Project description:BackgroundThe dual infection with SARS-CoV-2 is poorly described and is currently under discussion. We present a study of two strains of SARS-CoV-2 detected in the same patient during the same disease presentation.Case presentationA patient in their 90 s was hospitalised with fever. Oropharyngeal swab obtained on the next day (sample 1) tested positive for SARS-CoV-2. Five days later, the patient was transferred to the ICU (intensive care unit) of the hospital specialising in the treatment of COVID-19 patients, where the patient's condition progressively worsened and continuous oxygen insufflation was required. Repeated oropharyngeal swab (sample 2), which was taken eight days after the first one, also tested positive for SARS-CoV-2. After 5 days of ICU treatment, the patient died. The cause of death was a coronavirus infection, which progressed unfavourably due to premorbid status. We have performed sequencing of full SARS-CoV-2 genomes from oropharyngeal swabs obtained eight days apart. Genomic analysis revealed the presence of two genetically distant SARS-CoV-2 strains in both swabs. Detected strains belong to different phylogenetic clades (GH and GR) and differ in seven nucleotide positions. The relative abundance of strains was 70% (GH) and 30% (GR) in the first swab, and 3% (GH) and 97% (GR) in the second swab.ConclusionsOur findings suggest that the patient was infected by two genetically distinct SARS-CoV-2 strains at the same time. One of the possible explanations is that the second infection was hospital-acquired. Change of the dominant strain ratio during disease manifestation could be explained by the advantage or higher virulence of the GR clade strain.
Project description:BackgroundThe recent COVID-19 pandemic has raised concerns about patient diagnosis and follow-up of chronically ill patients. Patients suffering from chronic illnesses, concomitantly infected by SARS-CoV-2, globally tend to have a worse prognosis and poor outcomes. Renal tropism and acute kidney injury following SARS-CoV-2 infection has recently been described in the literature, with elevated mortality rates. Furthermore, patients with pre-existing chronic kidney disease, infected by SARS-CoV-2, should be monitored carefully. Here, we report the case of a 69-year-old patient with splenic marginal zone lymphoma, suffering from longstanding chronic kidney disease following SARS-CoV-2 infection.Case presentationA 69-year-old male patient previously diagnosed with pulmonary embolism and splenic marginal zone lymphoma (Splenomegaly, Matutes 2/5, CD5 negative and CD23 positive), was admitted to the hospital with shortness of breath, fever and asthenia. A nasopharyngeal swab test was performed in addition to a CT-scan, which confirmed SARS-CoV-2 infection. Blood creatinine increased following SARS-CoV-2 infection at 130 μmol/l, with usual values at 95 μmol/l. The patient was discharged at home with rest and symptomatic medical treatment (paracetamol and hydration), then readmitted to the hospital in August 2020. A kidney biopsy was therefore conducted as blood creatinine levels were abnormally elevated. Immunodetection performed in a renal biopsy specimen confirmed co-localization of SARS-CoV2 nucleocapsid and protease 3C proteins with ACE2, Lewis x and sialyl-Lewis x antigens in proximal convoluted tubules and podocytes. Co-localization of structural and non-structural viral proteins clearly demonstrated viral replication in proximal convoluted tubules in this chronically ill patient. Additionally, we observed the co-localization of sialyl-Lewis x and ACE2 receptors in the same proximal convoluted tubules. Reverse Transcriptase-Polymerase Chain Reaction test performed on the kidney biopsy was negative, with very low Ct levels (above 40). The patient was finally readmitted to the haematology department for initiation of chemotherapy, including CHOP protocol and Rituximab.ConclusionsOur case emphasizes on the importance of monitoring kidney function in immunosuppressed patients and patients suffering from cancer following SARS-CoV-2 infection, through histological screening. Further studies will be required to decipher the mechanisms underlying chronic kidney disease and the putative role of sialyl-Lewis x and HBGA during SARS-CoV-2 infection.
Project description:Introduction and importanceGranulomatous chronic invasive fungal rhinosinusitis (GCIFR) is a rare entity with scarce cases reported mainly in subtropical areas. Its prevalence among individuals with clinical suspicion of fungal rhinosinusitis has been reported in approximately 20% in subtropical populations, unlike North America with a prevalence of 0.5%. It is typically associated with Aspergillus flavus and the presence of noncaseating granulomas or Langerhans giant cells on histopathologic examination.Case presentationWe describe a case of a patient with clinical history of recent SARS-CoV-2 infection and development of intense cephalalgia, visual impairment, palpebral ptosis, and limitation of extraocular movements. MRI demonstrated the presence of opacification of paranasal sinuses, and a left intraconal abscess. A surgical endoscopic approach was performed and histopathologic examination revealed frontal GCIFR and maxillary fungus ball. Treatment with IV azoles provided adequate clinical response.Clinical discussionThe spectrum of the fungal rhinosinusitis disease is not clear. However, non-invasive fungal rhinosinusitis is not often found concomitantly with invasive types. GCIFR typically manifests with an indolent and gradual progression at early stages. Advanced stages can exhibit orbital and intracranial involvement leading to visual impairment, frequent relapses, and a poor prognosis. A higher incidence of invasive fungal rhinosinusitis has been reported in patients with SARS-CoV-2 infection despite an unremarkable medical history, associated with immune dysregulation.ConclusionGCIFR is a rare condition with few cases reported in America. Because of its uncommonness, its diagnosis is often delayed leading to increased morbidity and mortality.
Project description:BackgroundCoronavirus disease 2019 (COVID-19) is a rapidly spreading pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It is a multisystemic disease associated with micro- and macrovascular thrombo-embolic complications, including intracardiac thrombosis, which has not been previously reported in the literature.Case summaryWe report a case of a 68-year-old woman with COVID-19 admitted to our intensive care unit with acute respiratory distress, undifferentiated shock, hyperkalaemia, acute kidney injury, and coagulopathy. She received crystalloid infusion, broad-spectrum antibiotics, hydroxychloroquine, insulin-dextrose, calcium gluconate, sodium bicarbonate, and i.v. vasopressors. Continuous renal replacement therapy (CRRT) was started for refractory hyperkalaemia and metabolic acidosis. Transthoracic echocardiogram obtained for concern of pulmonary embolism found bi-atrial thrombosis with normal bi-ventricular dimensions and function. Systemic anticoagulation was provided, but this was stopped soon afterwards due to worsening coagulopathy and bleeding. Despite intensive measures and supportive therapy, the patient developed worsening hypoxia, refractory shock, and multiorgan failure. After discussion of goals of care with her family, a decision was made to initiate hospice care. The patient died within 72 h of hospital admission.DiscussionInfection with SARS-CoV-2 is a multisystemic disease that primarily affects the lungs, but also predisposes to rare thrombo-embolic phenomena such as intracardiac thrombosis.
Project description:Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here we uncover a role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.
Project description:Adolescents with coronavirus disease 2019 (COVID-19) associated multisystem inflammatory syndrome (MIS) can present with shock and myocardial injury and mimic Kawasaki disease. We describe 4 previously well adolescents (age 13-14 years), presenting with clinical features of MIS in children (MIS-C). All patients had nearly similar clinical presentation. Hematological investigations revealed elevated inflammatory markers, anemia, thrombocytopenia, and decreased neutrophil:lymphocyte ratio. All patients were negative on real-time polymerase chain reaction against severe acute respiratory syndrome coronavirus 2, but had elevated immunoglobulin G titers. Two patients had atypical Kawasaki disease. Three patients had severe disease with hypotensive shock and required intensive care with fluids and inotropes. Two patients required non-invasive respiratory support for dyspnea and one patient had biventricular dysfunction. All received empiric antibiotics, low-molecular weight heparin, steroids, and intravenous immunoglobulin. One patient succumbed, while others recovered well. MIS-C may be a late presentation in adolescent with COVID-19. Individualized treatment with empiric antibiotics, immunomodulation, and thromboprophylaxis can result in significantly better outcome.
Project description:In the current scenario, in which an elevated number of COVID-19 survivors present with severe physical deconditioning, exercise intolerance, persistent symptoms, and other post-acute consequences, effective rehabilitation strategies are of utmost relevance. In this study, we report for the first time the effect of home-based exercise training (HBET) in a survivor patient from critical COVID-19 illness. A 67-year-old woman who had critical COVID-19 disease [71 days of hospitalization, of which 49 days were in the intensive care unit (ICU) with invasive mechanical ventilation due to respiratory failure] underwent a 10-week HBET aiming to recovering overall physical condition. Before and after the intervention, we assessed cardiopulmonary parameters, skeletal muscle strength and functionality, fatigue severity, and self-reported persistent symptoms. At baseline (3 months after discharge), she presented with severe impairment in cardiorespiratory functional capacity (<50% age predicted VO2peak). After the intervention, remarkable improvements in VO2peak (from 10.61 to 15.48 mL·kg-1·min-1, Δ: 45.9%), oxygen uptake efficiency slope (OUES; from 1.0 to 1.3 L·min-1, Δ: 30.1%), HR/VO2 slope (from 92 to 52 bpm·L-1, Δ: -43.5%), the lowest VE/VCO2 ratio (from 35.4 to 32.9 L·min-1, Δ: -7.1%), and exertional dyspnea were observed. In addition, handgrip strength (from 22 to 27 kg, Δ: 22.7%), 30-s Sit-to-Stand (30-STS; from 14 to 16 repetitions, Δ:14.3%), Timed-Up-and-Go (TUG; from 8.25 to 7.01 s, Δ: -15%) performance and post-COVID functional status (PCFS) score (from 4 to 2) were also improved from baseline to post-intervention. Self-reported persistent symptoms were also improved, and Fatigue Severity Scale (FSS) score decreased (from 4 to 2.7) from baseline to post-intervention. This is the first evidence that a semi-supervised, HBET program may be safe and potentially effective in improving cardiorespiratory and physical functionality in COVID-19 survivors. Controlled studies are warranted to confirm these findings.
Project description:We reported a 33-year-old female case with novel coronavirus disease 2019 (COVID-19) accompanied by Acute tubular necrosis (ATN). She had a gestational age of 34 weeks. The patient referred to treatment clinic for COVID-19 in Imam Reza hospital of Tabriz (Iran) after having flu-like symptoms. In radiologic assessment, ground glass opacity (GGO) with consolidation was found in upper right lobe. Lopinavir/ritonavir (200mg/50mg) two tablet tow times, Ribavirin 200mg every 6 h, and Oseltamivir 75mg tow times were given for the treatment of COVID-19. The medications used for treatment of pneumonia were Meropenem, Ciprofloxacin, Vancomycin. All doses of medications were administrated by adjusted dose assuming the patient is anephric. Also, a few supplements were also given after ATN development including daily Rocaltrol and Nephrovit (as a multivitamin appropriate for patients with renal failure), Folic acid and Calcium carbonate. The patient is still under ventilator with a Fraction of inspired oxygen (FiO2) of 60% and Positive end-expiratory pressure (PEEP) of eight. SpO2 is 94% but the patient's ATN problem has been resolved. We started weaning from mechanical ventilator. The patient is conscious with full awareness to time, person and place. The maternal well-being is achieved and her neonate was discharged.
Project description:We reported a 33-year-old female case with novel coronavirus disease 2019 (COVID-19) accompanied by Acute tubular necrosis (ATN). She had a gestational age of 34 weeks. The patient referred to treatment clinic for COVID-19 in Imam Reza hospital of Tabriz (Iran) after having flu-like symptoms. In radiologic assessment, ground glass opacity (GGO) with consolidation was found in upper right lobe. Lopinavir/ritonavir (200mg/50mg) two tablet tow times, Ribavirin 200mg every 6 h, and Oseltamivir 75mg tow times were given for the treatment of COVID-19. The medications used for treatment of pneumonia were Meropenem, Ciprofloxacin, Vancomycin. All doses of medications were administrated by adjusted dose assuming the patient is anephric. Also, a few supplements were also given after ATN development including daily Rocaltrol and Nephrovit (as a multivitamin appropriate for patients with renal failure), Folic acid and Calcium carbonate. The patient is still under ventilator with a Fraction of inspired oxygen (FiO2) of 60% and Positive end-expiratory pressure (PEEP) of eight. SpO2 is 94% but the patient's ATN problem has been resolved. We started weaning from mechanical ventilator. The patient is conscious with full awareness to time, person and place. The maternal well-being is achieved and her neonate was discharged.
Project description:Introductionand Importance: COVID-19 infection presents various symptoms that may resemble signs and symptoms of other underlying diseases. Pleural effusion in a confirmed COVID-19 patient with a history of malignancy is found to be rare, and the exact pathogenesis is still unclear. Hence RT-PCR COVID-19 assay from pleural effusion fluid is essential.Case presentationA 62-year-old female patient was admitted to the emergency department with a complaint of shortness of breath and headache. Previously, the patient was diagnosed with stage III breast carcinoma. The chest radiograph showed massive pleural effusion. The SARS-CoV-2 was found in the nasopharyngeal and oropharyngeal sample, but the RT-PCR COVID-19 assay of pleural fluid was negative.Clinical discussionPleural effusion can be an uncommon manifestation of COVID-19, but there are many other etiologies. Malignancy is a commonly encountered underlying cause of the pleural effusion. Since it presents similar respiratory signs and symptoms, awareness of possible etiologies is pivotal. A strict examination, assessment, and protocol should be done to prevent the intervention's potential hazard.ConclusionPleural effusion related to COVID-19 infection can resemble the clinical presentation in a patient with a malignancy history. SARS-CoV-2 can be found in the nasopharyngeal and oropharyngeal sample but absent in pleural effusion fluid.