Abstract
BackgroundThe first influenza pandemic of the 21th century was ignited by a new strain of influenza A virus (A/H1N1pdm). Specific patient groups, including those with comorbidities, pregnant women, young children, older and immunocompromised patients, are at increased risk for serious influenza-related disease. This study was aimed at investigating the influence of clinical presentation, antiviral treatment and possible drug resistance-associated mutations, on the extent and duration of viral shedding in patients infected with A/H1N1pdm.MethodsAn observational study was performed, based on retrospective review of clinical and laboratory records of patients who were hospitalized for A/H1N1pdm infection at the National Institute for Infectious Diseases "L. Spallanzani", Rome, Italy, between April 24 and December 31, 2009. Among 119 hospitalized patients, 39 were selected for a post hoc analysis, based on the availability of serial nasopharyngeal swabs samples and related information.ResultsEleven out of the 39 study patients (28.2%) presented with pneumonia; 29 (74.4%) received antiviral treatment. Patients with pneumonia were significantly older than patients without pneumonia. The mean values of viral RNA concentration were not significantly increased in patients with pneumonia, but a significant increase in the duration of viral shedding was observed as compared to patients without pneumonia. In patients receiving antivirals, the viral RNA concentration was significantly reduced in comparison to untreated patients at days 4-5 after symptom onset, while the overall duration of viral shedding was only marginally affected. A significant correlation between duration of viral shedding and time elapsed between symptom onset and therapy start was observed, with a significant reduction of days of viral shedding when therapy was initiated within 2 days of symptoms appearance. No known drug resistance mutations were detected in patients with prolonged viral shedding.ConclusionsOur results show that severe respiratory illness is associated with delayed virus clearance in patients with A/H1N1pdm infection. Antivirals caused an early reduction of viral load, but only marginally affected the overall duration of shedding. Prolonged shedding was not associated with the emergence of strains carrying known drug-resistance mutations.
Highlights
The first influenza pandemic of the 21th century was ignited by a new strain of influenza A virus (A/ H1N1pdm)
In patients treated with oseltamivir, younger age (< 13 years) has been associated with prolonged viral shedding, while clinical severity has been associated with a higher viral load in the upper respiratory tract [15]
Viral load according to the time lapse between symptom onset and presentation for diagnosis During the whole observation period, nasopharyngeal swab samples from 2,609 patients were analysed by realtime reverse trascriptase-polymerase chain reaction (RT-PCR), to establish an A/H1N1pdm diagnosis; among them, 870 samples (33.3%) were A/H1N1pdmpositive
Summary
The first influenza pandemic of the 21th century was ignited by a new strain of influenza A virus (A/ H1N1pdm). This study was aimed at investigating the influence of clinical presentation, antiviral treatment and possible drug resistance-associated mutations, on the extent and duration of viral shedding in patients infected with A/H1N1pdm. Prolonged course of illness and severe complications seem to be associated with a delayed presentation for care, higher initial viral loads in upper respiratory samples [4] and emergence of antiviral-resistance [5]. In case of an uncomplicated illness, the early use of oseltamivir is usually associated with prompt clearance of infectious influenza A/H1N1pdm virus from the upper respiratory tract [10]. The rapid curtailment of active viral replication in the respiratory tract, determined by antiviral therapy, may reduce the duration of hospitalization [11] and the risk of progression to severe disease [12,13]. In patients treated with oseltamivir, younger age (< 13 years) has been associated with prolonged viral shedding, while clinical severity has been associated with a higher viral load in the upper respiratory tract [15]
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