**3. Routes of entry of mastitis pathogens to the udder**

In general, it is believed that mastitis pathogens gain entrance to the udder through teat opening into the teat canal and from the teat canal into the intramammary area during the reverse flow of milk due to vacuum pressure fluctuation of the milking machine [9]. However, the detailed mechanism of mastitis pathogen colonization of the mammary gland may vary among species of bacteria and the virulence factors associated with particular strain in each species. An example of this is in some cases; it has been shown that *E. coli* can penetrate the teat canal without the reverse flow of milk [9]. Some of the major mastitis pathogens, such as *E. coli* [140], *Staphylococcus aureus*, and *Streptococcus uberis* [20–22] can adhere to and subsequently invade into the mammary epithelial cells. This adherence and subsequent invasion into mammary epithelial cells allow them to persist in the intracellular area as well as to escape the host immune defenses attack and action of antimicrobial drugs [120, 140–144]. Dogan et al. [145] compared *E. coli* strains known to cause chronic infections with strains known to cause acute infections and found that chronic strains were more invasive to the epithelial cells, leading to the difficulty in clearance and persistent infection compared to acute strains. *S. aureus* enters the mammary gland through the teat opening and subsequently multiply in the mammary gland where they may form biofilms, attach to, and internalize into the mammary epithelial cells causing inflammation of mammary glands characterized by swelling, degeneration of epithelial cells, and epithelial erosions and ulcers [146, 147].

**157**

[149, 150].

*Bovine Mastitis: Part I*

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

**4. Clinical manifestation of mastitis**

Depending on clinical signs, mastitis can also be divided into clinical and subclinical mastitis. Clinical mastitis is characterized by visible inflammatory changes (abnormalities) in the mammary gland tissue such as redness, swelling, pain, increased heart, and abnormal changes in milk color (watery, bloody, and blood tinged) and consistency (clots or flakes) [9]. Clinical mastitis can be acute, peracute, subacute, or chronic. Acute mastitis is a very rapid inflammatory response characterized by systemic clinical signs which include fever, anorexia, shock, as well as local inflammatory changes in the mammary gland and milk. Peracute mastitis is manifested by a rapid onset of severe inflammation, pain, and systemic symptoms that resulted in a severely sick cow within a short period of time. Subacute mastitis is the most frequently seen form of clinical mastitis characterized by few local signs of mild inflammation in the udder and visible changes in milk such as small clots. Chronic mastitis is a long-term recurring, persistent case of mastitis that may show few symptoms of mastitis between repeated occasional flare-ups of the disease where signs are visible and can continue over periods of several months. Chronic mastitis often leads to irreversible damage to the udder from the repeated occur-

Subclinical mastitis is the inflammation of the mammary gland that does not create visible changes in the milk or the udder. Subclinical mastitis is an infection of mammary gland characterized by non-visible inflammatory changes such as a high somatic cell count coupled with shedding of causative bacteria through milk [9]. During this inflammatory process, the milk samples showed a rapid increase of somatic cells, characterized by increased number of neutrophils in the secretion [146, 148]. Despite increased recruitment of somatic cells into infected mammary glands, evidenced by an increased number of neutrophils, infection usually does not clear but became subclinical. Intramammary infections during early lactation may become acute clinical mastitis characterized by gangrene development due congestion and thrombosis (blockage) of blood supply to the tissue but most new infection during late lactation or dry period become acute or chronic mastitis

The increase in somatic cell count during subclinical infections leads to a decrease in useful components in the milk, such as lactose and casein [151]. Lactose is the sugar found in milk, and casein is one of the major proteins in milk and decreases in these two components affect the quality and quantity of milk yield [9]. During mastitis, there is an increase in lipase and plasmin, which have a detrimental effect on the quantity and quality of milk due to the breakdown of milk fat and casein [9]. Subclinical infections can reduce milk production by 10–12% when just one-quarter is infected [152]. These subclinical infections cause some of the greatest unseen economic [20] losses because of their detrimental impact on production and

There are host-, pathogen-, and environmental-related risk factors that predispose dairy cows to mastitis. The host risk factors include age (parity), stage of lactation, somatic cell count, breed, the anatomy of the mammary glands/morphology of udder and teat (diameter of teat canal and conformation of the udder), and immune competence (immunity) [153] (**Figure 1**). The environmental risk factors include the proper functioning status of milking machine, udder trauma, sanitation, climate, nutrition, management, season, and housing condition [154]

rences of the inflammation, and often these cows are culled.

milk quality without showing visible signs of infection [152].

**5. Risk factors for mastitis**

*Animal Reproduction in Veterinary Medicine*

The most important virulence factor of *S. agalactiae* is the capsular polysaccharide [133], which protects this bacterium from being engulfed by macrophages and subsequently phagocytosed [133]. Another virulence factor of *S. agalactiae* is the Rib protein, which confers resistance to proteases. Emaneini et al. [133] found that the Rib encoding gene (*rib)* was detected in 89% of the isolates from bovine origin. *Streptococcus agalactiae* causes persistent infections that are usually difficult to clear without antibiotic treatment [134]. Though *Streptococcus agalactiae* is highly contagious, it has good response to treatment with antibiotics, which makes it possible to eliminate from herds with current mastitis control measures [129]. Since the adoption of hygienic milking practices, the incidence of mastitis caused by *S. agalactiae* has dramatically decreased and is now rarely observed in dairy herds [135].

Mastitis caused by *Mycoplasma* spp. is a growing concern in the United States. It is believed that this organism has been underreported due to the difficulty of isolation by culture method [136]. The incidence of *Mycoplasma* mastitis varies across the globe, with a 3.2% prevalence rate in the United States that may increase to 14.4% in larger herd size of greater than 500 cows [47, 48, 62, 137]. A risk factor for *Mycoplasma* mastitis increase with herd size, and most of the *Mycoplasma* mastitis cases are subclinical infections with outbreaks linked to asymptomatic carriers [138]. Pathogenesis of most *Mycoplasma* spp. infection is characterized by adherence to and internalization into host cells resulting in colonization of the host with immune modulation without causing severe disease [138]. *Mycoplasma* species lack a cell wall, thus not sensitive to beta-lactam antibiotics, but showed sensitivity to

In general, it is believed that mastitis pathogens gain entrance to the udder through teat opening into the teat canal and from the teat canal into the intramammary area during the reverse flow of milk due to vacuum pressure fluctuation of the milking machine [9]. However, the detailed mechanism of mastitis pathogen colonization of the mammary gland may vary among species of bacteria and the virulence factors associated with particular strain in each species. An example of this is in some cases; it has been shown that *E. coli* can penetrate the teat canal without the reverse flow of milk [9]. Some of the major mastitis pathogens, such as *E. coli* [140], *Staphylococcus aureus*, and *Streptococcus uberis* [20–22] can adhere to and subsequently invade into the mammary epithelial cells. This adherence and subsequent invasion into mammary epithelial cells allow them to persist in the intracellular area as well as to escape the host immune defenses attack and action of antimicrobial drugs [120, 140–144]. Dogan et al. [145] compared *E. coli* strains known to cause chronic infections with strains known to cause acute infections and found that chronic strains were more invasive to the epithelial cells, leading to the difficulty in clearance and persistent infection compared to acute strains. *S. aureus* enters the mammary gland through the teat opening and subsequently multiply in the mammary gland where they may form biofilms, attach to, and internalize into the mammary epithelial cells causing inflammation of mammary glands characterized by swelling, degeneration of epithelial cells, and epithelial erosions and

*2.4.3 Streptococcus agalactiae*

*2.4.4 Mycoplasma mastitis*

non-beta-lactam antibiotics [139].

**3. Routes of entry of mastitis pathogens to the udder**

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ulcers [146, 147].
