**1. Introduction**

*Staphylococcus aureus* is a symbiotic and opportunistic microorganism that can colonize various sites of different animals and humans. This bacteria can cause serious infections in humans and animals [1]. In animals, bovine mastitis, commonly caused by various bacteria, is one of the most devastating disease in dairy farming worldwide. Of these bacteria, *Staphylococcus aureus* is the leading pathogen causing the most dangerous mastitis in cattle and the most difficult dairy product in most countries. *Staphylococcus aureus* has emerged as superbug of dairy udder, compromising animal health and economy [2]. Its virulence is due to its

ability of producing wide array of virulence factors that enhances its attachment, colonization, longer persistence and escaping the immune response. Such resistant strains are distinguished by systemic heterogenicity, genetic variety, interactions between complex community and the extracellular matrix of macromolecular substances [3].

*Staphylococcus aureus* has a variety of strains, most notably multi-drug resistance and biofilm formation. The latter has received a lot of attention due to its ability to minimize the effects of antibiotics, colonize the mucous membrane of the epithelium, last longer, avoid immune reactions, and contribute to etiology [4]. Methicillin resistant *S. aureus* strains have been designated as emerging pathogen in livestock and dairy animals. Hospital acquired MRSA and community associated MRSA are limited to humans only, but livestock occupational personals may have infections with human originated MRSA [5].

The successful mastitis therapy depends on various factors such as accurate diagnosis, elimination of causative agent, stage of disease, severity of the infection, selection of the drugs, route of drugs administration along with other supportive treatments [6, 7] and some other factors regarding mastitis causing organisms. However, irrespective of the appropriate use of antibiotic, the mastitis may not be treated successfully [8]. The treatment failure mainly occurs due to insufficient contact of antimicrobials and disease-causing microorganisms in the udder. Mastitis can incur economic losses in both ways either directly and indirectly [9]. The direct losses include veterinary expenditure, labor costs, reduced production, poor quality milk and discarded milk. Whereas, the indirect losses are not obvious to the producers and are termed as "hidden losses" which include increased risk of other diseases, poor fertility rate, increased culling rate and sometime mortality. So, total cost can be much more than the direct losses [10–12]. This chapter addresses the following aspects such as transmission, pathogenesis, strains spectrum, economic impact, emerging treatment and prevention strategies to control *S. aureus* dairy udder infection.

## **2. Transmission of** *Staphylococcus aureus* **in udder infections**

The main reservoirs of *Staphylococcus aureus* are infected mammary glands, ducts, and papillary lesions. However, this bacteria also found on the skin, nose and teat passages. The bacteria spread to uninfected areas through the lining of the teat cups, milker's hands, towels and fruit flies. *Staphylococcus aureus* does not persist on healthy teat skin, but tends to colonize damaged skin and teat lesions. The body reproduces the infected lesion, increasing the likelihood of teat colonization and subsequent udder infection. Heifers infected during calf pregnancy are an important reservoir that can be passed on to uninfected *Staphylococcus aureus* herds. There has been much controversy over the route of infection with *Staphylococcus aureus* in early prenatal heifers, but it is possible that the cause is a calf that was fed on a mother infected with *Staphylococcus aureus*. Data is limited, but if you have a problem with *Staphylococcus aureus* on your farm, you should definitely consider choosing scrapes carefully (such as cryo-sterilization). Obviously, a good treatment plan for mastitis will take into account the absence of this disease in heifers [13].

### **3. Pathogenesis of** *S. aureus* **in udder infection**

Bacterial pathogens can recognize, respond and adapt to the harsh environmental conditions that prevail in mammalian hosts during infection. Despite the

## Staphylococcus aureus *and Dairy Udder DOI: http://dx.doi.org/10.5772/intechopen.95864*

host's immune response and antibacterial treatment, it helps to invade, calm, and survive within the host [14]. *Staphylococcus aureus* produces a variety of enzymes, including coagulase, which can coagulate plasma, converting plasma fibrinogen to fibrin, coat bacterial cells, and inhibit nutrition. Hyaluronidase (also called diffusion factor) can break down the hyaluronic acid present in tissues and support the spread of *Staphylococcus aureus* in the host. It also produces DNase (deoxyribonuclease), an enzyme that breaks down DNA. Lipase, which breaks down lipids, and staphylokinase, which breaks down fibrin. It is also known that *Staphylococcus aureus* produces β-lactamase, esterase, elastase and phospholipase for drug resistance, and these enzymes promote colony formation and pathogenicity. Other toxic factors of *Staphylococcus aureus* include leukocidin (which can cause cytolytic destruction of phagocytic cells in some animals) and toxic shock syndrome toxin (TSST). The latter can cause an overproduction of lymphokine, which can lead to tissue damage [15]. Depending on the strain, *Staphylococcus aureus* can release some toxins that are major virulence factors. These toxins act on cell membranes containing superantigens, exfoliating toxins, and some two-component toxins such as alpha toxins, beta toxins, gamma toxins, delta toxins and Panton Valentine's toxins and leukocidin (PVL). It can be divided into three categories, for example toxins [16]. Protein A, which plays an important role in strategies for evading immunity, is immobilized on the staphylococcus-peptide-glycan-pentaglysin bridge using transpeptidase sortase (**Figure 1**). Protein A is able to bind to fragments of the crystal region (Fc) of IgG antibodies (γ-immunoglobulins). This phenomenon is due to the fact that Protein A binds to an IgG antibody produced against the target microorganism and reacts with the corresponding antigen usually present in the patient sample to perform an aggregation test in which a visible aggregation reaction can be observed. The *Staphylococcus aureus* strain is known to produce pigments such as staphyloxanthin and gold carotenoid pigments. These pigment acts primarily as a toxic factor, acting as a bacterial antioxidant and helping microorganisms escape the host's immune system and kill reactive oxygen species used by the pathogen [18]. The toxins produced by *Staphylococcus aureus* destroy the cell membranes and tissues that directly produce milk. White blood cells (leukocytes) are attracted to the area of inflammation and try to fight the infection. First, bacteria damage the tissues lining the teat and mammary gland within 1/4 of a second, eventually leading to scar tissue formation. The bacteria

**Figure 1.** *Various virulence factors of S. aureus [17].*

then migrate into the duct system, forming deep-rooted infectious pockets in the lactating (alveolar) cells. The second is the formation of abscesses that prevent their spread, thus avoiding detection by the immune system. Abscesses prevent antibiotics from entering bacteria. This is the main reason for poor response to treatment. However, bacteria can also escape the lethal effects of some antibiotics by hiding in neutrophils (white blood cells) and other host cells preventing exposure to antibiotics. When the white blood cells die (usually within a day or two), the bacteria are released and the infection continues [19].

During infection, the destruction of alveolar and tubular cells reduces the lactation yield. These damaged cells can attach to leukocytes and block the mammary canal that drains the alveolar region, resulting in additional scar tissue, blockage of the canal, and decreased lactation. The teat canal can be opened later, but this usually results in the release of *Staphylococcus aureus* to other areas of the udder. The spread of *Staphylococcus aureus* in the glands leads to the formation of additional abscesses, which can become very large and appear as lumps in the udder (**Figures 2** and **3**). Most cases of *S. aureus* mastitis are asymptomatic, but chronic cows typically have high SCC, abnormal udder tissue, and recurrence of clinical mastitis. Clinically infected areas are usually swollen, milk has visible clots (large clots). Acute infections with *Staphylococcus aureus* usually develops late in lactation. Clinical symptoms such as udder swelling and hardness, milk appearance change) do not appear until the start of the next stage. It is difficult to cure an infection well, because the drug cannot penetrate all foci of infection, and bacteria can avoid contact with antibiotics in the white blood cells. Many strains of *Staphylococcus aureus* have acquired antibiotic resistance (the ability to produce enzymes that

**Figure 2.** *Immune response to* S. aureus *and vice versa inside the mammary gland [20].*

**Figure 3.** *Intracellular invasion of* S. aureus *inside mammary gland [20].*

inactivate penicillin and other antibiotics), making treatment impossible. The development of antibiotic resistance during treatment with certain β-lactam antibiotics (such as penicillin) is another reason for treatment failure [20].
