearing surface it courses upward on the axial side of the claw. This
white line is a unique and important structure. It is the softest horn within the claw
capsule. This permits it to provide a flexible junction between the harder horn of the wall
and the softer horn of the sole. On the other hand, because of its softer nature it also
represents a weak spot on the weight-bearing surface that is vulnerable to damage.
Suspensory Apparatus and Supporting Structure of the Bovine Digit
Cattle (and all animals with claws or hooves) are suspended in their feet, that is,
they stand in their feet, not on them. In other words, the bone within the claw (also
known as P3) is suspended within the claw horn capsule by the laminar corium and a
series of collagen fibers bundles that stretch from the insertion zone on the surface of P3
to the basement membrane of the epidermis (the line of demarcation between dermis and
epidermis). The interface between dermal and epidermal components is the
interdigitating dermal and epidermal laminae. The result is that P3 hangs within the claw
capsule and weight is transferred as tension onto the wall of the claw capsule.
The suspensory system in cattle differs significantly from that in horses. First, the
laminar corium is much less extensive in cattle as compared to horses. Secondly, there
are no secondary laminae in the laminar corium of cattle. Therefore, capabilities with
respect to mechanical load carried on the claws of cattle vary significantly. In the horse
load bearing is primarily on the wall. Cattle, on the other hand, simply cannot handle the
same amount of mechanical load on the walls of their claws. Instead, weight-bearing in
cattle requires displacement of load to the wall, and support structures within the sole and
The primary structures within the supportive apparatus of the bovine claw are the
solar corium and associated connective tissue, and the digital cushion, which consists of
loose connective tissue and varying amounts of adipose (fat) tissue. The digital cushions
are arranged in a series of three parallel cylinders similar to the design used in the
cushion of a running sole. In the cows foot these cushions act like shock absorbers within
the claw protecting the corium and permitting limited movement of P3 in the region of
Horn Formation and Growth
The horn-producing germinal layer of the epidermis and its supporting structure,
the corium, consist of four different regions, each producing a structurally different type
of horn (Budras et al., 1996). Perioplic horn, overlying the perioplic corium, is found just
below the skin-hom junction and extends to the back of the claw to include the heel horn
(Budras et al., 1996). Horn of the wall is produced in the area of the coronary corium and
it is situated between the perioplic corium and the sensitive laminae. The area overlying
the laminar corium produces the horn of the white line, also known as laminar horn. The
solar horn overlies the solar corium and is situated between the laminar hom of the white
line and the perioplic hom of the heel (Budras et al., 1996; van Amstel and Shearer,
Horn production and growth are supported by the corium, which corresponds to
the dermis. The corium consists of a rich vascular network that terminates in dermal
papillae, also called vascular peg (Greenough, 1997). A vascular peg consists of a main
arteriole and a venule, which are connected at the tip. Between the arteriole and the
venule is an extensive capillary network, and there are also several vascular shunts
between such arterioles and venules. These shunts may open under certain circumstances,
cutting of the blood supply to the tip of the vascular peg, which adversely affect horn cell
formation. The epidermal layer overlying the vascular pegs produces horn cells in the
form of tubules (tubular horn) (Budras et al., 1996; Greenough, 1997). Intertubular horn
is produced between the papillae and interconnects the tubular horn. There are
approximately 80 vascular pegs or dermal papillae per square millimeter of coronary
corium surface (Greenough, 1997), which means that the wall consists of tightly packed
tubular homn that is cemented together by intertubular horn. The perioplic corium of the
heel horn and the solar corium has fewer vascular pegs per square millimeter. Because
tubular homn supplies structural strength to the homn capsule, it follows that the horn of the
wall is structurally the strongest, followed by the sole and the heel. Keratin filaments
produced by horn cells enhances the rigidity and strength of homn cells as they progress to
Laminar horn is immature, nontubular, so it is soft and flexible and has a high
turnover rate. Homn cells, whether tubular or nontubular, are cemented by a substance
known as membrane-cementing substance (Budras et al., 1998). This substance, a
lipoprotein, is permeable and holds water, giving the horn its flexibility (Budras et al.,
Horn quality is dependant on internal and external and factors. Internal factors
relates to blood and nutrient supply, whereas external factors relates to environment
where the claw is found. Any compromise in blood flow has a negative effect on horn
Microanatomy of the Claw: Structure of the Wall
The structure of the claw consists of modified skin that is a continuation of the
epidermis of the coronary band. The claw has the same basic structures as the skin. It has
an epidermis (horny wall), a dermis coriumm or quick), and a subcutis (Hibroelastic heel
pad and coronary and digital cushion). The epidermis itself is divided into basement
membrane, germinal epithelium (stratum germinativum), stratum spinosum (layers of
horn undergoing keratinization) and stratum corneum (the layer of comified epithelium).
The basement membrane is the junction between the epidermis and corium. The stratum
germinativum is the germinative layer responsible for horn growth. The stratum corneum
is the cornified epithelium forming the claw hom. Cells are arranged into tubular and
intertubular horn. The mechanical strength of the bovine claw is a function of the
keratinization of cells in the germinal layers of the epidermis (Hendry et al., 1994).
Etiology of Lameness
Lameness in cattle can be caused by a variety of reasons. The purpose of the next
section is to describe the different causes of lameness in cattle.
Infectious Diseases of the Digits
Several systemic diseases can be associated with digital lesions potentially
leading, as a result of localized pain, to stiffness and lameness. They include
Foot-and-Mouth Disease (FMD), Bovine Virus Diarrhea (BVD), Bovine Malignant
Catarrh, Bluetongue and Vesicular Stomatitis. This review of lameness is focused on
maj or specific infections of the digits: Interdigital Phlegmon (Foot-Rot), Interdigital
Dermatitis and Digital Dermatitis.
Interdigital phlegmon (Foot-rot, Interdigital necrobacillosis)
Interdigital Phlegmon is characterized by fissuring, caseous necrosis of the
subcutis in the interdigital space and diffuse digital swelling. Pain, moderate to severe
lameness, and pyrexia are also common signs of this disease. A characteristic fetid odor
is usually present because of the presence of Fusobacterium necrophorum which if not
treated early a common sequela is septic arthritis (Berry, 2001).
Although the pathogenesis of foot rot is not understood completely, bacteria gain
entry through abraided skin on the lower part of the foot. Hard surfaces contribute to foot
injury, and continuous wetting likely favors abrasions by softening the interdigital skin
(Radostits et al., 2000). The greatest economic impact of bovine foot rot is in dairy
operations, where milk production may be affected (Hernandez et al., 2002). In this
study, cows affected with foot rot produced 10% less milk than normal cows. Also this
disease can affect feedlots where antimicrobial treatments require withdrawal times that
could delay marketing of products (Radostits et al., 2000). Although spontaneous
recovery may occur, lameness may persist for several weeks when infections are left
untreated, and complications may cause more severe problems that could eventually lead
to death or euthanasia of the animal (Radostits et al., 2000).
Treatment of foot rot can be accomplished with a variety of antimicrobials (Cook
et al., 1995; Morck, 1998; Berry, 2001). A recent study looked at the efficacy of Ceftiofur
Sodium and Hydrochloride formulation for the treatment of foot rot (Kausche et al.,
2003). This was a multilocation study conducted on 11 farms in the US to compare the
efficacy of Ceftiofur at a dose of 1.1 mg/kg once a day for 3 consecutive days with a
placebo group. Results of this study indicated that cure rate for Ceftiofur was 62.2%
versus 14% for the placebo group (P < 0.003). These same authors did another study to
compare the efficacy of Ceftiofur versus Oxytetracycline at 10 mg/kg. Results of this
study indicated that Ceftiofur and Oxytetracycline were comparable in efficacy, with
Ceftiofur having excellent inj ection-site tolerance and a short or no milk discard or
pre-slaughter withdrawal (Kausche et al., 2003). Treatment can also be accomplished by
the use of Sulfadimethoxine orally (25 g/1b followed by 12.5 g/1b SID for no more than 5
days) or intravenously (55 mg/kg followed by 27.5 mg/kg SID for 2 days after remission
of clinical signs). Good results also can be obtained with Penicillin G intramuscularly for
3 days (Bergsten, 1997).
Prevention and control of foot rot can be accomplisheded by the use of foot baths
with 5% to 10% copper sulfate or zinc sulfate (Rebhun, 1982). Formaldehyde solutions
of 3 to 5% in water have been reported to be effective in the prevention of foot-rot
(Bergesten, 1997). Caution should be emphasized when using formaldehyde due to
potential hazards for handlers as well as contamination of the environment. Other
measures recommended to prevent foot rot are to maintain clean passageways to reduce
the exposure of the feet to feces, maintaining a dry environment and avoiding rough floor
surfaces that can traumatize the interdigital skin and allow the entry of bacteria (Blowey,
1994). Efforts to produce vaccines against Fusobacterium necrophorum have failed
because of the weak immune response to the bacterium (Smith, 1992). There are vaccines
available in the US market but there are no peer-reviewed studies to support their use.
Interdigital dermatitis occurs as an acute or chronic inflammation of the
interdigital skin that does not usually cause lameness (Blowey, 1994; Guard, 1995). The
inflammation does not extend to the subcutaneous tissues and in this respect differs from
foot-rot, where infection extends to the dermis, leading to fissure formation, infection of
deeper structures, and cellulitis of the pastern and fetlock (Blowey, 1994). Some authors
implicate F.necrophorum, Dichelobcater nodosus and Bacetroides sp as the causative
agents of interdigital dermatitis (Toussaint Raven, 1989, Peterse, 1982).
Interdigital dermatitis occurs in dairy cattle, especially in wet environments. It is
usually an incidental finding when trimming feet because it rarely causes lameness. A
study conducted in 17 Danish dairy herds reported that interdigital dermatitis occurred in
4.5% and 7.6% of first and 2+ lactation cows, respectively (Enevoldsen et al., 1991). In
this study, severity of disease increased with parity and risk increased with stage of
lactation. In a Dutch study on 86 dairy farms, researchers reported that the prevalence of
interdigital dermatitis and heel horn erosion was 24% (range = 3 to 92%) (Manske et al.,
Clinical signs of interdigital dermatitis include hyperemia of the interdigital skin,
including the palmar and plantar areas, superficial erosion and ulceration followed by
hyperemia with serious or grayish exudates. More aggressive forms interfere with the
horn formation in the bulbs, where fissures, hemorrhages and necrosis can arise. The
subcutaneous tissue is inflamed secondarily. Swelling and hyperkeratosis may develop in
a more chronic stage. Chronic interdigital irritation may cause slight to severe interdigital
hyperplasia (Bergsten, 1997). The most common complication of interdigital dermatitis is
heel horn erosion. Results of a study conducted by Enevoldsen (1991) support the
hypothesis that severe heel erosion and interdigital dermatitis are two manifestations of
the same disease with Dichelobacter nodosus as an important component and are closely
related. In this study (Enevoldsen, 1991) the incidence of heel erosions in 1st and 2+
lactation cows was 43% and 69%, respectively. This study (Enevoldsen, 1991) also
reported unhygienic and moist conditions as important risk factors for interdigital
Prevention and treatment is usually accomplished by the use of 5 to 10% copper
sulfate footbath or zinc sulfate (10 to 20%), or formalin (3 to 5%) footbaths. Care must be
taken to ensure that the footbath remains clean. Interdigital dermatitis can persist in
dairies that practice regular footbaths (Guard, 1995). This same report suggested that the
causative organisms may survive within deep heel cracks that are not permeated by
footbath solutions; hence, heel cracks must be trimmed during hoof trimming to allow for
exposure to footbath solutions. Claw trimming causes a mechanical cleansing of affected
tissues and an exposure to air that might be beneficial for the curing of dermatitis lesions
(Manske et al., 2002b). As reported in this same study, every third hoof affected with a
severe dermatitis and concurrent heel-horn erosion had recovered 1 month after
Digital dermatitis (DD) (Footwarts, Hairy heel warts, Heel warts)
Digital dermatitis is an important cause of lameness in dairy cattle. It was first
reported by Cheli and Mortellaro in 1974 (Mortellaro, 1994) as a mysterious cause of
epidemic lameness affecting up to 70% of adult cattle in the Po Valley of Italy. Since
then, the disease has been reported in other countries such as the Netherlands, France,
England, Czechoslovakia, Germany, and Ireland (Bassett et al., 1990; Brizzi, 1993). In
the United States, Rebhun (1980) first reported the disease as outbreaks of lameness in
New York dairy herds.
Clinically, digital dermatitis typically appears within dairy herds as outbreaks of
lameness. It is a superficial skin disease of the bovine digit with variable presentation
(i.e., depending upon the stage of the lesion), from painful, moist, strawberry-like lesions
to raised, hairy, wart-like lesions (Read and Walker, 1998). These lesions (i.e., usually
located on the rear of the foot between the bulbs of the heel) have been referred to by
several names, including: hairy footwarts, strawberry (or raspberry) heelwarts, and
papillomatous digital dermatitis. Early lesions produce matting of the hairs, which stand
erect in thick, light brown exudates, which have a characteristic pungent odor (Blowey et
al., 1994). A study conducted in California described the lesions as being distinctly
demarcated, circumscribed, spherical to oval, 0.5 cm to 6 cm across, partially or
completely alopecic, moist, painful-to-touch, prone-to-bleed plaques of flat or raised
proliferative tissue. Lesion surfaces vary in appearance from being extensively red and
granular (3 1%), often with patches of yellow or gray filiform papillae (41%) to
extensively gray, brown or black with papillary outgrowth of the epithelium (28%) (Read
and Walker, 1994).
In spite of many studies and specific research, the exact etiology of DD is still
unknown. Researchers still believe that DD is a multifactorial disease, even though in
some cases high morbidity, apparent contagiousness and response to antimicrobial
treatments suggest that an infectious agent is primarily involved (Mortellaro, 1994). In
one study the incidence of DD was higher in heifers a few months after they entered the
milking herd and may be due to lack of immunity (Read et al., 1992). Initial studies
(Rebhun et al., 1980; Cheli and Mortellaro, 1986; Peterse, 1982) were unable to identify
any viral pathogens, and results of bacteriology were inconsistent. Peterse (1982) was
able occasionally to isolate Dichelobacter nodosus from some typical lesions. Bassett
(1990) was unsuccessful in isolating a microorganism from DD lesions and also failed to
replicate the disease after inoculation of heifers with homogenate from fresh lesions.
Read (1992) examined histological lesions and were able to demonstrate the presence of
large numbers of spirochetes invading the stratum spinosum and dermal papillae (Blowey
et al., 1994). In a more recent study, Walker (1995) isolated two different spirochetes
from cows with DD lesions in California dairy herds. These spirochetes were further
categorized based on morphology (intracytoplasmatic tubules), antigenicity and
enzymatic activity in the genus Treponema. This finding was supported later by another
study (Demirkan et al., 1999) where serological evidence suggested that spirochetes are
involved in the pathogenesis of DD. Also, this study (Demirkan et al., 1999) supports the
hypothesis that Borrelia burgdorferi may be involved in the pathogenesis of DD, as first
proposed by Blowey (1994). To date, there is still no isolation of the bovine spirochete.
In a study conducted in California dairy herds (Read and Walker, 1994), the
prevalence of DD was approximately 90%. Between-herd morbidity varied from 0.5 to
12% per month. Within-herd morbidity was generally greater during spring and summer
months. Most lesions occur on the plantar interdigital cleft of the rear foot and less
common sites for lesions are the palmar interdigital ridge of a front foot or a dorsal aspect
of any foot (Mortellaro, 1994; Read and Walker, 1998). Another study conducted by the
National Animal Health Monitoring System involving 83% of US dairy cows in 20 states
observed the incidence of digital dermatitis and risk factors (Wells et al., 1999). This
study reported, that within the last 12 months of the study, 43.5% of the US dairy herds
had cows that showed clinical signs of DD with variation by herd size and region (Table
The study by Wells (1999) reported that the average percent of cows affected was
18.9%. A high percentage of digital dermatitis-affected cattle were also reported lame
(81.9% of affected cows and 85.9% of bred heifers). This study also looked at risk factors
associated with digital dermatitis. Interesting results from this study identified several
factors that contribute to herd incidences > 5%. The percent of cows not born on the dairy
operation was strongly associated with high digital-dermatitis incidence, and there was
evidence for a dose-response relationship.
Table 2-3. Incidence of Digital Dermatitis in US dairy herds by herd size and region
.aibe ee Herds with digital dermatitis in the
previous 12 months (%)
Herd Size < 100 cows 36.4
100 to 199 cows 61.9
>200 or more cows 80.3
Region Northwest 56.1
North Midwest 35.4
South Midwest 45.5
Wells et al., 1999
Rodriguez-Lainz (1996) showed a strong association between introduction of
heifers and digital-dermatitis prevalence in southern California dairy herds. These results
were in agreement with results from Argaez Rodriguez (1997) who reported that
purchased animals were 3.4 times more likely to be affected than animals born on the
farm. Farm factors such as type of concrete flooring with concrete abrasive floors or
slippery floors were associated with > 5% incidence of DD. Rodriguez-Lainz (1996)
reported an association between the incidence of digital-dermatitis and corral moisture in
southern California dairy operations with dirt dry lot corrals. Some biosecurity factors
identified were hoof trimmers that trim cows on other farms. Herds in which the primary
hoof trimmer also trimmed cows hooves on other operations were 2.8 times more likely
to have > 5% incidence of digital dermatitis compared to herds where the primary hoof
trimmer did not trim hooves on other operations or where cows hooves were not
trimmed. Also, herds in which hoof-trimming equipment was not washed between cows
were 1.9 times more likely to have > 5% incidence of digital dermatitis than those where
the equipment was washed or where no hooves were trimmed (Wells et al., 1999).
Blowey (1988) reported different treatments when describing one of the first
outbreaks of the disease in the UK. Treatment of DD started by the application of
parenteral injections of penicillin, streptomycin, tetracyclines, cephalexin, and
sulphonamides, but none of these treatments proved effective and most cases recovered
on their own. The most effective treatment in this report appeared to be deep scraping of
the lesion with a hoof knife, followed by topical oxytetracycline/genti an violet aerosol
spray. This treatment led to a reduction of lameness in 6 to 12 hours and complete
resolution in 2 days. In this study, footbaths with 5% formalin or 2.5% copper sulfate
were used to try to control the outbreak with poor results. Sheldon (1994) further
supported treatment with oxytetracycline spray (4 g/L), although this was not a controlled
study. Further research conducted by Britt (1996) confirmed the efficacy of
Oxytetracycline (100 mg/mL) as a treatment for digital dermatitis applied as a spray.
Manske et al., (2002c) reported that Oxytetracycline applied as a bandage was
significantly more effective than hoof trimming alone of the affected foot (P < 0.001).
This study was done to try to Eind an alternative treatment to antibiotics and
Glutaraldehyde bandage was tested as the alternative non- antibiotic treatment. Results of
this study did not support the use of this product. Treatment of DD with topical
oxytetracycline does not require any milk withdrawal as shown by Britt (1999) who was
unable to demonstrate antibiotic residues in milk using standard routines after cows were
treated topically with this antibiotic. The most common treatments for digital dermatitis
involve the use of topical antibiotics (Blowey, 1988; Blowey, 1994; Guard, 1995; Berry
et al., 1996; Britt et al., 1996; Britt et al., 1998; Read et al., 1998; Berry et al., 1999a;
Berry et al., 1999b, Hernandez et al., 1999; Shearer et al., 2000; Manske et al., 2002c).
Some of the antibiotics used in these studies were Oxytetracycline, Tetracycline,
Li ncomy cin/S p ecti nomy ci n, and Erythromy ci n.
There also are reports of non-antibiotic products being effective in the treatment
of DD (Shearer and Hernandez, 2000; Hernandez et al., 1999). Hernandez (1999) used a
topical spray with four different non-antibiotic products in the lame cow with DD.
Treatment with an Oxytetracycline solution, or a soluble copper, peroxide compound and
a cationic agent appeared to be effective for the treatment of DD, compared to a 5%
copper sulfate (CuSO4) Solution, or acidified copper solution, or hydrogen
peroxide-peroxyacetic acid (HPPA) solution. In another study (Shearer et al., 2000)
non-antibiotic compounds were used to treat DD in 78 cows affected with lameness. In
this study (Shearer et al., 2000), a previously tested product (Hernandez et al., 1999) was
modified to improve its handling and storage characteristics. There were four treatment
groups in this study: cows in group A were treated with oxytetracycline solution, cows in
group B were treated with the original formulation also containing soluble copper,
peroxide compound and a cationic agent, cows in group C were treated with a modified
formulation with reduced soluble copper, peroxide compound but increased levels of
cationic agent and cows in group D were treated with a modified formulation containing
levels of soluble copper and cationic agent similar to the original formulation but reduced
concentrations of peroxide compounds. Results of this study (Shearer et al., 2000)
indicated that the modified non-antibiotic formulation used on cows in group C appeared
to be the most effective treatment of papillomatous digital dermatitis compared to the
other formulations as the proportion of cows with signs of pain was significantly lower in
this group of cows (group C). Also this study reported an unexpected low efficacy of the
oxytetracycline treatment suggesting the possible development of resistance in dairy
cows affected with DD. This study supports the use of non-antibiotic products as an
efficacious tool for the treatment of DD, thus minimizing the potential risk for residues in
milk and meat.
Control measures of biosecurity, as stated in a previous study (Wells et al., 1999),
includes examination of animals entering the herd, cleaning hoof trimming equipment
between cows, and to have a farm-set of trimming tools available for the hoof trimmer to
avoid contamination incoming from other farms. Footbaths can be used as a part of
control measures of DD on infected herds (formalin 5%; copper sulfate 2.5%;
oxytetracycline 1 to 4 g/L; zinc sulfate 20%) (Blowey et al., 1988; Brizzi, 1993;
Mortellaro, 1994; Guard, 1995). If no preventive herd measures are taken, a relapse may
be expected within 5 to 7 weeks after a successful single topical treatment of DD (Berry
et al., 1999a) (Guard and Williams, 1995). Although the efficacy of footbaths remains
controversial, individual treatment of affected cows combined with the use of footbaths
for the herd represent the most effective method of prevention (Mortellaro, 1994).
Metabolic Hoof Horn Disease: Claw Horn Disruption
Hoof horn of low quality is a frequent cause of lameness in cattle. Studies in the
UJK reported that claw disorders accounted for 70 to 90% of diagnosed cases of lameness
in dairy cattle (Whitaker et al., 1983; Clarkson et al., 1996; Murray et al., 1996). These
researchers identified subclinical laminitis related disorders, such as sole ulcers and white
line disease, as the most important conditions affecting dairy cattle in the UK. Laminitis
was regarded by some authors (Bradley et al., 1989; Greenough and Vermunt, 1991) as
an important predisposing factor in lameness caused by claw disorders such as sole
ulcers, white line disease, and abscesses in the subsole. Subclinical laminitis has been
identified as the underlying cause of abnormalities of hoof horn formation which results
in claw disorders (Hoblet et al., 2001). To better understand the pathophysiology of
lameness, it is important to review the anatomy of the bovine foot.
Laminitis, or pododermatitis a~septica diffuse, is an aseptic inflammation of the
dermal layers of the claw (Nielsson, 1963) characterized by defective claw horn
production with thrombosis and hemorrhages in the digital corium (Mortensen, 1994). It
was originally described as consisting of three clinical forms (acute, subacute, chronic),
but Peterse (1979) later described a fourth form of laminitis, "subclinical laminitis".
Because the disease process finally affects horn formation at the cellular level, regardless
of whether an initial primary inflammatory response had occurred, the term claw horn
disruption has been proposed (Logue et al., 1998). Although many different terms have
been proposed for this disorder, I will refer to it as laminitis for the purpose of this
Laminitis has a multifactorial etiology and is thought to be associated with
several, largely interdependent factors such as genetic predisposition, claw size, body
weight, architecture of limb angles, claw hardness, pigmentation of the claw and the
quality of the surface over which the animal walks (Mortensen, 1994; Nordlund and
Garret, 1994). Nutritional management has been identified as a key component in the
development of laminitis, particularly the feeding of increased fermentable carbohydrates
which result in an acidotic state. There seems to be no doubt that the disease is related to
high energy intake, frequency and quantity of consumption. Factors such as body
condition, body weight, and feet and leg structure, can unnaturally increase the weight
load and stress on feet and exacerbate the internal mechanical damage that is associated
with laminitis (Nocek, 1997).
Nocek (1997) has described the mechanisms causing development of laminitis in
detail on a recent review of the topic. The mechanistic phases of laminitic development
were described as alternating stages of disturbances relating to metabolic and subsequent
mechanical degradation of the internal foot structure (Mortensen, 1994; Nordlund and
Garret, 1994). The process can be segmented into various phases (Nocek, 1997).
Phase 1. The initial activation phase of laminitis, phase 1, is associated with a
systemic metabolic insult. This phase is a result of ruminal acidosis, and subsequently an
altered systemic pH. The reduction in systemic pH activates a vasoactive mechanism that
increases digital pulse and total blood flow. Depending upon the insult that initiates the
process, endotoxins, histamine and lactate can be released, which create increased
vascular constriction and dilation and, in turn, cause the development of several
unphysiological arteriovenous (AV) shunts, further increasing blood pressure. The
increased blood pressure causes seepage of serum through vessel walls, which ultimately
are damaged. Damaged vessels then exude serum, which results in edema, internal
hemorrhaging of the solar corium from thrombosis, and ultimately expansion of the
corium, causing severe pain.
Phase 2. As a result of the initial insult, there is mechanical damage, phase 2,
which is associated with the vascular system. Once vascular edema has occurred,
ischemia results in hypoxemia of the local internal digital tissue causing tissue hypoxia
which results in fewer nutrients and less oxygen reaching the epidermal cells. Ischemia
itself can trigger a further increase in AV shunting. Trauma and stress can increase AV
shunting. As a result of previous events, increased blood pressure further increases
vascular seepage in the lower part of the digit as well as edema and ischemia. This cycle
continues as long as the initial insult continues.
Phase 3. In phase 3, as a result of the mechanical damage associated with
microvasculature and fewer nutrients provided to the epidermal cells, the stratum
germinativum in the epidermis breaks down. These events ultimately cause corium
degeneration and breakdown of the laminar region associated with the dermal-epidermal
Phase 4. Ultimately, in phase 4, local mechanical damage occurs. A situation
develops in which the epidermal junction is broken down which results in the separation
of the strata germinativum and corium. This separation results in a breakdown between
the dorsal and lateral laminar supports of the hoof tissue. Ultimately, the laminar layer
separates, and P3 takes on a different configuration in relationship to its position in the
corium and dorsal wall. As the bone shifts in position it causes a compression of the soft
tissue between the bone and sole which is extremely susceptible to damage. The
compression of this soft tissue results in hemorrhage, thrombosis, and further
enhancement of edema and ischemia which result in a necrotic area within the solar
region of the foot. Small areas of scar tissue accumulate because of the necrotic process.
Once this process is triggered, continued potential for tissue degeneration persists
because cellular debris is incorporated into the cellular matrix and the production and
integrity of new horn tissue layers are hindered. Ultimately, a variety of processes can
occur as a result of the incorporation of scar tissue intervention, which includes double
sole phenomenon, sole hemorrhages (red blood patches), bruises, white line lesions, and
sole ulcers (Vermunt, 1994).
Forms of laminitis
Acute and subacute laminitis. In the acute and subacute stage of the disease, an
aseptic inflammation of the corium coincides with a systemically sick animal. At this
stage, the claw horn shows few, if any, visible changes. Vessel seepege, edema of
capillary beds, and AV shunting are all initiated. Vascular congestion is present. The
maj or clinical sign in addition to pain includes swelling and temperatures that are slightly
warmer than normal above the coronary band in the soft tissue (Nocek, 1997). These
forms of laminitis are prone to recurrence at varying intervals and often progress to the
chronic form (Vermunt, 1994).
Chronic laminitis. Chronic laminitis has no systemic symptoms and changes are
localized to the claw. A disturbed horn growth pattern and an alteration in the shape of
the claw with an elongated flattened and broadened sole are characteristic (Vermunt,
1994; Greenough, 1997). Internally P3 has separated from the dorsal aspect of the wall.
Continued ischemia results in destruction of the capillary beds and development of AV
shunts. Cellular destruction results in separation of the dermal-epidermal junction, and
internal foot destruction (Nocek, 1997). Grooves and ridges caused by irregular episodes
of horn growth can be seen in the claw wall. This deformation of the claw shape often
predisposes to sole ulcers, white line disease or subsolar abscesses (Greenough and
Vermunt, 1991; Mortensen, 1994).
Subclinical laminitis. Subclinical laminitis was first described in 1979 by Peterse
and later by others (Bradley et al., 1989; Greenough and Vermunt, 1991). Lameness is
usually not observed with this form of laminitis, but changes in the hooves can lead to
chronic laminitis. The horn becomes softer, discolored, and waxy in appearance. It often
stains yellow and hemorrhages can be seen in the weight-bearing surface of the claw, in
particular the white zone, apex of the sole and the axial side of the sole-bulb junction
(Bradley et al., 1989; Greenough and Vermunt, 1991). Internally, ischemia, hypoxia and
epidermal damage are key aspects associated with this stage (Nocek, 1997). The concept
of subclinical lameness is now universally accepted (Mortensen, 1994).
Claw Lesions Associated with Laminitis
Hemorrhages of the sole and sole ulcer
Hemorrhages in the sole are the maj or and characteristic indication of past
laminitic insults. The hemorrhages can take the form of a slight pink tinge, a pronounced
brush stroke of red coloration, or a dark solid red stain. Hemorrhages of the sole are
considered part of the same pathologic process as sole ulcers and are represented by a
continuum that ranges, from barely perceptible hemorrhages to severe ulceration of the
sole with exposed corium (Leach et al., 1997). Sole hemorrhages have a particularly high
incidence in first lactation heifers managed in confinement in the interval from 60 to 100
days after calving (Greenough and Vermunt, 1991; Smilie et al., 1996). The most
common spot for sole hemorrhages and sole ulcers is the so-called typical spot of the
lateral claw of the hind limb under the flexor tuberosity (axial prominence) of P3 (Smilie
et al., 1996).
Softening of the horn of the sole
Although obj ective evidence is not available, it has been proposed that sole horn
produced after an episode of laminitis is softer than normal (Mortensen, 1994).
White line disease
There are a number of names for the lesions in the White Line (WL): WL disease,
WL abscess, WL separation, WL fissure, WL lesions, widening of the WL, WL
hemorrhages (Bergsten, 2000; Blowey, 1993; Kempson and Logue, 1993; Leach, 1997).
These names describe clinical signs or morphological changes in the WL. Different
names are descriptions of different stages of development and degree of diseases whose
pathogenesis has a common origin (Miilling, 2002). This condition is also considered to
be associated with laminitis (Mortensen, 1994).
Heel erosion has been described as one of the infectious diseases affecting the
bovine foot in this manuscript, but there are some authors that also relate this disease with
laminitis (Mortensen, 1994).
Diagnosis of Lameness
Several locomotion scoring systems have been developed to standardize gait
analysis in cattle. Manson and Leaver (1988) devised a system of locomotion scoring
which is a subj ective assessment based on observation of cows walking away from the
observer on a level concrete surface (Table 2-4). Using this scoring system, cows
classified with a score of 3 or higher were counted as lame for calculation of prevalence
of lameness. Two problems with this system were its subj activity and complexity (Ward,
1998). Collick (1989) used this system and factored percentage reduction of weight
bearing for the affected foot, foot structure affected and duration of lameness, which
made this system more complicated.
Table 2-4. Locomotion scoring developed by Manson and Leaver (1988)
1.0 Minimal abduction/adduction, no unevenness of gait, no tenderness
1.5 Slight abduction/adduction, no unevenness or tenderness
2.0 Abduction/adduction present, uneven gait, perhaps tender
2.5 Abduction/adduction present, uneven gait, tenderness of feet
3.0 Slight lameness, not affecting behavior
3.5 Obvious lameness, some difficulty in turning, not affecting behavior
4.0 Obvious lameness, difficulty in turning, behavior pattern affected
4.5 Some difficulty in rising, difficulty in walking, behavior affected
5.0 Extreme difficulty rising, difficulty walking, adverse effect on behavior
Wells (1993) described a similar but different locomotion scoring system (Table
2-5) arguing that simplicity was necessary when using this type of scoring. This system
was used to estimate the prevalence of lameness in 17 dairies in Wisconsin and
Minnesota and cows with a score of 2 or higher were classified as lame
Table 2-5. Locomotion scoring used described by Wells (1993)
Score Gait abnormality Description
0 None Gait abnormality not visible at walk; not reluctant to walk.
1 Mild Mild variation from normal gait at walk; includes
intermittent mild gait asymmetry or mild bilateral or
quadrilateral restriction in free movement.
2 Moderate Moderate and consistent gait asymmetry or symmetric gait
abnormality, but able to walk
3 Sever Marked gait asymmetry or severe symmetric abnormality
4 Nonambulatory Recumbent
This system was used to estimate the prevalence of lameness in 17 dairies in
Wisconsin and Minnesota and cows with a score of 2 or higher were classified as lame.
In 1997, Boelling (1998) used the locomotion system developed by Manson and Leaver
(1988) and described it using a 9 point-scale, from 1 (perfect walk) to 9 (near inability to
walk). A score of 1 to 4 was considered sound locomotion, while a score of 5 or higher
was regarded as clinical lameness. They used this to estimate the heritability of
locomotion, which they found to be 0.06 to 0. 11. Sprecher (1997) based on an
observation of Morrow in 1966, where an arched-back posture was associated with acute
and chronic laminitis, developed a simple locomotion scoring system. He developed this
method of classification of lameness to try to predict future reproductive performance and
culling risk of cows classified within different scores. This locomotion scoring system
was based on gait and back posture (Table 2-6).
If used consistently, all these scoring systems are useful to screen cows and
identify early lesions associated with lameness. Early intervention prevents the more
serious stages of a claw disorder (Toussaint Raven, 1989).
Table 2-6. Locomotion scoring system developed by Sprecher et al., 1997
1 Normal The cow stands and walks with a level-back posture. Her
gait is normal
2 Mildly lame The cow stands with a level-back posture but develops an
arched-back posture while walking
3 Moderately An arched-back posture is evident both while standing and
lame walking. Her gait is affected and is best described as short-
striding with one or more limbs
4 Lame An arched-back posture is always evident and gait is best
described as one deliberate step at a time. The cow favors
one or more limbs/feet
5 Severely The cow additionally demonstrates an inability or extreme
lame reluctance to bear weight on one or more of her limbs/feet
If used consistently, all these scoring systems are useful to screen cows and identify
early lesions associated with lameness. Early intervention prevents the more serious
stages of a claw disorder (Toussaint Raven, 1989).
On the basis of differences in anatomic location and morphologic characteristics,
it is possible to make a clinical diagnosis of interdigital phlegmon, digital dermatitis, or
claw lesions in cows affected with lameness. Lame cows with interdigital phlegmon will
be cows characterized by Hissuring, caseous necrosis of the subcutis in the interdigital
space, and swelling of the entire foot above the dewclaws and separation of the digits.
Pain and moderate to severe lameness are often seen with this disease. A characteristic
fetid odor is usually present (Berry, 2001). Lame cows with digital dermatitis will have
demarcated lesions, circumscribed, spherical to oval, 0.5cm to 6cm across, partially or
completely alopecic, moist, painful-to-touch, prone-to-bleed plaques of flat or raised
proliferative tissue on the interdigital cleft, heels, or dewclaw (Read and Walker, 1994).
Lame cows with claw lesions will be cows that have white line lesions, abscess, or sole
ulcers and will be treated by use of corrective foot trimming techniques (Shearer and van
Lameness and Animal Welfare
Because of the pain, discomfort, and high incidence of lameness in dairy cows,
lameness is an animal welfare issue. Disturbed claw health is an unequivocal source of
suffering for cows, because the disorder is usually long term and painful (Alban, 1995).
Some countries are already setting acceptable levels of clinical lameness. As an example,
the Dutch Advisory Board for Animal Affairs (RDA) has considered the actual levels of
clinical and subclinical claw disorders (30% cow cases per year) in The Netherlands as
unacceptable from an animal welfare point of view (Somers et al., 2003). In other
countries as well, the prevalence of lameness has also stated as not acceptable and have
give rise to a growing concern about animal welfare.
Welfare can be defined as the state of animals regarding their attempts to cope
with their environment (Broom, 1988). A lame cow is less able to cope with her
environment, as pain might seriously affect walking and other movements (Hassall et al.,
1993). The secondary effects of a reduced ability to walk may impact important
physiological activities such as reduction in the time feeding (Hassall et al., 1993;
Galindo et al., 2002), also affecting their behavior as suggested by Peeler and Esslemont
(1994), were lame cows experienced similar inhibitions as cows on poor footing and
would less likely be observed in estrus. These welfare factors are important to consider
when evaluating the effects of lameness disease on production.
In most US dairies, incidence of lameness is underestimated because only cows
affected with severe signs of lameness are detected and treated; cows with mild or
moderate signs of lameness are often not diagnosed. In a study by Wells (1993) the
prevalence of lameness diagnosed by farmers in 17 dairies was compared to that by
researchers in the same farms. The prevalence of lameness reported by researchers was
three times higher than that by farmers. The underestimation of prevalence of lameness
keeps farmers and the industry unaware of the importance of this disease.
Lameness and Milk Production
Several studies have been carried out around the world to test the effect of
lameness on milk production. Results of these studies are conflicting. Some authors
reported a decrease in milk yield after diagnosis of lameness (Whitaker et al., 1983;
Tranter and Morris, 1991; Rajala-Schultz et al., 1999; Warnick et al., 2001), a decrease in
milk yield before and after treatment (Lucey et al., 1986; Green et al., 2002) or no change
in milk yield (Cobo-Abreu et al., 1979). Another study (Barkema et al., 1994) reported an
increase in milk yield from 100 to 270 DIM during the same lactation in lame cows with
sole ulcers. Green (2002) reported an increase in 100-day cumulative milk volume in the
previous lactation for cows with any cause of lameness. Culling bias may in part account
for these results because cows with both lameness and low production would be expected
to be culled more often than cows with lameness and high production. Argaez-Rodriguez
(1997) did a retrospective study a in Mexico to examine the effects of digital dermatitis in
milk production. The authors (Argaez-Rodriguez et al., 1997) reported a statistically non-
significant difference between milk production of lame cows due to DD and healthy
cows, with cows experiencing DD producing less milk. In this study lame cows due to
DD were compared with healthy cows and lame cows for other reasons were included as
healthy which can mask the effects of DD on milk production.
Three studies have examined the relationship between lameness and milk yield in
US dairy herds. In a study conducted on a 500-cow dairy in California (Deluyker et al.,
1991), cows diagnosed as lame during the first 49 days postpartum coincided with higher
milk yield. The positive association of lameness and high milk yield during early
lactation found in this study suggested that high yield was a risk factor for lameness.
Although diseases or foot lesions associated with lameness were not investigated, white
line and sole lesions were the most common lesions in this study. In another study
conducted on two dairy herds in New York (Warnick et al., 2001), lame cows with claw
lesions or interdigital phlegmon produced less milk than healthy cows. Lameness was
more common in early lactation and more likely to occur in older cows. Finally, in a
study conducted in Florida, lame cows with interdigital phlegmon produced 10% less
milk, compared to non-lame cows (Hernandez et al., 2002). The authors (Hernandez et
al., 2002) estimated that such a decrease in milk yield of 1,885 lb/cow represented a loss
of $301/cow (assuming a milk value of $16.00/100 lb). In that study, most lame cows
with interdigital phlegmon were affected during early lactation (within 100 days
postpartum), when cows reach peak yields and 60% were culled during lactation. These
findings may suggest that lame cows affected with interdigital phlegmon during early
lactation may be sufficiently compromised to adversely affect a cow's ability to achieve
its own milk yield potential during the current lactation (Hernandez et al., 2002).
Lameness and Reproductive Performance
A relationship between lameness and reproductive performance has been
established in several studies in the United States and in other parts of the world. In 1985,
Weaver postulated lameness as a possible cause of reduced fertility because animals
spend more time lying down, are less willing to demonstrate standing heat, and are less
able to compete for available feed. Some of these suggestions were later confirmed by
different studies. Varner (1994) looking at pedometer readings, reported that cows in
estrus move and interact with other cows significantly more than the rest of the herd.
Britt (1986) found that excellent footing greatly increases the duration of estrus
activity in dairy cows. Peeler and Esslemont (1994) reported that lame cows experience
similar inhibitions as cows on poor footing and would less likely be observed in estrus.
These Eindings may in part explain results of studies indicating that lameness has a
detrimental effect on reproductive performance. In a study conducted on Hyve dairy farms
in the UK, Lucey (1986) found that lame cows affected with sole ulcer and white line
disease between 36 and 70 days after calving were associated with longer calving to
conception intervals (17 and 30 days, respectively). Collick (1989) did a larger study on
17 dairy farms in the UK involving 427 cases of lameness. The authors reported that
lameness happening before 120 days after calving was associated with significantly
increased intervals from calving to conception. The largest increase in the intervals from
calving to conception were associated with sole ulceration (40 days, P < 0.01). In a
retrospective study of digital dermatitis in a commercial dairy in Mexico Argaez-
Rodriguez (1997) reported that healthy cows conceived 93 days after calving (median),
compared to affected cows with digital dermatitis which conceived 113 days after calving
(P < 0.0 1).
Three previous studies have examined the relationship between lameness and
reproductive performance in US dairy herds. In one study conducted in five dairy herds
in Pennsylvania, cows affected with lameness had a 28-day-longer calving to conception
interval, compared to healthy cows (Lee et al., 1989). In another study, a scoring system
was developed to identify lameness and predict future reproductive performance in dairy
cows, lame cows were 15.6 times more likely to require an interval greater than the mean
for days open compared to healthy cows (Sprecher et al., 1997). In a study conducted on
a 500-cow dairy in Florida (Hernandez et al., 2001), claw lesions were the most
important cause of lameness and impaired reproductive performance in dairy cows, as
indicated by a higher incidence of affected cows, a greater time from calving to
conception (median, 140 days), and a higher number of services required per conception
(median, 5), compared to non-lame cows (100 days and 3 services, respectively). In this
study herd, cows were synchronized and time-inseminated; thus the authors were not able
to assess the calving to first breeding interval nor to draw any conclusion that lameness
has an effect on estrus behavior. Conversely, the significantly higher number of services
required per conception and the longer time from calving to conception in lame cows
with claw lesions, compared to healthy cows, may suggest that lameness has an effect on
Melendez (2003) examined the association between lameness, ovarian cysts, and
fertility on a 3000-cow dairy in Florida. Results of this study showed that cows that
became lame within the first 30 days postpartum were associated with higher incidence
of ovarian cysts, a lower likelihood of pregnancy, and a lower fertility than non-lame
cows. Although all these studies found a significant association between lameness and
reproductive performance, the relationship between lameness and ovarian activity was
Resumption of Ovarian Activity Postpartum
Early resumption of ovarian cyclicity postpartum is important for high
reproductive efficiency in dairy cows. Delays in the commencement of ovarian cyclicity
and estrous expression are associated with reduced conception rates, pregnancy rates and
an increased interval from calving to conception (Thatcher and Wilcox, 1973; Stevenson
and Call, 1983; Lucy et al., 1992; Senatore et al., 1996). The study done by Thatcher and
Wilcox, (1973) reported that cows exhibiting 0 or 1 heat postpartum required
significantly more services per conception than cows exhibiting 2 to 4 heats. These
authors reported that non-return rates improved as frequency of postpartum heats
increased (0 and 1 heat, 37%; 2 to 4 heats 44%; P < 0.05). In a study conducted to
identify the influence of early estrus, ovulation and insemination on fertility in
postpartum dairy cows, Stevenson and Call (1983) reported that the interval to first
detected heat had a significant influence on first service intervals and days open. When
estrus was not expressed before 60 days postpartum, average days to first service were 18
days longer and days open were 19 days longer than in cows that expressed heat before
60 days postpartum (P < 0.05). These authors concluded that more expressed heats early
postpartum were associated with positive effects on fertility.
A study conducted by Lucy (1992) who monitored the interval to first ovulation to
clarify the importance of milk production, dry-matter intake and energy balance in the
interval to first ovulation, reported that cows having first ovulation before 42 days tended
to have a shorter interval from calving to detected estrus, required fewer services per
conception and had a shorter interval from calving to conception compared with cows
having first ovulation after 42 days postpartum. More recently, Darwash (1997) reported
that the interval to postpartum commencement of luteal activity was correlated favorably
with measures of fertility such that for every day delay in the interval to commencement
of ovarian activity, there was an average delay of 0.24 and 0.41 (P < 0.001) days in the
interval to first service and conception respectively. These studies pointed out the
importance of early resumption of ovarian cyclicity postpartum as a factor contributing to
high reproductive efficiency on dairy cows.
Following calving, the reproductive strategy of the cow is transformed from
delivering and nourishing a healthy calf to reestablishing pregnancy. The dormancy of
ovarian follicular development that prevailed during late pregnancy must now be
replaced by a sequence of events culminating with behavioral estrus, ovulation of healthy
follicles and normal luteal function. These are the requirements for successful
reproductive performance in any type of cattle production system (Rhodes et al., 2003).
After regression of the corpus luteum of pregnancy, there is a variable
anovulatory period before first ovulation takes place (Savio et al., 1990a). This period is
characterized by an absence of estrus behaviour and lack of progesterone secretion by the
ovary and a return to basal concentrations of estradiol during the first week postpartum
(Echternkamp and Hansel, 1973; Stevenson and Britt, 1979; Webb et al., 1980;
Humphrey et al., 1983; Peters, 1984; Savio et al., 1990a; Rhodes et al., 2002). Following
parturition, a wave of follicular development occurs in 5 to 7 days regardless of negative
energy balance and in response to an elevation in plasma FSH concentrations (Beam and
Butler, 1997). As reported by Savio (1990a), ovarian follicular turnover starts early after
calving and is similar to that observed during normal estrous cycles. In this study Savio
(1990a) reported that the postpartum interval to the detection of the first dominant follicle
was 11.6 & 8.9 days and the interval to first ovulation was 27.4 & 23 days. Beam and
Butler (1997) reported that the emergence of the first follicular wave postpartum occurred
after a peak in mean peripheral FSH levels and rather synchronously with the clearance
of gestational estradiol from blood. Subsequent, mean levels of FSH increased in the first
5 days postpartum and decreased from 5 to 11 days. This is in accordance with previous
work (Butler et al., 1983; Price and Webb, 1988) that indicated that removal of estradiol
negative feedback inhibition of FSH release would account for the increase in mean
plasma FSH observed between days 2 and 9 postpartum. After returning to basal levels,
estradiol concentrations fluctuate or remain low until 2 to 3 days before estrus when they
peak (Echtemnkamp and Hansel, 1973; Stevenson and Britt, 1979). Estradiol levels
declined from the 1st day postpartum until day 7, when estradiol levels slowly increase
with the concurrent development of a dominant ovarian follicle (Beam and Butler, 1997).
Plasma estradiol concentration is related with the degree of the peak of LH release in
response to GnRH as reported by Zolman (1974); Kesler (1977); and Fernandes (1978).
These studies agreed with that of Moss (1985) who reported that pituitary responsiveness
to GnRH is not restored until approximately 8 to 10 days post-partum. As described by
Savio (1990a), follicular growth is accompanied by episodic LH secretion of variable
amplitude and frequency. The use of ultrasound techniques allowed Savio (1990a) to
relate the stage of follicular development and the pulsatile secretion of LH. Within a
6-hour period, 2 to3 LH pulses occurred when concentrations of estradiol were low (< 5
pg/mL), and the frequency of LH pulses increased to 6 when estradiol concentrations
increased (> 10 pg/mL) coinciding with a dominant follicle. Stevenson and Britt (1979)
reported that the interval from calving to first postpartum ovulation was associated
inversely with the number of episodic LH surges and magnitude of the largest LH surge.
This high frequency mode of pulsatile LH secretion has been identified as necessary for
the final phase of maturation of ovarian follicles and thus induction of estrus and
ovulation (Webb et al., 1980; Humphrey et al., 1983; Randel, 1990). Canfield and Butler
(1990a) reported a high correlation between the interval from parturition to the highest
LH pulse frequencies and first ovulation, emphasizes the importance of achieving this
pattern of secretion for the stimulation of first ovulation, support this.
These series of events can lead to three different outcomes of follicular
development as described by Beam and Butler (1997):
a. Ovulation of the first dominant follicle;
b. Non-ovulation of the first dominant follicle followed by turnover and a new
c. The dominant follicle fails to ovulate and becomes cystic.
The development of non-ovulatory dominant or cystic follicles prolongs the
interval from calving to first ovulation. In dairy cattle, the interval from calving to first
ovulation has been reported to be between 17 and 34 days (Table 2-7) The variation
observed between some of these studies may be due to differences in study populations
such as animal breeds, production systems, level of production, feeding systems, or it
might be as concluded by Opsomer (2000) that the first postpartum ovulation in modern
high-yielding dairy cows tends to occur later than it did a decade ago. Results of these
studies are difficult to compare since mean days to first ovulation were calculated only
for normal cows in some of these studies, which excluded cows that had follicular cysts
or those who did not ovulate early postpartum; while in other studies, all cows were in
Table 2-7. Days from calving to 1st ovulation reported in the literature
Author, year Days to 1st postpartum ovulation (d)
Schams (1978) 17
Stevenson (1979) 18
Webb (1980) 17
Butler (1981) 36
Stevenson (1983) 19
Fonseca (1983) 20
Meisterling (1987) 33 Short luteal phase 25 Normal luteal phase
Butler (1989) 30
Canfield (1990) 19
Harrison (1990) 29
Staples (1990) 22
Savio (1990) 22
Spicer (1990) 24
Canfield (1990) 29
Etherington (1991) 24
Nakao (1992) 30
Zurek (1995) 24
Darwash (1997) 22
Opsomer (2000) 32
Reist (2000) 34
If ovulation occurs then plasma progesterone concentrations increase to greater
than Ing/mL within 2 to 3 days after ovulation (Schams et al., 1978; Stevenson and Britt,
1979). An elevation of plasma Progesterone concentration above 1 ng/mL has been used
as an indication of resumption of postpartum ovarian cyclicity in several studies (Butler
et al., 1981; Harrison et al., 1990; Staples et al., 1990; Canfield et al., 1991; Zurek et al.,
1995; Beam and Butler, 1997; Beam et al., 1998)
The duration of the first postpartum estrous cycle can be variable, being shorter
than normal or normal, and it can occur with or without estrus behavior. Stevenson and
Britt (1979) reported 32% of first estrous cycles were shorter (16 d vs. 20 d) than
subsequent estrous cycles. These observations have been supported by different studies
(Schams et al., 1978; Webb et al., 1980; Stevenson and Call, 1983; Fonseca et al., 1983;
Savio et al., 1990b; Staples et al., 1990; Senatore et al., 1996).
Among dairy cows, those that have not ovulated by 60 days post partum have been
defined as having a delayed resumption of ovarian cyclicity (Humboldt and Thibier,
1980; Stevenson and Call, 1983; Staples et al., 1990; Moreira et al., 2001). Incidence
rates of delayed cyclicity reported in the literature are summarized in Table 2-8.
Table 2-8. Incidence rates of delayed cyclicity reported in the literature
Incidence of delayed
Author, year Delayed cyclicity Milk/Plasma yit )
Humboldt (1980) P4 > 1.5 ng/mL 60d Plasma 29
Bartlett (1987) Palpation 70d 23
Miesterling (1987) P4 > 4 ng/mL 65d Milk 21
Presence of CL and P4 >
Archbald (1990) stPlasma 30
Ing/mL 1~ month PP
Nakao (1990) P4 < 1 ng/mL 50d Milk 25
Staples (1990) P4 < 1 ng/mL 63d Plasma 28
Etherington (1991) P4 > 2ng/mL 50d Milk 33
Lamming (1998) P4 > 3 ng/mL 45d Milk 11
Opsomer (2000) P4 < 15 ng/mL 50d Milk 21
Moreira (2001) P4 < 1 ng/mL 63d Plasma 23
Several factors can affect the interval between calving and first postpartum
ovulation, the incidence rate of delayed cyclicity, and the reproductive performance of
affected cows. Some of theses factors cited in the literature are energy balance, season,
parity, and periparturient diseases (Butler et al., 1981; Fonseca et al., 1983; Canfield et
al., 1990b; Lucy et al., 1992; Senatore et al., 1996; Beam and Butler, 1997; Darwash at
al., 1997; Jonsson et al., 1997; Opsomer et al., 2000; Moreira et al., 2001).
Several studies have found associations relating energy balance to ovarian activity
postpartum, and some of these studies have proposed a casual path to this association.
However, the effects of energy balance affecting postpartum ovarian activity are not
completely elucidated. Milk production and dry matter intake increase after calving but at
different rates with the maximum feed intake occurring some weeks after maximum milk
production. The result of this delay is negative energy balance that persists for 4 to 12
weeks of lactation (Butler at al., 1981), when most dairy cows must mobilize body
reserves to support milk production (Bauman and Currie, 1980). Negative energy balance
is usually maximal during the first 3 weeks of lactation (Canfield et al., 1990b). Butler
(1981) reported that first ovulation occurred 10 days after the negative energy balance
nadir was reached, and energy balance was still negative at ovulation, but was returning
towards zero. The authors (Canfield et al., 1990b) concluded that there was an inverse
relationship between the interval from parturition to first normal ovulation and the
average energy balance during the first 20 days postpartum. These results were further
supported by other studies (Staples et al., 1990; Canfield and Butler, 1990a; Lucy et al.,
1992; Senatore et al., 1996).
The greater the average energy deficit incurred, the longer the delay to ovulation.
Canfield and Butler (1990b) showed a high correlation between days to negative energy
balance nadir and days to first ovulation. This relationship suggested that first ovulation
does not occur in an individual animal until energy balance progresses beyond its most
negative value and is returning toward balance. In this study, 1st ovulation also occurred
10 and 13 days following negative energy balance nadir in non-lactating and lactating
cows respectively. It was proposed from this study that energy status could be acting to
slow an increasing LH pulse frequency until the cow has begun to return to a positive
energy balance. Cows that reached the energy balance nadir earlier postpartum (4 d vs. 14
d) ovulated earlier (14 d vs. 27 d) and had higher concentrations of insulin. These results,
together with the finding that the pulse frequency of LH was not different for both
groups, made the authors propose that insulin levels may act permissively on the ovary to
enhance follicular responsiveness. These same authors (Canfield and Butler, 1990a)
examined the effect of energy balance and changes in plasma concentrations of glucose,
insulin, non-esterified fatty acids (NEFA), and ketones on pulsatile LH secretion in early
postpartum period. They reported a direct relationship between postpartum energy
balance and first ovulation, and between negative energy balance nadir and changes in
pulsatile LH secretion, suggesting that as negative energy balance reaches it's nadir and
starts returning towards balance, LH secretion is disinhibited and first ovulation occurs.
The relationship between energy balance and first ovulation was further supported
by different studies. A study by Staples (1990) examined the relationship between
ovarian activity and energy status during the early postpartum period. In this study, cows
were classified according to the time of first ovulation as early responders (resume
ovarian activity within 40 days postpartum), late responders (resume ovarian activity
between 40 and 60 days postpartum), and no responders (resumption of ovarian activity
after 63 days PP). These authors concluded that the early and late responders cows were
in less negative energy balance than non-responders and were able to restore ovarian
activity during the first 63 days postpartum. On the other hand, the non-responder cows
did not have the capability to consume as much dietary energy, produced less milk and
were more dependent on energy from body reserves to produce milk. As a consequence,
metabolic status inhibited the initiation of postpartum ovarian activity in cows during the
first 63 days postpartum. In addition, an increased loss of body weight during the first 2
weeks of lactation coincided with decreased ovarian activity; early responder cows losing
the least weight and non-responder cows losing the most weight.
Lucy (1992) examined the influence of diet composition, dry-matter intake, milk
production, and energy balance on time to post-partum ovulation. Results of this study
confirmed those of Staples (1990) where the interval to first ovulation was shorter in
cows that consumed more dry-matter and produced more milk. In contrast, low milk
producing cows consumed less dry-matter and were more likely to be classified as late
responders. These two studies suggested that the fact that higher producing cows
ovulating earlier than low producing cows did not contradict the effects of energy balance
on the interval to first ovulation, as higher producing cows can be in a less negative
energy balance and thus ovulate earlier. It was also reported that cows ovulating earlier
(before day 42 postpartum) had a superior reproductive performance. Also results from
the study done by Lucy (1992) are in agreement with those of Fonseca (1983) where
Jersey cows producing more milk ovulated earlier than lower producing herdmates.
These two studies concluded that the data do not support linear relationships
between days to first estrus, days to first insemination, and days open with increasing
milk yield as suggested by others. They proposed that this contradiction occurred because
lowest producing cows in commercial herds are culled before they have the opportunity
to express their reproductive potential. As stated by Staples (1990) and supported by
several studies (Fonseca et al., 1983; Harrison et al., 1990; Lucy et al., 1992), if energy
status of the cow is more important than milk yield in determining return to estrus, then
milk yield alone may be either positively or negatively correlated with days to first
ovulation. Although an association between energy balance and postpartum ovarian
activity has been clearly established, the causal path remains unclear. Detrimental effects
of negative energy balance on ovarian activity could be due to effects on any of the
components of the reproductive endocrine axis.
Physiological Factors Involved in Ovarian Activity Potentially Affected by Energy
Effects of negative energy balance in LH secretion
It has been already mentioned the importance of a high frequency mode of
pulsatile LH secretion in the final phase of maturation and ovulation of ovarian follicles.
Although pituitary content of gonadotropins increase rapidly after calving and are
capable of supporting ovulation by day 8 to 10 postpartum (Kesler et al., 1977; Fernandes
et al., 1978; Moss et al., 1985), however, pulsatile LH secretion capable of inducing
ovulation generally occurs near 1st ovulation which usually takes place at 17 to 34 days
(see table 2.4). There is strong evidence that secretion of LH is impaired in cows not
recovering from negative energy balance. Peters (1985) reported that very few lactating
cows ovulated in response to pulsatile administration of LHRH when delivered at a time
when animals were in a negative energy balance.
Canfield (1988) compared LH secretion at 2 weeks postpartum and again at the
energy balance nadir (during the return towards EB), and reported an increase in LH
frequency and a decrease in pulse amplitude. These authors concluded that energy
balance plays an important role in the control of first ovulation by suppressing LH pulse
frequency following calving. Canfield and Butler (1990a) demonstrated a direct
relationship between postpartum energy balance and 1st ovulation, and between negative
energy balance nadir and changes in pulsatile LH secretion. Therefore, it was concluded
that as negative energy balance reaches it nadir and starts returning towards balance, LH
secretion is disinhibited and 1st ovulation occurs. Canfield and Butler (1991) reported that
dairy cows in a negative energy balance had similar LH patterns but ovulated later than
cows in positive energy balance. In another study, increased energy balance was
associated with increase pulse amplitude of LH secretion (Lucy et al., 1991). Schillo
(1992), in a review of the topic proposed that, the reduction on the LH pulse frequency
observed during negative energy balance, represents one of the most important means by
which energy balance impairs reproductive activity in cattle. The above results are
consistent with Eindings of Beam and Butler (1997) which reported that follicles
emerging after the negative energy balance nadir, rather than before, exhibited greater
growth and diameter, enhanced estradiol production, and were more likely to ovulate.
There is evidence that metabolic hormones such as growth hormone, insulin,
IGF-I, and leptin have important roles in the control of ovarian follicular development
and are likely to be important mediators of the effects of dietary intake and energy
balance on cow fertility.
Insulin -like growth factor-I. IGF-I and insulin are effectors of follicle cell
function in vitro with stimulation of steroidogenesis and cell proliferation in granulosa
and thecal cells (Monniaux et al., 1992; Spicer et al., 1993; Magoffin et al., 1993; Spicer
et al., 1996). Insulin-like growth factor-1 (IGF-I) is decreased in postpartum cows when
experiencing negative energy balance (Spicer et al., 1990; Beam and Butler, 1999) Cows
in poor body condition or cows not recovering body condition during lactation have also
been identified as having low blood IGF-I concentrations. Beam and Butler (1997)
reported that levels of plasma IGF-I averaged approximately 40% higher during the first
2 weeks postpartum in cows ovulating during the first follicular wave postpartum than in
cows not ovulating. Plasma IGF-I in cows ovulating the 1st follicular wave was higher at
day 1 postpartum, before the establishment of follicular dominance and subsequent
increases in peripheral estradiol. Therefore, the authors suggested that higher IGF-I in
ovulatory cows did not result from greater dominant follicle estradiol production, but
preceded and possibly contributed to differences in follicular function (Beam and Butler,
1997). Results of this study also suggest that low concentrations of circulating IGF-I are
related to low steroidogenic output of dominant ovarian follicles early post partum.
Results of another study (Cohick et al., 1996) also suggested that changes in systemic
levels of IGF-I and IGFBP affect their concentrations in follicular fluid and follicular
development. Finally, Beam and Butler (1999) proposed that during the negative energy
balance period, the ability of follicles to produce sufficient estradiol for ovulation seems
to depend on the availability of insulin and IGF-I in serum and the changing energy
Insulin. There is significant evidence that dietary restriction and negative energy
balance reduce circulating concentrations of insulin (Vizcarra et al., 1998; Mackey et al.,
2000). In vitro studies (Stewart et al., 1995) showed that insulin at physiological levels
affected proliferation of bovine thecal cells, and acted synergistically with luteinizing
hormone in stimulating steroidogenesis. Spicer (2001) reported that insulin by itself was
a more effective stimulator of aromatase activity than FSH in vitro. Beam and Butler
(1997) reported a greater insulin:GH ratio during the first week postpartum in cows
ovulating during the first follicular wave than those that did not, suggesting that levels of
insulin and GH during the very early stages of follicular recruitment may be important to
later follicular function. Gong (2002) showed that dairy cows fed a diet that increased
circulating concentrations of insulin during the first days 50 postpartum had shorter
postpartum anestrus intervals, and an increased conception rate to first service
independent of any effects on LH or FSH and without affecting milk yield or energy
balance. The authors proposed that the increase in insulin concentrations promoted
differentiation and maturation of dominant follicles during early lactation, thereby
increasing the chance of these dominant follicles of ovulating in response to the LH
surge. These results suggest that insulin may have a direct effect at the ovarian level.
Thyroid hormones (T3 and T4). Reist (2003) examining associations between
postpartum reproductive function and metabolic status in high yielding cows, reported
that cows with higher plasma levels of thyroid hormones (T3 and T4), WeTO aSsociated
with early start of ovarian cycle; proposing that Thyroid hormones can also play an
important role in the resumption of ovarian activity postpartum. These results are
supported by previous findings of Spicer (2001) who provided evidence for a role of T3
and T4 in regulating steroidogenesis of bovine follicles. The author proposed that T3 and
T4 may have a minor positive impact on FSH-induced progesterone production by bovine
granulosa cells, and a maj or positive impact on LH-induced androstenedione production
by bovine thecal cells, both of which would result in a net increase in estrogen production
by the follicle, however, T3 and T4 have little or no direct effect on aromatase activity.
This evidence supports a role of Thyroid hormones as part of a multihormonal complex
regulating ovarian activity in cattle.
Leptin. Leptin is a protein hormone secreted by adipocytes (Bradley et al., 2000)
and acts on the central nervous system to reduce voluntary feed intake (Schwartz et al.,
2000). Block (2001) reported that postparturient cows undergoing negative energy
balance had significantly lower plasma concentrations ofleptin compared with
postparturient cows in positive energy balance. In addition, at the first week of lactation
the plasma concentration of leptin was correlated positively with plasma concentrations
of glucose and insulin and negatively correlated with plasma concentrations of GH and
NEFA. The author concluded that these correlations could represent a co-regulation by
energy balance and these factors in mediating the effect of energy balance on leptin
Leptin has diverse effects on the neuroendocrine axis in addition to appetite and
body weight regulation (Ahima and Flier, 2000). Leptin stimulated gonadotropin release
and inhibited insulin-like growth factor-mediated release of estradiol in ovarian follicular
cells in rat ovarian granulosa cells (Zachow and Magoffin, 1997). Another study (Chehab
et al., 1996) reported that correction of the sterility defect in homozygous (ob/ob) obese
female mice could be accomplished by repeated administration of human recombinant
leptin, resulting in ovulation, pregnancy and parturition. Williams (2002) reported that
short term fasting of growing prepubertal heifers causes marked reductions in circulating
leptin, concomitant with declines in LH pulse frequency, and serum concentrations of
insulin and IGF-I. In this same study results could not be repeated for mature cows under
the same short term fasting. Altogether, these results may indicate that leptin signals the
adequacy of energy stores for reproduction, by interacting with different target organs in
the hypothalamic-pituitary-gonadal axis in cattle and other species. It has been proposed
that the effects of leptin might be mediated in part by NPY, which in turn has been shown
to regulate gonadotrophin release by inhibiting LH secretion in ewes (McShane et al.,
NPY is a potent inhibitor of LH release and unlike leptin, is a potent stimulator of
food intake (Houseknecht et al., 1998) Concentrations ofNPY increase in cerebrospinal
fluid during undernutrition and can negatively modulate the secretion of LH when
centrally infused in cattle (Gazal et al., 1998). These results may stimulate future research
to explore the role and potential interactions between hormones, neuropeptides and
resumption of ovarian cyclicity under negative energy balance in postpartum dairy cattle.
It has been well established in cattle that ovarian function is controlled primarily
by an integrated GnRH-gonadotrophin-ovari an axi s. Recent work has shown that factors
classically thought to be mainly involved in the regulation of metabolic processes, such
as GH, insulin and IGF-I, thyroid hormones, leptin,and neuropeptide-Y may play an
important role in the control of ovarian activity in the postpartum dairy cow (Spicer at al.,
1995; Reist et al., 2003; Williams et al., 2002). Metabolic hormones can act either
directly to control gonadotrophin -independent stages of follicle development (Gong et
al., 1996), or in synergy with gonadotrophins to modulate follicular recruitment and final
development and maturation of preovulatory follicles (Spicer et al., 1995; Armstrong et
al., 2002). These effects could represent at least part of the mechanism underlying well
documented but not completely understood nutritional influence on reproductive function
Season. The effect of season has been reported as having an effect on resumption
of ovarian activity postpartum. In a study conducted in North Carolina, Fonseca (1983)
reported that cows calving in the winter had 6.5 more days to first ovulation compared
with cows calving in the fall. Peters (1984) reported that cows calving in the spring
underwent longer periods between calving and first ovulation than autumn calvers. Savio
(1990a) reported that the postpartum interval to detection of the first dominant follicle
was shorter in autumn than in the spring. When only normal dominant follicles were
considered, the cows that calved in autumn tended to have a shorter, and less variable,
intervals from calving to first ovulation. In Australia, cows calving in summer had
significantly longer intervals from calving to first postpartum ovulation than those
calving in winter (23d vs. 18d) (Jonsson et al., 1997). In addition, cows losing more
bodyweight had longer intervals from calving to first ovulation. In Belgium, cows calving
in the winter (stable housing) were more prone to delayed ovarian function compared to
cows calving in the spring (pasture housing) (Opsomer et al., 2000). None of these
studies proposed a path as to how season affects ovarian cyclicity. In Switzerland, Reist
(2003) examined the relationship between reproductive function and metabolic and
endocrine status in dairy cows. Results of this study showed a significant effect of season
in resumption of ovarian activity. Cows calving in the fall were more likely to start
ovarian cyclicity earlier postpartum than cows calving in the spring.
Parity. The data on the effect of parity on the interval to first ovulation is
contradictory and does not support an effect of parity on resumption of ovarian cyclicity.
Stevenson and Britt (1979) reported that interval to first ovulation tended to be longer for
pluriparous than for primiparous cows (18.7 vs 16.3 days), but the interval to first estrus
was not different between parity groups (26.1 vs 27.7 days). Fonseca (1983) reported that
in cows between 33 and 60 months of age, younger cows had their first ovulation earlier
than older cows. In this study, there were very few observations in older cows. In
contrast, Lucy (1992) reported that ovarian activity was delayed in primiparous cows
compared with multiparous cows. However, primiparous cows were similar to
multiparous cows with respect to first service, first service conception rate, services per
conception, and days open. Moreira (2001) reported that the incidence of anestrus at 63
days was greater in primiparus than in multiparous cows.
Periparturient diseases. The effects of periparturient diseases in resumption of
ovarian cyclicity in dairy cows have been reported. Fonseca (1983) reported that cows
with abnormalities after calving had 8.8 more days to first ovulation than cows without
abnormalities after calving. In this study the main abnormalities at parturition were
retained placenta and milk fever in Holstein cows and Jersey cows, respectively. During
the postpartum period, uterine infection was the most frequent clinical abnormality in
Holsteins, while ovarian cysts ranked first (followed by injury or disease and uterine
infection) in Jerseys. Opsomer (2000) conducted a study to identify risk factors
associated with postpartum ovarian dysfunction in dairy cows. In this study, cows
suffering from clinical diseases such as mastitis, severe lameness, or pneumonia during
the first month of lactation, were 5 times more at risk of developing delayed resumption
of ovarian activity than healthy cows. In addition, cows developing clinical symptoms of
ketosis with a positive prussiate test were 1 1 times more at risk of delayed resumption of
ovarian cyclicity than normal cows. Cows with abnormal calvings and abnormal vaginal
discharges were 3.6 and 4.5 times more likely to develop delayed ovulation compared to
cows with normal vaginal discharges respectively. Similar results were reported by
Etherington (1991) where cows with retained placenta were associated with longer
intervals to first ovulation.
Loss of body condition early in the postpartum period was another factor
increasing the risk of delayed cyclicity. Cows losing more in body condition were 19 and
11 times more at risk of delayed cyclicity at 30 days and 2 months after calving. Cows
with normal progesterone profiles lost on average 0.26 points during the first month after
calving and 0.29 points during the first 2 months after calving, while cows with delayed
ovarian function lost 0.39 and 0.49 points, respectively (Opsomer et al., 2000). These
results were in agreement with those of Moreira (2001), where an effect of body
condition at 63 days was associated with the frequency of cows classified as anestrus. As
body condition increases the incidence of anestrus decreases. In another study conducted
by Mateus (2003) a relationship between endotoxin concentrations in blood from cows
with endometritis and a prolonged anestrus period was observed. This result is in
agreement with a previous study from Peter (1990) where intrauterine infusions of
endotoxins reduced the preovulatory LH surge in cows. This could have been mediated
by high cortisol levels and resulted in ovulation failure. Ketosis is another periparturient
disorder related to delayed resumption of ovarian activity. Reist (2000) examined the
relationship between ketone body concentration and first ovulation in dairy cows. Cows
classified as late responders (cows with a first ovulation between 31 and 87 days
postpartum) had higher blood and milk ketone bodies concentrations compared to early
responders (cows with first ovulation within 30 days postpartum), with no significant
differences in body condition scores between groups.
Lameness and Ovarian Activity
While several studies have shown a relationship between lameness and
reproductive performance, the relationship between lameness and ovarian activity in
dairy cows has not been investigated using obj ective research methods. To our
knowledge, there is only one study that looked at the relationship between lameness and
ovarian activity in dairy cows. This study was conducted in 335 dairy cows on six high
producing dairy herds in Belgium. Cows diagnosed with clinical mastitis, severe
lameness, or pneumonia by farmers were at higher risk of delayed cyclicity, compared to
cows classified as clinically healthy (Opsomer et al., 2000); however, the actual number
of cows affected with clinical mastitis, severe lameness, or pneumonia was not reported.
In Florida, clinical observations by veterinarians and dairy farmers suggest that
cycle cows affected with lameness experience anestrus, and the duration of anestrus is
associated with severity, duration, and diseases or lesions associated with lameness (eg,
interdigital phlegmon, papillomatous digital dermatitis, claw lesions). We hypothesized
that as lame cows experience a more pronounced loss in body condition (hence a
prolonged state of negative energy balance) during the early post partum period, lame
cows are at higher risk of delayed ovarian cyclicity than non-lame cows. Lame cows eat
less and go into a negative energy state. In order to meet energy deficit, body reserves are
mobilized resulting in body weight loss. The output of energy in lame cows (body
maintenance and milk yield) may exceed the energy input in the form of feed. It is
possible that cows that become lame are in a progressive negative energy state, go into
anestrus and experience long delays to restore ovulation.
Results of previous studies suggest that as cows experience increasing positive
energy status, there is increased ovarian follicle activity leading to early return to
ovulation (Butler et al., 1981, Staples et al., 1990; Lucy et al., 1991). As energy status
becomes more positive for cows in early postpartum, diameter of the largest follicle
increases, the number of double ovulations increases, and time for detection of the first
corpus luteum decreases. (Lucy et al., 1991).These changes in follicle size and numbers
and the number of ovulations are thought to be aroused by increases in luteinizing
hormone (LH), follicle stimulating hormone (FSH), insulin, BST, insulin-like growth
hormone-1 (IGF-1), and possibly other yet-to-be determined compounds as activated by
improving energy status (Beam and Butler, 1998). Therefore, lameness may have an
effect on feed intake and energy status leading to changes in concentrations of
reproductive hormones. Under field conditions, evidence of corpus luteum function can
be determined by monitoring plasma progesterone (P4) COncentrations weekly during
lactation, before and after diagnosis of lameness in dairy cows.
MATERIALS AND METHODS
Cows and Herd Management
Cows in this study were from a high-producing dairy herd (rolling herd average
milk production, approx 12,000 kg) of approximately 600 Holstein cows located in
Florida. Cows were milked and fed a TMR ration three times per day. Cows were housed
in lots equipped with sprinklers, fans and shade cloth over the feed bunks to reduce the
effects of heat stress. This herd was selected for study on the basis of a history of
lameness, quality of veterinary records, and willingness of the owner to participate in the
This study was designed as an observational cohort study. Sample size calculations
were made on the basis of our estimate of the number of cows affected with delayed
ovarian cyclicity increasing from 10% in non-lame cows to 30% in lame cows (type I
error = 0.05; type II error = 0.20). A total of 253 (45%) of 563 Holstein cows identified
with an even numbered ear-tag that calved from June 1, 2002 until May 31, 2003 was
used in the study. Cows with an even numbered ear-tag were enrolled in the study as they
calved (instead of cows randomly selected) to overcome logistical identification
procedures and to reduce disruption of routine veterinary medical and management
procedures at the study farm. Cows were classified into one of six categories of lameness
during the first 3 5 days post partum using a modification of the locomotion scoring
developed by Sprecher et al., 1997. Blood samples were obtained for weekly for
detection of plasma progesterone (P4) COncentrations during the first 60 days post partum.
Risk of delayed cyclicity was compared between cows classified as non-lame, moderately
lame, or lame.
Using farm records, the following data were collected for each cow: lactation
number, calving date, calving season (winter months: Jan to Apr and Oct to Dec; summer
months: May to Sep), dystocia (yes, no), retained placenta (yes, no), metritis (yes, no),
mastitis (yes, no), ketosis (yes, no), body condition score at calving (Edmonson et al.,
1989), change in body condition score in the first 50 days post partum, use of PGF2a
(Lutalyse, Pharmacia, Kalamazoo, MI) prior to resumption of ovarian activity (yes, no),
and 305-day mature equivalent milk yield. From Dairy Herd Improvement Association
(DHIA) records, proj ected 305 day ME milk yield data were collected based upon
production at 60 days post partum. Levels of milk yield were defined as low (5,530 to
10,619 kg), medium (10,620 to 12,978 kg) and high (12,979 to 15,137 kg) on the basis of
the frequency of distribution (first, second and third, and fourth quartiles, respectively).
Diagnosis of Lameness
During the first 35 days post partum, study cows were examined weekly (Tuesday)
for diagnosis of lameness using a locomotion scoring system described by Sprecher
(1997) with modifications (Table 1). Cows were observed and scored by the same
veterinarian (EJG) as they walked-out of the wash pen to the holding area prior to
milking. Cows with a locomotion score of 4 or 5 were further examined on a tilt table for
diagnosis and treatment of lameness, noting lesions observed and date of occurrence.
Lame cows with claw lesions had white line lesions or sole ulcers and were treated by
corrective foot trimming techniques (Shearer and van Amstel, 2001). Lame cows with
subacute laminitis were those with yellow and red discoloration of the sole and white
line, and in most cases they had thin soles and were sensitive at examination with hoof
testers (Mortensen, 1994; Toussaint Raven, 1989). Lame cows with interdigital dermatitis
were those with inflammation confined to the epidermis and in some cases
hyperkeratosis, which creates a roughened appearance to the interdigital skin (Blowey,
1994); a fetid serious exudate could be present, and there was mild sensitivity to pressure.
This condition was frequently accompanied by cracks in the heel, heel horn erosion, with
potential under-running of the heel horn (Berry, 2001).
Collection of Blood Samples and Detection of Plasma P4 COncentrations
Cows were blood-sampled and scored for body condition (Edmonson et al., 1989)
weekly (Thursday) for detection of plasma progesterone concentrations during the first
60 days post partum. Cows were blood-sampled via coccygeal venipuncture using
vacutainer collection tubes containing K3 EDTA (Becton, Dickinson, and Company,
Franklin Lakes, NJ). Blood samples were refrigerated until and during transportation to a
laboratory at the University of Florida where they were centrifuged for 20 min at 3000
RPM at room temperature for plasma harvest. Plasma samples were frozen at 20 C until
tested for P4 COncentrations using the Coat-A-Count@ Progesterone Kit (DPC@
Diagnostics Products Corporation) radioimmunoassay. The Coat-A-Count@ Progesterone
procedure is a solid-phase radioimmunoassay where 125I-labeled progesterone competes
for a fixed time with the progesterone content of the cow' s plasma sample. Because
antibody is bound to the wall of the polypropylene tube, simply decanting the supernatant
is enough to terminate the competition and to isolate the antibody-bound fraction of the
radiolabeled progesterone. A standard curve dilution was prepared using coated tubes and
non-coated tubes were used for total counts and non-specific binding. A 100 Cl~ volume of
increasing concentrations of progesterone calibrators, (0, 0.1i, 0.25, 0.5, 2, 5, 10, 20, and
40 ng/mL) were placed in the tubes. Plasma samples (100 Cl) were added to coated tubes
and 1 mL of 125I-labeled progesterone (25000 cpm) to all tubes. Every 6th plasma sample
was evaluated in duplicate. After an incubation period of 3 hours, the supernatant was
discarded and tubes were dried for 15 minutes. They were then placed in a gamma
counter. Calculation of the progesterone concentration in the plasma sample was made by
computerized data process using a spline fitting curve.
Accuracy of assay procedures was determined by measuring known quantities of
exogenous progesterone (0.625, 1.25, 2.5, and 5.0 ng/mL) in plasma in seven different
assays. Recovery of added (x) versus measured (Y) P4 COncentrations was described by
linear regression (Y= 0.57 + 0.93x; R2 = 0.89). The regression intercept value (0.57
ng/mL) represented original P4 COncentrations measured in a plasma pool prior to
addition of exogenous masses.
Parallelism of logit plots between the displacement curves for different volumes of
a plasma pool containing 8 ng/mL of P4 (i.e., 25, 50 and 100 Cl~) and standard P4 amOunts
(i.e., 0.1, 0.25, 0.5, 1.0, 2.0, 5.0, 10.0 and 20.0 ng/mL) was tested for homogeneity using
regression analysis (Wilcox et al., 1990). The linear regression curves for plasma and P4
standards were parallel (Yp= 0.60 1.44x, R2 = 0.99; Ys = 0.21 1.61x, R2 = 0.99; where
Yp and Ys = In B/F, x = loglo of assay volume or loglo standard P4 COncentrations,
respectively). The slopes were not different.
Coefficients of variation were calculated from a reference sample (luteal phase) and
duplicate samples obtained from all assays. Duplicate plasma concentrations of P4 were
categorized into high (2 3.0 ng/mL; n = 359), medium ( 1.0 and <3.0 ng/mL; n = 128),
and low (> 0.3 and <1.0 ng/mL; n = 52), and the coefficients of variation were 12.4%,
12.4%, and 14.2%, respectively. Inter-and intraassay coefficients of variation for the
luteal phase reference sample were 8.9% and 8.34%, respectively.
Resumption of Ovarian Cyclicity
Cows with evidence of normal ovarian cyclicity during the first 60 days post
partum were those with: i) weekly plasma P4 COncentrations > 1 ng/mL for 2 or 3
consecutive samples followed by a decline in P4; Or ii) if P4 COncentration > 1 ng/mL was
followed by a marked decrease after PGF2a inj section and this followed by an increase in
P4 COncentration. Cows with a delayed resumption of ovarian cyclicity were those with
consistently low P4 COncentrations < 1 ng/mL during the first 60 days post partum
(Staples et al., 1990). For the purpose of this study, cows with P4 values above 1 ng/mL
for 4 or more consecutive samples were classified as cows with extended luteal phases
(Opsomer et al., 1999). First luteal phase was defined as the first rise in P4 above 1
Reproductive and Health Management
All cows were subj ected to a pre-synchronization program. After days 30 to 3 5
postpartum cows received an inj section of prostaglandin F2a and then again at 44 to 49
days. Cows observed in heat after the second inj section of prostaglandin F2a were
inseminated, and those that did not demonstrate behavioral signs of estrus were enrolled
in a timed insemination program. This program involved the use of GnRH on Day 0, 7
days later prostaglandin F2a, a second GnRH on Day 9, and timed inseminated 16 to 18
hours later. All cows were examined for pregnancy at 42 to 49 days post insemination by
palpation of the uterus and its contents by the attending veterinarian.
Farm personnel examined cows for the detection of health problems several times
post partum following a pre-established protocol (Table 3-1). Cows were grouped by
days in milk and a group of fresh cows (less than 30 DIM) were kept together. Cows
were examined after each milking. On Day one cows were checked for retained fetal
membranes (fetal membranes visible at the vulva for more than 24hs after calving), udder
edema (by observation and palpation of the udder), and mastitis (by stripping all four
quarters). On Day 4, cows were checked for production (using Afimilk@ computerized
system), udder edema, metritis (Table 3-2) and rectal temperatures were taken. On day 7
cows were checked for Ketonuria (using Ketostixs@), metritis, body temperature, and
using a stethoscope, rumen movements, and displaced abomasum (DA) tympanicc sound
on the left side at simultaneous auscultation-percussion of the left paralumbar fossa). This
7-day check was repeated at day 10 and 15. In all checks, daily milk yield was monitored
for every cow for deviations in production.
Table 3-1. Protocol for examination of cows postpartum
Check day Health checks
1 Retained fetal membranes (RFM), udder edema, mastitis
4 Temp, udder edema, metritis, production, mastitis, manure consistency
7 Temp, ketosis, DA, rumen, metritis, mastitis, manure consistency
10 Temp, ketosis, DA, rumen, metritis, mastitis, manure consistency
15 Temp, ketosis, DA, rumen, metritis, mastitis, manure consistency
Table 3-2. Definitions of metritis done by farm personnel based on discharge and
Metritis code Definition
Ul Normal size and abnormal discharge.
U2 Abnormal size and abnormal discharge (pus discharge)
U3 Abnormal size and abnormal discharge (watery and foul smelling)
U4 Abnormal size, abnormal discharge and the cow looks sick
Cows with Ul and some with U2 were treated with an inj section of prostaglandin
F2a. Some cows with U2 and all with U3 were treated with an intrauterine infusion of
tetracycline (100 mg/mL) solution. Cows with U4 were treated with systemic antibiotics.
Other health codes recorded were calving outcomes (See table 3-3)
Table 3-3. Definition of calving outcomes
Calving code Definition
Pull 1 Easy pull, 1 person.
Pull 2 Difficult pull, 1 person
Pull 3 Easy for 2 persons
Pull 4 Difficult pull for 2 persons
Pull 5 Extreme pull.
Cows with pulls 4 and 5 were started with systemic antibiotics after calving.
All cows in the herd were monitored daily for deviations in milk (Afimilk@) production,
and milk conductivity for detection of mastitis following a pre-established criteria. (Table
3.4). All health events and treatments were recorded on a cow-side computer program
(Visi-Cow@) used by farm personnel.
Table 3-4. Criteria for monitoring production health and mastitis using Afimilk@ system
Population % Decrease in daily milk Increase in daily Increase daily milk
production (%) conductivity (%) production (%)
1 to 15 DIM ---- ---- < 10
1 to 40 DIM 15 12--
41 to 100 DIM 20 15--
> 100 DIM 25 18--
The null hypothesis that risk of delayed ovarian cyclicity is the same in cows
classified as non-lame, moderately lame, or lame was tested using logistic regression. In
the analysis, non-lame cows were those with a score of 3 for one week only, or scores of
< 2. Cows classified as moderately lame were those with a score of 3 on two consecutive
weeks. Lame cows were those classified at least once with a locomotion score of 4 or 5.
Additional independent variables (lactation number, calving season, milk yield, dystocia,
retained placenta, metritis, ketosis, body condition score, use of PGF2a) were included in
the analysis to address possible modifying or confounding effects of these factors on risk
of delayed ovarian cyclicity. Stepwise forward regression was used, and a variable had to
be significant at the 0.20 level before it could enter the model. A variable remained in
the model when its significance level was < 0.10. Variables for lactation number and
calving season were forced into the model.
In the Einal model, adjusted odds ratios (OR) and 95% confidence intervals (CI)
were reported. The OR was used as an epidemiologic measure of association between a
variable (i.e., lameness) and the outcome of interest (i.e., delayed ovarian cyclicity). In
each variable, the reference category had an OR = 1. An assessed OR > 1.0 indicates that
the probability of delayed ovarian cyclicity increased, compared with cows in the
reference category. The attributable proportion was estimated as (OR 1)/OR, and
interpreted to represent the proportion of lame cows that experienced delayed ovarian
cyclicity because of lameness (Martin et al., 1987).
The null hypothesis that number of days post partum to first luteal phase did not
differ among groups of cows classified as non-lame, moderately lame, or lame was tested
by use of the Kruskal-Wallis nonparametric test (because the dependent variable failed to
meet assumptions of parametric testing), and multiple ANOVA for the dependent
variable of days to first luteal phase (ranked data) while simultaneously adjusting for
variables related to ovarian cyclicity (i.e., lactation number, calving season, ketosis, milk
yield). Significance was set at P < 0.05.
7 14 21 28 35 42 49 56 63 70 77
Figure 1. Normal ovarian cyclicity
7 14 21 28 35 42 49 56 63 70 77 84
Figure 2. Normal ovarian cyclicity for cows treated with PGF2
7 14 21 28 35 42 49 56 63 70 77 84
Figure 3. Delayed resumption of ovarian cyclicity
7 14 21 28 35 42 49 56 63 70 77 84 91 98 105
Figure 4. Extended luteal phase
All 253 cows enrolled in the study were followed-up successfully during the
60-day study period. Two hundred and thirty-eight (94%) cows met the criteria for
ovarian delayed cyclicity used in this study. A visual examination of plasma P4
concentration patterns revealed that 15 cows (6%) experienced an extended luteal phase.
A total of 101 of 23 8 (42%) cows were classified as moderately lame (locomotion score
= 3) and 41 (17%) as lame (score = 4) (Table 4-1). The mean number of days post partum
when cows were classified as lame was 15 days (1 34 days). The most common lesions
observed were subacute laminitis (26/41 = 63%), and claw lesions such as sole ulcers and
white line disease (9/41 = 22%).
The overall incidence of delayed ovarian cyclicity was 11%. The incidence of
delayed ovarian cyclicity was higher in cows classified as moderately lame (14/101;
14%) or lame (7/41; 17%), compared to non-lame cows (6/96; 6%). In the univariable
analysis, cows classified as moderately lame were 2.4 times at higher risk of delayed
ovarian cyclicity compared to non-lame cows (OR = 2.4; 95% CI = 0.9 6.7; P = 0.07)
(Table 4-2). Cows classified as lame were 3.1 times at higher risk of delayed ovarian
cyclicity compared to non-lame cows (OR = 3.1; 95% CI = 0.9 9.9; P = 0.05).
In the multivariable analysis, lameness, lactation number, season, ketosis and milk
yield were retained in the final modeling process (Table 4-3). Addition oftwo-way
interaction terms did not contribute to the final model for risk of delayed ovarian
cyclicity, and these terms were removed from the model. Cows classified as moderately
lame were 2. 1 times at higher risk of delayed ovarian cyclicity, compared to non-lame
cows (OR = 2.1; 95% CI = 0.7 6.1; P = 0.15). Cows classified as lame were 3.5 times at
higher risk of delayed ovarian cyclicity compared to non-lame cows (OR = 3.5; 95% CI =
1.0 12.2; P = 0.04). The attributable proportions of cows that experienced delayed
ovarian cyclicity associated with moderate lameness and lameness were 0.52 and 0.71,
respectively (Table 4-4).
Overall, the time interval (median) from calving to first luteal activity in the study
population was 31 days. This time period was more prolonged in cows classified as lame
(median = 36; range = 17 to 97) or moderately lame (median = 32; range = 4 to 146),
compared with non-lame cows (median = 29; range = 2-172) (P < 0.05).
Table 4-1. Frequency distribution of cows classified as lame or non-lame using a
modification of the locomotion scoring system developed by Sprecher, 1997
Locomotion Clinical Assessment criteria Cows
score description n = 238
No. of cows (%)
0 Normal The cow stands and walks with a 3 (1)
level-back posture. Gait is normal.
The cow stands with a level-back
posture but develops an arched
back posture while walking. Gait
An arched-back posture is evident
both while standing and walking.
An arched-back posture is evident
both while standing and walking.
Gait is affected and best described
as short strides with one or more
An arched-back posture is always
evident and gait is best described
as one deliberate step at a time.
The cow favors one or more
In addition to criteria in LS4, the
cow demonstrates an inability or
extreme reluctance to bear weight
on one or more of her limbs/feet.
Table 4-2. Descriptive statistics and unadjusted odds ratios for risk of delayed ovarian
cyclicity in post-partum Holstein cows
Variable Delayed cyclicity Delayed cyclicity OR 95% CI P
n = 27 n= 211
No. of cows (%) No. of cows (%)
Locomotion score <: 2
BCS at calving
BCS change (0.75)
Use of PGF2a,
2.4 0.9 6.7
3.1 0.9 9.9
1.0 Reference NA
0.9 0.4 2.2 0.95
1.0 Reference NA
0.7 0.3 1.6 0.40
1.0 0.4 2.5
0.2 0.05 0.9
0.3 5.3 0.58
0.3 3.2 0.93
0.5 2.5 0.73
1.0 Reference NA
0.3 0.09 1.6 0.19
1.0 Reference NA
2.6 1.0 6.2 0.03
0.6 0. 1 2.3
1.1 0.3 3.6
0.6 4.0 0.32
1.0 Reference NA
0.8 0.3 1.9 0.70
Table 4-3. Final logistic regression model for risk of delayed ovarian cyclicity in
post- partum Holstein cows
Variable Adjusted odds 95% confidence interval P value
Locomotion score <;2 1.0 Reference NA
3 2.1 0.7 6. 1 0.15
4 3.5 1.0 -12.2 0.04
1 1.0 Reference NA
> 2 1.2 0.5 2.3 0.65
Winter 1.0 Reference NA
Summer 0.9 0.3 2.3 0.90
No 1.0 Reference NA
Yes 2.7 1.0 7.0 0.03
Low 0.9 0.3 2.5 0.98
Medium 1.0 Reference NA
High 0.2 0.05 0.9 0.04
NA = Not applicable
Table 4-4. Attributable proportion of cows that experienced delayed resumption of
Locomotion score N OR Attributable proportion
< 2 6/96 1 NA
3 14/101 2.1 0.52
4 7/41 3.5 0.71
The results of the study reported here support the hypothesis that lameness has a
detrimental effect on ovarian activity in Holstein cows during the early post partum
period. Cows classified as lame were 3.5 times at higher risk of delayed cyclicity,
compared to non-lame cows. Attributable proportion analysis indicated that delayed
ovarian cyclicity in lame cows would be reduced by 71% if lameness had been prevented.
In addition, cows classified as moderately lame were 2. 1 times at higher risk of delayed
ovarian cyclicity compared to non-lame cows (OR = 2. 1; 95% CI = 0.7 6. 1; P = 0. 15).
Even though this association was not statistically significant, the OR and the position of
the confidence interval (Szklo and Nieto, 2000) suggest that cows classified as
moderately lame were at high risk of delayed ovarian cyclicity. This observation is
further supported by the fact that the interval from calving to first luteal phase was more
prolonged in both lame cows (median = 36 days) or moderately lame cows (32 days)
compared with non-lame cows (29 days) (P < 0.05). Thus preventive measures (such as
examination of cows feet and, if necessary, use of corrective foot trimming techniques)
should be targeted at the group of moderately lame cows since as they represented 42%
of the study population. We examined a second logistic regression model which included
the 15 cows that experienced an extended luteal phase (in addition to the 238 cows that
met the criteria for ovarian cyclicity used in this study), and the effect of lameness on
delayed cyclicity did not disappear. Cows classified as moderately lame and lame were 2
(OR = 2.0; 95% CI = 0.7, 5.9; P = 0.17) and 3 times (OR = 3.0; 95% CI = 0.9, 10.3; P =
0.07) at higher risk of delayed cyclicity, respectively, compared to non-lame cows. To
our knowledge, only one previous study has examined the relationship between lameness
and ovarian activity. In a study conducted in 335 dairy cows on six high producing dairy
herds in Belgium, cows diagnosed with clinical mastitis, severe lameness, or pneumonia
by farmers were at higher risk of delayed ovarian cyclicity compared to cows classified
as clinically healthy (Opsomer et al., 2000). However, the actual number of cows
affected with clinical mastitis, severe lameness, or pneumonia was not reported.
The incidence of cows classified as moderately lame and lame during the first 35
days post partum was 42% and 17%, respectively. In a previous study involving 66 dairy
cows on a farm in Michigan (Sprecher et al., 1997), a locomotion scoring system similar
to that in our study was used for diagnosis of lameness. In the Michigan study, 27 (49%)
cows and 14 (24%) cows were classified as moderately lame and lame, respectively.
Results from that study are difficult to compare with results of the present study because
of differences in the scoring system. After testing the locomotion scoring system
(Sprecher et al., 1997) weekly for two months in the study herd, a new category was
added to include cows that were observed with an arched-back posture that was evident
both while standing and walking, but their gait seemed normal (score = 2, mildly lame);
76 (32%) cows were included in this category. In our analysis, this group of cows was
classified as non-lame. Assuming that this group of cows was misclassified as non-lame,
the incidence of cows classified as moderately lame (score = 3) would have been higher
(76 + 101 = 177 cows or 74%).
However, study results support our clinical observations and locomotion scoring
system for diagnosis oflameness. The possibility that cows classified as mildly lame
were misclassified is unlikely since the incidence of delayed ovarian cyclicity was lower
in mildly lame cows (3/76 or 4%) compared to moderately lame cows (14/101 or 14%). If
mildly lame cows were misclassified, there would have been an expected an incidence of
delayed ovarian cyclicity similar to that observed in cows classified as moderately lame.
Although we established an association between lameness and delayed ovarian
cyclicity, we failed to identify loss of body condition (or a modifying effect of lameness
and loss of body condition) as a significant risk factor associated with delayed ovarian
cyclicity. The risk of delayed ovarian cyclicity was 1.5 times higher in cows that had a
change in BCS > 0.75 in the first 50 days post partum compared to cows with a change in
BCS < 0.75. Therefore, this association was not significant
(OR = 1.5; 95% CI = 0.6 4.0; P = 0.32). The observed incidence of delayed ovarian
cyclicity in the study population was low (11%) compared to other studies (23 to 29%),
(Humboldt and Thibier, 1980; Bartlett et al., 1987; Staples et al., 1990), creating a sample
size limitation. In the previous study conducted in 335 dairy cows in Belgium, cows
losing more body condition during the first and second month after calving were at higher
risk of delayed ovarian cyclicity (Opsomer et al., 2000).
In our study, ketosis was, by itself, a risk factor for delayed resumption of ovarian
cyclicity. This result is in agreement with a study conducted in 84 dairy cows on 8 farms
in Switzerland (Reist et al., 2000) where blood serum and milk ketone body
concentrations during the first 6 weeks post partum were higher in cows classified as late
responders (i.e., cows started post partum ovarian cyclicity after 30 days) than in early
responders, with no significant differences in body condition scores between groups. It is
possible that lameness and ketosis may additionally interact with each other to affect the
risk of delayed ovarian cyclicity, but the small sample size was too small in the present
study did not allow detection of such an interaction.
Lameness can depress dry matter intake (Hassall et al., 1993; Galindo and Broom,
2002) and result in negative energy balance. It has been reported that negative energy
balance contributes to increased ketone body formation and delays the onset of ovarian
activity (Reist et al., 2000). A negative energy balance post partum not only contributes
to increased ketogenesis, but also delays the onset of ovarian cyclicity, especially if
energy deficiency is prolonged (Butler and Smith, 1989; Staples et al., 1990; Lucy et al.,
1992). Furthermore, results of the study reported here revealed that the risk of delayed
ovarian cyclicity was lower in high milk producing cows, compared to medium or low
producing cows. The results of previous studies suggested that low producing cows have
reduced inferior dry matter intake, a more negative energy balance, and are less likely to
restore ovarian activity during the first 63 days post partum compared to high producing
cows (Staples et al., 1990; Lucy et al., 1992).
Although is clear that lameness has an effect on resumption of ovarian cyclicity in
postpartum cows, we could not establish the cause of this effect. We hypothesized that
energy balance would be responsible for the delayed in resumption of ovarian cyclicity,
but our study could not support such pathway. Even though there are no studies reporting
a pathway to explain the effect of lameness on ovarian activity, we cannot ignore other
proposed mechanisms by which lameness may affect the hypothalamus-pituitary-ovarian
Dobson (2000) proposed that activation of the hypothalamus-pituitary-adrenal axis
by stressors reduces the pulasatility of GnRH/LH by actions at both the hypothalamus
and pituitary gland, depriving the ovarian follicle of adequate LH support. This will lead
to reduced estradiol production by slower growing follicles. A combination of a reduced
GnRH/LH pulsatility with a reduced production of estradiol, contributes to the delay and
reduced magnitude of the LH surge and a delayed or absence of ovulation (Dobson et al.,
1999; Dobson et al., 2000). Phogat (1997; 1999) provided evidence that the effect of
increased concentrations of ACTH either exogenously, or after transport, reduced the
amounts of LH released after challenges with small doses of GnRH, providing support
for additional effects at the pituitary level. Dobson (2000) proposed that in situations such
as during chronic stress of severe lameness or fever, the pulse GnRH/LH frequency will
be so slow that initial follicular growth will occur but will be unable to continue into the
later stages that depend on faster pulse frequencies. Thus the animal fails to maintain an
estrus cycle developing anestrous.
Another hypothesis is that the effect of lameness on cyclicity could be driven by
endotoxins released after an event of ruminal acidosis (Nocek, 1997). As shown by Peter
(1990) increases in cortisol concentrations after the infusion of endotoxin might block the
synthesis of estradiol at ovarian level resulting in failure of a preovulatory LH surge. This
may lead to anovulation or delayed ovarian cyclicity. Supporting the effects of
endotoxins, Bataglia (1997) found that the suppressive effects of endotoxins on the
reproductive axis can be mediated centrally through an inhibition of GnRH and thus LH
pulsatile secretion. Ruminal acidosis has been identified as risk factor for lameness
(Nocek, 1997; Hoblet et al., 2001). So if lame cows are suffering from acidosis with
endotoxin released by gram-negative bacteria, endotoxins can mediate the effect of
lameness in delayed resumption of ovarian cyclicity. At this point these hypotheses are
only speculative and need further research to be proved.
Analysis of results of the study reported here support the hypothesis that lameness
has a detrimental effect on ovarian activity in Holstein cows during the early post partum
period. The locomotion scoring system used in this study is a useful management tool
that veterinarians and dairy farmers can adopt for early detection of lameness in dairy
cows. The use of corrective foot trimming techniques in moderately lame cows may help
reduce the risk of delayed ovarian cyclicity associated with the more severe forms of
lameness (i.e., score = 4 and 5) in dairy cows.
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