Staphylococcus aureus Pneumonia

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J15.211 – Pneumonia due to Methicillin susceptible Staphylococcus aureus

441658007 – Pneumonia due to Staphylococcus aureus


Staphylococcus aureus are aerobic gram-positive cocci that form clusters and short chains. They are responsible for a wide variety of diseases ranging from superficial skin and soft tissue infections to deep-seated and life-threatening infections with high morbidity and mortality rates, such as endocarditis and septicemia. In addition, S. aureus is capable of secreting toxins that mediate illnesses like the toxic shock syndrome (TSS) and the staphylococcal scalded skin syndrome (SSSS).

S. aureus is a ubiquitous colonizer of the skin and mucosal surfaces and can be found in the nares of 10–40% of individuals in the community and in the hospital. Nasal carriage is also a source for the transmission of multiresistant staphylococci. Certain patient populations like dialysis patients, diabetics, IV drug users, alcoholics, and HIV-infected individuals are at a high risk for infections from staphylococci.

S. aureus in responsible for about 1–10% of community-acquired pneumonias and 20–30% of hospital-acquired pneumonias. S. aureus pneumonia may result from air-borne contamination or aspiration or hematogenous seeding of the lungs from bacteremia or right-sided endocarditis. There may be a history of recent viral or influenzal illness. The clinical manifestations of staphylococcal pneumonia are similar to other causes of pneumonia except for a tendency to cause necrotizing infection with tissue destruction and cavitation. The patient will present with an abrupt onset of fever, tachypnea, pleuritic chest pain, and a productive cough with purulent sputum, which can be blood-tinged. S. aureus is also one of the most common causes of empyema. In cases with accompanying endocarditis, stigmata-like subungual hemorrhages, murmur of aortic, tricuspid or mitral regurgitation, palmar Janeway lesions, and digital Osler nodes may be found.

Methicillin-resistant S. aureus (MRSA) first emerged as an important nosocomial pathogen in the 1960s. In more recent years, community-acquired outbreaks of MRSA (CA-MRSA) have been described increasingly among healthy individuals lacking the traditional risk factors for staphylococcal infections.

A rapidly progressive necrotizing pneumonia in young, healthy adults and children has been described due to infection with strains of CA-MRSA containing the gene for the Panton-Valentine leucocidin (PVL), a toxin that induces lysis of host macrophages, thus impairing host response and facilitating tissue necrosis. The mortality from pneumonias caused by the PVL strains is very high.

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