SYMPOSIUM: MASTITIS AND GENETIC EVALUATION

FOR SOMATIC CELL COUNT

Physiology of Mastitis and Factors Affecting

Somatic Cell Counts'
R. J. HARMON
Department of Animal Science
University of Kentucky
Lexington 40546

ABSTRACT proximately $2 billion in the United States

Inflammation of the mammary gland alone. This number excludes the additional
that results from the introduction and untold losses from altered milk quality and
multiplication of pathogenic microorgan- composition and the effects on dairy products
isms in the mammary gland is a complex that occur once milk has left the farm. The
series of events leading to reduced syn- complexity is reflected in the numerous causa-
tive pathogens, the variety and magnitude of
thetic activity, compositional changes,
the physiological responses to these pathogens,
and elevated SCC. The magnitude and
and the variation in efficacy of control meas-
temporal relationships of these responses
ures for different causative organisms. The
vary with nutritional status, other animal
purpose of this review is to describe the in-
factors, and the pathogen involved. Be-
flammatory response in the bovine mammary
cause the elevation of SCC is a response gland and the factors that influence SCC in
to an insult to the mammary gland and is milk.
modulated by inflammatory mediators,
the major factor influencing SCC is in-
fection status. The effects of stage of DISCUSSION
lactation, age, season, and various
stresses on SCC are minor if the gland is Mastitis Pathogens
uninfected. Except for normal diurnal 'Ihe causative bacteria can be categorized as
variation, few factors other than infection major or minor pathogens (13,23, 27, 54). The
status have a significant impact on milk
most common major pathogens include
SCC. Staphylococcus aureus, Streptococcus agalac-
(Key words: mastitis, somatic cell count) riae, and coliforms, streptococci, and en-
Abbreviation key: BTSCC = bulk tank SCC, terococci of environmental origin. Individual
GSH-Px = glutathione peroxidase, PMN = cases or sporadic outbreaks of mastitis may be
polymorphonuclear neutrophil leukocyte. caused by Pseudomonas spp., Actinomyces
pyogenes, Serratia spp., or other unusual
pathogens. Mastitis caused by the major patho-
INTRODUCTION
gens results in the greatest compositional
Mastitis, or inflammation of the mammary changes of milk, including increases in SCC,
gland, is one of the most complex and costly and has the most economic impact of all
diseases of the dairy industry (13). The wide- causative organisms. Coagulase-negative
spread occurrence of the disease in dairy herds staphylococci and Corynebacterium bovis are
creates an estimated loss to producers of ap- considered to be minor pathogens (23, 24).
Infections by these organisms cause only
moderate inflammation with SCC exceeding
those of uninfected glands by only two- to
Received June 16, 1993. threefold. Minor pathogen infections are infre-
Accepted November 4, 1993.
'This manuscript (93-5-105) is published with the ap-
quently associated with clinical mastitis,
proval of the director of the Kentucky Agricultural Experi- marked compositional changes in milk, or dra-
ment Station. matic decreases in milk production.

1994 J Dairy Sci 77:2103-2112 2103

2104
Staphylococcus aureus and Strep. agalac-
tiae are contagious mastitis pathogens (13) for
which the major reservoir is the infected udder,
and infections are spread among cows during
the milking process. Infections tend to be
chronic and subclinical but with periodic clini-
cal episodes. The environmental pathogens in-
clude the coliforms and environmental strep-
tococci and enterococci. The coliforms are a
group of Gram-negative pathogens that include
Escherichia coli, Klebsiella spp., Enterobacter
spp., and Citrobacter spp. Streptococcus dys-
galactiae, Streptococcus uberis, Streptococcus
bovis, Enterococcus faecium and Enterococ-
cus faecalis are common environmental strep-
tococci and enterococci (27,63). The source of
environmental pathogens, as the term suggests,
is the surroundings of the cow (e.g., bedding,
manure, and soil). Although new infections by
environmental pathogens can occur at milking,
primary exposure appears to be between milk-
ings. Approximately 70 to 80% of coliform
infections become clinical (abnormal milk, ud-
der swelling, or systemic symptoms), and
about 50% of environmental streptococcal in-
fections display clinical symptoms. Sixty to
70% of environmental pathogen infections ex-
ist for less than 30 d.
Inflammation
Infections of the mammary gland by patho-
genic bacteria result in decreased milk produc-
tion and compositional changes that vary with
the intensity and duration of the infection (13,
54). Subclinical infections are those for which
no visible changes occur in the appearance of
the milk or the udder, but milk production
decreases, bacteria are present in the secretion,
and composition is altered. Clinical mastitis is
characterized by abnormal milk and swelling
or pain in the udder and may be accompanied
by systemic signs such as elevated rectal tem-
perature, lethargy, or anorexia. As in subclini-
cal mastitis, milk production declines, bacteria
are present in the milk, and dramatic changes
in milk composition are usually present.
An inflammatory response is initiated when
bacteria enter the mammary gland through the
teat canal and multiply in the milk (13). Bac-
terial toxins, enzymes, and cell-wall compo-
nents may have a direct effect on the function
of the mammary epithelium but also stimulate
Journal of Dairy Science Vol. 77. No. 7, 1994
HARMON
the production of numerous mediators of in-
flammation by inflammatory cells that may be
directly involved in the pathogenesis of the
disease (18). These mediators include comple-
ment components (18, 30), prostaglandins (1,
19). leukotrienes (52). histamine (54, 68),
serotonin, interleukins (10, 61), tumor necrosis
factor (2, 61), interferon (2), and other
cytokines (2, 10, 29). The classical symptoms
of inflammation include increased vascular
permeability, vasodilation, edema, increased
blood flow, neutrophil margination and migra-
tion, decreased mammary synthetic activity,
pain, and fever (18). Marked mononuclear leu-
kocyte infiltration may be noted with chronic
infections (44).Elevated serum cortisol (59)
and decreased plasma iron and zinc (34) have
been observed in clinical models for mastitis.
The new infection rate, as well as the mag-
nitude of the inflammatory response once an
infection occurs, may be influenced by the
causative pathogen (13, 54, 63), stage of lacta-
tion (27,63), age (27,63), immune status of the
cow (9, 41), genetics (30), and nutritional sta-
tus. Deficiencies in dietary selenium and vita-
min E result in increased incidence of mastitis,
but supplemental dietary Se and vitamin E
lower the frequency and shorten the duration
of clinical mastitis (62). Herd prevalence of
intramammary infection decreased as mean ac-
tivity of glutathione peroxidase (GSH-Px) in-
creased; Se is an essential component of this
enzyme (17). Erskine et al. (16) showed that
experimental E. coli mastitis was less severe
and shorter for cows supplemented with Se
than for cows deficient in Se. Killing of E. coli
by milk neutrophils from cows deficient in Se
was decreased. Also, diets deficient in vitamin
A or &carotene resulted in increased incidence
of mastitis (7).
There is considerable current interest in the
role of free radical biology and antioxidant
systems in health and disease. Highly reactive
oxygen species or free radicals can be gener-
ated in the presence of oxygen during normal
cellular metabolism or during inflammation
(4). These free radicals or other reactive
molecules can result in tissue damage through
lipid peroxidation of cellular membrane com-
ponents, inactivation or denaturation of en-
zymes, DNA damage, or damage to carbohy-
drates that can alter cellular receptor function
(4). Several naturally occumng antioxidant
 SYMPOSIUM:MASTITIS AND GENETIC EVALUATION FOR SOMATIC CELL COUNT 2105
compounds can inactivate these free radicals or TABLE 1. Compositional changes in milk constituents
prevent their generation. Naturally occurring associated with elevated SCC.1
antioxidants include superoxide dismutase, Milk
GSH-Px, vitamin E, catalase, ascorbic acid, Normal with high Percentage
and &carotene. Increased dietary Se resulted Constituent milk SCC of normal
in increased activities of GSH-Px, a selenoen- (W
zyme (17). The benefits of supplemental die- SNF 8.9 8.8 99
tary Se and vitamin E on mastitis (16, 17, 62) Fat 3.5 3.2 91
may be related to their effects on antioxidant -0% 4.9 4.4 90
mechanisms. Total protein 3.61 3.56 99
Total casein 2.8 2.3 82
One of the initial components of the i d a m - whey protein .8 1.3 162
matory response that is a major line of defense Scnun albumin .a .07 350
for the udder is the influx of polymor- Lactofenin .02 .10 500
phonuclear neutrophil (PMN) leukocytes into Immunoglobulins .10 .60 600
sodium .057 .lo5 184
the mammary tissue (8, 21, 22, 42, 47). The Chloridt ,091 .147 161
P M N normally flow freely through capillaries Potassium .173 ,157 91
with only minimal adherence to vessel walls. Calcium .12 .04 33
During infection and inflammation, adhesion 1Examples of compositional changes found in various
molecules are expressed, and P M N marginate studies. Adapted from work of Eberhart et al. (13) and
or adhere to the endothelium of smaller blood Kitchen (31).
vessels and pass between cells lining the ves-
sel. Chemical messengers or chemotactic
agents released from leukocytes normally in
the milk or from damaged tissues attract PMN In addition to elevated SCC, infection
into milk in large numbers (8). The PMN causes a number of other events in the mam-
appear in large numbers lined up outside some mary gland. Toxins produced by bacteria or
alveoli (22, 42). In other areas, damage to mediators of inflammation damage milk-
milk-synthesizing cells may be apparent, and producing tissue, resulting in less total synthe-
masses of PMN may pass between epithelial sis of milk (8, 13, 59, 60,61). Changes in the
cells into the lumen of the alveolus. Thus, the permeability of blood vessels and mammary
end result of this process is an increase in the epithelium lead to the leakage of blood compo-
SCC in milk resulting from P M N migration to nents into milk and the movement of some
the site of infection. The PMN also infiltrate normal milk components out of the alveolar
the linings of teat and duct cisterns and the teat lumen into the perivascular space. Clots
duct (22, 42, 43). These areas may be sites of formed by the aggregation of leukocytes and
migration during the initial response to inva- blood clotting factors may block small ducts
sion. and prevent complete milk removal (13). Dam-
The function of PMN in milk is to engulf age to epithelial cells and blockage of small
and to digest the invading bacteria (8, 47). ducts can result in the formation of scar tissue
When PMN enter milk, they also engulf other in some cases with a permanent loss of func-
particles such as fat globules and casein, which tion of that portion of the gland. In other cases,
decreases their efficiency compared with that inflammation may subside, tissue repair may
of blood cells. However, P M N still remain a occur, and function may return in that lactation
key defense mechanism in the udder. The leu- or the subsequent one.
kocytes in milk may also release specific sub-
stances that change the permeability of blood Comporltlonal Changm
vessels or attract more leukocytes to the area
to fight the infection (8, 18). With persistent Compositional changes accompany the ele-
bacterial infections, leukocyte numbers may vation of SCC and inflammation in an infected
fluctuate, but generally remain abnormally mammary gland (31, 36). Table 1 lists exam-
high. Such abnormal numbers of somatic cells ples of some changes in milk components that
continue after bacteria are eliminated until accompany mastitis. Mastitis or elevated SCC
healing of the gland occurs. are associated with a decrease in lactose, a-
Journal of Dairy Science Vol. 77, No. 7, 1994
2106
lactalbumin, and fat in milk because of
reduced synthetic activity of the mammary tis-
sue. Some studies [review (31)] have shown no
change in fat content, yet total fat yield
decreases because of a decline in milk produc-
tion. Some components, such as lactose (60)
and a-lactalbumin (38), may leak out of the
alveolus between epithelial cells; these compo-
nents have been measured in urine or blood of
cows with mastitis. Although total protein con-
tent may undergo little change, the types of
proteins present change dramatically. The con-
tent of casein, the major milk protein of high
nutritional quality, declines, but lower quality
(for dauy products) whey proteins increase.
Serum albumin, immunoglobulins, transfemn,
and other serum proteins pass into milk be-
cause vascular permeability changes (31, 36).
Lactofemn, the major antibacterial iron-
binding protein in mammary secretions, in-
creases in concentration, likely because of in-
creased output by the mammary tissue and a
minor contribution from PMN (25).
Mastitis also markedly changes the ionic
environment and increases the conductivity of
milk (32,36). Sodium and chloride increase
because of passage from blood into milk.
Potassium, normally the predominant mineral
in milk, declines because of paracellular pas-
sage out of the alveolar lumen between
damaged epithelial cells. Because most cal-
cium in milk is associated with casein, the
disruption of casein synthesis contributes to
lowered calcium in milk.
The pH may increase from a normal of 6.6
to 6.9or higher because of movement of blood
components into milk (31). Many enzymes and
other whey proteins originating from damaged
tissue, the blood, or leukocytes are elevated in
milk. Examples of enzymes that may have
increased activity are acid phosphatase, al-
antitrypsin (antitrypsin or al-protease inhibi-
tor), alkaline phosphatase, arylsulfatase, 8-
glucuronidase, catalase, glutamic-oxaloacetic
transaminase, lactate dehydrogenase, lipase,
lysozyme, NAGase, plasmin, xanthine oxidase,
and various esterases (31). Increased free fatty
acids also occur in milk with high SCC.
Kitchen (31) suggested that the lysosomal en-
zyme NAGase is an indicator of tissue damage
during mastitis.
Milk protein breakdown that is dependent
on time and temperature can occur for milk of
Journal of Dairy Science Vol. 77, No. 7, 1994
HARMON
cows with clinical or subclinical mastitis from
proteolytic enzymes. Plasmin, an important
proteolytic enzyme in milk with high SCC (3,
65). is normally found in milk; however, there
may be more than 2-fold increases in its ac-
tivity in milk during mastitis. Plasminogen, the
inactive precursor to plasmin, normally occurs
in plasma. From a series of proteolytic
cleavages, plasminogen is converted to the ac-
tive form of plasmin (65). The activation is
thought to occur in the lumen of the alveolus
or early during the process of milk synthesis.
Plasmin and enzymes derived from somatic
cells can cause extensive damage to casein in
the udder before milk removal. One study
showed a drop of approximately 20% for the
intact casein content of fresh raw milk from
proteolysis during Strep. ugulucriue infections
(53). Although the rate of plasmin-related
casein breakdown is slowed at refrigeration
temperatures, plasmin is extremely heat stable.
Normal milk pasteurization times and tempera-
tures are not adequate to inactivate elevated
plasmin activities in abnormal milk. Thus, de-
terioration of milk protein as a result of masti-
tis may continue during processing and stor-
age, and further activation of plasmin may
continue.
Because of a strong relationship between
some of the inflammatory or compositional
changes in milk and the presence of infection
(8, 31, 36, 37), the measurement of certain
components has been used to monitor udder
health and, thus, milk quality. Milk SCC prob-
ably has been most widely used as a measure
of milk quality worldwide since the develop-
ment of rapid, electronic cell counting tech-
niques. Other proposed screening tests or tests
to monitor the course of infections have in-
cluded the measurement of catalase, NAGase,
antitrypsin, chloride, sodium, and serum albu-
min in milk (31, 36, 37).
Factors Affwlng Milk SCC
Somatic cell counts are readily available to
most dauy farmers today on a monthly basis
through the Dairy Herd Improvement program.
Extensive data are now available on large
numbers of cows concerning factors affecting
SCC in milk. When these data are combined
with bacteriological culture results, the factors
 SYMPOSIUM:MASTITIS AND GENETIC EVALUATION FOR SOMATIC CELL COUNT
TABLE 2. Estimated infection prevalence and losses in
milk production associated with elevated bulk tank SCC
(SncC).
Infected
quarters Production
BTSCC in herd loss'
(103/ml) (%I
200 6 0
500 16 6 200,000 (12). A higher elevation is abnormal
lo00 32 18
1500 48 29
1Produaion loss calculated as a percentage of p d u c -
tion expected at 2C0.000 celldml. From Eberhart et al.
(14).
of greatest importance can be determined, and
some misconceptions concerning changes in
SCC can be clarified. Several comprehensive
reviews and individual studies over the past 20
yr have addressed issues surrounding SCC,
their variation, and the potential use of SCC
for monitoring milk quality (5, 6, 11, 12, 14,
39, 48, 49, 50, 51, 55, 58). The previous
discussion of the inflammatory response in the
mammary gland is helpful for considering
those factors that influence SCC in milk.
Milk somatic cells are primarily leukocytes
or white blood cells, which include macro-
phages, lymphocytes, and PMN. Studies iden-
tifymg cell types in milk have shown that
epithelial cells infrequently occur in udder
secretions, including those from the dry gland,
and range from 0 to 7% of the cell population
(32). Thus, increases in SCC at the end of
lactation are not from sloughing of epithelial
cells. During inflammation, the major increase
in SCC is because of the influx of PMN into
the milk (8, 22, 39, 42, 47). At this time, over
90% of the cells may be PMN.
Infecrion Status. The major factor affecting
SCC at the quarter, cow, or bulk tank level is
an infection of the mammary gland (11).
Eberhart et al. (14) studied infection prevalence
for 80 herds and related this to bulk tank SCC
(BTSCC),which ranged from 103,000 to
1,591,000 celldml. Table 2 shows estimates of
infection prevalence by major pathogens and
production losses reported in this study. Obvi-
ously, an increase in BTSCC is related to
increased infection prevalence and decreased
milk production. An analysis of these data
2107
showed that infection prevalence was the ma-
jor determinant of BTSCC.
At the cow and quarter levels, SCC from
normal (i.e., uninfected) quarters are generally
below 200,000 but may be below 100,000
during first lactations of cows. One study esti-
mated that 50% of uninfected cows have SCC
under 100,W/ml, and 80% have under
and an indication of inflammation in the udder.
The major pathogens cause the greatest SCC
increase and include Staph. uureus, Strep.
ugulucriue, coliforms, and Streptococcus spp.
other than Strep. ugulactiue (12, 58). As noted
earlier, the minor pathogens (C. bovis and
coagulase-negative staphylococci) usually
cause only a moderate increase in SCC over
that of uninfected quarters (23).
Most studies indicate that the use of SCC
alone to classify quarters as infected or unin-
fected results in error from false positives and
false negatives (11, 49, SO). These errors may,
in part, be because of the normal fluctuation of
SCC observed throughout the course of an
infection. Temporal changes in SCC following
experimental challenge of mammary glands
(16, 56, 60,61) suggest dramatic changes in
the magnitude of the SCC during the early,
acute stages of the infection reaching a peak
SCC within hours or days, depending on the
challenge organism. This peak may be fol-
lowed by a modest reduction in SCC as bacte-
ria are killed by PMN. The magnitude of de-
cline in SCC can vary considerably and may
be dependent upon the bacteriological outcome
of the infection, the pathogen involved, and
cow differences. Examples of SCC changes
with time during naturally occurring Staph.
uureus infections are shown in Table 3 for the
University of Kentucky herd. The SCC in in-
fected quarters apparently tend to fluctuate.
For chronic infections, SCC and bacterial num-
bers tend to fluctuate with time (40,56).Table
3 also shows variation in SCC for uninfected
quarters, but the SCC still remains below
200,000.
The magnitude of SCC responses to major
pathogens varies among cows, and differentia-
tion between the types of pathogens does not
seem possible with SCC alone (11). Schultz
(55) reported that days, weeks, or longer may
be required for SCC to decrease after the
pathogens have been eliminated from the
Journal of Dairy Science Vol. 77, No. 7, 1994
2108 HARMON

TABLE 3. The SCC of uninfectcd quarters or quarters infected with Stuphylococcus aureus.
cow 46 Cow 834 cow 602
Date Infcclcd Uninfd Infected Uninfected Infected
~ ~~~~~~~~~~

(x 103/ml)
Sep 16 Presh Fresh 62 1 182 5447
Sep 30 419 169 1484 124 1344
Oct 14 151 90 940 28 720
Oct 28 203 117 838 101 495
Nov 18 350 54 193 67 3371
Dec 09 243 117 220 81 837
Ian 06 278 128 385 87 464
Feb 04 1551 99 43 1 74 62 1
Mar 04 377 84 47 1 I40 Culled
1Negative culture.

gland. The SCC in the bucket or composite
milk would also be expected to be related to
the number of quarters infected and the
amount of milk being produced by each. How-
ever, if all quarters of a cow are uninfected,
generally SCC below 200,000 would be ex-
pected for bucket milk.
The DHI program has adopted an SCC
scoring system (48) that divides the SCC of
composite milk into 10 categories from 0 to 9
(Table 4). This system has an advantage over
BTSCC because changes in the SCC of a small
number of cows does not markedly change the
herd mean score. About 50% of the cows are
above, and 50% are below, the herd mean
score. Both the BTSCC and herd mean SCC
score indicate the state of udder health of the
herd and should be used to monitor trends and
alert the dauy producer of problems. Treat-
ment during lactation based solely on in-
dividual SCC has been shown to be impracti-
fxl (64).
Age and Stage of Lacfation.Generally SCC
increases with advancing age and stage of
lactation. However, work by Eberhart et al.
(12) showed that, if cows are separated into
groups by infection status, little change in SCC
occurs for uninfected cows, either as they age
or during late lactation (Tables 5 and 6). Shel-
drake et al. (58) confumed that milk from
uninfected quarters displays little change in
SCC as number of lactations increase. In addi-
tion, they (58) showed that the SCC of milk
from uninfected quarters rose from 83,000 at

TABLE 4. Estimated differences in lactation milk produc-

tion associated with an incnase in SCC score. TABLE 5. Mean SCC by cow age and infection status.l
Difference in Infection status
M a milk production' All
SCC Mean Age cows None Minor2 Major3
Score SCC Lactation1 Ladation2
@103/ml) -& m a - - - (yr)
2 232 126
(X103/d)
190 614
12.5 ... ... 3 314 149 218 661
25 ... ... 4 390 148 233 753
50 ... ... 5 564 180 308 977
100 -9 1 -181 6 544 194 322 880
200 -181 -363 7 654 25 1 320 986
400 -272 -544 >7 868 113 519 1207
800 -363 -726 ~~ ~

1600 454 -907 'Data from 3130 cows. From Eberhart et al. (12).
~Comparisoosare with lactation production at SCC 2lnfections by minor pathogens.
scores of 2. From Raubertas and Shook (48). 3Infections by major pathogens.

Journal of Dairy Science Vol. 77, No. 7, 1994

 SYMPOSIUM: MASTITIS AND GENETIC EVALUATION FOR SOMATIC CELL COUNT 2109
TABLE 6. Mean SCC by days of laaation and infection (uninfected and infected with Staphylococcus
status.'
spp.) subjected to either heat stress or housed
.___..
.
All
Infection status in a thermoregulated environment were
Lactation cows None Minor2 Major3
~

145,000 and 105,000/ml. A portion of this

difference in SCC may be because of the
(4 (XI@/ml) decreased milk production that is observed
049 380 164 247 839 with heat stress. A 10 to 20% decline in milk
50-99 429 138 286 861 production is not unusual for dairy cattle ex-
100-149 498 125 240 1068
150-199 399 126 295 735
periencing heat stress (57). Although stray volt-
200-249 452 208 240 902 age may result in behavioral changes in dairy
250-299 445 139 267 758 cattle, no evidence exists that stray voltage
>300 634 165 374 1031 directly influences SCC in healthy udders (33).
Guidry et al. (20) reported that estrus has no
~ ~

1Data from 3130 cows. From Eberhatt et al. (12).

zlnfections by minor pathogens.
3lnfections by major pathogens.
35 d postpartum to 160,OOO by 285 d. How-
ever, the SCC of milk from quarters infected
with Staph. aureus rose from 234,000 to
1,000,OOO over the same period. All quarters,
regardless of infection status, had elevated
SCC immediately postpartum, but those quar-
ters with no infections or with minor pathogen
infections showed a rapid decline in SCC to 35
d postpartum; SCC in uninfected cows should
be less than 300,000 by 5 d postpartum (50).
Bodoh et al. (5) found SCC at the end of
lactation rose only after production had
dropped below 4 kg/d, but the infection status
of these cows was not determined. Feed or
water deprivation results in dramatic decreases
in milk production and proportional increases
in SCC (35, 50). This result can be interpreted
as a dilution phenomenon. Some (50, 55) have
suggested that the modest rise in SCC of unin-
fected quarters at the end of lactation is in fact
a dilution effect. Thus, the major influence of
parity and stage of lactation on SCC is related
to intramammary infection status.
Stress and Season. Stresses of various types
have been implicated as causing increases in
SCC (11). However, attempts to induce SCC
changes experimentally for uninfected cows by
injection of ACTH or corticosteroids or by
placing cows in environmentally controlled
chambers have shown only modest or no ef-
fects on milk SCC (45, 56, 66). Although a
recent Florida study (15) showed a significant
increase in SCC of milk from heat-stressed
cows, the respective mean SCC from cows
significant effect on SCC.
Somatic cell counts are generally lowest
during the winter and highest during the sum-
mer (11). which coincides with an increased
incidence of clinical mastitis during the sum-
mer months (28, 46, 63). Smith et al. (63)
showed that rate of infection with environmen-
tal pathogens was highest during the summer
and coincided with highest number of coli-
forms in bedding. They suggested that the
stress of high temperatures and humidity could
have increased the susceptibility to infection as
well as increased the numbers of pathogens to
which cows were exposed. Additional data
support the association of rates of clinical
mastitis with bacterial counts in bedding (28).
These findings support the concept that tem-
perature stress per se is not the cause of in-
creased SCC, but the increased SCC is a result
of greater exposure of teat ends to pathogens,
resulting in more new infections and clinical
cases during the summer months.
Other Factors. A normal variation in SCC
occurs with the fraction of milk collected
throughout a milking, and diurnal variation
occurs during the time between milkings (1 1,
67). In general, SCC are highest in the strip-
pings and lowest immediately before milking.
The elevated SCC may persist for up to 4 h
after milking and then gradually decline. This
difference in high and low SCC varies from
4- to 70-fold for individual quarters (67). Be-
cause correlation is high (r = .86) between SCC
in foremilk and composite or bucket milk (ll),
either of these types of samples can be rou-
tinely used to collect SCC data.
Brolund (6) has reported that variability in
SCC within breed was greater than differences
in SCC among breeds. Neither of these factors
approaches the impact of bacteriological status
on SCC.
Journal of Dairy Science Vol. 77, No. 7, 1994
21 10
Limitations of SCC. Certainly the use of
SCC records on a monthly basis can be a
useful tool for monitoring udder health of a
dairy herd. Multiple SCC records for in-
dividual cows or the entire herd are most
useful, but a single SCC record is relatively
inconclusive for reasons cited (50). The in-
terpretation of SCC records is particularly ap-
plicable to herds experiencing infections from
contagious pathogens. Because infections by
these pathogens tend to be of long duration,
new infections in the herd may lead to in-
creased prevalence of infection and are
reflected in elevated SCC for bulk tank or herd
average SCC scores. Hoblet et al. (26)
documented that well-managed herds that have
controlled mastitis from contagious pathogens
can experience clinical mastitis problems be-
cause of environmental pathogens, yet main-
tain herd average SCC below 300,000.In this
case, the long-tern health status of the udder
may not be clearly reflected in monthly herd
SCC or BTSCC. Intramammary infections by
environmental pathogens tend to be shorter
than those caused by contagious pathogens; 60
to 70% of these environmental infections may
last less than 30 d (27). The period of elevated
SCC for these cows would be correspondingly
shorter as well. The prevalence of infection by
environmental pathogens at any point in time
also tends to be low (less than 10% of quar-
ters). Thus, herds that predominantly have en-
vironmental mastitis may have SCC below
300,000 (some may be below 200,000) because
the relatively small number of environmental
infections in the herd at any particular time
does not have a major impact on the herd
SCC. Exceptions may be during times of in-
creased clinical incidence. Over a year, en-
vironmental mastitis may have a marked finan-
cial impact because of clinical mastitis (26).
CONCLUSIONS
Mastitis is an extremely complex disease
that results in marked reduction in the amount
of milk synthesized and in changes in levels of
specific milk components, reducing the overall
milk quality. The SCC is the most common
measurement of milk quality and udder health.
The major factor affecting SCC at the herd and
cow level is the presence of intramammary
infections. Because marked increases in SCC
Journal of Dauy Science Vol. 77, No. 7, 1994
HARMON
are a result of cells being attracted to the
mammary tissue because of the mediators
produced during a local infection, events that
do not affect udder health are unlikely to have
a direct or dramatic effect on SCC. Little
evidence exists that any factor other than nor-
mal diurnal variation has a major influence on
SCC in the absence of intramammary infec-
tion.
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