• Jan-Willem van den Brink, Alberdina M Simoons-Smit, Albertus Beishuizen, Armand R J Girbes, Rob J M Strack van Schijndel, and A B Johan Groeneveld.
• Department of Intensive Care, Institute for Cardiovascular Research, Vrije Universiteit Medical Centre, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands.
• J. Clin. Virol. 2004 May 1; 30 (1): 68-72.

BackgroundThe clinical significance and pulmonary pathogenicity of herpes simplex virus type 1 (HSV-1) in mechanically ventilated, critically ill patients are unclear.ObjectiveTo determine the clinical features and course of respiratory HSV-1 infections/colonisations in the critically ill, in order to evaluate the contribution to outcome.DesignA retrospective cohort study in the intensive care unit of an university hospital, involving 22 patients with a HSV-1 isolated from bronchoalveolar lavage (BAL) fluid, divided into survivors (n = 13) and non-survivors (n = 9). All patients except for one survivor had been intubated and were mechanically ventilated.ResultsNon-survivors had acquired HSV-1 sooner on mechanical ventilation than survivors. Prior chronic heart disease was more prevalent in non-survivors than in survivors and, at the time of HSV-1 isolation, the mean creatinine level was higher (P < 0.05) in the former. Survivors had a somewhat greater fall in body temperature after a 10-day course of antiviral therapy than non-survivors, but the lung radiographic abnormalities prior to and after the course did not differ. There were no major differences in cardiorespiratory variables between outcome groups and causes of death and were judged not to relate, in general, to HSV-1.ConclusionsCritically ill patients in whom HSV-1 from BAL is isolated, have about 40% chance of dying, mainly because of severe underlying disease and comorbidity, which may predispose to endogenous reactivation of the virus. There is no clinical evidence for direct cardiorespiratory pathogenicity and beneficial effects of antiviral therapy. HSV-1 isolated from lung secretions may thus be a marker rather than a mediator of severe illness.

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