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Sir: Daubin and colleagues' recent report [1] addressed the possibility of viral ventilator-associated pneumonia (VAP) in adult ICU. However, several of their key conclusions are not supported by their study design and reported results. The investigators set to “determine the incidence … and clinical relevance of viral VAP”, hypothesizing that a proportion of VAP may be caused by nosocomial transmission of viruses. While commonly employed criteria were used to define bacterial VAP, no comparably explicit definition was provided for viral VAP. The mere demonstration of a virus in the tracheobronchial secretions of a patient with suggestive clinical features does not allow a conclusion on the presence or absence of causality for viral VAP, and as herpes simplex virus 1 (HSV) constituted 86% of viral isolates in patients suspected of VAP, it deserves further comment. The suggested use of incubation and excretion periods for influenza virus A and enterovirus, along with previously described definitions of viral hospital-acquired infections, can certainly assist in crafting working definitions for viral VAP, but are no substitute for explicit proposed diagnostic criteria. Similarly, the methods used by the investigators precluded proper exploration of nosocomial viral transmission, through tools such as serial staff and patient surveillance and genomic fingerprinting of viral isolates.
HSV can be isolated in the saliva of 1–5% of asymptomatic subjects [2], and its frequency in tracheobronchial secretions in ICU patients is roughly in direct relation to patients' severity of illness [3, 4], noted in up to 65% in patients with the acute respiratory distress syndrome [3]. HSV pneumonia has been described mostly in severely immunocompromised patients, while its risk in general critically ill patients appears low [3]. Nosocomial, strain-specific transfer of HSV from patients to staff and family in adult ICU has been documented [5], while transfer to adult critically ill patients has been reported rarely and only on epidemiological grounds [5]. It has been expert opinion [3] that viral reactivation and shedding at the oral level (with subsequent aspiration to the tracheobronchial tree) or by transmission down superior cervical and jugular portion of vagal ganglia [6] is the major source of HSV isolated from tracheobronchial secretions in critically ill, mechanically ventilated patients. Demonstration of HSV in tracheobronchial secretions in these patients cannot by itself distinguish between plain viral shedding due to reactivation vs. resultant tracheobronchitis or pneumonia, and the tracheobronchial tree can appear normal on bronchoscopic examination [7], thus not supporting authors' use of the term “lower respiratory tract HSV-1 infection” referring to 11 of their VAP patients. The independent prognostic role of HSV demonstration in tracheobronchial secretions of critically ill, mechanically ventilated patient, with or without clinical features of pneumonia, remains unsettled [3, 4, 7].
Given the above considerations, the data reported by Daubin et al. preclude credible insight on their study objectives and hypothesis, does not support their assertion that 12 of the viral isolates (and especially HSV) upon enrollment were hospital-acquired, and preclude defining the causal role of the most common viral isolate in their VAP patients.
References
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Oud, L. Comment on: “Nosocomial viral ventilator-associated pneumonia in the intensive care unit” by Daubin et al.. Intensive Care Med 32, 613 (2006). https://doi.org/10.1007/s00134-005-0034-0
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DOI: https://doi.org/10.1007/s00134-005-0034-0