Dr. Isaacs is a clinical assistant professor of emergency medicine at the Temple University School of Medicine and the director of the emergency department at Virtua Hospital-Voorhees Division in Voorhees, NJ.
The emergence of community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) is nothing new. Anyone practicing medicine in almost any specialty (if not all specialties) has encountered a patient infected with an invasive form, usually an abscess or cellulitis. The lay press and scientific literature have been filled with reports, advisories, and clinical research, but one form of the invasive disease, pneumonia, accounts for only two percent of all cases but has a 42 percent mortality rate. (Emerg Med Clin North Am 2008;26: 431.) This type of pneumonia poses a challenging clinical picture, where high suspicion is the first step in making the diagnosis.
In the late 1990s, the first cases of patients developing infections with CA-MRSA appeared, interestingly, in children with pneumonia. (JAMA 1999;282: 1123.) Since then, the incidence of pneumonia and skin and soft tissue infections (SSTIs) has shifted dramatically toward the latter. It has now been shown that CA-MRSA and hospital-acquired MRSA (HA-MRSA) have different genetic profiles, leading to a clinically relevant exotoxin. This toxin, Panton-Valentine leukocidin (PVL), is lethal to leukocytes.
PVL was first discovered in 1932, and is associated with skin and lung abscesses and clindamycin sensitivity. (Chest 2007; 131:1718.) Most strains of CA-MRSA carry the gene to manufacture PVL while very few strains of HA-MRSA do. PVL is thought responsible for the necrotizing aspect of the clinical effects. Another difference, well documented in the lay and clinical literature, is that HA-MRSA is sensitive to very few antibiotics while there are several effective antibiotic choices for CA-MRSA. HA-MRSA also generally infects a defined subset of patients while CA-MRSA has no definite pattern except for one notable exception, patients with pneumonia.
Unlike the skin and soft tissue manifestation of CA-MRSA, the invasive pneumonia follows an epidemiologic pattern. Colonization with MRSA (nasal or skin), a prior history of a CA-MRSA SSTI, and close contact with an infected person are all risk factors for developing pneumonia. (Emerg Med Clin North Am 2008;26: 431.) A previous or current influenza-like illness is a strong risk factor. Staphylococcal pneumonias always have been associated with viral respiratory infections, especially influenza A. During the 1958 influenza outbreak, there was an association between a recent SSTI and nasal colonization and S. aureus pneumonia. (Lancet 1959;2:428.) The current theory is that the viral illness damages the respiratory epithelium to which the PVL(+) S. aureus then attaches.
The typical CA-MRSA patient is generally young and healthy, and has severe pneumonia. There is often a previous influenza-like illness, usually in the winter months. Hemoptysis is common due to erosion of lung tissue into pulmonary vessels. Hypotension, leukopenia, high fevers, tachycardia, and tachypnea are common. Chest x-ray findings usually show unilobar or multilobar infiltrates and sometimes an ARDS-like pattern. Later, effusions and cavitary lesions occur.
Treatment begins with the usual emergency department care of a patient with pneumonia. Oxygenation status, IV fluids, and early antibiotics are all obviously indicated. I hate to say it, but blood cultures may be helpful. These patients are sicker than the average community-acquired pneumonia patient so even those most skeptical about the utility of blood cultures send them. If the clinician can obtain sputum, certainly it should be sent for gram stain and culture. Antibiotic selection begins with the usual choices for community-associated pneumonia, and when CA-MRSA is suspected, the current Infectious Diseases Society of America/American Thoracic Society guidelines say to add vancomycin or linezolid.
Historically, vancomycin is the drug of choice, but with case reports of treatment failures (Chest 2005;128:2732) and improved survival with linezolid (Chest 2003;124:1789, a retrospective review), it may replace vancomycin someday. Linezolid and clindamycin significantly reduce PVL production, but linezolid is far more expensive and can cause myelosuppression and serotonin syndrome. In pediatric patients with suspected CA-MRSA pneumonia, most suggest vancomycin plus clindamycin.
Since fall and winter are just around the corner and the incidence of viral syndromes and influenza will be climbing, awareness of this very dangerous pneumonia with its different clinical characteristics and treatment is paramount. Adding CA-MRSA to a patient's differential may be the difference between a good and bad outcome.
Diagnosing CA-MRSA Pneumonia
▪ Suspect CA-MRSA pneumonia in the fall and winter in patients with previous or concurrent viral syndrome or influenza.
▪ Clinical features of severe pneumonia include hypotension, leukopenia, hemoptysis, and fever.
▪ A chest x-ray may show unilobar or multilobar infiltrates, effusions, and cavities.
▪ Add vancomycin, linezolid, or clindamycin to the antibiotic regimen.