As community-acquired infections due to meticillin-resistant Staphylococcus aureus (CA-MRSA) increase, so lethal cases of CA-MRSA pneumonia are also on the rise. A paper in the June edition of the Lancet Infectious Diseases looks at the emerging and deadly threat of community-acquired necrotising pneumonia due to CA-MRSA. CA-MRSA pneumonia appears to occur most commonly following an influenza-like illness and may have special relevance given the emergence of H1N1 influenza.
Dr Alicia Hidron, Emory University School of Medicine, Atlanta, GA, USA, and colleagues say that many of the published cases of community-acquired Staphylococcus aureus pneumonia report a preceding influenza-like illness, and generally affect young and previously healthy patients. They analyse two recent cases from the USA in which were caused by the specific MRSA strain USA300 which is the most common genotype of CA-MRSA causing infections in the US.
The authors say: "CA-MRSA infections are no longer restricted to certain risk groups or to the geographic areas where outbreaks first occurred. They now occur widely both in the community as well as health care facilities, and have been reported in nearly every continent…the spectrum of disease caused by CA-MRSA occurs worldwide and primarily encompasses skin and soft-tissue infections...[however] severe infections such as necrotising pneumonia and bacteraemia have also been reported." They add that, in the USA, 6% of CA-MRSA infections cause serious invasive disease. Clinical presentation of CA-MRSA pneumonia usually features high fever and low blood pressure with rapid progression to septic shock and an urgent requirement for mechanical ventilation. Many reports from the USA and Europe have noted mortalities greater than 50%.
CA-MRSA has genetic differences from its related infection healthcare-associated MRSA (HA-MRSA). Panton valentine leukocidin (PVL) is a toxin which is present in most CA-MRSA isolates, but rarely in HA-MRSA isolates. The ability of PVL to kill white blood cells and increase inflammatory response has been suggested by some (but discounted by other) investigators as a contributory factor to the lethality of CA-MRSA pneumonia, although other virulence factors are under scrutiny. There remains significant debate about the importance of PVL in the pathogenesis of CA-MRSA pneumonia or whether PVL is merely a marker of CA-MRSA infections.
CA-MRSA is generally more susceptible to antibiotic treatment than HA-MRSA, probably because HA-MRSA has developed resistance to survive in the hospital setting. Whether screening and prophylactic treatment could be an effective way to reduce CA-MRSA cases in family members or close contacts of CA-MRSA infected patients is not known. Nasal colonisation with S aureus is a known risk factor for subsequent infection with this organism, but no guidelines for decolonisation of infected close contacts exist. The authors say: "Whereas antimicrobial/antiseptic regimens that were intended for the eradication of S aureus colonisation have been used in some community settings to prevent autoinfection of colonised patients and transmission to contacts, the effectiveness of this approach has not been established...treatment decisions are often made on an individual basis by the physicians who provide care to the patients and their families to prevent recurrent diseases or intrafamilial spread."
The authors conclude by discussing their concerns that, with the advent of CA-MRSA USA300 in hospitals, "it is unclear whether severe health-care-associated pneumonias due to MRSA USA300 will also emerge".
For Dr Alicia Hidron, please contact Holly Korschun, Director, Research Communications, Woodruff Health Sciences Center of Emory University. T) +1 404-727-3990 E) hkorsch@emory.edu / ahidron@emory.edu
For full Grand Round paper, see: http://press.thelancet.com/tlidpneumonia.pdf
Journal
The Lancet Infectious Diseases