Acute Respiratory Syndrome Disease Research Articles

Spatial Aspects of Acute Respiratory Disease Syndrome: An Application of Scan Statistics Using SaTScan in Identification and Analysis of Hotspot in India

Spatial Aspects of Acute Respiratory Disease Syndrome: An Application of Scan Statistics Using SaTScan in Identification and Analysis of Hotspot in India

Nurses Experience of Prone Position in The Absence of Positioning Tool, and Suggestion of Prone Position Tool: A Phenomenology Study

During the COVID-19 pandemic which is a non-natural disaster, the ARDS cases (Acute Respiratory Disease Syndrome) rocketed. Despite the advantages of prone positioning for ARDS care, ICU staff seldom use it due to the unavailability of positioning tools, making it a challenging task for nurses. This study aims to investigate nurses' experiences with manual prone positioning and propose ICU-friendly prone position tools. This research method used a qualitative phenomenology theory study to 15 ICU nurses who were experienced in prone positioning at least 10 times to intubated patients and had complaints about the intervention. The experience was gathered using structured questions and recorded. The data was analyzed following Colaizzi’s thematic method, and all the emerged themes were collected and reported. The research results show that fifteen interviewed nurses noted that prone positioning is physically demanding and requires a coordinated team with a minimum of three staffs, 2 handles patient positioning, 1 leader securing the intubation tube. Before starting, the team assesses the difficulty level. Recommended tools include a slide sheet with handles, a modified Vollman prone positioner, and a crane-like prone harness. The conclusion is nurses find tools highly beneficial for prone positioning but will improvise with available resources like underpads as a ring-shaped pillow if tools are unavailable.

Gut microbiota-derived acetate attenuates lung injury induced by influenza infection via protecting airway tight junctions

BackgroundGut microbiota (GM) have been implicated as important regulators of gastrointestinal symptom which is commonly occurred along with respiratory influenza A virus (IAV) infection, suggesting the involvement of the gut-to-lung axis in a host’s response to IAV. IAV primarily destroys airway epithelium tight junctions (TJs) and consequently causes acute respiratory disease syndrome. It is known that GM and their metabolism produce an anti-influenza effect, but their role in IAV-induced airway epithelial integrity remains unknown.MethodsA mouse model of IAV infection was established. GM were analyzed using 16S rRNA gene sequencing, and short-chain fatty acids (SCFAs) levels were measured. GM depletion and fecal microbiota transplantation (FMT) were conducted to validate the role of GM in IAV infection. A pair-feeding experiment was conducted to reveal whether IAV-induced GM dysbiosis is attributed to impaired food intake. Furthermore, human bronchial epithelial (HBE) cells were cocultured with IAV in the presence or absence of acetate. TJs function was analyzed by paracellular permeability and transepithelial electronic resistance (TEER). The mechanism of how acetate affects TJs integrity was evaluated in HBE cells transfected with G protein-coupled receptor 43 (GPR43) short hairpin RNA (shRNA).ResultsIAV-infected mice exhibited lower relative abundance of acetate-producing bacteria (Bacteroides, Bifidobacterium, and Akkermansia) and decreased acetate levels in gut and serum. These changes were partly caused by a decrease in food consumption (due to anorexia). GM depletion exacerbated and FMT restored IAV-induced lung inflammatory injury. IAV infection suppressed expressions of TJs (occludin, ZO-1) leading to disrupted airway epithelial barrier function as evidenced by decreased TEER and increased permeability. Acetate pretreatment activated GPR43, partially restored IAV-induced airway epithelial barrier function, and reduced inflammatory cytokines levels (TNF-α, IL-6, and IL-1β). Such protective effects of acetate were absent in HBE cells transfected with GPR43 shRNA. Acetate and GPR43 improved TJs in an AMP-activated protein kinase (AMPK)-dependent manner.ConclusionCollectively, our results demonstrated that GM protected airway TJs by modulating GPR43-AMPK signaling in IAV-induced lung injury. Therefore, improving GM dysbiosis may be a potential therapeutic target for patients with IAV infection.

Predicting the Length of Mechanical Ventilation in Acute Respiratory Disease Syndrome Using Machine Learning: The PIONEER Study.

Background: The ability to predict a long duration of mechanical ventilation (MV) by clinicians is very limited. We assessed the value of machine learning (ML) for early prediction of the duration of MV > 14 days in patients with moderate-to-severe acute respiratory distress syndrome (ARDS). Methods: This is a development, testing, and external validation study using data from 1173 patients on MV ≥ 3 days with moderate-to-severe ARDS. We first developed and tested prediction models in 920 ARDS patients using relevant features captured at the time of moderate/severe ARDS diagnosis, at 24 h and 72 h after diagnosis with logistic regression, and Multilayer Perceptron, Support Vector Machine, and Random Forest ML techniques. For external validation, we used an independent cohort of 253 patients on MV ≥ 3 days with moderate/severe ARDS. Results: A total of 441 patients (48%) from the derivation cohort (n = 920) and 100 patients (40%) from the validation cohort (n = 253) were mechanically ventilated for >14 days [median 14 days (IQR 8-25) vs. 13 days (IQR 7-21), respectively]. The best early prediction model was obtained with data collected at 72 h after moderate/severe ARDS diagnosis. Multilayer Perceptron risk modeling identified major prognostic factors for the duration of MV > 14 days, including PaO2/FiO2, PaCO2, pH, and positive end-expiratory pressure. Predictions of the duration of MV > 14 days showed modest discrimination [AUC 0.71 (95%CI 0.65-0.76)]. Conclusions: Prolonged MV duration in moderate/severe ARDS patients remains difficult to predict early even with ML techniques such as Multilayer Perceptron and using data at 72 h of diagnosis. More research is needed to identify markers for predicting the length of MV. This study was registered on 14 August 2023 at ClinicalTrials.gov (NCT NCT05993377).

Molybdenum Nanodots for Acute Lung Injury Therapy.

Acute respiratory disease syndrome (ARDS) is a common critical disease with high morbidity and mortality rates, yet specific and effective treatments for it are currently lacking. ARDS was especially apparent and rampant during the COVID-19 pandemic. Excess reactive oxygen species (ROS) production and an uncontrolled inflammatory response play a critical role in the disease progression of ARDS. Herein, we developed molybdenum nanodots (MNDs) as a functional nanomaterial with ultrasmall size, good biocompatibility, and excellent ROS scavenging ability for the treatment of acute lung injury (ALI). MNDs, which were administered intratracheally, significantly ameliorated lung oxidative stress, inflammatory response, protein permeability, and histological severity in ALI mice without inducing any safety issues. Importantly, transcriptomics analysis indicated that MNDs protected lung tissues by inhibiting the activation of the Nod-like receptor protein 3 (NLRP3)-dependent pyroptotic pathway. This work presents a promising therapeutic agent for patients suffering from ARDS.

Neutrophil extracellular traps induce persistent lung tissue damage via thromboinflammation without altering virus resolution in a mouse coronavirus model

BackgroundDuring infection, neutrophil extracellular traps (NETs) are associated with severity of pulmonary diseases such as acute respiratory disease syndrome. NETs induce subsequent immune responses, are directly cytotoxic to pulmonary cells, and are highly procoagulant. Anticoagulation treatment was shown to reduce in-hospital mortality, indicating thromboinflammatory complications. However, data are sparsely available on the involvement of NETs in secondary events after virus clearance, which can lead to persistent lung damage and postacute sequelae with chronic fatigue and dyspnea. ObjectivesThis study focuses on late-phase events using a murine model of viral lung infection with postacute sequelae after virus resolution. MethodsC57BL/6JRj mice were infected intranasally with the betacoronavirus murine coronavirus (MCoV, strain MHV-A95), and tissue samples were collected after 2, 4, and 10 days. For NET modulation, mice were pretreated with OM-85 or GSK484 and DNase I were administered intraperitoneally between days 2 to 5 and days 4 to 7, respectively. ResultsRapid, platelet-attributed thrombus formation was followed by a second, late phase of thromboinflammation. This phase was characterized by negligible virus titers but pronounced tissue damage, apoptosis, oxidative DNA damage, and presence of NETs. Inhibition of NETs during the acute phase did not impact virus burden but decreased lung cell apoptosis by 67% and oxidative stress by 94%. Prevention of neutrophil activation by immune training before virus infection reduced damage by 75%, NETs by 31%, and pulmonary thrombi by 93%. ConclusionNETs are detrimental inducers of tissue damage during respiratory virus infection but do not contribute to virus clearance.

The Role of Toll-like Receptor-4 in Macrophage Imbalance in Lethal COVID-19 Lung Disease, and Its Correlation with Galectin-3.

To the current data, there have been 6,955,141 COVID-19-related deaths worldwide, reported to WHO. Toll-like receptors (TLRs) implicated in bacterial and virus sensing could be a crosstalk between activation of persistent innate-immune inflammation, and macrophage's sub-population alterations, implicated in cytokine storm, macrophage over-activation syndrome, unresolved Acute Respiratory Disease Syndrome (ARDS), and death. The aim of this study is to demonstrate the association between Toll-like-receptor-4 (TLR-4)-induced inflammation and macrophage imbalance in the lung inflammatory infiltrate of lethal COVID-19 disease. Twenty-five cases of autopsy lung tissues were studied by digital pathology-based immunohistochemistry to evaluate expression levels of TLR-4 (CD 284), pan-macrophage marker CD68 (clone KP1), sub-population marker related to alveolar macrophage Galectin-3 (GAL-3) (clone 9C4), and myeloid derived CD163 (clone MRQ-26), respectively. SARS-CoV-2 viral persistence has been evaluated by in situ hybridation (ISH) method. This study showed TLR-4 up-regulation in a subgroup of patients, increased macrophage infiltration in both Spike-1(+) and Spike-1(-) lungs (p < 0.0001), and a macrophage shift with important down-regulation of GAL-3(+) alveolar macrophages associated with Spike-1 persistence (p < 0.05), in favor of CD163(+) myeloid derived monocyte-macrophages. Data show that TLR-4 expression induces a persistent activation of the inflammation, with inefficient resolution, and pathological macrophage shift, thus explaining one of the mechanisms of lethal COVID-19.

Association of ovine gammaherpesvirus 2 with an outbreak of acute respiratory disease in dairy cattle

This study investigated the cause of an outbreak of an acute respiratory disease syndrome followed by episodes of diarrhea in a dairy cattle herd from Southern Brazil. Deep nasal swabs (DNS) from asymptomatic calves, calves with pulmonary discomfort, and diarrheic calves after episodes of respiratory distress were used in molecular assays designed to detect the principal pathogens associated with bovine respiratory disease (BRD). Fecal samples were used for the molecular detection of bovine enteric disease agents. Pulmonary tissues from three calves and a cow that died were evaluated by molecular assays to identify 11 agents associated with the development of BRD. The intestinal and pulmonary fragments of one calf and the cow revealed atrophic enteritis and interstitial pneumonia by histopathology, respectively. Immunohistochemistry (IHC) identified intralesional antigens of a malignant catarrhal fever virus, genus Macavirus, within epithelial cells of the lungs and intestines. Molecular assays amplified ovine gammaherpesvirus 2 (OvGHV2) from most of the DNS, and the pulmonary and intestinal fragments from the animals that died, confirming that the Macavirus identified by IHC was OvGHV2. Concomitant pulmonary infections of OvGHV2 with bovine gammaherpesvirus 6 and bovine coronavirus were identified. Additionally, bovine viral diarrhea virus 1b and Aichivirus B were detected in the fecal samples. These findings demonstrated that OvGHV2, a Macavirus, was the disease agent most frequently (81.2%; 13/16) associated with singular pulmonary infections during this outbreak of BRD, suggesting that this virus may be another potential agent of respiratory disease of cattle.

Echocardiography Before Extracorporeal Membrane Oxygenation in Refractory Respiratory Failure: SARS-CoV-2 Infection Versus Other Etiologies

The study authors hypothesized that in patients with SARS-CoV-2, COVID-19-related refractory respiratory failure requiring extracorporeal membrane oxygenation (ECMO) support echocardiographic findings (just before ECMO implantation) would be different from those observed in patients with refractory respiratory failure from different etiologies. A single-center observational study. At an intensive care unit (ICU). A total of 61 consecutive patients with refractory COVID-19-related respiratory failure (COVID-19 series) and 74 patients with refractory acute respiratory disease syndrome from other etiologies (no COVID-19 series), all needing ECMO support. Echocardiogram pre-ECMO. Right ventricle dilatation and dysfunction were defined in the presence of the RV end-diastolic area and/or left ventricle end-diastolic area (LVEDA >0.6 and tricuspid annular plane systolic excursion [TAPSE] <15 mm. Patients in the COVID-19 series showed a higher body mass index (p < 0.001) and a lower Sequential Organ Failure Assessment score (p=0.002). In-ICU mortality rates were comparable between the 2 subgroups. Echocardiograms performed in all patients before ECMO implantation revealed an incidence of RV dilatation that was higher in patients in the COVID-19 series (p < 0.001), and they also showed higher values of systolic pulmonary artery pressure (sPAP) (p < 0.001) and lower TAPSE and/or sPAP (p < 0.001). The multivariate logistic regression analysis showed that COVID-19-related respiratory failure was not associated with early mortality. The presence of RV dilatation and the uncoupling of RV function and pulmonary circulation were associated independently with COVID-19 respiratory failure. The presence of RV dilatation and an altered coupling between RVe function and pulmonary vasculature (as indicated by TAPSE and/or sPAP) are associated strictly with COVID-19-related refractory respiratory failure needing ECMO support.

Postoperative Respiratory Failure and Advanced Ventilator Settings.

Postoperative respiratory failure has a multifactorial etiology, of which atelectasis is the most common mechanism. Its injurious effects are magnified by surgical inflammation, high driving pressures, and postoperative pain. Chest physiotherapy and noninvasive ventilation are good options to prevent progression of respiratory failure. Acute respiratory disease syndrome is a late and severe finding, which is associated with high morbidity and mortality. If present, proning is a safe, effective, and underutilized therapy. Extracorporeal membrane oxygenation is an option only when traditional supportive measures have failed.

Lung ultrasound to evaluate aeration changes in response to recruitment maneuver and prone positioning in intubated patients with COVID-19 pneumonia: preliminary study

BackgroundThis single-center preliminary prospective observational study used bedside ultrasound to assess the lung aeration modifications induced by recruitment maneuver and pronation in intubated patients with acute respiratory disease syndrome (ARDS) related to coronavirus 2019 disease (COVID-19).All adult intubated COVID-19 patients suitable for pronation were screened. After enrollment, patients underwent 1 h in a volume-controlled mode in supine position (baseline) followed by a 35-cmH2O-recruitment maneuver of 2 min (recruitment). Final step involved volume-controlled mode in prone position set as at baseline (pronation). At the end of the first two steps and 1 h after pronation, a lung ultrasound was performed, and global and regional lung ultrasound score (LUS) were analyzed. Data sets are presented as a median and 25th–75th percentile.ResultsFrom January to May 2022, 20 patients were included and analyzed. Global LUS reduced from 26.5 (23.5–30.0) at baseline to 21.5 (18.0–23.3) and 23.0 (21.0–26.3) at recruitment (p < 0.001) and pronation (p = 0.004). In the anterior lung regions, the regional LUS were 1.8 (1.1–2.0) following recruitment and 2.0 (1.6–2.2) in the supine (p = 0.008) and 2.0 (1.8–2.3) in prone position (p = 0.023). Regional LUS diminished from 2.3 (2.0–2.5) in supine to 2.0 (1.8–2.0) with recruitment in the lateral lung zones (p = 0.036). Finally, in the posterior lung units, regional LUS improved from 2.5 (2.3–2.8) in supine to 2.3 (1.8–2.5) through recruitment (p = 0.003) and 1.8 (1.3–2.2) with pronation (p < 0.0001).ConclusionsIn our investigation, recruitment maneuver and prone positioning demonstrated an enhancement in lung aeration when compared to supine position, as assessed by bedside lung ultrasound.Trial registration: www.clinicaltrials.gov, Number NCT05209477, prospectively registered and released on 01/26/2022.

Correlation between serum autotaxin level and pulmonary ultrasound score with the disease severity and 28-day mortality in patients with acute respiratory disease syndrome

Objective: To investigate the relationship between serum autocrine motor factor (Autotaxin) level and pulmonary ultrasound score (LUS) and the disease severity and 28-day mortality of patients with acute respiratory distress syndrome (ARDS). Methods: Totally 142 ARDS patients admitted to Danzhou People's Hospital from January 2019 to December 2021 were selected, and serum Autotaxin level and LUS score of ARDS patients on the day of onset were detected. According to the survival within 28 days after entering the intensive care unit, ARDS patients were divided into survival group (86 cases) and death group (56 cases). According to the oxygenation index, ARDS patients were divided into mild group (200 mmHg<oxygenation index≤300 mmHg, 36 cases), moderate group (100 mmHg<oxygenation index≤200 mmHg, 61 cases) and severe group (oxygenation index≤100 mmHg, 45 cases). The receiver operating characteristic curve (ROC) was performed to analyze the value of serum autotaxin level and LUS score to predict the death of patients with ARDS. Kaplan-Meier method was used to draw the survival curve, and Log-rank test was used for comparison between groups. Cox multivariate regression analysis was used to analyze the risk factors of death in patients with ARDS. Results: The LUS score [(26.50±5.20 vs 13.45±3.70, t=11.974,P<0.01] and serum Autotaxin level [(54.83±16.28)μg/L vs (32.70±11.85) μg/L,t=13.842,P<0.01] in the death group were significantly higher than those in the survival group, the difference is statistically significant. The serum autotaxin level and LUS score in severe group were significantly higher than those in mild group and moderate group (all were P<0.001). ROC curve showed that the combino ation of autotaxin and LUS score had the largest AUC to predict the AUC of death in patients with ARDS (0.904, 95CI:0.847-0.962), with the highest accuracy of 88.2%. Survival curve analysis showed that the survival rate of high autotaxin group was significantly lower than that of low autotaxin group (44.1% vs 75.7%,P<0.001), and the survival rate of high LUS score group was significantly lower than that of low LUS score group (49.4% vs 73.8%,P=0.003). Cox multivariate regression analysis showed that elevated LUS score (HR=1.983, 95%CI: 1.402-4.715,P<0.001) and Autotaxin level (HR=2.604, 95%CI: 1.853-6.317,P<0.001) were risk factors for death in patients with ARDS (P<0.05). Conclusion: The increase of serum autotaxin level and LUS score is related to the severity and death of patients with ARDS, which are risk factors for 28-day death in ARDS patients, and can be used as a reference mdicator to predict death in ARDS patients.

Clinical Impact of Hydrocortisone Uses on Patient with COVID-19: A Case Report

COVID-19 can cause anything from no symptoms at all to severe breathing problems, organ failure, and even death. Currently, there is no cure for COVID-19, thus treatment focuses on providing the patient with as much comfort as possible. Hydrocortisone are utilized for patients with acute respiratory disease syndrome and septic shock because they shorten the need for mechanical ventilation, ICU stay, and perhaps mortality. This prospective case report study showed the intravenously administered Hydrocortisone response on a patient admitted to the Elekahia COVID-19 treatment centre, located in Port Harcourt, Rivers State, Nigeria. The patient was a 47-year-old man of Asian descent; he presented with pneumonia-like symptoms and developed severe breathlessness. Treatment started on 6th June 2020 and ended on 16th June 2020. &#x0D; There was a marked improvement in peripheral capillary oxygen saturation (SpO2) after hydrocortisone intervention; respiratory rate reduced from 40 cycles per minute to 18 cycles per minute, and the patient could complete sentences without developing breathlessness, three hours after receiving the first dose of intravenous hydrocortisone.&#x0D; The use of Hydrocortisone therapy could be of tremendous benefit in the treatment of COVID-19 patients who present with severe respiratory distress. Controlled randomized clinical trials are required to assess steroid use in COVID-19 treatment properly. And to assess its use as a prophylactic in the early management of severe COVID-19 cases.

Regulation of cellular senescence by innate immunity.

During the COVID-19 pandemic, the interplay between the processes of immunity and senescence is drawing more and more intensive attention. SARS-CoV-2 infection induces senescence in lung cells, failure to clear infected cells and increased presence of inflammatory factors could lead to a cytokine storm and acute respiratory disease syndrome (ARDS), which together with aging and age-associated disease lead to 70% of COVID-19-related deaths. Studies on how senescence initiates upon viral infection and how to restrict excessive accumulation of senescent cells to avoid harmful inflammation are crucially important. Senescence can induce innate immune signaling, and innate immunity can engage cell senescence. Here, we mainly review the innate immune pathways, such as cGAS-STING, TLRs, NF-κB, and NLRP3 inflammasome, participating in the senescence process. In these pathways, IFN-I and inflammatory factors play key roles. At the end of the review, we propose the strategies by which we can improve the immune function and reduce inflammation based on these findings.

IL-33 and the Cytokine Storm in COVID-19: From a Potential Immunological Relationship towards Precision Medicine.

Coronavirus SARS-CoV-2 has represented, and still represents, a real challenge from a clinical, diagnostic and therapeutic point of view. During acute infection, the increased levels of pro-inflammatory cytokines, which are involved in the pathology of disease and the development of SARS-CoV-2-induced acute respiratory disease syndrome, the life-threatening form of this infection, are correlated with patient survival and disease severity. IL-33, a key cytokine involved in both innate and adaptive immune responses in mucosal organs, can increase airway inflammation, mucus secretion and Th2 cytokine synthesis in the lungs, following respiratory infections. Similar to cases of exposure to known respiratory virus infections, exposure to SARS-CoV-2 induces the expression of IL-33, correlating with T-cell activation and lung disease severity. In this work, we analyse current evidence regarding the immunological role of IL-33 in patients affected by COVID-19, to evaluate not only the clinical impact correlated to its production but also to identify possible future immunological therapies that can block the most expressed inflammatory molecules, preventing worsening of the disease and saving patient lives.

A Comparative Study of Rapid SARS-Cov-2 Antigen Detection Assay against RT-PCR Assay for Diagnosis of COVID-19 in a Tertiary Hospital of Kathmandu

Background The Coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus (SARS-CoV-2) has spread worldwide since its first recorded case in the city of Wuhan, China, in December 2019. SARS-CoV-2 infection causes asymptomatic to sever pneumonia. Severe cases may develop acute respiratory disease syndrome (ARDS), with an average mortality rate of 6.9%. Real Time Reverse Transcriptase Polymerase Chain Reaction (rRT-PCR) assay is the current reference standard laboratory method for the diagnosis of SARS-CoV-2 infection. However, it takes around 6-8 hours to get the result and is time consuming. Therefore, rapid and accurate tests for SARS-CoV-2 screening are essential to expedite disease prevention and control. Lateral flow immunoassay using monoclonal anti SARS-CoV-2 antibodies which target for SARS-CoV-2 antigen can be complimentary screening test if their accuracy were comparable to that of the real time reverse transcription-polymerase chain reaction (RT-PCR) assay.&#x0D; Objective To find the sensitivity and specificity of a rapid antigen test kit in comparison to reverse transcription-polymerase chain reaction (RT-PCR).&#x0D; Method A cross-sectional hospital based study was carried out at Shree Birendra Army Hospital, Kathmandu for a period of four months.&#x0D; Result Our finding shows sensitivity and specificity of rapid diagnostic tests (RDT) Ag kit as 60.6% and 96.4% respectively. Positive and negative predictive value was 83.7% and 89.0%. Likewise, positive and negative likelihood ratio was 17.0 and 0.4. The overall accuracy of the antigen kit was 88.1% in comparison to reverse transcription-polymerase chain reaction (RT-PCR) as the gold standard.&#x0D; Conclusion Our study concluded the use of rapid antigen kit is mainly useful for screening purposes.

Molecular characterization of avian metapneumovirus subtype C detected in wild mallards (Anas platyrhynchos) in The Netherlands.

Avian metapneumovirus (AMPV) represents a long-term threat to the poultry industry due to its etiological role in the induction of acute respiratory disease and/or egg drop syndrome in domestic turkeys, chickens, and ducks. Although this disease is commonly referred to as turkey rhinotracheitis, the host range of AMPV encompasses many avian species. We have screened 1323 oropharyngeal- and cloacal swab samples obtained from wild mallards in the Netherlands from 2017 to 2019 by RT-PCR using a degenerate primer pair to detect all members of the Paramyxoviridae and Pneumoviridae or an avian metapneumovirus subtype C (AMPV-C)-specific RT-qPCR assay. We identified a total of seven cases of AMPV-C infections in wild, healthy mallards (Anas platyrhynchos), of which two AMPV-C positive samples were further processed using next-generation sequencing. Phylogenetic analysis of the two complete genomes showed that the newly identified AMPV-C strains share closest sequence identity (97%) with Eurasian lineage AMPV-C strains identified in Muscovy ducks in China that presented with severe respiratory disease and egg production loss in 2011. Further analysis of Gprotein amino acid sequences showed a high degree of variability between the newly identified AMPV-C variants. PONDR scoring of the G protein has revealed the ectodomain of AMPV-C to be partitioned into a long intrinsically disordered and short ordered region, giving insights into AMPV G protein structural biology. In summary, we provide the first report of full-length AMPV-C genome sequences derived from wild birds in Europe. This emphasizes the need for further surveillance efforts to better characterize the host range, epidemiologic distribution, and pathogenicity of AMPV-C to determine the risk posed by cross-species jumps from wildfowl to domesticated avian species.

Clinical characteristics and outcomes of hospitalized COVID-19 patients with diabetes mellitus in East Java, Indonesia: A cross-sectional study

Introduction: Diabetes mellitus has been perceived as the worsening factor for coronavirus disease 2019 (COVID-19), where diabetes mellitus patients with pre-existing inflammatory condition could develop acute respiratory disease syndrome as well as multi-organ dysfunction. Managing diabetes mellitus amidst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also a matter of concern as several antidiabetic therapies could affect the progression of COVID-19. This study aimed to provide the clinical characteristics and outcomes of patients with both COVID-19 and diabetes mellitus receiving blood glucose lowering therapies and COVID-19 symptomatic treatments. Methods: This retrospective study was performed on 260 medical records of patients hospitalized between May 2020 to February 2021 in East Java, Indonesia. Patients were confirmed COVID-19 positive based on the results from real time polymerase chain reaction (RT-PCR) using nasal swab samples collected on hospital admission. Data included were demographic characteristics, COVID-19 symptoms, severity of COVID-19, comorbidities (other than diabetes mellitus), fasting blood glucose (FBG), and 2-hours post-prandial blood glucose (2hPBG), and outcomes. Results: Most of the patients had age range of 41–60 years old (76.1%) with more than a half of the subjects (60%) were obese. Patients with uncontrolled diabetes were distributed evenly among the COVID-19 severities (74.3% in asymptomatic group, 73.6% in mild group, and 74.1% in moderate group). There were reductions in FBG and 2hPBG levels measured before (210.75±81.38 and 271.19±100.7 mg/dL, respectively) and after the treatment (181.03±68.9 and 222.01±86.96 mg/dL, respectively). All patients received multivitamin and symptomatic treatment for COVID-19. Oral antidiabetic drug (57.6%) and insulin (28.8%) were administered to lower the blood glucose level of the patients. As many as 96.9% patients survived, while 3.1% died. Conclusion: COVID-19 could affect the blood glucose level, suggesting the importance of antihyperglycemic therapies among patients with both COVID-19 and diabetes mellitus.

Clinical characteristics and outcomes of hospitalized COVID-19 patients with diabetes mellitus in East Java, Indonesia: A cross-sectional study.

Introduction: Diabetes mellitus has been perceived as the worsening factor for coronavirus disease 2019 (COVID-19), where diabetes mellitus patients with pre-existing inflammatory condition could develop acute respiratory disease syndrome as well as multi-organ dysfunction. Managing diabetes mellitus amidst severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also a matter of concern as several antidiabetic therapies could affect the progression of COVID-19. This study aimed to provide the clinical characteristics and outcomes of patients with both COVID-19 and diabetes mellitus receiving blood glucose lowering therapies and COVID-19 symptomatic treatments. Methods: This retrospective study was performed on 260 medical records of patients hospitalized between May 2020 to February 2021 in East Java, Indonesia. Patients were confirmed COVID-19 positive based on the results from real time polymerase chain reaction (RT-PCR) using nasal swab samples collected on hospital admission. Data included were demographic characteristics, COVID-19 symptoms, severity of COVID-19, comorbidities (other than diabetes mellitus), fasting blood glucose (FBG), and 2-hours post-prandial blood glucose (2hPBG), and outcomes. Results: Most of the patients had age range of 41-60 years old (76.1%) with more than a half of the subjects (60%) were obese. Patients with uncontrolled diabetes were distributed evenly among the COVID-19 severities (74.3% in asymptomatic group, 73.6% in mild group, and 74.1% in moderate group). There were reductions in FBG and 2hPBG levels measured before (210.75±81.38 and 271.19±100.7 mg/dL, respectively) and after the treatment (181.03±68.9 and 222.01±86.96 mg/dL, respectively). All patients received multivitamin and symptomatic treatment for COVID-19. Oral antidiabetic drug (57.6%) and insulin (28.8%) were administered to lower the blood glucose level of the patients. As many as 96.9% patients survived, while 3.1% died. Conclusion: COVID-19 could affect the blood glucose level, suggesting the importance of antihyperglycemic therapies among patients with both COVID-19 and diabetes mellitus.

Health outcomes and comorbidities among Covid-19 patients from a Peri urban community of Chandigarh

Introduction: Covid-19 is a respiratory disease caused by severe acute respiratory disease syndrome Coronavirus 2(sars-cov-2). Health outcomes varies broadly in patients with and without comorbidities. Objectives: The purpose of the study was to assess the prevalence of comorbidities and health outcomes among Covid-19 patients residing in Indira colony, Chandigarh. Method: A descriptive cross-sectional study was conducted to enroll all Covid-19 patients over a period of two weeks. The list of patients was obtained from ANM’s of the selected area. A semi structured interview schedule was developed to collect information telephonically and responses were recorded on Google forms. Result: A total of 110 participants were enrolled in the study. The results revealed that 81% of participants were having Covid-19 symptoms. Fever was the most common symptom (88.8%) A total of 25 patient (22.7%) person having comorbidities diabetes mellitus was the most common comorbidity (44%) seen in participants. About 27.2% of the total patients required hospitalization. Only few participants required mechanical ventilation. Zero deaths were reported in the present study. Conclusion: Fever was the most common symptom in symptomatic patients followed by cough. The most prevalent comorbidity in patient was diabetes mellitus and there was no fatality seen in studied population.