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Mastitis: Comparative Etiology and Epidemiology

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J Mammary Gland Biol Neoplasia (2011) 16:339–356
DOI 10.1007/s10911-011-9234-0
Mastitis: Comparative Etiology and Epidemiology
G. Andres Contreras & Juan Miguel Rodríguez
Received: 5 July 2011 / Accepted: 16 September 2011 / Published online: 27 September 2011
# Springer Science+Business Media, LLC 2011
Abstract Mastitis is broadly defined as the inflammation
of the mammary gland; however, the concept of mastitis is
customized to address its social and clinical impact in the
case of humans and the health, welfare, and economic
consequences for other mammals. There are many micro-
bial, host, and environmental factors that influence the
development of mastitis. Some are common to all mammals
as well as inherent to each species. Together these factors
influence the most prevalent etiological agents for each
species and might determine the possibility of interspecies
transmission with its consequences to public health. The
present review will summarize and compare reports on
mastitis etiology and its epidemiology in humans and food
animal species.
Keywords Mastitis . Lactational . Puerperal
Abbreviations
CNS Coagulase-negative staphylococcus
GBS Group B streptococci
IMI Intramammary infection
PDS Post-partum dysgalactia syndrome
SCC Somatic cell count
G. A. Contreras (*)
Department of Large Animal Clinical Sciences,
Michigan State University,
D202 VMC,
East Lansing, MI 48824, USA
e-mail: contrera@cvm.msu.edu
J. M. Rodríguez
Departamento de Nutrición, Bromatología y Tecnología de los
Alimentos, Complutense University of Madrid,
28040 Madrid, Spain
Introduction
The lactation process has been remarkably successful since
the earliest mammals, allowing them to occupy a vast range
of ecological niches. However, lactation is seriously
impacted by the development of mastitis among most, if
not all, mammalian species [1]. This condition alters milk
composition and reduces milk secretion, facts that impair
infant/offspring growth and development. In humans,
mastitis is the main cause of early weaning, and in food
animal species, it is one of the diseases with highest
economic impact and a major animal welfare concern. This
review summarizes different elements of mastitis etiology
and epidemiology across species, complementing other
mastitis aspects addressed in this special issue.
Definition of “mastitis”: Is There Only One?
A broad definition of mastitis is inflammation of the
mammary gland, including not only intramammary tissues
but also related anatomical structures such as nipples,
mammary areolas, milk ducts, etc. In Veterinary Medicine,
mastitis is referred to an intramammary inflammatory
reaction caused by an infectious agent. In contrast, some
authors in human literature consider mastitis as either an
infectious or non-infectious disease [2]. This distinction
seems to be no longer valid, since in the past, most
diagnoses were based on visual assessment of the affected
breast and not on microbiological analysis [3]. Currently,
the use of bacteriological cultures for human mastitis
diagnosis reveals that the term “infectious mastitis” was
being applied only to describe acute cases caused by
Staphylococcus aureus and by some streptococcal species.
These cases usually included both local (breast redness,
340
engorgement and pain) and systemic symptoms. In contrast,
subacute mastitis caused by coagulase negative staphylococci
(CNS) and other bacterial agents was generally misdiagnosed
as “non-infectious” or as “mammary candidiasis” because
there were only local symptoms, such as breast engorgement
and pain, often without redness [4, 5]. In addition, in the
few instances in which human milk cultures were
performed, CNS were always considered as “commensal”
or “saprophytic” bacteria, independent of their concentration.
Defining human mastitis as an infectious disease could
differentiate the condition from other inflammatory
processes of the mammary gland, such as those associated
with different types of breast/mammary cancer [6], and
from Raynaud’s disease, a painful vasoconstriction of
the nipple during human breastfeeding [7]. Another
complication to a general definition of mastitis in humans
is the use of mastitis related terms such as “milk stasis”,
“retention”, “obstruction” or “breast engorgement”. These
processes are usually considered as predisposing factors
for mastitis, however, such findings usually represent a
direct consequence of the disease.
A better approach to the definition of human and food
animal mastitis is to classify it into subgroups depending on
different criteria including: lactation stage (lactational,
non-lactational), clinical manifestations (clinical or subclinical),
or its course (peracute, acute, subacute, chronic or
recurrent) (Fig. 1). In humans, lactational mastitis is
defined as an acute inflammation of the interlobular
connective tissue within the mammary gland [8]. Non
lactational mastitis is a localized inflammatory reaction
of secretory or non-secretory structures in the breast and
comprises mainly periductal mastitis, and breast abscesses [9].
Both definitions are easily adapted to food animals where
mastitis affects the mammary gland in lactating and non-
lactating stages including mammary gland development
during gestation and in young individuals [10].
In humans and animals, clinical mastitis is characterized
by signs of inflammation in the mammary gland including
hyperemia, pain, and increased gland size and density.
These symptoms may be accompanied or not by systemic
signs, such as fever or depression. Clinical mastitis in dairy
animals such as cows, buffaloes, does, and ewes is also
often detected by direct observation because of changes in
the organoleptic characteristics of milk. In sows, clinical
mastitis is often accompanied by metritis in what is known
as the mastitis, metritis, agalactia syndrome or post-partum
dysgalactia syndrome (PDS) [11].
Subclinical mastitis is defined by quantification of
somatic cells in milk. In dairy cows and buffaloes, a
somatic cell count (SCC) higher than 200,000 cells/mL
defines the diagnosis of subclinical mastitis [12, 13]. In
does and ewes a subclinical mastitis case is defined as an
animal or half gland producing milk with SCC higher than
J Mammary Gland Biol Neoplasia (2011) 16:339–356
1,000,000 cells/mL [14, 15]. Subclinical mastitis is not
well defined in sows and beef cows as a SCC limit has not
been established. In humans, there is not a routine
quantitative approach to diagnose subclinical mastitis. In
this context, the term “subclinical” should be used to
describe those cases characterized by the absence of external
inflammatory changes, a reduced milk secretion, an increase
in the sodium/potassium (Na+/K+) ratio, and a high bacteria
count in a milk sample obtained manually [16, 17].
The course of mastitis cases is directly related to its
clinical manifestations and the etiological agent. For
example, in periparturient and early lactation dairy cows,
intramammary infections (IMI) caused by coliform patho-
gens are often the cause of peracute or acute mastitis. These
cases have systemic symptoms that can be fatal or lead to
quarter losses [18]. Similarly in does, enterotoxin secreting
Staphylococcus aureus IMI are associated with peracute or
acute cases of gangrenous mastitis, especially during the
puerperium [19]. Both coliforms and Staphylococcus
aureus can cause chronic mastitis cases in dairy animals
that are usually diagnosed by high SCC and therefore
considered subclinical mastitis. In the case of coliforms,
strains isolated from chronic cases have a better capacity for
intracellular growth in bovine mammary epithelial cells
than strains isolated from acute clinical cases [20]. Peracute
or acute mastitis cases in sows are usually associated with
PDS. In these animals, there are also cases of chronic
mastitis characterized by abscesses and granulomas in the
mammary tissue that may diminish milk production
although these cases are often not diagnosed and only
observed at abattoirs [21].
Mastitis Diagnosis
Mastitis may lead to clinical symptoms and, as a
consequence, it is often diagnosed directly by visual
assessment of breast/udder inflammation or by changes
in milk’s organoleptic properties. In addition, there are
several ancillary tests that are used to detect both
clinical and especially subclinical mastitis and these
include: SCC, which is considered the standard method,
milk microbiological cultures, N-acetyl-beta-D-glucosamini-
dase activity, pH, lactose content, electrical conductivity,
flow measurements, and quantification of acute phase
proteins [22]. The choice of one or more of these
procedures usually depends on the availability, proximity
to a diagnosis laboratory, personal experience and/or
technical skills. Microbiological analysis of milk is the
only method that allows for an etiological diagnosis of
mastitis, however, there are relevant factors that have to be
considered when using this diagnostic tool. These factors
include: use of standard protocols for milk sample
J Mammary Gland Biol Neoplasia (2011) 16:339–356 341

Figure 1 Mastitis classification

across species depending on
Mastitis
lactation stage, clinical signs
and etiological agent. CNS,
coagulase negative
Staphylococcus Non
Lactational
Lactational

Etiological
Clinical Signs
Agents

Periductal
Clinical Infectious Non Infectious
Mastitis

Subclinical Contagious Environmental Breast Abscess

S. aureus
Strep. agalactiae
Bacterial Non Bacterial
Mycoplasma spp.

Algae Prototheca

Gram Positive Gram Negative

Herpesvirus
Viruses
Escherichia coli Food and mouth
CNS
Streptococcus Klebsiella spp
Pseudomonas spp

collection, correct identification and quantification of
bacterial isolates, and the relevance of clinical symptoms
in the patient/animal [23].
The collection of a representative sample for microbial
analysis is of outmost importance for good etiological
diagnosis. In food animal medicine, there are standard
protocols for milk sample collection proposed by the
National Mastitis Council (NMC) and the International
Dairy Federation (IDF) [24, 25]. In human hospitals and
private physician offices, however, milk sampling
procedures are usually not standardized. Recently,
Arroyo et al., [26] proposed a protocol that avoids
common sampling-related factors that may affect final
bacteriological results. For example, the use of milk
pumps for sample collection is associated with high
concentrations of enterobacteria, Pseudomonas spp.,
Stenotrophomonas spp., Bacillus spp., and yeasts (Candi-
da spp.), that usually are not etiological factors in the
particular mastitis case [27]. Furthermore, milk contam-
ination during pumping is constantly reported and seems
to be of particular concern for premature infants or ill
infants in neonatal intensive care units [28, 29]. A possible
cause is that most milk pumps and/or their accessories
cannot be properly sanitized and/or sterilized and such
microorganisms usually persist after application of current
cleaning protocols.
A reliable etiological analysis must identify the causing-
organism(s) at least at the species level. Many phenotypic
assays traditionally used for taxonomical purposes, such as
the carbohydrate fermentation pattern, are no longer valid
due to low specificity or non-conclusive results. Recently,
the introduction of molecular microbiology techniques such
as PCR and matrix-assisted laser desorption/ionization
time-of-flight mass spectrometry (MALDI-TOF MS) have
improved the sensitivity, specificity, and processing time of
bacterial identification procedures [30]. Furthermore, real-
time PCR assays performed directly on milk samples
(without culturing) have benefits over conventional culture,
including higher speed, automated interpretation of results,
and increased sensitivity [31, 32]. However, implementa-
tion of this technique must take into account that, in
addition to live bacteria, milk contains a high quantity of
dead bacteria and free bacterial DNA, thus reducing its
specificity [33]. As a consequence, bacterial cultures are
still required for routine etiological diagnosis of mastitis.
There is no doubt that ongoing and future improvements on
the application of Omics in mastitis diagnosis will provide
powerful tools with high specificity and sensitivity.
342
Mastitis Etiology: From a Mammary Microbiota
to Mastitis?
Culture-dependent and -independent analyses of bacterial
diversity in milk from healthy women revealed that this
biological fluid is a source of live staphylococci and
streptococci, and to a minor extent of lactic acid bacteria,
bifidobacteria and enterobacteria, to the infant gut [33–36].
Physiologically, concentration of bacteria in fresh human
milk is lower than 3 log10 colony-forming units (CFU)/mL.
At the same time, the number of bacterial species is
relatively low (from 2 to 12 different species) and the
species profile is host-specific [37]. Similar findings were
obtained by microbiological analysis of swine and canine
milk [36, 38]. These facts can explain why gut microbiota
of healthy breast-fed infants usually comprises a narrow
species spectrum and also, why the development of a more
diverse microbiota coincides with the weaning period.
Furthermore, these studies suggest that at least some of
the bacteria present in milk are not the result of skin
contamination but reflect a true intramammary microbiota.
These bacteria may also play an important role in the
reduction of the incidence and severity of infections in the
mother-infant/offspring pair [34]. In fact, some of these
milk bacterial strains have the ability to inhibit growth of a
wide spectrum of pathogenic bacteria, including those
causing mastitis. This bacteriostatic activity may be
explained by competitive exclusion and/or through the
production of antimicrobial compounds, such as bacteriocins,
organic acids or hydrogen peroxide [39–41].
More recently, microbial identification techniques based
on pyrosequencing of the 16S ribosomal RNA gene were
used to obtain a description of the human milk microbiome
[42]. Results indicated that milk bacterial communities are
more complex than expected, with several genera representing
greater than 5% of the relative community abundance.
Staphylococci (particularly Staphylococcus epidermidis) and
streptococci were the dominant genera. Bacterial populations
were usually, although not always, stable over time within
the same individual. These findings open a new concept
regarding the role of mammary microbiota in maintaining
mammary health, not only in humans but also in other
mammalian species.
The elucidation of the origin of human mammary
microbiota will be an attractive research target in the next
years. Traditionally, it was considered that mammary flora
was acquired by skin contamination. Obviously, sampling
of breast milk for microbiological analysis will collect some
skin contamination, and this fact is almost unavoidable.
However, doubts on the original source, internal mammary
gland or skin, of the isolated bacteria arise, especially for
some bacterial groups including bifidobacteria or lactobacilli
where skin origin is unlikely due to their unique growth
J Mammary Gland Biol Neoplasia (2011) 16:339–356
requirements [38]. Previously, it has been reported that
lactobacilli and enterococcal isolates present in human milk
are genetically different from those isolated from the skin
[35]. This suggests that, the origin of these bacterial isolates
found in breast milk could be the maternal gut and that
bacteria could have migrated to the mammary gland through
an endogenous route also called entero-mammary pathway
involving maternal dendritic cells and macrophages [35].
These viable bacteria and a wide range of free bacterial DNA
signatures found in maternal milk may help in the
development of the neonatal immune system [4]. More
recently, oral administration of probiotic lactobacilli strains
to women with mastitis not only led to a notable improve-
ment of the condition but also to the transfer of such strains
from the gut to the mammary gland [5, 43].
Metagenomic and transcriptomic analysis of milk sam-
ples from healthy and mastitis-affected women are in
progress. Preliminary results indicate that human mastitis
may be characterized by a mammary bacterial disbiosis, a
process in which the population of mastitis agents increases
while other bacteria, normal mammary microbiota, decrease
[4, 44, 45] (Fig. 3). As pathogenic bacteria concentration
increases, it induces a series of biochemical and immuno-
logical changes in mammary gland and milk that are later
expressed as clinical symptoms. These changes can be
specific to the etiological agent as recently demonstrated by
Hettinga’s group, who classified cow’s mastitic milk in five
groups (mastitis by Staph. aureus, mastitis by CNS, mastitis
by streptococcus, mastitis by E. coli, and uninfected
quarters) on the basis of the volatile bacterial metabolites
[46, 47]. Systems biology and omics-related research
approaches, as those discussed in other articles of this
issue, will help to provide new insights on the process
leading from a “healthy” mammary microbiota to mastitis.
Main Etiological Agents of Mastitis
Globally, staphylococci (S. aureus and CNS) are the most
common mastitis-causing agents in cows, buffaloes, ewes,
does, llamas, dromedaries, rabbits, dolphins and women
[13, 48–50]. They are closely followed by streptococci and
E. coli which in some species or settings may have a similar
or higher prevalence than that of staphylococcal mastitis.
Less commonly, other Gram-positive (Actinomyces spp.,
Corynebacterium spp., Bacillus spp., Mycobacterium spp.,
Enterococcus spp., Clostridium spp.) and Gram-negative
(Klebsiella spp., Enterobacter spp., Citrobacter spp.,
Serratia spp., Proteus spp., Pasteurella spp., Mannheimia
haemolytica) bacteria and mycoplasma may be involved in
the etiology of mastitis while cases due to molds or yeasts
are rare. In dairy animals, mastitis causing pathogens are
classified depending on their epidemiological behavior in
J Mammary Gland Biol Neoplasia (2011) 16:339–356
contagious and environmental [51]. Among contagious
pathogens S. aureus, Streptococcus agalactiae, and Myco-
plasma spp. are included. Contagious pathogens’ main
reservoir is the mammary gland; consequently, these
bacteria are spread from cow to cow or between quarters/
halfs of the same animal during the milking process. In
contrast, environmental pathogen reservoirs include
bedding, pasture, and other unanimated objects. These
bacteria are isolated from the skin, teat ends, and teat
canals where they can gain access to the gland causing
IMI. Streptococcus other than agalactiae, Enterococcus
sp, CNS, and coliform bacteria including Escherichia coli
and Klebsiella spp. are included in this group. It is
important to note that certain microbial, host and/or
environmental factors may induce environmental agents
to behave as contagious pathogens or vice versa [52, 53].
Independent of their classification in dairy animal
medicine, the main mastitis causing infectious agents will
be described below. Although there may be other infectious
agents implicated in the development of the disease in
certain species or under specific circumstances, their
epidemiological relevance is minimal and, therefore, are
not included in this review.
Staphylococcus aureus
In women, the main etiological agent of acute mastitis and
breast abscesses is S. aureus. This Gram positive bacteria is
isolated in 40 to 50% of lactational mastitis cases and in the
majority of non-lactational mastitis including periductal
mastitis and breast abscesses [54–58]. In dairy cows,
reported prevalence for S. aureus. mastitis worldwide
varies between 5% to 18% [59–61]. At the same time,
herd prevalence are very high with values ranging from
30% to 85% [62–64]. S. aureus is responsible for up to
40% of clinical mastitis cases in ewes and its prevalence is
linked with high somatic cell counts [65]. In does, S.
aureus is the etiological agent of gangrenous mastitis, a
disease with high mortality rates. However, there is a low
prevalence in caprine herds and its transmission between
does is infrequent [66].
Coagulase Negative Staphylococcus (CNS)
These Gram-positive bacteria have become the most
common mastitis isolate in ruminants in many countries
and are now described as emerging mastitis pathogens [52].
CNS are not as pathogenic as S. aureus and infections
usually remain subacute or subclinical. However, CNS
cause persistent infections that may result in increased milk
SCC, udder damage and decreased milk quality and
production. CNS include various species, but only a few
prevail in ruminant mastitis.
343
Staphylococcus chromogenes is commonly associated
with mastitis in nulliparous (heifers) and primiparous cows
whereas Staphylococcus simulans is frequently isolated in
older cows [52]. Furthermore, different studies reported
isolation of Staphylococcus epidermidis in 10% to 12% of
mastitis cases in dairy cows [67, 68]. A recent study
showed that there were no differences between these three
CNS species in their association with daily milk produc-
tion, cow milk somatic cell count, and month of lactation in
cows with subclinical mastitis [69]. In dairy ewes S.
epidermidis is the main pathogen causing clinical mastitis
and its prevalence is associated with high SCC in the flock,
however, S. chromogenes, S. xylosus, and S. simulans are
frequent isolates in subclinical and clinical mastitis milk
samples [14, 70]. In caprine mastitis, S. epidermidis IMI are
associated with subclinical mastitis where it is identified in
20% to 30% of cultured samples and S. caprae is
commonly isolated in dairy goats IMI [15, 66, 71]. In sows
with PDS, S. simulans and hiycus are the most prevalent
CNS isolated in milk [11]. Knowledge of the CNS species
involved in food animal mastitis is increasing, for example,
recent findings suggest that some CNS such as Staphylo-
coccus chromogenes and S. epidermidis could behave as
contagious mastitis pathogens in dairy cows, while others
like S. haemolyticus and S. simulans have an environmental
reservoir [72]. Remarkably, resistance to various antimicro-
bials is more common in CNS than in S. aureus, however,
CNS mastitis respond much better to antimicrobial
treatment than S. aureus mastitis [52].
In contrast to ruminants, S. epidermidis is the CNS
species most commonly associated with lactational
mastitis in women. This species is isolated at a high
concentration in at least 30% of the clinical cases and
in most subacute or subclinical cases [73]. Currently,
this is a frequent but largely underrated cause of human
mastitis. S. epidermidis is a commensal inhabitant of the
healthy human skin and mucosal surfaces, but also a
common nosocomial pathogen [74]. Living at the edge
between commensalism and pathogenicity, S. epidermidis
has developed interesting strategies to transform into a
notorious pathogen [75]. Recent progress in genome
analysis and molecular epidemiology gave interesting
insights into the enormous flexibility by which this
species generates continuously novel phenotypic and
genotypic variants. A comparison between the genomes
of several S. aureus and S. epidermidis strains confirmed
the relative abundance of virulence factors in S. aureus
compared to S. epidermidis; this fact reflects the propen-
sity of S. aureus to cause acute and sometimes life-
threatening infections, as opposed to the more subacute or
chronic infections caused by S. epidermidis [76].
S. chromogenes, S. epidermidis and other CNS may have
a probiotic function by preventing colonization of the host
344
by more severe pathogens, such as S. aureus [74, 77].
Quorum sensing interference favors at least one subtype of
S. epidermidis over S. aureus in vitro but its efficiency has
not been tested in vivo yet [78]. In primiparous and
multiparous dairy cows, quarters infected with CNS had
lower SCC and were less susceptible to development of
new mastitis cases caused by S. aureus during intra-
mammary challenge [79, 80]. However, a potential CNS
probiotic approach should take into account that CNS
provide a reservoir function for the transfer of genetic
elements to enhance the pathogenic success and antibiotic
resistance to S. aureus, and therefore, have an important
role in human and animal disease [76].
Streptococcus Species
Streptococcus agalactiae (Group B Streptococci; GBS) is
an obligate parasite of the mammary gland of cattle,
where it causes contagious mastitis [81]. GBS is the
most significant cause of neonatal bacterial sepsis, and
there is indirect evidence that human GBS is derived
from a bovine ancestor [82]. In addition, a common
strain was isolated from a pet heifer suggesting the
possibility of interspecies transmission and a zoonotic
risk [83]. However, it is important to mention that
preventive intramammary antibiotics at the end of lacta-
tions and appropriate hygiene have eradicated Strep.
agalactiae in a high percentage of commercial dairy
herds, thus reducing its prevalence in North American
and European countries [63, 64, 84]. GBS are only
occasionally implicated in mastitis cases in goats and
ewes and, up to the present, they have not been reported as
mastitis agents in sows [11, 14, 66].
Other Streptococcus species associated with mastitis
seem to be species-specific. In cattle the most prevalent
are Streptococcus uberis and Streptococcus dysgalactiae,
both considered environmental mastitis pathogens, however,
some authors described contagious transmission for the
species dysgalactiae [85, 86]. In buffaloes the most
common isolates are Streptococcus dysgalactiae and
Streptococcus bovis [87, 88]. Common species in women
include Streptococcus mitis and Streptococcus salivarius
[73]. Streptococcus equinus, Streptococcus mutans and
Streptococcus mitis were isolated from mammary gland of
sows with PDS [11]. Streptococcal mastitis are less
common in goats and ewes; however, a contagious
agalactia with concomitant arthritis was reported to be
caused by Streptococcus equi [89, 90]. It is important to
note that streptococci have been submitted to important
taxonomical rearrangements and that many novel strep-
tococcal species have been described recently; therefore,
the implication of streptococci in mastitis should be
carefully reevaluated [91].
J Mammary Gland Biol Neoplasia (2011) 16:339–356
Other Gram-Positive Bacteria
Actinomyces pyogenes and Corynebacterium bovis are
common mastitis pathogens in ruminants. In Europe,
Actinomyces pyogenes is the etiological cause of summer
mastitis together with some strains of Streptococcus
dysgalactiae and its main reservoir and transmission
vector are flies [24, 92]. This type of mastitis usually
affects non lactating cows and heifers producing significant
suppurative inflammation and a rapid loss of secretory
tissue [93]. Corynebacterium bovis is considered a minor
mastitis pathogen that lives as a commensal in the teat
canal of lactating cattle causing clinical or subclinical
mastitis when it colonizes the mammary gland [24]. In
fact, specific diagnosis of mastitis caused by this agent
should include milk sampling from the infected quarter
using a teat cannula to bypass the teat canal [94].
Corynebacterium kroppenstedtii, Corynebacterium
amycolatum and Corynebacterium tuberculostearicum
are often involved in human granulomatous lobular
mastitis, a chronic inflammatory disease that was previously
considered of unknown etiology [95–97]. Patients usually
exhibit an enlarging, mildly tender breast lump, which is
sometimes associated with local inflammation, tenderness,
and sinus formation and can become chronic and disfiguring
in a large number of patients. Corynebacteria stain
poorly using the Gram technique and often fail to grow
on routine media. These organisms are found in
histological specimens from deep in the breast tissue
surrounded by granulomatous inflammatory reaction
relatively early in the clinical presentation. These facts
could have led to decreased diagnosis of human mastitis
caused by corynebacteria in the past
Other Gram-positive bacteria that are associated with
mastitis in cattle, sheep, goats and swine include Enterococcus
faecium and Enterococcus faecalis, which are associated, at
least in cattle, with poor bedding and inadequate hygiene
practices [98]. Similarly, Bacillus species may be an
important cause of cow mastitis in some regions. As an
example, Bacillus spp., including Bacillus pumilus and
Bacillus licheniformis, were identified as the major organ-
isms in 23 out of 100 milk samples of mastitic cows in
Finland [99]. Some other species, such as Bacillus cereus
and Bacillus anthracis are unusual mastitis agents but have
been reported to cause mastitis in beef cattle [100].
Commensal Bacillus strains isolated from the udder micro-
biota of healthy cows have been proposed as a probiotic
approach for mastitis prevention or treatment [101].
Mastitis and breast abscesses due to clostridia (Clostridium
perfringens, Clostridium difficile) are not frequent in sows
and humans [102, 103]; however, they may lead to gangrene
in ewes and clinical cases in cows and buffaloes [104].
Finally, another pathogen associated with mastitis across
J Mammary Gland Biol Neoplasia (2011) 16:339–356
species is Mycobacterium tuberculosis. This bacterium is
isolated from granulomatous mastitis cases in humans and
from clinical mastitis cases in cattle where the lesion is
secondary to pulmonary tuberculosis [105]. The incidence of
human mammary tuberculosis is of approximately el 0.3–5%
in endemic regions [106].
Gram-Negative Bacteria
Escherichia coli, Klebsiella pneumoniae and Enterobacter
spp. are isolated in less than 3% of lactational mastitis cases
in women [73]. Salmonella typhi and Salmonella paratyphi
were reported to cause non-lactational mastitis and
mammary abscesses [107, 108]. In dairy cows, these
Gram-negative bacteria, and particularly E. coli, are a
common cause of mastitis in both lactating and non-
lactating animals. Other organisms isolated from clinical
and subclinical mastitis in cows belong to the genera
Pasteurella, Proteus, Pseudomonas or Serratia [109]. All
are considered environmental mastitis pathogens [24].
These organisms typically cause clinical mastitis that
is, in some cases, life-threatening. The severity of the
disease is due to the release of endotoxin during the
host immune response [110]. In sows, coliform bacteria
are known to be among the causative agents of PDS [11].
In does and ewes the most common Gram-negative
mastitis pathogens belong to the species M. haemolytica
or to the genuses Pastereulla and Pseudomonas, although
these infections are of low prevalence, especially in
pasture grazed herds and flocks [14, 111, 112].
Mycoplasma
Mycoplasma species including Mycoplasma bovis, Myco-
plasma californicum, and Mycoplasma bovigenitalum are
contagious mastitis pathogens in dairy cattle. IMI caused by
these agents are particularly difficult to treat since they are
unresponsive to antibiotics [113]. In does Mycoplasma
agalactiae, Mycoplasma mycoides and Mycoplasma capri-
colum are the etiologies of contagious agalactia and are
endemic in Mediterranean countries [66]. Ewes are only
affected by Mycoplasma agalactiae where it also causes
contagious agalactia [114]. In women, the genus Mycoplasma
is not linked to breast infections although it is considered
among the potential agents of preterm labor [115].
Non-Bacterial Pathogens
Prototheca spp, an unicellular algae is reported to infect the
mammary gland of dairy cattle causing moderate to severe
subclinical or clinical mastitis [116, 117]. Prototheca spp is
classified as an environmental pathogen isolated from
water, soil, and bedding in the farms. This algae does not
345
respond to antibiotic treatment and may pose a zoonotic
threat since it is resistant to pasteurizing temperatures
(62 to 75°C for 15 to 30 min), and only ultra-high
temperatures treatments (100°C for 1 min) can effectively
inhibit its growth [118].
Yeasts are a very rare cause of mastitis. Traditionally,
many human cases of painful breastfeeding and/or sore
nipples were considered as “mammary candidiasis” on the
basis of visual assessment without taking into account
Koch’s postulates. However, effective isolation of the
pathogen in milk samples from mastitis cases diagnosed
as “mammary candidiasis” by a clinician is very rare [119,
120]. A recent prospective study showed that Candida
albicans was not present in milk ducts of women suffering
from symptoms of severe nipple and deep breast pain that
were empirically diagnosed as “mammary candidiasis”
[121]. Similarly, there are very few reports of yeast mastitis
in other mammals including dairy cattle where its world-
wide prevalence is very low [122].
Viruses can cause IMI leading to subclinical and clinical
mastitis cases. In cattle, even though its diagnosis is
difficult and rarely performed in clinical cases, several
viruses (including bovine herpesvirus 1, herpesvirus 4,
foot-and-mouth disease virus, and parainfluenza 3) have
been isolated from mastitic milk [123]. In goats, caprine
arthritis encephalitis virus is recognized as an etiological
cause of mastitis, furthermore, this virus exhibits great
tropism towards the mammary gland turning the secretory
epithelium into its reservoir [66, 124]. Although lactational
or non-lactational mastitis cases caused by viruses are not
reported in women, it is worthy of mention that the
presence of subclinical mastitis increases the risk of
transmission of HIV from mother to child [125].
Occurrence of Mastitis
Mastitis is a relatively common condition, developing in 5–
33% of women at some point during lactation [126, 127].
Incidence and prevalence of human mastitis are difficult to
calculate because of differences in case definition and
reporting [3]. A good example comes from a recent Spanish
study that followed approximately 9,000 lactating women
during a 5-year period. Based on clinical symptoms, only
3–5% of the clinical cases were initially diagnosed as
mastitis and all of them involved Staphylococcus aureus as
etiological agent. Mastitis cases caused by CNS or
viridans streptococci were initially misdiagnosed by the
medical staff as “milk stasis”, “retention”, “obstruction”
or “breast engorgement” on the exclusive basis of visual
assessment. By the end of the study, authors reported that
approximately 30% of women suffered at least one case of
infectious mastitis. [5, 44].
346
Mastitis most frequently develops in the early stages of
lactation, with a higher incidence during the first 4 weeks
after parturition and with 74–95% of cases observed in the
first 3 months [1, 127–129]. This condition may be
unilateral or bilateral and, in the last case, one of the
breasts is usually more affected than the other. The
incidence of mastitis complicated with breast abscess is
approximately 0.4–0.5% in lactating mothers [1, 128]. S.
aureus is, by far, the most common pathogenic organism
isolated in these abscesses [130]. Community-acquired
methicillin-resistant S. aureus (MRSA) strains are com-
mon etiological agents in these cases [57, 131, 132].
Interestingly, several socio-economic characteristics in-
cluding: ethnicity, age, time to presentation, parity,
insurance, or mode of delivery do not affect MRSA
infection risk [132]. Readers are referred to the MRSA
chapter in this special issue for current information about
this mastitis pathogen.
Incidence of mastitis in dairy cows varies depending on
geographical location and housing environment. In North
America and Europe, the incidence of clinical mastitis in
dairy cows ranges from 7 to 30 cases per 100 cows-years at
risk [63, 133, 134]. In grazing herds from New Zealand, a
lower incidence rate of 10% and 19% was reported, but in
one of the studies only cows with less than 100 days after
parturition were evaluated [135, 136]. Similarly, in the New
South Wales region of Australia clinical mastitis incidence
was 16% [137]. Reports on clinical mastitis incidence and
prevalence from other countries are scarce. In Africa for
example, a study from Tanzania reported clinical mastitis
incidence of 43 cases per 100 cow-years at risk [23].
Subclinical mastitis prevalence is reported to be 31% in
USA, 20 to 40% in Western Europe, and 29% in Australia
[64, 138–141]. In other countries with developing dairy
industries, subclinical mastitis prevalence is much higher. A
survey from a dairy province in China reported 54%
prevalence at the cow level and 28% at the quarter level
[142]. Similarly, cow level prevalence in Brazil was 47%
[143]. All these reported values should be considered
historical, since the incidence and prevalence of mastitis
in dairy cows is largely determined by conditions in each
geographical region and individual herd and are constantly
evolving. For example, some studies demonstrated a direct
relation between herds’ bulk tank SCC and clinical mastitis
incidence. This approach reveals a higher incidence of
clinical cases for herds with lower SCC than those with
high counts, possibly due to a reduction in the total amount
of immune cells in the mammary gland [63, 133, 134].
In does and ewes, clinical mastitis incidence is usually
below 5% per year. However, certain herds and flocks with
management problems may experience rates above 30%
[24, 25]. Similar to dairy cows, subclinical mastitis
incidence and prevalence are defined by the bulk SCC of
J Mammary Gland Biol Neoplasia (2011) 16:339–356
the herd. In French does, SCC of 750,000, 1,000,000 and
1,500,000 cells/mL correspond to 30%, 39%, and 51%
prevalence of subclinical mastitis [24]. Similarly, Spanish
flocks with SCC values of 250 000 or 1,000,000 cells/mL
corresponded to subclinical mastitis prevalence of 16 and
35% respectively. In the U.S. subclinical mastitis
prevalence at parturition was reported to be 35.5 and
19.0% in goats and sheep respectively [26]. In buffaloes,
mastitis frequencies are similar to those in dairy cows,
however, their IMI rate is much higher than in cows [13].
Furthermore, certain management factors largely affect
mastitis occurrence, in Pakistan for example, peri-urban cows
have higher mastitis prevalence than rural cows [144].
The majority of clinical cases of mastitis in sows are
related to PDS. Incidence in Europe and North America
vary between 1% to 60% with average of 13% [27, 28].
Chronic mastitis prevalence as assessed in abattoirs is
18% to 25%, however, its primary pathogen remains
unidentified and its real economic impact is unknown
[11]. Finally, incidence of clinical mastitis in beef cows is
not reported; instead, the literature describes IMI rates of
20 to 66.7% [29–31]. Beef cows affected with clinical or
subclinical mastitis wean calves with lower weights and
at higher risk of developing disease.
Epidemiological Aspects of Mastitis
Breast/udder health depends on a balanced interaction
between host and its microbiota, which may contain
microorganisms ranging from probiotic to potentially
infectious. Obviously, there are relevant differences
among mammals regarding the number, size, position
and structure of the mammary glands. In addition,
mammals (even within a same species) differ widely
in their ecosystems, management and use (e.g., milk-
producing versus meat-producing domestic species).
Therefore, there are many microbial, host and/or
environmental factors that may play important roles in
the development of mastitis (Figs. 2 and 3) [1, 145].
Microbial Factors
The mammalian ecosystem is hospitable, or at least
receptive, to many microorganisms including most of
the bacterial groups that have potential to cause mastitis.
The evolutionary process has led to state of mutual
acceptance or tolerance. However, upon disturbance
localized or disseminated invasive infections can occur.
Unfortunately, the exact causal events leading to the
transition from colonization to infection still are ill-
defined in vivo [146]. The ability to colonize and,
eventually, infect a host depends on several microbial
J Mammary Gland Biol Neoplasia (2011) 16:339–356
Figure 2 Epidemiological
factors influencing mastitis
etiology and pathophysiology
Microbial
Genetic
Pathogen
Virulence Factors
Antibiotic
resistance
Herd
Nutritional
practices
Management
practices
characteristics, including the expression of several viru-
lence factors, e.g. the formation of biofilms, expression of
super antigens, and antimicrobial resistance.
At the species level, pathogen-specific transcriptomic
disruptions are observed in the mammary gland as well as
in peripheral organs [147]. As an example, two major
mastitis pathogens, such as E.coli and S. aureus, elicit
differential innate immune responses following IMI in
cows, which may determine the course and severity of the
disease [148]. In relation to different staphylococcal
species, genomic analysis reveals that S. aureus is more
suited to develop acute infections than CNS. Conversely,
CNS have a tendency to cause subacute, subclinical or
chronic infections. As an example, members of the
enterotoxin and exotoxin families, which function as super
antigens and inducers of a proinflammatory cytokine
response, are unique to S. aureus and have not been
identified in characterized isolates of S. epidermidis or
other CNS.
Several virulence factors or toxins are included in certain
pathogenicity genomic islands (vSa). In S. aureus seven
islands carry approximately one-half of the virulence
factors that have been identified. Variations in the patho-
genic potential of strains belonging to this species depends
largely on allelic variation of the virulence genes, on the
presence or absence of individual vSas, and on the presence
of single nucleotide polimorphysms (SNPs) in key genes.
Such differences are the most significant factor contributing
347
Mastitis Epidemiological
Factors
Host
Lactation stage Age
Number of Mammary gland
lactations factors
Milking and Breast feeding Nutritional and
practices Immune status
Socio-economic
Education
Income
Habits
to observed variations in antibiotic resistance and virulence
among S. aureus strains [76].
The expression of super antigens enhances bacterial
capacity to colonize the mammary gland. These molecules
are potent stimulants of the immune system and function by
activating a large number of T cells through the major histo-
compatibility complex class II. Bovine mammary S. aureus
isolates usually harbor genes encoding superantigens, such
as tst, exfoliative toxins, and enterotoxins [149]. However,
S aureus is not the only mastitis pathogen carrying super
antigens. Recently, the presence of 19 classical and newly
described staphylococcal super antigen genes was demon-
strated in 263 CNS isolates from bovine IMI [150]. The
most prevalent combination of these genes (seb, seln and
selq; n=45) was found in common bovine mastitis CNS
including S. chromogenes, and S. xylosus.
Biofilm formation is another important virulence
factor. A recent study compared 200 S. epidermidis
strains isolated from women with mastitis with 105 S.
epidermidis strains isolated from milk of healthy women.
Interestingly, the number of strains carrying the biofilm-
related icaD gene and showing resistance to oxacillin,
erythromycin, clindamycin and mupirocin was significantly
higher among mastitis isolates [44]. The authors sug-
gested that resistance to diverse antibiotics and a higher
ability to form biofilms found among mastitis specific
strains may explain the chronic and recurrent nature of this
infectious condition.
348 J Mammary Gland Biol Neoplasia (2011) 16:339–356

(A) Healthy mammary gland

Mammary
Mammary epithelium areola

Bacteria Milk culture

Normal milk • Bacteria:
flow ≤3 log 10 CFU/ml
Bacteria • Heterogeneous
population

Nipple

Microbial factors
Genetic factors
(virulence, biofilm
(HLA status,
formation, resistance to
Lewis antigens,
antibiotics, immune
autoimmune thyroid
evasion, molecular
disease…)
mimetism…)
Other factors
Immune factors (smoking…)
(innate system,
Medical factors
neutrophil recruitment,
(antibiotics)
cytokine pattern…) Feeding factors
Biochemical factors
(nursing technique,
(milk oligosaccharides,
tongue tie…)
polyamines,
antioxidants,…)
(B) Mastitis
Cracking,
sore nipples
Mammary epithelium
Inflammation Withish spots
Bacteria Milk culture
Reduced milk • Bacteria:
flow > 4 log 10 CFU/ml
Bacteria Homogeneous
population
Decreased
milk secretion
obstruction
Obstructions, milk retention, ingurgitation, milk stasis

Figure 3 Schematic representation of the etiopathogeny of human mastitis as suggested by the “disbiosis” model [73]; human mammary
epithelium in physiological conditions (a) and during mastitis (b). Red arrows indicate the typical burning and/or needle-like pain

There are several other virulence factors that modify
bacterial ability to colonize and cause IMI but the combination
of genes associated to pathogenicity is strain-specific [58,
145, 151, 152]. In Veterinary Medicine, this could possibly
lead to the use of bacterial genetic characterization as a
management tool. For instance, animal culling or segregation
could be determined on the bases of infectious status with
strains expressing specific virulence factors.
Host Factors
In order to ask why evolution has not managed to sort out
the problem of mastitis or what mechanisms exist to
prevent it from developing, an insight into host differences
is required. Although contemporary environmental factors
such as breastfeeding frequencies, the wearing of a tight
brassière, or maternal hygiene might increase this problem
in humans, these are not relevant throughout mammalian
evolutionary history [1]. In contrast, the genetic back-
ground and the structure and immunology of the mammary
gland differ notably among the mammalian species, and
breed or individual differences may also be observed even
within the same species. The interactions between the host
immune system and the pathogen seem to be of particularly
relevance in the etiopathogeny of mastitis [153]. Recently,
E. coli-infected mammary gland tissue was found to
J Mammary Gland Biol Neoplasia (2011) 16:339–356
significantly up-regulate expression of genes related to the
immune response and down-regulate genes related to fat
metabolism [154].
The hypothesis that a mastitis-causing bacterial species
may show host specificity has been largely debated [146].
The studies dealing with this subject have been mainly
focused on S. aureus since most of the isolates recovered
from either serious infections in humans or from mastitis in
cattle usually represent genetically distinct sets of clonal
groups. Whole genome sequencing and comparative
genomic analyses revealed a set of molecular genetic
features that distinguish clones of highly successful
bovine-associated S. aureus optimized for mastitis patho-
genesis in cattle from those that infect human hosts or are
only infrequently recovered from bovine sources [155].
Probably, only a handful of genes or gene combinations
may be responsible for host specificity [156]. Previously,
it was observed that mastitis-associated S. aureus strains
isolated in diverse farm animal species form a distinct
genetic cluster, characterized by an overrepresentation of
the toxic shock syndrome toxin super antigen-encoding
gene [149].
The existence of a genetic basis for host responses to
bacterial IMI has been widely documented, but the
underlying mechanisms and the genes are still largely
unknown. In this frame, quantitative trait loci affecting the
risk of clinical mastitis and that exhibit pathogen-specific
effects against S. aureus or E. coli have been discovered
[157]. Fine mapping studies in Norwegian Red cattle
chromosome 6 (BTA6) revealed an additional quantitative
trait locus for clinical mastitis [158]. In addition, the link
between DNA polymorphisms of the osteopontin gene
(SPP1), the number of milk immune cells, and increased
susceptibility to mastitis by E. coli was reported recently in
dairy cattle [159]. Two divergent lines of sheep selected
for high/low milk somatic cell scores were shown to be
respectively susceptible and resistant to IMI by Staphylococ-
cus [160]. Gene profiling in resistant and susceptible lines
has provided good candidates for mapping the biological
pathways and genes underlying genetically determined
resistance and susceptibility towards Staphylococcus infec-
tions, and opens new fields for further investigation.
Besides genetic background, mastitis occurrence is
affected by the stage of lactation in all species. The vast
majority of human mastitis cases are reported during the
first 8 weeks of lactation [126]. In dairy cattle, clinical
mastitis incidence peaks around parturition and early in
the dry period [161]. This period is the interval between
two lactations during which the cow is not being
milked. In sows, PDS is a disease exclusively of the
immediate postpartum, causing a severe reduction in
milk production from 12 h to 48 h after farrowing
[162]. In contrast, does are at higher risk of clinical
349
mastitis during late lactation at least in tropical grazing
systems [163]. In ewes, there are no differences in mastitis
incidence related to lactation stage [89].
Age and number of lactations in women affect mastitis
incidence. In non-lactational mastitis, older women (42–
85 years) are at a higher risk of developing duct ectasia,
while younger women (19–48 years) are more prone to
periductal mastitis. For lactational mastitis, studies from
North America and Oceania reported that women older than
35 years are more likely to have puerperal mastitis and
especially if they had a history of mastitis with their
previous child [126, 164]. In cattle, older animals with 3 or
more lactations have a higher prevalence of subclinical and
clinical mastitis during middle and late lactation [165]. In
contrast, primiparous cows have a higher incidence and
prevalence of clinical mastitis immediately after parturition
[166]. In does and ewes, number of lactations and mastitis
incidence and prevalence are positively correlated [89]. In
contrast, primiparous sows are more prone to coliform
mastitis (PDS) than older sows; this is aggravated if their
litter has more than 13 piglets born alive [167].
Certain species-specific anatomic characteristic could
also affect mastitis susceptibility. In women, the outer upper
quadrants of breasts are found to be the most frequent sites
of initial clinical signs during lactational mastitis [168]. In
the nipple, cracks and sores were associated with a higher
risk of developing lactational mastitis [126, 164]. However,
recent studies suggested that nipple lesions can be an
additional clinical sign of mastitis rather than a predispos-
ing factor [73] In dairy cows rear quarters of the udder are
at higher risk of subclinical and clinical mastitis specially if
they had a previous IMI [169]. Regarding teat morphology,
dairy cows with small teat’s cistern diameters and shorter
teat canals are predisposed to mastitis [170]. Teat end
hyperkeratosis is associated with clinical mastitis cases
where Kl. pneumoniae and E. aerogenes were isolated as
etiological pathogens [171]. Dairy goats with longer teats
are more likely to develop clinical and subclinical mastitis
than does with short teats [163]. Mastitis in PDS is more
common in the posterior mammary complex of sows when
compared to the anterior mammary glands [11].
Breastfeeding practices in women can modify their suscep-
tibility to puerperal mastitis. Inappropriate or infrequent milk
removal may increase the risk of mastitis [172]. In order to
increase milk evacuation, the use of breast pumps and/or
frequent feeding is recommended [164]. Conversely, feeding
the baby 10 or more times per day increases the risk of
lactational mastitis compared to feeding 6 or less times [126].
Other practice that increases the incidence of mastitis in
lactational women is the use of creams in the nipple area,
including antifungal ointments [126, 164]. Certain habits,
such as smoking, are directly linked with the development of
primary breast abscesses and its recurrence [173]. Similarly,
350
chronic disseminated infections such as tuberculosis and
certain cultural practices such as nipple piercing are associated
with increased risk of developing breast abscess specially those
localized in the subareolar area [1, 174, 175]. Peripartum
antibiotherapy, usually related to Caesarean section or GBS
intrapartum prophylaxis, has emerged as a strong risk factor
for human mastitis because it induces selection for antibiotic
resistant staphylococci in the mammary gland and the
elimination of potential competitors [45, 73].
Nutritional status affects mastitis incidence and prevalence
in both women and animals. In African countries under
nutrition, reduced plasma levels of micronutrients, including
zinc and vitamin A, and antioxidants including selenium and
vitamin E are associated with subclinical mastitis [55, 176].
Limited availability of the same antioxidants is a known risk
factor for clinical and subclinical mastitis in dairy cattle
[177]. Dairy cows produce more milk than needed for their
offspring, and as a result, major nutritional imbalances can be
observed particularly at the onset of lactation leading to a
higher risk for mastitis. Cows around parturition and during
early lactation often experience negative energy balance. This
status is caused by a reduced dry matter intake and increased
energy expenditure in fetal growth and milk synthesis [178].
Cows in a negative energy balance have high plasma levels of
non-esterified fatty acids and betahydroxybutyrate. Prolonged
high concentrations of these markers in early lactation cows
and periparturient cows are associated with subclinical mastitis
and cases of clinical mastitis in early lactation [179]. Similarly,
sudden diet changes especially energy concentration may
increase the risk for coliform mastitis in sows [162].
Besides energy and antioxidant availability, plasma calcium
is limited in periparturient dairy animals (cattle, sheep and
goats) due the massive secretion of this mineral into colostrum
and milk. Clinical or subclinical hypocalcemia impairs
systemic and mammary gland immune function thus increasing
the risk for clinical mastitis [180]. Furthermore, reduced
plasma calcium impairs muscle contraction and therefore
efficient closing of the teat sphincter allowing bacteria to enter
the teat canal [181]. Around parturition there are also changes
in dairy animals’ innate and specific immune function that
diminish their resistance to IMI [161]. In periparturient cows
for example, macrophage and neutrophil functions including
phagocytosis, respiratory burst activity, superoxide anion
production, random cellular migration, and chemotaxis are
impaired [182]. The same immune functions are impaired in
sows and are likely predisposing factors for PDS [162].
Socio-Economic Factors
Literature reporting epidemiological factors related to socio-
economic status and mastitis in women is scarce. However,
family income, economic status, and higher education are risk
J Mammary Gland Biol Neoplasia (2011) 16:339–356
factors for lactational mastitis. In North America, women with
a full time employment and higher education degree were at
higher risk (2.65) of developing mastitis [183, 184]. In fact, a
study following 946 breastfeeding mothers in Michigan and
Nebraska found higher relative risks in women with income
over $100,000 and college, graduate or professional degrees
[126]. Similarly, in an Australian cohort of breastfeeding
mothers, higher income and education, and full time
employment were associated with lactational mastitis [185].
Another study following 1,352 breastfeeding Australian
mothers found that women with college education were at
a higher risk for mastitis (1.93) [164]. Also, higher economic
status was linked with a higher relative risk (1.13) of
developing mastitis in New Zealand women during the first
year postpartum [127]. Nevertheless, a higher economic and/
or educational status may not be actually associated with a
higher mastitis incidence, but with a higher likelihood of
reporting the condition to a health professional or a lactation
counselor. In contrast to developed countries, in African
nations nutritional deficiencies are risk factors for
lactational mastitis. For example, Gambian lactating
women with reduced caloric intake had lower concen-
trations of IgA in milk and a higher incidence of
clinical mastitis [186, 187].
Herd Factors
Dairy, flock, or sow barn management practices right from the
moment a female is born until first parturition and into
consequent lactations may increase or reduce mastitis inci-
dence and prevalence. In calves, the use of milk from mastitic
cows increases the incidence of mastitis caused by Strep
agalactiae [166]. Preventing calf cross sucking during rearing
decreases the transmission of the same pathogen and thus
reduced mastitis incidence after parturition [188]. Around the
time of calving, herds that separate mature cows from
primiparous heifers have a lower incidence of clinical mastitis
in the heifers [189]. At the milking parlor, the use of dipping
teats with germicides before and after milking, and the
implementation of a milking routine, have a positive impact
in the transmission of contagious mastitis pathogens and SCC
in dairy cows, does and ewes [24, 90]. However, teat dipping
does not prevent IMI with coliform or other environmental
pathogens, and if not used or mixed adequately,
contaminated teat dip solution could be a pathogen
reservoir. In fact, these solutions have been the cause of
several clinical mastitis outbreaks [190]. Good hygiene
conditions in the parlor and the stalls are positively
correlated with udder health in dairy herds and flocks
[89, 90, 191]. Similarly, sanitation and hygiene practices
and animal cleanliness are especially important in
reducing PDS and chronic mastitis in sows as both are
J Mammary Gland Biol Neoplasia (2011) 16:339–356
caused by pathogens of fecal origin [21, 162]. Along the
same line, stall and parlor preventive management tools,
such as fly control, help in the reduction of mastitis caused
by Actinomyces pyogenes and S. aureus [192, 193]. The
use of antibiotic and teat sealant infusions in each
productive quarter or half at the end of lactation reduces
the incidence of new clinical mastitis cases and helped
eradicate GBS in several dairy cow herds, and reduced the
incidence of gangrenous mastitis in sheep [81, 90, 194]. In all
cases and operations, mastitis control is largely influenced by
owner/manager motivation, and effective programs to reduce
this disease must take into account this factor [195]. Finally,
reduction of mastitis by the use of vaccines is an effective
practice for specific etiological agents. In dairy cattle, the use
of E coli bacterins reduced the rate of clinical mastitis caused
by gram-negative pathogens during early lactation, and also
diminished the severity of the disease [196]. Vaccines against
CNS and S. aureus (gangrenous mastitis etiological agent)
reduced prevalence and severity of the clinical signs in sheep
and goats [197, 198].
Conclusion
Mastitis is a disease with high economic, social, and public
health impact. In humans, the number of women voluntarily
opting for breastfeeding is increasing in the developed world;
furthermore in developing countries, maternal breast milk is
the best (and usually only) nutritional option for children
under 1 year of age. Unfortunately, puerperal mastitis
frequently results in early weaning, depriving many children
from the benefits of breastfeeding. In food producing animals,
mastitis is the disease with highest economic impact and one
of the diseases with deepest implications for animal welfare
and public health. Despite the importance of this disease, the
research effort devoted to mastitis in human medicine is
minimal while in food producing animals is declining at a
steadily rate. Positive actions from world and national public
health agencies, universities, and research organizations are
needed to reduce the impact of mastitis on human and animal
health and food safety around the world.
Acknowledgements The authors thank Drs John Caron and Ronald
Erskine for their helpful comments. Juan Miguel Rodriguez research is
supported by CSD2007-00063 (FUN-C-FOOD, Consolider-Ingenio
2010) and AGL2010-15420 projects from the Ministerio de Ciencia e
Innovación (Spain).
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