STAPHYLOCOCCUS AUREUS PNEUMONIA
Staphylococcus aureus is a necrotizing gram-positive coccus that often appears in a grapelike cluster when stained in tissues and secretions. It can lead to infection at a variety of sites in the body, including the lung, and can be responsible for all forms of pneumonia, including community-acquired pneumonia (CAP), health care–associated pneumonia (HCAP), and nosocomial pneumonia. Although the organism can lead to a deepseated lung infection, it can also spread hematogenously from the lung to multiple sites throughout the body. Lung involvement may not only be the result of a primary pneumonia but can also be secondary to bacteremia from a variety of sites, including the skin and from right-sided endocarditis. The virulence of this organism is promoted by its ability to acquire from other organisms exogenous genetic material (insertion sequences, transposons, and bacteriophages) that are responsible for tissue invasion and the acquisition of antibiotic resistance. CAP can be caused by antibiotic- sensitive organisms or by methicillin-resistant S. aureus (MRSA), the latter being seen in both the community as well as in hospital-acquired infections.
S. aureus is generally not a common cause of CAP but has traditionally been seen in elderly individuals, in those with chronic lung disease (cystic ﬁbrosis and bronchiectasis), and as a cause of bacterial pneumonia complicating inﬂuenza. In the past several years, community-acquired strains of methicillin-resistant S. aureus (CA-MRSA) have emerged, primarily in skin and soft tissue infections but also as a cause of severe CAP. The frequency of CAP caused by CA-MRSA is still relatively low, but it does occur sporadically, with certain geographic areas having a high frequency, especially during inﬂuenza season. CA-MRSA is a clonal disease, emanating from the USA 300 clone of S. aureus, and is clinically and bacteriologically different from the strains of MRSA that cause nosocomial pneumonia. CA-MRSA can infect previously healthy individuals, usually as a complication of preceding viral infection, although nosocomial MRSA tends to infect chronically ill and debilitated individuals. CA-MRSA is often a necrotizing infection that may be mediated by a variety of staphylococcal toxins, including the Panton-Valentine leukocidin toxin.
Hematogenous seeding of the lung, leading to staphylococcal pneumonia, can occur in drug addicts with right-sided endocarditis or from septic venous thrombophlebitis (from central venous catheter or jugular vein infection). In patients with primary pulmonary infection, the disease tends to be severe and is often bilateral, multilobar, rapidly progressive, and necrotizing. Patients present with a sudden onset of fever, tachypnea, and cough with purulent sputum, and the condition can progress rapidly to septic shock and respiratory failure. The radiograph may show pleural effusion, cavitary inﬁltrates, lung abscess, or pneumatoceles (a late sequela of infection). Empyema is a common complication, but extrapulmonary complications include endocarditis and meningitis.
Therapy for antibiotic-sensitive organisms is with an antistaphylococcal penicillin (e.g., oxacillin or nafcillin) or a ﬁrst-generation cephalosporin. For MRSA, vancomycin may be used, but linezolid may be a more effective agent because it penetrates better to respiratory sites of infection. Therapy should be continued for 4 to 6 weeks in complicated infections, such as those complicated by bacteremia or distant seeding to extrapulmonary sites. Reinfection can occur, and the mortality rate may exceed 30%. Because the pathogenesis of CA-MRSA pneumonia may be related to bacterial toxin production, therapy may need to involve both an antibacterial agent and an antitoxin-producing agent (e.g., linezolid alone or the combination of vancomycin and clindamycin).