Adenovirus Induced Acute Respiratory Distress Syndrome Review of Literature

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• Published: 12 August 2014

Emergent severe acute respiratory distress syndrome caused by adenovirus type 55 in immunocompetent adults in 2013: a prospective observational study

• Hangyong He^1,2,
• Zheng Wang^one,2,
• Jiuxin Qu^2,three,
• Xuyan Li^1,2,
• Chengjun Ban^1,2,
• Jun Wan^1,2,
• Bin Cao^2,three,
• Zhaohui Tong^1,2 &
• Chen Wang^two,4

Critical Care book 18, Article number:456 (2014) Cite this article

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Abstract

Introduction

Since 2008, severe cases of emerging human being adenovirus type 55 (HAdV-55) in immunocompetent adults have been reported sporadically in China. The clinical features and outcomes of the nigh critically ill patients with severe astute respiratory distress syndrome (ARDS) caused by HAdV-55 requiring invasive mechanical ventilation (IMV) and/or extracorporeal membrane oxygenation (ECMO) are lacking.

Methods

Nosotros conducted a prospective, single-center observational study of pneumonia with ARDS in immunocompetent adults admitted to our respiratory ICU. We prospectively collected and analyzed clinical, laboratory, radiological characteristics, sequential tests of viral load in respiratory tract and blood, treatments and outcomes.

Results

The results for a total of v consecutive patients with severe ARDS with confirmed HAdV-55 infection were included. All five patients were immunocompetent young men with a median age of 32 years. The mean time from onset to dyspnea was five days. Arterial blood gas analysis at ICU access revealed profound hypoxia. Hateful partial oxygen pressure level/fraction of inspired oxygen was 58.1. Mean durations from onset to a single-lobe consolidation shown on chest Ten-rays (CXRs) and, from the beginning positive CXR to bilateral multilobar lung infiltrates, were 2 days and 4.8 days, respectively. The viral load was higher than 1 × 10^viii copies in three patients and was one × 10⁴ in one patient. It was negative in the but patient who survived. The hateful duration for noninvasive positive pressure ventilation (NPPV) failure and IMV failure were 30.eight hours and vi.ii days, respectively. Four patients received venovenous ECMO. 4 (80%) of the 5 patients died despite receiving appropriate respiratory support.

Conclusions

HAdV-55 may cause severe ARDS in immunocompetent immature men. Persistent loftier fever, dyspnea and rapid progression to respiratory failure within ii weeks, together with bilateral consolidations and infiltrates, are the virtually frequent clinical manifestations of HAdV-55-induced severe ARDS. Viral load monitoring may help predict illness severity and consequence. The NPPV and IMV failure rates were very high, but ECMO may still be the respiratory back up therapy of option.

Trial registration

Clinicaltrials.gov NCT01585922. Registered 20 Apr 2012

Introduction

Human adenoviruses (HAdVs) are notorious pathogens in people with compromised immune function and a frequent crusade of outbreaks of acute respiratory illness among young children. Life-threatening adenoviral pneumonia has previously been documented among military trainees, patients with AIDS and transplant recipients [1]–[5]. Human adenovirus type 55 (HAdV-55), which is emerging equally a highly virulent pathogen for astute fatal adenoviral pneumonia among immunocompetent adults in China, has gained increasing attending [6]. HAdV-55 is a newly identified, emergent acute respiratory affliction pathogen causing 2 contempo outbreaks in Mainland china in 2006 [7] and in Singapore in 2005 [eight]. In 2011, this pathogen apparently re-emerged in Beijing, China, causing several cases of astringent community-caused pneumonia [9]. This pathogen was fully characterized by whole-genome sequencing [x]. Comparative studies showed that the ability of HAdV to cause severe illness may relate to the serotypes of HAdVs. Severe adenoviral pneumonia induced by HAdV-55 has been reported to exist more closely related to severe cases compared to other serotypes (HAdV-3, HAdV-7 and HAdV-xiv) [six].

Current knowledge of HAdV-55-induced severe astute respiratory distress syndrome (ARDS) requiring invasive mechanical ventilation and/or extracorporeal membrane oxygenation (ECMO) support in immunocompetent adults is derived from single case reports or relatively modest, single-heart series. As a issue, piddling information is available on HAdV-55 pneumonia complicated with severe ARDS, the frequency of which is expected to increase in the coming years. Here we describe the clinical features and outcomes of five prospective cases of HAdV-55 pneumonia complicated with astringent ARDS in immunocompetent adults in our ICU.

Material and methods

Study population

Commencement in May 2012, a randomized trial of noninvasive positive force per unit area ventilation (NPPV) in ARDS patients was carried out in our center (ClinicalTrials.gov ID: NCT01585922). From May 2012 to April 2014, all adult patients with ARDS caused by pneumonia who were admitted to the respiratory ICU of Beijing Chao-Yang Hospital were prospectively enrolled. Severe ARDS was diagnosed co-ordinate to the Berlin definition: (one) developing within 1 calendar week of a known clinical insult or new or worsening respiratory symptoms; (ii) bilateral opacities non fully explained by effusions, lobar and/or lung collapse, or nodules; (3) respiratory failure non fully explained past cardiac failure or fluid overload; (4) partial oxygen pressure/fraction of inspired oxygen (PaO₂/FiO_ii) ≤100 mmHg with positive end-expiratory pressure (PEEP) ≥v cmH₂O; and (five) a chest radiograph with three or four quadrants with opacities. Patients with HAdV-55 infection and severe ARDS who failed conventional NPPV and invasive mechanical ventilation (IMV) were included in the assay. This study was approved by the Institutional Review Board of Beijing Chao-Yang Hospital (LLKYPJ2012031). Information were analyzed anonymously. Each patient gave written informed consent for their information to be used for research and publication.

Clinical data collection

Clinical information collected by investigators with a standardized information form included the post-obit: demographic characteristics (age and sexual activity), comorbidities, clinical symptoms (fever, cough, sputum, dyspnea, chest pain, rash, nausea, vomiting, abdominal pain, diarrhea and headache), signs (torso temperature, heart rate, respiratory frequency, blood pressure and crackles in the lungs), laboratory tests (whole-blood jail cell count and blood chemistry) and microbiological findings and images of the lung (chest X-ray (CXR) and computed tomography). Concomitant medications, respiratory support, complications and outcomes were also recorded.

Microbiological tests

Patients' specimens, including sputum, whole claret and serum samples, were collected upon admission and during hospitalization. Microbiological tests were performed at the Department of Infectious disease and Clinical Microbiology in our center, and the detection methods used were described in our previous report [6]. Mutual viruses causing respiratory affliction were screened using a kit with 15 unlike viral assays. Serum samples were used for Mycoplasma pneumoniae, Chlamydia pneumoniae and Legionella pneumophila antibodies. All patients had their HAdV-55 infection confirmed past RT-PCR analysis. Partial sequences of the hexon gene were analyzed to type the phylogeny of HAdV-55 strains. The adenoviral load was also performed on both respiratory specimens and claret by multiplex RT-PCR assay.

Criteria for human being adenoviral pneumonia

Viral pneumonia was diagnosed based on the presence of HAdV detected in sputum or throat swab samples past molecular methods.

Statistical analysis

Continuous variables were summarized every bit mean ± standard deviation (SD) or median (interquartile range).

Results

During the study menses, a total of eight patients diagnosed with HAdV infection and respiratory failure were admitted to our ICU, and vii of them received a diagnosis of ARDS. 5 consecutive patients with severe ARDS with confirmed HAdV-55 infection were admitted to our ICU between Apr and July 2013. They were included in the analysis. The other 2 patients had mild ARDS and were infected with other types of HAdVs.

Demographics

All v patients were immunocompetent young men with a median historic period of 32 years (range, 28 to forty years). All of the patients shared a B blood type and came from the same city: Baoding urban center, Hebei province, northern Mainland china. All patients had no exposure to farm animals, corn or hay. Patient 3 had tuberculosis pleuritis and received antituberculosis therapy at ICU admission. His blood tests, including the T-SPOT tuberculosis assay (Oxford Immunotec, Marlborough, MA, USA) and antibiotic of Mycobacterium tuberculosis, were negative.

Clinical characteristics

Flulike symptoms, such as fever, coughing and little sputum, were commonly observed at the onset of illness. All patients presented with a high fever, with a mean body temperature of 39.5°C (range, 39.0°C to twoscore.0°C), which persisted for 8 days (range, six to 11 days). Productive cough was observed in ii patients. Ho-hum substernal chest pain and rash were as well observed in two patients. All patients had dyspnea. The mean time from onset to dyspnea was 5 days (range, one to 10 days). Afterwards the onset of dyspnea, patients commonly progressed to respiratory failure or hypoxemia. The mean time from onset to ICU admission was 9.half dozen days (range, 8 to xi days) (Table i).

Table 1 Demographic, clinical characteristics and laboratory values for immunocompetent adults with human adenovirus blazon 55 on the first day of admission ^a

Full size tabular array

All patients had tachypnea when admitted to the ICU, with a mean rate of 43 breaths per infinitesimal (range = 38 to 52). Arterial blood gas analysis at ICU admission revealed profound hypoxia, with a hateful PaO₂/FiO₂ of 58.1 (range = 49 to 62.five). White claret cell counts were low or in the normal range. All patients had elevated serum aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and hydroxybutyrate dehydrogenase (HBDH) (Table 1). At admission, all patients' levels of immunoglobulin (serum immunoglobulins G and Chiliad) and components C3 and C4 were in the normal range. Four patients had lower than normal T-cell subset counts (Table 2).

Table ii Humoral amnesty and cell-mediated amnesty on the immunocompetent adult infection with human adenovirus type 55 ^a

Total size table

Radiographic features

CXRs revealed multiple bilateral lobar or segment consolidation in the lungs of all five patients, and radiographic lesions progressed quickly after ICU admission (Figure 1). Iii patients were examined past high-resolution computed tomography (HRCT). Unilateral or bilateral consolidations and infiltrates were plant on HRCT scans of all three of these patients. Consolidations within a unmarried lobe or several lobes with a clear border and air bronchogram were the most common findings on HRCT scans. Nodules, patches, pleural effusion, abscess and a cavity were also seen visualized by HRCT (Figure ii). The mean duration from onset to a single-lobe consolidation on CXRs was 2 days (range = 1 to v days). The hateful duration from the start positive CXR to bilaterally multilobar lung infiltrates was 4.viii days (range = 4 to 7 days).

Figure 1

Radiographic findings and their relationship to viral load monitoring in patient four. (Picture one) Radiographs show widespread bilateral interstitial infiltrates at the onset of the disease. (Flick 2) The patient's condition rapidly deteriorated inside 3 days, and mechanical ventilation was required. (Picture iii) The patient'due south adenoviral infection progressed, so supplementary oxygen was given on solar day 3 of admission. (Picture 4–8) Radiographs evidence gradual recovery with supportive therapy. Also shown are the trends of viral load detected with endotracheal aspirates (ETAs) and their relationship to radiological changes.

Full size paradigm

Figure ii

Dynamic changes on computed tomography scans for human adenovirus type 55 pneumonia in patient 3. Chest computed tomography scans taken on day 1 evidence a nodular shadow in the right upper lobe. The nodular shadow expanded dramatically within three days and was surrounded past basis-glass opacity on day 4. The lesion was diffuse in both lung fields on mean solar day 8. A cavity was observed on day 23, and the mediastinum window shows the formation of pulmonary abscess in the upper right lobe (red pointer). The lung abscess tested negative for Legionella, Staphylococcus and tuberculosis.

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Detection of adenoviruses by RT-PCR

All patients had HAdV-55 viremia. In 4 of the five patients, it was first detected in endotracheal aspirate (ETA) samples. The time between initial ETA sample drove of adenoviruses and positive results for HAdV-55 nucleic acrid in the blood was 1 to 10 days (Table iii). Virus DNA copies in ETAs were determined for all patients during their ICU stay. The viral load was college than 1 × 10^viii copies in three patients and ane × 10^iv in one patient. The viral load became negative in the merely patient who survived. In the four patients who did non survive, Dna copies did non decrease, fifty-fifty with antiviral therapy (Figure three).

Table 3 Common respiratory pathogen coinfection with human adenovirus type 55 and patients' clinical outcomes ^a

Full size table

Figure 3

Changes in human adenovirus type 55 concentration measured in endotracheal aspirates from all five acute respiratory distress syndrome patients. Patient 4, whose viral Deoxyribonucleic acid copies in ETA became negative, was the only patient who survived.

Full size image

Respiratory support

Oxygenation was not maintained with conventional NPPV or IMV support in whatsoever of the patients. The hateful duration until NPPV failure was 30.8 hours (range = 22 to 48 hours), and the mean time until IMV failure was 6.2 days (range ii = to xiii days) (Tabular array 1). Four patients received venovenous ECMO to maintain oxygen saturation, and one patient refused ECMO support and received high-frequency oscillatory ventilation instead. Tabular array 4 gives the oxygenation information of patients before and after venovenous ECMO support.

Table 4 Oxygenation response to venovenous extracorporeal membrane oxygenation support ^a

Full size tabular array

Antimicrobiological therapy and result

All patients received antiviral therapy, including acyclovir (10 mg/kg, every 8 hours, intravenous drip), ganciclovir (v mg/kg, every 12 hours, intravenous drip) and ribavirin (250 mg, twice daily, intravenous drip). Considering that bacterial coinfection may combine with a severe viral infection, broad-spectrum intravenous antibiotics were given to all patients. Tests for bacterial pathogens were negative for only 1 patient (Table 3). Four (80%) of the 5 patients died. Amid the 4 patients receiving venovenous ECMO, only one patient survived. The other four patients died due to ARDS, Aspergillus fumigatus coinfection, septic shock and catheter-related bloodstream infection due to Acinetobacter baumannii, respectively.

Give-and-take

To the best of our knowledge, this is the starting time cohort observational study on the clinical characteristics of patients with severe ARDS caused by emergent HAdV-55 infection and likewise the first on the evaluation of a viral load test for monitoring the reaction to therapy and for prediction of patient effect. The post-obit are the master findings of this study. (1) HAdV-55 may cause astringent ARDS in immunocompetent young men with blood type B. All of our patients were from the same metropolis of Hebei province, northern China. (ii) Persistent high fever, dyspnea and rapid progression to respiratory failure inside ii weeks, together with bilateral consolidations and infiltrates at the same time, are the well-nigh frequent clinical manifestations of severe HAdV-55-induced ARDS. (iii) Viral load monitoring may help predict affliction severity and patient outcome. (iv) The NPPV and IMV failure rates were very high, and ECMO may be the last support method for this group of patients. (5) HAdV-55-induced severe ARDS has a very high mortality rate (80%) despite appropriate respiratory support.

Desultory severe adenoviral infection in healthy adults has historically been described for serotype iv [11], serotype vii [4],[12] and, more recently, serotype 14 in the general population and in military trainees [xiii],[fourteen]. HAdV-55 was first completely characterized in Shaanxi, Mainland china [7] and then reemerged in Hebei, a province close to Beijing, where it caused several cases of acute respiratory illness [9]. It was presumed that HAdV-55 was a recombinant course of the B2 species of HAdV-xiv and HAdV-11 [7],[15] due to its sharing a hexon factor with the HAdV-eleven and HAdV-14 chassis [16]. The results of our study evidence that HAdV-55, as an emerging pathogen among immunocompetent adults, may cause severe ARDS.

The prevalence of severe fatal adenoviral pneumonia induced by HAdV-55 in our study is somewhat similar to that described past Cao and colleagues [half-dozen]. All cases of reported HAdV-55 in our written report were from the aforementioned city: Baoding, Hebei province, northern China. They occurred between April and July 2013, just partly overlapping or post-obit the flu epidemic. The patients with severe disease also came from the same region and were treated during a similar time period, which suggests that HAdV-55 may be an of import viral pathogen derived from this region.

Our study results advise that the following may be clinical features of ARDS caused by HAdV-55: persistent high fever, rapid progression of dyspnea, demand for mechanical ventilation support, elevated AST level and rapid progression from unilateral infiltrates to bilateral consolidations. These clinical features are highly similar to those of ARDS acquired by other types of HAdV described in previous reports [six],[9].

Contempo studies have shown that the immune system plays a crucial role in the clearance of HAdV viremia and survival of the host [17]. Chen et al. reported that, in the acute phase of HAdV-55 infection, patients with severe disease may have high levels of dendritic cells and Th17 cells [18]. In our report, the but patient who recovered from astringent infection had higher T-cell counts. Three of the five patients had relatively depression T-cell counts when admitted. Our results suggest that these 3 patients may have been relatively immunocompromised and that a lower T-cell count may be a take a chance factor for HAdV-55 infection in young adults.

HAdV-55 DNA was previously reported in 41.2% of patients with severe infection [18]. In our study, HAdV-55 Dna was detected and monitored in all patients with severe ARDS. The initial, and tendency of, viral load that presented as HAdV-55 Dna copies in the respiratory tract samples and claret may advise the severity of infection and may predict both the reaction to therapy and patient result.

The use of mechanical ventilation and ECMO in patients with ARDS caused by HAdV-55 has not been detailed in previous studies. In our cohort, we found that severe HAdV-55 infection could cause a rapid progression of respiratory failure, with a very high failure charge per unit for NPPV and IMV. This failure rate may be a result of the large area of consolidation that induced a severe shunt in the lung, which may atomic number 82 to lack of response to positive pressure ventilation. For patients with astringent ARDS, ECMO should be considered a better choice for oxygenation.

Our written report has limitations. It is an observational written report with no comparison group, so the deviation betwixt the astringent and modest infections could not exist clarified in terms of allowed status, clinical features, radiological findings, viral load and handling effects on respiratory support and antiviral therapy. Sequential dynamic analysis is needed to determine the relationship between HAdV-55 viremia and treatment response.

Conclusions

Our data provide new insight into the clinical features of HAdV-55 infection in patients with severe ARDS. HAdV-55 may cause severe ARDS in immunocompetent young men. Persistent loftier fever, dyspnea and rapid progression to respiratory failure within ii weeks, together with bilateral consolidations and infiltrates during the same catamenia, are the well-nigh frequent clinical manifestations of astringent HAdV-55-induced ARDS. Viral load monitoring may help predict disease severity and patient outcome. NPPV and IMV failure rates were very high, and thus ECMO may exist a improve choice of respiratory back up in this group of patients. HAdV-55-induced severe ARDS has a very high mortality rate (eighty%) despite appropriate respiratory support.

Primal messages

• HAdV-55 infection may be a crusade of severe ARDS in immunocompetent immature male adults.

• Persistent loftier fever, dyspnea, rapid progression to respiratory failure within 2 weeks, together with bilateral consolidations and infiltrates during the same period, are the almost frequent clinical manifestations of severe HAdV-55-induced ARDS.

• Viral load monitoring may be helpful in predicting patients' disease severity and issue.

• NPPV and IMV failure rates were very high, and thus ECMO may be a ameliorate choice for respiratory back up in this grouping of patients.

• HAdV-55-induced severe ARDS has a very high mortality rate of 80% despite appropriate respiratory support.

Abbreviations

ARDS:

Acute respiratory distress syndrome

CXR:

Chest Ten-ray

ECMO:

Extracorporeal membrane oxygenation

ETA:

Endotracheal aspirate

HAdV-55:

Human adenovirus type 55

IMV:

Invasive mechanical ventilation

NPPV:

Noninvasive positive pressure ventilation

PEEP:

Positive cease-expiratory pressure

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Author data

Affiliations

1. Department of Respiratory and Critical Intendance Medicine, Beijing Chao-Yang Infirmary, Upper-case letter Medical Academy, No. 8 Gongti Nanlu, Chaoyang district, Beijing, 100020, Communist china

   Bing Sun, Hangyong He, Zheng Wang, Xuyan Li, Chengjun Ban, Jun Wan & Zhaohui Tong

2. Beijing Found of Respiratory Medicine, Beijing Key Laboratory of Respiratory and Pulmonary Apportionment, Capital letter Medical Academy, No. 8 Gongti Nanlu, Chaoyang commune, Beijing, 100020, China

   Bing Dominicus, Hangyong He, Zheng Wang, Jiuxin Qu, Xuyan Li, Chengjun Ban, Jun Wan, Bin Cao, Zhaohui Tong & Chen Wang

3. Department of Infectious Diseases and Clinical Microbiology, Beijing Chao-Yang Hospital, Capital Medical University, No. 8 Gongti Nanlu, Chaoyang district, Beijing, 100020, Prc

   Jiuxin Qu & Bin Cao

4. Establish of Respiratory Medicine, Beijing Hospital, Ministry building of Heath, No. 1 Dahua Road, Dongcheng district, Beijing, 100730, Communist china

   Chen Wang

Corresponding author

Correspondence to Chen Wang.

Additional information

Competing interests

The authors declare that they have no competing interests.

Authors' contributions

CW takes total responsibleness for the integrity of the submission and publication and was involved in study design. BS, HH and ZW had full access to all the data in the study, take responsibility for the integrity of the data and the accuracy of the data analysis, and were responsible for data verification and assay and the drafting of the manuscript. ZT takes responsibleness for the acquisition of the information and the interpretation of the data assay. JQ, CB, BC, JW and XL were responsible for the microbiological examination and information drove. All authors read and approved the final manuscript.

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Dominicus, B., He, H., Wang, Z. et al. Emergent severe acute respiratory distress syndrome acquired by adenovirus blazon 55 in immunocompetent adults in 2013: a prospective observational study. Crit Intendance 18, 456 (2014). https://doi.org/ten.1186/s13054-014-0456-6

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• Received: xix May 2014

• Accepted: 15 July 2014

• Published: 12 Baronial 2014

• DOI : https://doi.org/10.1186/s13054-014-0456-6

Keywords

• Astute Respiratory Distress Syndrome
• Respiratory Back up
• Invasive Mechanical Ventilation
• Noninvasive Positive Pressure Ventilation
• Immunocompetent Adult

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