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I. DEFINITION

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Infection with methicillin-resistant Staphylococcus aureus (MRSA) (clustered gram-positive cocci) causes a variety of localized and invasive suppurative infections and toxin-mediated syndromes such as toxic shock syndrome and scalded skin syndrome. MRSA infections used to be limited to health care facilities (HC-MRSA) and were strictly nosocomial; however, a significant increase in community-acquired MRSA (CA-MRSA) has been seen in the last decade. The separation between HC-MRSA and CA-MRSA is becoming less distinct, as CA-MRSA is becoming more virulent and causing significantly more health care–associated infections.

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II. INCIDENCE

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The methicillin-sensitive Staphylococcus aureus normally colonizes the nose, umbilicus, and the groin area by 1 week of age, with a colonization rate of 20–90%. Maternal anogenital colonization with MRSA ranges from 0.5% to 10.4%, with little risk for early-onset disease in the newborn. There are several documented outbreaks of invasive CA-MRSA that developed in healthy newborn infants discharged from normal newborn nurseries as well as neonatal intensive care units (NICUs). The majority of MRSA infections in the NICU are of late onset. According to neonatal data reported from National Nosocomial Infections Surveillance System for the years 1995–2004, MRSA accounted for 23% of all hospital-associated S. aureus infections. The incidence of MRSA infections per 100,000 patient-days increased by 308% during the study period from 0.7 in 1995 to 3.1 in 2004. The NICU colonization rate is variable; one study showed a rate of 10.4%, with a mean time to acquire MRSA of 17 days.

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III. PATHOPHYSIOLOGY

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. If the newborn infant is exposed to MRSA, whether from the community or the hospital, then he or she will be colonized with more virulent strains that are more likely to cause invasive disease. MRSA has specific virulence factors that make it more invasive than methicillin-sensitive S. aureus. These include staphylococcal chromosome cassette (SCC) mecA, Panton-Valentine leukocidin (PVL), and staphylococcal enterotoxins. The SCC mecA has the genes that encode antibiotic resistance. PVL genes lead to the production of cytotoxins that form pores in the cellular membrane and cause tissue necrosis and cell lysis.

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IV. RISK FACTORS

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Include overcrowding, inconsistent hand washing, invasive procedures (eg, central lines, endotracheal intubations, nasogastric tubes), low birthweight, the practice of kangaroo (skin-to-skin) mother care, a high MRSA colonization rate, and prolonged hospital stay.

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V. CLINICAL PRESENTATIONS

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Invasive MRSA disease is likely to be preceded by colonization (skin, umbilicus, and nasopharynx). The source of the bacteria could be a health care worker, another patient, equipment, or a family member.

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  1. Bloodstream infections. These are usually catheter related. Common clinical signs are nonspecific and include apnea or hypoxia, fever, elevated C-reactive protein, and leukocytosis. The infant needs to be examined repeatedly and meticulously for subtle clues of focal infection (eg, phlebitis, pustulosis).

  2. Septic arthritis and osteomyelitis. Staphylococcus aureus is the primary cause of septic arthritis ...

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