Scientific Letter
Invasive Aspergillosis as a Complication of Influenza Virus H3N2 Infection
Aspergilosis invasora como complicación de infección por virus influenza H3N2
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the Editor</span>," "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "406" "paginaFinal" => "408" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Marta García Clemente, Lorena Martín Iglesias, Ana Isabel Enríquez Rodríguez, Marta Iscar Urrutia, Claudia Madrid Carbajal, Francisco Julián López González" "autores" => array:6 [ 0 => array:4 [ "nombre" => "Marta" "apellidos" => "García Clemente" "email" => array:1 [ 0 => "mgclemen@gmail.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "*" "identificador" => "cor0005" ] ] ] 1 => array:3 [ "nombre" => "Lorena" "apellidos" => "Martín Iglesias" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] ] 2 => array:3 [ "nombre" => "Ana Isabel" "apellidos" => "Enríquez Rodríguez" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 3 => array:3 [ "nombre" => "Marta" "apellidos" => "Iscar Urrutia" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 4 => array:3 [ "nombre" => "Claudia" "apellidos" => "Madrid Carbajal" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] 5 => array:3 [ "nombre" => "Francisco Julián" "apellidos" => "López González" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Servicio de Neumología, Área de Gestión del Pulmón, HUCA, Oviedo, Spain" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Servicio de Medicina Intensiva, HUCA, Oviedo, Spain" "etiqueta" => "b" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Aspergilosis invasora como complicación de infección por virus influenza H3N2" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 894 "Ancho" => 1074 "Tamanyo" => 76377 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Right basal lung condensation.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Invasive aspergillosis occurs frequently in immunocompromised patients, primarily in patients with neutropenia or individuals receiving treatment with corticosteroids, antibiotics, or cytotoxic drugs,<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a> while it is uncommon in patients with preserved cell immunity. Several cases of fungal infection caused by <span class="elsevierStyleItalic">Aspergillus</span> have been described in recent years, and this is a complication that should be taken into account in patients who present a pneumonic process during the course of an influenza virus infection.<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">We report the case of a patient with influenza virus infection who developed invasive aspergillosis as a complication that caused his death.</p><p id="par0015" class="elsevierStylePara elsevierViewall">A 50-year-old patient diagnosed with common variable immunodeficiency receiving treatment with intravenous immunoglobulins every 3 weeks, clinically stable, with no significant infections in the last 3 years, consulted his primary care physician with irritative cough, high fever, and dyspnea. He was treated with levofloxacin without improvement, so he attended the emergency room. Physical examination showed BP 133/85, pulse 111<span class="elsevierStyleHsp" style=""></span>beats per minute, 20<span class="elsevierStyleHsp" style=""></span>breaths per minute, no fever. Immunoglobulin serum values: IgA: 0<span class="elsevierStyleHsp" style=""></span>g/l; IgG: 7.05<span class="elsevierStyleHsp" style=""></span>g/l; IgM: 0.73<span class="elsevierStyleHsp" style=""></span>g/l. The chest X-ray showed loss of left volume and images of bilateral bronchiectasis without radiological changes. The patient was admitted for respiratory failure. PCR of pharyngeal exudate was positive for influenza virus (H3N2), so treatment began with systemic corticosteroids and oseltamivir, with the addition of piperacillin/tazobactam and intravenous amikacin. After an initial improvement, the patient deteriorated on day 5 of admission with tachypnea, tachycardia, and the appearance of a right basal pulmonary condensation on radiology (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>), so he was transferred to the intensive care unit, requiring intubation and invasive ventilation. Linezolid and intravenous colistin were added to his regimen. Bronchoscopy was performed, showing images of whitish membranes in the bronchial tree in both sides. Bronchial aspirate and bronchoalveolar lavage showed countless colonies of <span class="elsevierStyleItalic">Aspergillus fumigatus</span> and <span class="elsevierStyleItalic">Aspergillus terreus</span> sensitive to voriconazole and amphotericin B. Galactomannan testing in bronchoalveolar lavage and blood was negative. Treatment with voriconazole was added, with little improvement. Amphotericin B was then administered, and the patient developed refractory shock and acute respiratory distress syndrome, which caused his death.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">The most frequently described complications in patients with influenza virus infection are acute respiratory distress, bacterial superinfection, the selection of oseltamivir-resistant strains, and pulmonary hemorrhage, which can lead to a poor outcome in immunocompromised patients.<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">1</span></a> It is unusual to think of <span class="elsevierStyleItalic">Aspergillus</span> as a pathogen capable of causing invasive disease in patients with viral infection, yet since 2010 several cases of influenza virus infection complicated by post-onset invasive aspergillosis have been reported. Influenza virus infection, then, appears to be a new risk factor for invasive fungal infection.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Pathogenesis may be a result of the influenza virus (and the H1N1 virus more frequently) causing severe and diffuse damage to the respiratory mucosa, disrupting the respiratory mucosa, and altering normal ciliary clearance,<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3–5</span></a> thus permitting invasion by the fungus. The virus can also damage local defenses against <span class="elsevierStyleItalic">Aspergillus</span>, alter local phagocytosis produced by alveolar macrophages, and reduce the functionality of natural killer cells and other immune responses.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">6,7</span></a> A recent publication found that the virus also damages pulmonary and systemic levels of cytokines and the function of pulmonary phagocytes, producing a state of immune deficiency.<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">8,9</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">When influenza virus infection is complicated by fungal co-infection, mortality is approximately 50%–60%, 5 times higher than in hospitalized patients with viral infection only.<a class="elsevierStyleCrossRefs" href="#bib0090"><span class="elsevierStyleSup">3,10</span></a> In the series published by Van de Veerdonk et al.,<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">11</span></a> invasive aspergillosis mortality in influenza patients was 55%. Absence of suspicion, the interference of the underlying influenza virus infection, and the limited use of serological diagnostic methods prevent early diagnosis, delay treatment, and lead to increased mortality.</p><p id="par0035" class="elsevierStylePara elsevierViewall">Despite high mortality rates, this association is not routinely reported.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">12</span></a> The isolation of <span class="elsevierStyleItalic">Aspergillus</span> spp. observed in cultures obtained from bronchoscopic samples of patients admitted to the ICU with influenza virus infection can thus be underestimated, and they may be considered contaminants despite their potential to cause invasive disease. The presence of structural lung disease, high doses of corticosteroids, and T cell deficiencies during influenza virus infection may be responsible for an emerging group of patients at high risk of invasive aspergillosis.</p><p id="par0040" class="elsevierStylePara elsevierViewall">According to Wauters et al.,<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">13</span></a> steroid use within 7 days prior to ICU admission was an independent risk factor for fungal coinfection. Patients with influenza treated with corticosteroids before or after admission to the ICU should be carefully evaluated for possible <span class="elsevierStyleItalic">Aspergillus</span> coinfection; the authors suggest that systemic steroids should be avoided in patients with influenza, even in those who develop acute respiratory distress associated with their influenza infection.</p><p id="par0045" class="elsevierStylePara elsevierViewall">Our patient had common variable immunodeficiency treated with immunoglobulins, with normal immunoglobulin values except IgA, and no infections in recent years. The infections most frequently described in these patients are bacterial infections (otitis, sinusitis, pneumonia, diarrhea, etc.) associated with humoral immunity deficiencies, which play a lesser role in invasive aspergillosis than the more important cell immunity.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">14</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">The interest of this scientific letter is that it draws attention to the increased risk of invasive aspergillosis in patients with influenza virus infection (most often H1N1). In patients with worsening symptoms, a chest CT scan and bronchoscopy should be performed early to ensure early diagnosis and treatment of invasive aspergillosis if there are signs indicating its presence. Taking into account the results published in the literature, <span class="elsevierStyleItalic">Aspergillus</span> species in the respiratory cultures of critically ill patients, particularly those with influenza virus infection, should not necessarily be considered contaminants or colonizers. Early diagnosis and treatment strategies should be initiated in these patients and multicenter studies should be carried out to better define the incidence and outcome of this disease.<a class="elsevierStyleCrossRefs" href="#bib0135"><span class="elsevierStyleSup">12,15</span></a></p></span>" "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as: García Clemente M, Martín Iglesias L, Enríquez Rodríguez AI, Iscar Urrutia M, Madrid Carbajal C, López González FJ. Aspergilosis invasora como complicación de infección por virus influenza H3N2. Arch Bronconeumol. 2020;56:406–408.</p>" ] ] "multimedia" => array:1 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 894 "Ancho" => 1074 "Tamanyo" => 76377 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Right basal lung condensation.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:15 [ 0 => array:3 [ "identificador" => "bib0080" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Acute community-acquired pneumonia due to <span class="elsevierStyleItalic">Aspergillus</span> in presumably immunocompetent hosts: clues for recognition of a rare but fatal disease" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "C.J. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 5 | 7 | 12 |
| 2024 October | 51 | 25 | 76 |
| 2024 September | 48 | 10 | 58 |
| 2024 August | 60 | 40 | 100 |
| 2024 July | 51 | 19 | 70 |
| 2024 June | 48 | 43 | 91 |
| 2024 May | 57 | 32 | 89 |
| 2024 April | 43 | 27 | 70 |
| 2024 March | 27 | 22 | 49 |
| 2024 February | 22 | 22 | 44 |
| 2023 March | 6 | 4 | 10 |
| 2023 February | 55 | 16 | 71 |
| 2023 January | 28 | 31 | 59 |
| 2022 December | 52 | 29 | 81 |
| 2022 November | 47 | 24 | 71 |
| 2022 October | 54 | 34 | 88 |
| 2022 September | 39 | 21 | 60 |
| 2022 August | 34 | 39 | 73 |
| 2022 July | 25 | 32 | 57 |
| 2022 June | 33 | 29 | 62 |
| 2022 May | 27 | 32 | 59 |
| 2022 April | 25 | 27 | 52 |
| 2022 March | 26 | 22 | 48 |
| 2022 February | 18 | 22 | 40 |
| 2020 October | 2 | 0 | 2 |
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