**2.1 Environmental mastitis pathogens**

It is important to mention that all environmental mastitis pathogens may not be strictly environmental, and some of them may transmit both ways (contagious and environmental). However, the vast majority of these organisms are in the environment of dairy cows, and they transmit from these environmental sources to the udder of a cow at any time of the lactation cycle.

#### *2.1.1 Streptococcus uberis mastitis*

*Streptococcus uberis* is one of the environmental mastitis pathogens that accounts for a significant proportion of subclinical and clinical mastitis in lactating and nonlactating cows and heifers [14]. This organism is commonly found in the bedding material, which facilitates infection of mammary glands at any time [15]. Some report also indicated the possibility of contagious transmission of *Streptococcus uberis* [16].

*S. uberis* has various mechanisms of virulence that increases the chances of this organism establishing infection. These include a capsule, which evades phagocytosis, adherence to, and invasion into mammary epithelial cells [17, 18]. *S. uberis* adheres to epithelial cells using different mechanisms, including the formation of pedestals [19] and bridge formation through *Streptococcus uberis* adhesion molecule (SUAM) and lactoferrin [20–22]. This attachment is specific and mediated through a bridge formation between *Streptococcus uberis* adhesion molecule (SUAM) [23, 24]

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*Bovine Mastitis: Part I*

*DOI: http://dx.doi.org/10.5772/intechopen.93483*

mammary epithelial cells [14].

*2.1.3 Coliform mastitis*

*2.1.2 Coagulase-negative Staphylococcus species (CNS)*

efficient bacterial clearance are not clearly defined.

on *S. uberis* surface and lactoferrin, which is in the mammary secretion and has a receptor on the mammary epithelial surface [20, 22]. This interaction creates a molecular bridge that enhances *S. uberis* adherence to and internalization into mammary epithelial cells most likely via caveolae-dependent endocytosis and potentially allows *S. uberis* to evade host defense mechanisms [22, 24]. These factors increase the pathogenicity of *S. uberis* to cause mastitis. The *sua* gene is conserved among strains of *S. uberis* isolated from geographically diverse areas [9, 13], and a *sua* deletion mutant of *S. uberis* is defective in adherence to and internalization into

More recently, coagulase-negative *Staphylococcus* species (CNS) such as *S. chromogenes, S. simulans, S. xylosus, S. haemolyticus, S. hyicus*, and *S. epidermidis* are increasingly isolated from bovine milk [7, 25–27] with *S. chromogenes* being the most increasingly diagnosed species as a cause of subclinical mastitis. *Staphylococcus chromogenes* [28] and other CNS [4, 8] have been shown to cause subclinical infections in dairy cows that reduce the prevalence of contagious mastitis pathogens.

*Staphylococcus chromogenes* is most commonly isolated from mammary secretions rather than from the environment itself [8, 29]. *S. chromogenes* consistently isolated from the cow's udder and teat skin [30], and some studies showed that it causes long-lasting, persistent subclinical infections [26]. The CNS causes high somatic cell counts in milk on some dairy farms [29, 31]. Woodward et al. [32] evaluated the normal teat skin flora and found that 25% of the isolates exhibited the ability to prevent the growth of some mastitis pathogens. An *in vitro* study conducted on *S. chromogenes* showed that this organism could inhibit the growth of major mastitiscausing pathogens such as *Staph. aureus*, *Strep. dysgalactiae*, and *Strep. uberis* [28]. In a study conducted on conventional and organic Canadian dairy farms, CNS were found in 20% of the clinical samples [33]. Recently, mastitis caused by CNS increasingly became more problematic in dairy herds [30, 34–36]. However, mastitis caused by CNS is less severe compared to mastitis caused by *Staphylococcus aureus* [26].

Coliform bacteria such as *Escherichia*, *Klebsiella,* and *Enterobacter* are a common cause of mastitis in dairy cows [37]. The most common species, isolated in more than 80% of cases of coliform mastitis, is *Escherichia coli* [38, 39]. *E. coli* usually infects the mammary glands during the dry period and progresses to inflammation and clinical mastitis during the early lactation with local and sometimes severe systemic clinical manifestations. Some reports indicated that the severity of *E. coli* mastitis is mainly determined by cow factors rather than by virulence factors of *E. coli* [40]. However, recent molecular and genetic studies showed that the pathogenicity of *E. coli* is entirely dependent on the FecA protein that enables *E. coli* to actively uptake iron from ferric-citrate in the mammary gland [41]. The severity of the clinical mastitis and peak *E. coli* counts in mammary secretions are positively correlated. Intramammary infection with *E. coli* induced expression and release of pro-inflammatory cytokines [42, 43]. Recently, it has been shown with mouse mastitis models that IL-17A and Th17 cells are instrumental in the defense against *E. coli* intramammary infection [44, 45]. However, the role of IL-17 in bovine *E. coli* mastitis is not well defined. The result of recent vaccine efficacy study against *E. coli* mastitis suggested that cell-mediated immune response has more protective effect than humoral response [46]. However, the cytokine signaling pathways that lead to

### *Bovine Mastitis: Part I DOI: http://dx.doi.org/10.5772/intechopen.93483*

*Animal Reproduction in Veterinary Medicine*

pathogens lists as environmental or contagious may not be strictly environmental or strictly contagious; some of them may transmit both ways. Environmental mastitis pathogens exist in the cow's environment, and they can cause infection at any time. Environmental mastitis pathogens are difficult to control because they are in the environment of dairy cows and can transmit to the mammary glands at any time, whereas contagious mastitis pathogens exist in the infected udder or on the teat skin and transmit from infected to non-infected udder during milking by milker's hand or milking machine liners. Environmental mastitis pathogens include a wide range of organisms, including coliform bacteria (*Escherichia coli, Klebsiella* spp.*, Enterobacter* spp., and *Citrobacter* spp)*,* environmental Streptococcus spp. (*Streptococcus uberis, Streptococcus dysgalactiae, Streptococcus equi, Streptococcus zooepidemicus, Streptococcus equinus, Streptococcus canis, Streptococcus parauberis*, and others), *Trueperella pyogenes,* which was previously called *Arcanobacterium pyogenes* or *Corynebacterium pyogenes* and environmental coagulase-negative *Staphylococcus* species (CNS) (*S. chromogenes, S. simulans, S. epidermidis, S. xylosus, S. haemolyticus, S. warneri, S. sciuri, S. lugdunensis, S. caprae, S. saccharolyticus*, and others) [4, 6–9] and others such as *Pseudomonas*, *Proteus*, *Serratia*, *Aerococcus*, *Listeria*, Yeast and *Prototheca* that are

increasingly found as mastitis-causing pathogens on some farms [10, 11].

treatment and prevention of mastitis difficult.

udder of a cow at any time of the lactation cycle.

**2.1 Environmental mastitis pathogens**

*2.1.1 Streptococcus uberis mastitis*

Contagious mastitis pathogens primarily exist in the infected mammary glands or on the cow's teat skin and transmit from infected to non-infected mammary glands during milking by milker's hand or milking machine liners. *Mycoplasma* spp. may spread from cow to cow through aerosol transmission and invade the udder subsequent to bacteremia. The most frequent contagious mastitis pathogens are coagulase-positive *Staphylococcus aureus, Streptococcus agalactiae, Mycoplasma bovis,* and *Corynebacterium bovis* [11, 12]*.* The prevalence of mastitis caused by these different mastitis pathogens varies depending on herd management practices, geographical location, and other environmental conditions [13]. These different causative agents of mastitis have a multitude of virulence factors that make

It is important to mention that all environmental mastitis pathogens may not be strictly environmental, and some of them may transmit both ways (contagious and environmental). However, the vast majority of these organisms are in the environment of dairy cows, and they transmit from these environmental sources to the

*Streptococcus uberis* is one of the environmental mastitis pathogens that accounts for a significant proportion of subclinical and clinical mastitis in lactating and nonlactating cows and heifers [14]. This organism is commonly found in the bedding material, which facilitates infection of mammary glands at any time [15]. Some report also indicated the possibility of contagious transmission of *Streptococcus* 

*S. uberis* has various mechanisms of virulence that increases the chances of this organism establishing infection. These include a capsule, which evades phagocytosis, adherence to, and invasion into mammary epithelial cells [17, 18]. *S. uberis* adheres to epithelial cells using different mechanisms, including the formation of pedestals [19] and bridge formation through *Streptococcus uberis* adhesion molecule (SUAM) and lactoferrin [20–22]. This attachment is specific and mediated through a bridge formation between *Streptococcus uberis* adhesion molecule (SUAM) [23, 24]

**150**

*uberis* [16].

on *S. uberis* surface and lactoferrin, which is in the mammary secretion and has a receptor on the mammary epithelial surface [20, 22]. This interaction creates a molecular bridge that enhances *S. uberis* adherence to and internalization into mammary epithelial cells most likely via caveolae-dependent endocytosis and potentially allows *S. uberis* to evade host defense mechanisms [22, 24]. These factors increase the pathogenicity of *S. uberis* to cause mastitis. The *sua* gene is conserved among strains of *S. uberis* isolated from geographically diverse areas [9, 13], and a *sua* deletion mutant of *S. uberis* is defective in adherence to and internalization into mammary epithelial cells [14].
