J. Dairy Sci.
84:1407–1412
 American Dairy Science Association, 2001.
Influence of Subclinical Mastitis During Early Lactation
on Reproductive Parameters
F. N. Schrick, M. E. Hockett, A. M. Saxton,
M. J. Lewis, H. H. Dowlen, and S. P. Oliver
Department of Animal Science, Institute of Agriculture,
The University of Tennessee, Knoxville 37996
ABSTRACT
Our objective was to determine the effects of mastitis
during early lactation on the reproductive performance
of Jersey cows. From 1986 to 1997, quarter foremilk
samples were collected every 4 to 8 wk during lactation,
at drying off, near calving, and when clinical mastitis
was diagnosed and were evaluated microbiologically
to identify causative bacteria. Services per conception,
days open, and days to first service were obtained from
DHIA records on 752 cows. Cows were separated by
mastitis type (clinical, n = 186; subclinical, n = 240;
control, uninfected or infected after confirmed preg-
nancy, n = 326). Cows were reclassified based on the
time of clinical or subclinical mastitis as follows: period
1, before first service (n = 374); period 2, between first
service and pregnancy (n = 52); and period 3, after con-
firmed pregnancy or uninfected (control; n = 326). Milk
production did not differ for any group separations.
Reproductive performance did not differ between gram-
negative or gram-positive mastitis pathogens. Cows
with clinical or subclinical mastitis before first service
had increased days to first service (77.3 ± 2.7 and 74.8
± 2.7 d), days open (110.0 ± 6.9 and 107.7 ± 6.9 d),
and services per conception (2.1 ± 0.2 and 2.1 ± 0.2)
compared with controls (67.8 ± 2.2 d, 85.4 ± 5.8 d, 1.6
± 0.2; P < 0.05). Days to first service were not increased
in cows with clinical or subclinical mastitis during pe-
riod 2 (70.6 ± 3.3 and 61.2 ± 7.8 d). However, days open
(143.6 ± 8.5 d) and services per conception (3.0 ± 0.2)
were increased (P < 0.05) in cows with clinical mastitis
during period 2, but not in cows with subclinical masti-
tis (90.9 ± 20.2 d and 2.1 ± 0.5). Cows initially diagnosed
subclinical that became clinical during period 2 exhib-
ited increased days to first service (93.9 ± 10.1 d), days
open (196.0 ± 26.2 d), and services per conception (4.3
± 0.7) compared with control animals (P < 0.05). In
conclusion, subclinical mastitis reduced reproductive
Received July 31, 2000.
Accepted January 2, 2001.
Corresponding author: F. N. Schrick; e-mail: fschrick@utk.edu.
1407
performance of lactating cows similar to clinical masti-
tis. Subclinical mastitis followed by clinical mastitis
resulted in the most severe loss in reproductive per-
formance.
(Key words: mastitis, reproduction, dairy cattle)
Abbreviation key: DFS = days to first service, DO
= days open, S/C = services per conception, PGF2α =
prostaglandin F2α, P4 = progesterone.
INTRODUCTION
Mastitis is an inflammation of the udder that affects
a high proportion of dairy cows throughout the world.
Mastitis has been described as the most economically
imposing disease facing dairy producers in the United
States, costing an estimated $2 billion annually (De-
Graves and Fetrow, 1993). Mastitis significantly de-
creases production and alters milk composition. Several
species of bacteria are able to invade the mammary
gland, multiply there, and produce harmful substances
that result in an inflammatory response. Signs of clini-
cal mastitis include alterations in milk composition and
appearance; decreased milk production; elevated body
temperature; and swelling, redness, or heat in infected
quarters. Subclinical infections also decrease milk pro-
duction. Mastitis is difficult to control because several
different species have the ability to infect the udder.
Thus, even cows from well-managed dairy herds utiliz-
ing the most recent and effective control measures can
experience a high rate of mastitis, especially during
the first 90 d of lactation. Many of these IMI originate
during the dry or nonlactating period and result in
clinical and (or) subclinical mastitis during early lac-
tation.
Mastitis has also been implicated in decreasing repro-
ductive performance. Moore et al. (1991) reported a
negative correlation between clinical mastitis and re-
production due to altered interestrus intervals and de-
creased length of the luteal phase in cows with clinical
mastitis caused by gram-negative mastitis pathogens.
Cullor (1990) suggested that endotoxin might induce
luteolysis and influence conception and early embryonic
1408 SCHRICK ET AL.
survival by the release of inflammatory mediators.
Moore and O’Connor (1993) hypothesized that gram-
negative mastitis pathogens may stimulate production
of prostaglandin F2α (PGF2α), which subsequently
would cause luteal regression.
More recently, Barker et al. (1998) demonstrated that
onset of clinical mastitis before first service increased
the number of days to first service (DFS) and days open
(DO) compared with cows without clinical mastitis or
cows with clinical mastitis after establishment of preg-
nancy. Furthermore, services per conception (S/C) and
DO were both increased in cows with onset of clinical
mastitis between first service and conception compared
with cows without clinical mastitis or cows with clinical
mastitis after conception. However, little is known
about the effects of subclinical mastitis during early
lactation on reproductive performance. Thus, the objec-
tive of the present study was to determine the effects
of subclinical mastitis during early lactation on repro-
ductive performance of Jersey cows.
MATERIALS AND METHODS
Microbiological data on quarter foremilk samples col-
lected every 4 to 8 wk from all lactating cows in The
University of Tennessee Dairy Experiment Station re-
search herd from 1986 to 1997 were evaluated. In addi-
tion, microbiological data of foremilk samples obtained
near calving, at drying off, and when clinical mastitis
was diagnosed were evaluated to identify causative
bacteria.
Cows were milked twice daily in a 12-stall trigon
milking parlor equipped with automatic milking ma-
chine take-offs (Westfalia-Surge, Naperville, IL). Teat
dipping was routinely performed at milking. Milking
machines were backflushed (Surge Backflush II, West-
falia-Surge) after removal from cows. Milking equip-
ment was evaluated routinely and maintained per the
manufacturer’s recommendation. Cows were housed in
free stalls bedded, and dairy waste solids were sepa-
rated from a manure slurry (Alfa-Laval, Inc., Kansas
City, MO). Cows were pastured 4 to 6 h/d. All cows
were dried off approximately 8 wk before expected calv-
ing, and all quarters of cows were infused with an anti-
biotic preparation approved for use in nonlactating
cows following the last milking of lactation.
During lactation, cows were observed for estrus for
30 min at least three times daily. Milking personnel
observed cows at milking time and all farm personnel
participated regularly in detection of estrus throughout
the day. When weather permitted, cows were allowed
access to dirt and grass paddocks during detection of
estrus. After calving, cows were subjected to a voluntary
waiting period of 60 d before first insemination. Cows
Journal of Dairy Science Vol. 84, No. 6, 2001
were inseminated utilizing the a.m/p.m. rule following
detection of estrus. Postpartum reproductive exams
were performed on all cows during the voluntary wait-
ing period. Pregnancy examinations were performed 50
to 65 d after insemination.
Milking personnel identified cows with clinical masti-
tis, and treatment for mastitis was initiated after sam-
ples were collected. Treatment for clinical mastitis in-
cluded intramammary therapy with cephapirin (Bristol
Myers, Evansville, IN) and administration of an anti-
inflammatory agent depending on systemic severity of
the infection. Cows with severe cases of clinical mastitis
also received an antihistamine intravenously. Samples
of foremilk from all quarters of cows with clinical masti-
tis were collected aseptically upon diagnosis as de-
scribed by Oliver et al. (1994). Before sample collection,
teats of cows were cleaned thoroughly and dried with
individual disposable paper towels, and teat ends were
sanitized with swabs containing 70% isopropyl alcohol.
After sample collection, samples were stored frozen un-
til transported to the laboratory.
Milk samples for microbiological analysis were exam-
ined following procedures described by Oliver et al.
(1994). Briefly, foremilk (10 µl) from each quarter was
plated onto one quadrant of a trypticase soy agar plate
supplemented with 5% defibrinated sheep blood (Bec-
ton Dickinson Microbiology Systems, Cockeysville,
MD). Plates were incubated at 37°C and bacterial
growth was recorded at 24-h intervals for 2 d. Bacteria
on primary culture medium were identified tentatively
according to colony morphologic features, hemolytic
characteristics, Gram-stain reaction, and catalase test.
Isolates presumptively identified as staphylococci were
tested for coagulase by the tube coagulase method, and
all coagulase-positive isolates were plated on mannitol
salt agar slants. Isolates identified presumptively as
streptococci were evaluated initially for growth in 6.5%
NaCl, hydrolysis of esculin and sodium hippurate, and
cAMP reaction. Streptococcal organisms were identified
to the species level using the API 20 Strep system (bi-
oMerieux Vitek, Inc., Hazelwood, MO). Gram-negative
isolates were plated on MacConkey’s agar (Becton Dick-
inson Microbiology Systems) and evaluated initially by
the following biochemical tests: triple sugar iron, urea,
oxidase, motility, indole, and ornithine decarboxylase.
Gram-negative isolates were identified to the species
level using the API 20E Identification System (bioMer-
ieux Vitek, Inc.).
Measures of reproductive performance were obtained
from DHIA records on 758 Jersey cows. Reproductive
parameters included S/C, DO, and DFS. Cows were
first separated by type of mastitis (clinical, n = 186;
subclinical, n = 240; control, uninfected or infected after
pregnancy confirmation, n = 326). Subclinical mastitis
 SUBCLINICAL MASTITIS AND REPRODUCTION 1409
Table 1. Distribution of cows among various classifications.1

Time classification Uninfected Subclinical Clinical Sub to clinical2 Total clinical

Before first service NA 229 81 64 145
Between first service and
pregnancy NA 11 35 6 41
Control 326 NA NA NA NA
1
Number of cows per designated grouping.
2
Cows classified as subclinical either before first service (n=64) or during the breeding period (n=6) which
subsequently became clinical.
NA = not applicable.

was defined as the presence of the same pathogen in
at least two consecutive samples during lactation. Cows
were further reclassified based on the time of clinical
or subclinical mastitis as follows: period 1, before first
service (n = 374); period 2, between first insemination
and pregnancy (n = 52); and period 3, after confirmed
pregnancy or uninfected (n = 326). A subsequent analy-
sis evaluated cows with clinical mastitis that were in-
fected subclinically before detection of clinical mastitis.
These cows were divided into the same three groups as
described above and shown in Table 1, and reproductive
performance data were evaluated. Milk production (305
d mature equivalent), lactation number (range 1 to 10),
season of year, and bacterial type were included in the
model. Data were analyzed using the MIXED procedure
of SAS (SAS, 1996).
RESULTS
The majority of infections were due to Escherichia
coli, Streptococcus dysgalactiae, coagulase-negative
staphylococci, Staphylococcus aureus, and Streptococ-
cus uberis (Table 2). No differences in measures of re-
productive performance were detected due to milk pro-
duction or between gram-positive and gram-negative
mastitis pathogens (data not shown). Milk production
did not differ for any group separations (7465 ± 259 kg;
P = 0.9) and was removed from subsequent analyses.
Season of calving negatively affected DFS and DO (Ta-
ble 3) but had no effect on S/C.
Days to first insemination were greater (P = 0.01) in
cows that exhibited clinical or subclinical mastitis be-
fore first AI (75.7 ± 1.8 d) compared with animals that
were uninfected or exhibited mastitis after pregnancy
was confirmed (67.8 ± 2.2 d; Figure 1). Cows that demon-
strated either clinical or subclinical mastitis between
first AI and establishment of pregnancy were interme-
diate in DFS (75.2 ± 4.4 d) and did not differ from
control cows. However, DO and S/C were increased (P <
0.001) in cows with either clinical or subclinical mastitis
between first AI and establishment of pregnancy (143.5
± 11.4 d and 3.1 ± 0.3, respectively) compared with
control animals (85.4 ± 5.8 d and 1.6 ± 0.2; Figure 1).
Furthermore, cows that exhibited clinical or subclinical
mastitis before first insemination were intermediate for
DO and S/C (106.2 ± 4.8 d and 2.0 ± 0.1), which differed
from both comparative groups.

Table 2. Mastitis pathogens isolated from mammary glands of cows

with clinical or subclinical mastitis during early lactation or following
pregnancy confirmation.
Pathogen n

Coagulase-negative staphylococci 186

Staphylococcus aureus 29
Escherichia coli 48
Streptococcus uberis 39
Streptococcus dysgalactiae 33
Streptococcus equinus 30
Enterococcus faecalis 3 Figure 1. Effects of time of mastitis occurrence on days to first
Bacillus species 14 insemination, days open, and services per conception. Bars represent
Other pathogens (including multiple types) 47 clinical and(or) subclinical mastitis before first insemination (black),
Clinical mastitis—bacteriologically negative 70 mastitis between first insemination and pregnancy (gray), and masti-
Total 499 tis after pregnancy confirmation or uninfected (hatched). Means with
different superscripts within bar groups differ at P < 0.01.

Journal of Dairy Science Vol. 84, No. 6, 2001

1410 SCHRICK ET AL.

Table 3. Effect of calving date (season) on reproductive performance of lactating Jersey cows.

Services per
Season n Days to 1st service Days open conception
April to August 195 82.1 ± 2.0a 115.5 ± 5.2a 2.1 ± 0.1
September to November 231 68.7 ± 1.7b 103.5 ± 4.3b 1.9 ± 0.1
December to March 332 67.0 ± 1.6b 98.7 ± 4.1b 2.1 ± 0.1
Values with different superscripts within columns differ at P < 0.05.
a,b

Cows with clinical or subclinical mastitis before first
service had increased DFS (77.3 ± 2.7 and 74.8 ± 2.7
d, respectively), DO (110.0 ± 6.9 and 107.7 ± 6.9 d,
respectively), and S/C (2.1 ± 0.2 and 2.1 ± 0.2, respec-
tively) compared with control (67.8 ± 2.2 d, 85.4 ± 5.8
d, 1.6 ± 0.2; P < 0.05; Figure 2). Days to first service
were not increased in cows with clinical or subclinical
mastitis between first service and conception (period 2;
70.6 ± 3.3 and 61.2 ± 7.8 d; Figure 3). However, DO
(143.6 ± 8.5 d) and S/C (3.0 ± 0.2) were increased (P <
0.05) in clinical cows, but not subclinical (90.9 ± 20.2 d
and 2.1 ± 0.5). Cows with subclinical mastitis initially
that became clinical during period 2 exhibited increased
DFS (93.9 ± 10.1 d), DO (196.0 ± 26.2 d), and S/C (4.3
± 0.7; P < 0.05) compared with control animals (Figure
3). However, caution should be used when interpreting
these data for this grouping because the number of
animals was extremely low.
DISCUSSION
The occurrence of subclinical mastitis during early
lactation resulted in detrimental effects on reproductive
performance similar to those for cows exhibiting clinical
mastitis. The mechanism(s) by which clinical or subclin-
ical mastitis may influence reproductive performance
is unknown. Therefore, potential mechanisms through
which mastitis may affect reproductive efficiency will
be discussed.
Clinical or subclinical mastitis may influence repro-
ductive response by alterations in endocrine profiles
and follicular development. Battaglia et al. (1997)
treated ewes intravenously with endotoxin, a compo-
nent of the cell wall of gram-negative bacteria that
causes an inflammatory response, and sampled hypo-
physeal portal blood simultaneously with jugular blood
at 10-min intervals to observe GnRH, LH, cortisol, and
progesterone (P4). Ewes treated with endotoxin had a
significantly lower GnRH pulse amplitude, lower con-
centrations of GnRH and LH, elevated concentrations
of cortisol and P4, and a higher body temperature com-
pared with control animals. Peter et al. (1989) reported
that endotoxin administration to cycling heifers re-
sulted in elevated cortisol concentrations and smaller

Figure 2. Effects of mastitis type before first insemination on days
to first insemination, days open, and services per conception. Time of
mastitis occurrence for animals assigned to the subclinical to clinical
group (sub to clinical) was based upon timing of subclinical mastitis
diagnosis. Bars represent infection type before first insemination:
clinical (black), subclinical (gray), subclinical to clinical (striped),
and mastitis after a pregnancy confirmation or uninfected (control;
hatched). Means with different superscripts within bar groups differ
at P < 0.05.
Figure 3. Effects of mastitis type during the breeding period on
days to first insemination, days open, and services per conception.
Time of mastitis occurrence for animals assigned to the subclinical
to clinical group (sub to clinical) was based upon timing of subclinical
mastitis diagnosis. Bars represent infection type during, between,
before first insemination, and conception: clinical (black), subclinical
(gray), subclinical to clinical (striped), and mastitis after pregnancy
confirmation or uninfected (control; hatched). Means with different
superscripts within bar groups differ at P < 0.05.

Journal of Dairy Science Vol. 84, No. 6, 2001

 SUBCLINICAL MASTITIS AND REPRODUCTION
follicles on d 12 of the estrous cycle. Peter et al. (1989)
also observed that follicles failing to ovulate from
PGF2a-induced luteal regression resulted in cysts that
persisted for 7 to 21 d. The formation of follicular cysts
on ovaries might be a result of cortisol suppression of
the LH surge (Lopez-Diaz and Bosu, 1992).
Inflammation stimulates the immune system, re-
sulting in the release of cytokines which may inhibit
the action of FSH on LH receptor formation in cultured
rat granulosa cells and inhibit FSH-induced cAMP pro-
duction (Darbon et al., 1989). Other research (McCann
et al., 1997) indicates that cytokines, released following
endotoxin challenge, block the pulsatile secretion of LH
but not FSH through alterations in nitric oxide produc-
tion to inhibit GnRH. Consequently, mastitis could in-
fluence reproductive function via alterations in LH and
FSH activity or function, thus affecting follicular devel-
opment and (or) oocyte maturation.
Another possible action of mastitis involved in in-
creasing DO and S/C may be to influence the develop-
mental capabilty of the ovulatory oocyte. Luteinizing
hormone is responsible for the initiation of oocyte matu-
ration (Wise et al., 1994). Oocyte maturation is accom-
panied by an expansion of the cumulus cell layer medi-
ated by FSH and LH (Zuelke and Brackett, 1994). Fur-
thermore, LH has been reported to increase glucose and
pyruvate oxidation in cumulus cells in order to nourish
the oocyte (Zuelke and Brackett, 1994). Suppression of
LH experienced by cows with mastitis may affect the
ability of oocytes to mature and (or) alter expansion of
cumulus cells. Recent studies from our laboratory did
not reveal a suppression in GnRH-induced LH during
diestrus in lactating cows following experimentally in-
duced clinical mastitis (Hockett et al., 2000). Studies
investigating LH profiles during the preovulatory pe-
riod and estrus are ongoing.
Another symptom often associated with clinical mas-
titis is an elevated body temperature. Experimentally
induced S. uberis clinical mastitis resulted in elevated
body temperatures (Hockett et al., 2000). Thatcher and
Hansen (1993) documented that cows exposed to heat
stress experienced increased embryonic mortality. Fur-
thermore, it has been reported that effects of hyperther-
mia were greatest when experienced between the onset
of estrus and insemination (Putney et al., 1989) or dur-
ing early embryonic development (Ealy et al., 1993).
Edwards and Hansen (1996) reported that exposure
of bovine oocytes to elevated temperatures decreased
blastocyst formation.
A third mechanism by which mastitis may negatively
affect the oocyte is a secondary response to changes in
endocrine status. Suppressed LH surge (delayed ovula-
tion) or elevation of PGF2α (decreased P4) may result
in persistent follicles (Savio et al., 1993; Ahmad et al.,
1411
1995). Ahmad et al. (1995) reported decreased recovery
of embryos on d 6 postmating in cows with persistent
follicles than in cows with growing follicles. Further-
more, fewer embryos reached the 16-cell or morula
stage of development from persistent follicles than from
growing follicles. Peter et al. (1989) reported that intra-
uterine infusion of endotoxin suppressed LH and re-
sulted in follicles that did not ovulate. Therefore, cows
with clinical or subclinical mastitis may have increased
S/C and DO due to the formation of persistent follicles
or follicular cysts.
During the postovulatory period, mastitic infections
may influence the embryo or uterus. One component
normally elevated in animals infected by gram-negative
pathogens is PGF2α (Janosi et al., 1998). Gilbert et al.
(1990) reported that intrauterine infusion of E. coli re-
sulted in shortened estrous cycles in Holstein heifers,
implying that prostaglandins were stimulated and lu-
teolysis occurred. Hockett et al. (2000) observed an in-
creased sensitivity of the uterus to release of PGF2α in
cows with experimentally induced S. uberis mastitis
during the luteal phase of the estrous cycle and hypoth-
esized that prostaglandins may decrease reproductive
efficiency by decreasing luteal life span or by decreasing
embryo quality and development. Giri et al. (1991) re-
ported that endotoxin exposure caused a dose-depen-
dent increase in the concentration of plasma PGF2α
with a subsequent drop in P4 concentrations.
Schrick et al. (1993) reported a negative correlation
between bovine embryo quality and uterine luminal
concentrations of PGF2α. Seals et al. (1998) showed that
administration of PGF2α from d 5 through 8 postmating
to progestogen-supplemented cows resulted in de-
creased pregnancy rates compared with cows adminis-
tered saline only. Administration of PGF2α to progesto-
gen-supplemented cows on d 5 through 8 resulted in a
decreased percentage of embryos that developed beyond
the morula stage and a decrease in embryo quality
scores (Hockett et al., 1998). Elevated concentrations
of serum PGF2α associated with mastitis may cause
a decrease in embryonic development and ultimately
result in an increased number of services per conception
and number of DO.
CONCLUSIONS
Cows from well-managed dairy herds utilizing the
most recent and most effective mastitis control mea-
sures continue to experience a high rate of subclinical
and clinical mastitis, especially during the first 90 d of
lactation. Results of this study demonstrate clearly that
mastitis decreases reproductive performance of dairy
cows. Reproductive efficiency is of great concern to dairy
producers. Each day an animal fails to establish preg-
Journal of Dairy Science Vol. 84, No. 6, 2001
1412 SCHRICK ET AL.
nancy over 90 d is associated with monetary losses
(Britt, 1974; Fetrow and Blanchard, 1987). These losses
are in addition to other well known costs associated
with mastitis such as decreased milk production, al-
tered milk composition, treatment costs, discarded
milk, and increased involuntary culling rates. Collec-
tively, economic losses associated with mastitis and re-
duced reproductive performance are obviously signifi-
cant and merit further investigation. In conclusion, sub-
clinical mastitis was equal to clinical mastitis in its
detrimental effects on reproductive performance of lac-
tating cows. Reproductive performance is most severely
impacted when subclinical infections develop, then
progress to the clinical stage.
ACKNOWLEDGMENTS
This research was funded, in part, by the American
Jersey Cattle Association (Reynoldsberg, OH) Research
Foundation and supported by the Tennessee Agricul-
tural Experiment Station, and The University of Ten-
nessee, College of Veterinary Medicine, Center of Excel-
lence Research Program in Livestock Diseases and Hu-
man Health.
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