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Commentary |
1 Department of Radiology, University of New Mexico, 1 University of New Mexico, MSC10 5530, Albuquerque, NM 87131-0001.
Received October 6, 2009; accepted after revision October 7, 2009.
Address correspondence to L. H. Ketai
(lketai{at}unm.edu).
Keywords: CT imaging • H1N1 • S-OIV • swine-origin influenza A
It is unsettling when clinical observations contradict conventional wisdom; three articles in this issue of AJR are unsettling. These articles detail imaging findings of patients infected with swine-origin influenza A (H1N1), S-OIV [1–3]. The patients described in these articles vary widely with respect to underlying illnesses, severity of infection, and the point in the course of the disease when imaging was performed. Nevertheless, the articles are more than sufficient to disrupt assumptions about the imaging appearance of novel influenza.
While most patients with S-OIV infection were not ill enough to require diagnostic imaging of any kind, CT of more severely affected patients showed localized groundglass opacities and consolidation. In some cases these opacities were subpleural, similar to the appearance of opacities seen on CTs performed early in the course of severe acute respiratory syndrome (SARS) infections [4]. In other patients opacities were observed in a central or peribronchovascular distribution. None of the series published here describes the findings of small airways disease that are commonly associated with viral pulmonary infection. Centrilobular nodules, tree-in-bud opacities, and mosaic perfusion were conspicuously absent. Nodular consolidation was observed in a few patients, but neither size nor distribution of the opacities suggested small airways disease.
Other emerging diseases have challenged previously held concepts about the imaging findings of viral respiratory infections. In several of these infections the lack of apparent small airways disease is easy to explain. North American Hantaviruses attack the lung endothelium rather than the airway epithelium and H5N1 influenza may preferentially damage alveoli because it binds to the epithelium there more tightly than it does in the small airways [5]. The lack of small airways disease in SARS is more difficult to explain. The SARS organism infects airway epithelium but most of its radiologic findings can be attributed to alveolar damage caused through cytokine release or, perhaps, by novel mechanisms involving angiotensin-converting enzyme.
The lack of small airways disease in S-OIV infection is still more difficult to explain than the imaging appearance of SARS. One explanation would be that our imaging concepts of viral lower respiratory tract infections have been overly influenced by their appearance in abnormal hosts. In that setting, infections with adenovirus, respiratory syncytial virus, metapneumovirus, and other pathogens have been associated the presence of centrilobular nodules on CT images [6]. A second possibility is that patients with S-OIV infections develop small airways disease early in the course of the disease and then either improve clinically or progress to a different pattern of lung involvement by the time they become sufficiently ill to seek medical attention (in the Mexico City series, symptoms began approximately 6 days before hospital admission) [7]. The peribronchovascular pattern in many of these more severely ill patients favors involvement of large rather than small airways.
The apparent absence of small airways disease is not the only unexpected finding related to S-OIV pneumonia. The University of Michigan series reports both a high prevalence of obesity and a high incidence of pulmonary emboli among its most severely affected patients. An association of viral infection and thromboembolic disease has been questioned on occasion, including with SARS, but is not common [8]. It is possible that the causal association is between obesity and severe S-OIV infection, and the increased rate of thromboembolic disease a secondary phenomenon related to obesity [9]. Similar uncertainty remains about the role of bacterial superinfection on the clinical and imaging presentation of S-OIV. On the basis of clinical findings (e.g., bronchoalveolar lavage), none of these three articles suggests a major role for bacterial infection in contributing to imaging abnormalities. Recent analysis of postmortem material by the Centers for Disease Control, however, identified bacterial infection in approximately 30% of patients, half due to pneumococcus [10]. The latter findings are more congruent with recent evaluation of pathologic specimens from the 1918 influenza pandemic that show bacterial superinfection to have been the principal cause of mortality.
The questions about the role of small airways disease, predilection for thromboembolic disease, and bacterial superinfection in the setting of S-OIV are important ones. Unfortunately, with the approach of the influenza season much more clinical and radiologic data are likely to be accrued in the months ahead. As those data accumulate we will need to keep an open mind to possible imaging presentations and causal associations and not be confined by conventional wisdom. Three millennia ago physicians realized that experience is treacherous. It remains so today.
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