Staphylococcus Aureus Pneumonia: Emergence of MRSA in the Community

Suzanne F. Bradley, MD

Disclosures

Semin Respir Crit Care Med. 2005;26(6):643-649. 

In This Article

The Role of Toxins in the Changing Epidemiology and Clinical Presentation of Staphylococcal Pneumonia

In recent years, increasingly severe cases of MSSA community-acquired primary pneumonia have also been recognized among persons who should not be at risk of the infection.[10,33,34,35,36,37] In many instances, MSSA isolates contained the toxin Panton-Valentine leukocidin (PVL).

PVL is a member of the synergohymenotropic toxin family that induces pores in the membranes of cells.[2,37,41,42,43] Pairs of secretory proteins S and F work synergistically on cell membranes (hymen) as superantigens with release of intracellular interleukin-8, leukotrienes, proteases, and oxygen metabolites with resulting chemotaxis, vasodilitation, infiltration and death of neutrophils, and tissue necrosis.[2,37,42] SF protein pairs composed of S and F PVL-associated proteins (LukSPV + Luks FPV) and S and F α-hemolysin-associated proteins (HlgA (class S), HlgB (class F), HlgC (class S) have been found in various combinations in necrotizing pneumonia.[2,37,42] The presence of PVL in severe staphylococcal pneumonia isolates appears to be a recent phenomenon; in the past, the toxin had been identified in < 5% of strains.[37,40,42]

The clinical presentation of pneumonia appears to be different in PVL-producing strains. In cases of staphylococcal necrotizing CAP, 85% were PVL positive, whereas none of HAP strains were positive for the toxin.[42] Patients with PVL-positive strains were significantly more likely to have had an antecedent influenzalike illness, fever > 39°C, tachycardia, hemoptysis, pleural effusion, and leukopenia.[37] PVL-positive patients were also younger and less likely to survive their infection; overall mortality was > 40%.[37,38,42] Necrosis and hemorrhage of the trachea, alveoli, and blood vessels were commonly seen on autopsy and bronchoscopy specimens.[37,38] The presence of PVL may, in part, explain the changing epidemiology and clinical presentation of staphylococcal pneumonia whether it is due to MSSA or MRSA.

CA-MRSA infecting strains are more likely to have genes for toxins such as the leukocidins, staphylococcal enterotoxins B, C, and K (SEB, SEC, and SEK), and toxic shock staphylococcal toxin-1 (TSST-1) than HA-MRSA strains, but not all CA-MRSA strains are toxin producing.[10,18,34,36,43] Genetic factors that control the regulation and expression of toxins and other virulence factors, such as agr, may be important; most CA-MRSA strains contain agr1 and agr3.[18,35,44] Therefore, the presence of toxin genes and the ability to express those genes may explain, in part, how CA-MRSA causes severe and frequently fatal respiratory tract infections in healthy people.

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