**1. Introduction**

The emergence of community-acquired methicillin resistant *Staphylococcus aureus* (CA-MRSA) strains in individuals without traditional risk factors, has caused a drastic change in MRSA epidemiology since community acquired infections are etiologically caused by MSSA (methicillin sensitive *S. aureus*). Initially the most affected social groups were soldiers, men who have sex with men, prisoners, illicit injection drug users, and athletes; people with compromised skin and mucosa, poor hygiene habits and postpartum mastitis; Native Americans of the United States, and children due to their close contact with contaminated nasal secretions.

This change in epidemiology lead to molecular studies aimed at determining pathogenicity, virulence, resistance to different antimicrobial classes and the behavior of these strains against selective pressure of the human immunological system. Associating risk factors with the molecular studies gave rise to Molecular Epidemiology.

Humans are the main source of *Staphylococcus* spp., which can be found in the skin, throat, intestine and nose without causing damage to the host. In hospitals, the asymptomatic host can disseminate *S. aureus* to immunocompromised patients. Since they are ubiquitous, these bacteria can cause several types of infections such as: necrotizing pneumonia, skin and soft tissue infections, bacteremia, as well as food poisoning through enterotoxin production.

Individuals affected by CA-MRSA strains can develop from mild to metastatic and lethal infections, which are directly related to the synthesis of certain toxins, antimicrobial resistance and individual health conditions. One of the most discussed virulence factors is PVL (Panton-Valentine Leukocidine). Since its first association with skin and soft tissue infections, PVL is now believed to contribute to the elevated virulence potential attributed to CA-MRSA.

Methicillin resistance is conferred by *mecA* gene inserted in a mobile genomic island, the Staphylococcal cassette chromosomal (SCC*mec*). Some different SCC*mec* regions are responsible for mobility and regulation, and others for resistance to several antimicrobial classes. According to the presence, lack or genomic variations in these regions, the cassettes

CA-MRSA: Epidemiology of a Pathogen of a Great Concern 55

search for alternatives, and in 1959, adding the acid 6-aminopenicilanic in the penicillin molecule allowed for protecting the precursor of penicillin beta-lactam ring. This semisynthetic penicillin (Named methicillin (and the analog oxacillin, used in Brazil) proved to be resistant to the action of beta-lactamase. However, both were effective for a short period of time, and in 1961, strains resistant to semisynthetic penicillins emerged. These emerging new strains were named MRSA (Methicillin-Resistant *Staphylococcus aureus*), so far unique to

In the 1980s the first reports emerged of infections caused by *S. aureus* in patients without risk factors for acquisition of nosocomial MRSA (HA-MRSA), resulting in the designation of CA-MRSA (Community-Acquired Methicillin-Resistant *S. aureus*) in the 1990s when reports of CA-MRSA increased (Ricardo, 2004). The community-acquired infections are usually distinct from hospitals in terms of susceptibility and the carriage of the gene that codifies for the synthesis of Panton-Valentine Leukocidin (PVL) responsible for tissue invasion

According to criteria, it is considered that individuals affected by CA-MRSA should not report previous MRSA infections; the patient must have a positive culture for MRSA within 48 hours after hospital admission, and must not be hospitalized in the last 12 months, or admitted to nursing homes or homecare, and did not report undergoing dialysis, surgery, catheters or any prior or invasive treatment at the time of MRSA

The transmission of the bacteria occurs through direct contact of susceptible individuals with asymptomatic carriers. There are frequent reports of the spread of CA-MRSA among men who have sex with men, soldiers, athletes, intravenous illicit drug users, prisoners, people with compromised skin and mucous membranes, poor hygiene, postpartum mastitis (Reddy et al., 2007), Native Americans from the U.S. (Klevens et al., 2007; Stemper et al., 2006) and among children due to the contact with contaminated nasal discharge (Klevens et

The transmission of MRSA among family members was reported in a study with 10 families. Strains with PFGE ST8 (USA 300), ST59 (USA 1000), and ST80 PVL-positive were found in this investigation (Huijsdens et al., 2006). Lung infections caused by these strains can be serious because the symptoms are similar to pneumonia in children; therefore, it is important to consider infection by MRSA especially if there were previous reported.

Among pathogens that can cause pulmonary infections, CA-MRSA is associated with pneumonia and is frequently associated with pulmonary viral coinfection. Studies indicate that CA-MRSA agents are commonly found in pneumonia during the influenza season, and about 85% of *S. aureus* strains isolated contained the PVL gene. In three cases of severe necrotizing pneumonia, strategies were carried out to prevent the synthesis of Leukocidin, including the administration of antibiotics such as rifampicin, linezolid and clindamycin, and/or applying intravenous immunoglobulin to block the lytic effect of PVL under polymorphonuclear cells (Rouzic et al., 2010). During the influenza season of 2006 and 2007, there were 51 reported cases of pneumonia in health centers caused by *S. aureus*, and 79% were MRSA. Most cases of pneumonia due to MRSA occurred during or after viral infection

hospital settings (Ricardo, 2004; Salgado et al., 2003).

preceding the skin infections (Klevens et al., 2007).

isolation (Salgado et al. 2003).

al., 2007).

(Huijsdens et al., 2006).

(Kallen et al., 2008).

can be classified in a range from type I to XI largely used to discriminate hospital and community types.

Community strains are usually more sensitive to other antimicrobial classes compared to multiresistant health care associated strains. In fact, CA-MRSA can be resistant to other antimicrobials besides beta-lactams, thus decreasing the options of drug choices. Another subject of concern is resistance to the drug of choice for treating MRSA, vancomycin. There are few antimicrobials to control the infections caused by MRSA and vancomycin is one of them. Reports of resistance and low level of sensitivity to this drug in health care environments have been reported worldwide.

All of the issues mentioned above, underscore the importance of further research on the behavior of CA-MRSA at the epidemiological and molecular levels enabling establishment and application of preventive measures and treatment in view of infections. The present chapter will outline the main features of CA-MRSA and epidemiological principles involved in the outcome briefly described above.
