FINAL DIAGNOSIS - Staphylococcus aureus pneumonia complicating influenza.
In this particular case, a nasal specimen was reported positive for influenza A ribonucleic acid one hour before the patient arrested in the wee hours of the morning. Sputum culture from admission had been reported positive for heavy methicillin-resistant Staphylococcus aureus. The autopsy showed diffuse severe bilateral acute necrotizing and hemorrhagic pneumonia in all lobes of both lungs, with Gram-positive bacterial cocci visible in lung tissue sections and postmortem lung culture positive for methicillin-resistant Staphylococcus aureus. There was early abscess formation in right upper lobe lung. The lungs also demonstrated severe pulmonary diffuse alveolar damage (acute lung injury). Other findings included extensive severe acute ulcerative tracheobronchitis with staphylococcal superinfection, hypopharyngeal mucosal edema and hemorrhage, mild lymphocytic myocarditis (primarily in the right ventricle), numerous microscopic pulmonary thromboemboli, bilateral psoas muscle hemorrhages, multiple acute cerebral white matter hemorrhages and hypocellular bone marrow with myeloid immaturity, some hemophagocytic histiocytes and atypical megakaryocytes.
Influenza virus causes tracheitis and bronchitis with sloughing of the mucosa and without viral inclusions on light microscopy. The repair response commonly features prominent squamous metaplasia. Diffuse alveolar damage (acute lung injury) is typically prominent in influenza pneumonia, when the infection gets into the alveoli. Superinfection with bacteria is very common with influenza pneumonia. Staphylococcus aureus has been recognized as particularly adept at causing secondary infection with influenza pneumonia as far back as 1957 (1). Methicillin-resistant Staphylococcus aureus has shown the same predilection as its methicillin-sensitive counterpart (2). Virulent strains of methicillin-resistant Staphylococcus aureus can cause co-infection, secondary infection, superinfection or subsequent infection (whatever term you prefer) in patients with influenza, which may be fatal (2,3). Some believe that these strains are more likely to cause simultaneous co-infection because they are commonly isolated in the same initial stage in which the influenza virus is demonstrated to be present. There is evidence to suggest that influenza may interact synergistically with Staphylococcus aureus to increase the risk for co-infection, by enhancing the adhesion of Staphylococcus aureus throughout the respiratory tract (4).
Contributed by Timothy Gorrill, MD, PhD and Larry Nichols, MD