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1.
Malaysian Journal of Medical Sciences ; JOUR:83-92, 29(5).
Article in English | EMBASE | ID: covidwho-2100663

ABSTRACT

Background: COVID-19 was declared a pandemic by the World Health Organization (WHO). COVID-19 is highly contagious, making it a threat to healthcare workers, including those working in mortuaries. Therefore, it is important to determine if the cause of death (COD) could be identified using limited autopsy, diagnostic tests and post-mortem imaging modalities instead of full autopsy. This study aims to examine the effectiveness of post-mortem imaging, specifically post-mortem computed tomography (PMCT) at determining the COD during a pandemic. Method(s): This cross-sectional study included 172 subjects with suspected or unknown COVID-19 status brought in dead to the institute's mortuary during the pandemic in Malaysia. PMCT images reported by forensic radiologists and their agreement with conventional autopsy findings by forensic pathologists regarding COD were analysed to look at the effectiveness of PMCT in determining COD during a pandemic. Result(s): Analysis showed that 78.7% (133) of cases reported by forensic radiologists concurred with the COD certified by forensic pathologists. Of these cases, 85 (63.9%) had undergone only external examination and real-time reverse transcriptase polymerase chain reaction (rRT-PCR) COVID-19 testing, meaning that imaging was the sole method used to determine the COD besides history from available medical records and the investigating police officer. Conclusion(s): PMCT can be used as a complement to medicolegal autopsies in pandemic contexts, as it provides significant information on the possible COD without jeopardising the safety of mortuary health care workers. Copyright © 2022, Penerbit Universiti Sains Malaysia. All rights reserved.

2.
Journal of Infection and Public Health ; JOUR
Article in English | ScienceDirect | ID: covidwho-2095664

ABSTRACT

Background At what rate does the RNA of SARS CoV-2 shed from cadavers? Although, there have been numerous studies which have demonstrated the persistence of the virus on dead bodies, there is a lack of conclusive evidence regarding the variation of viral RNA content in cadavers. This has led to a knowledge gap regarding the safe handling/management of COVID-19 decedents, posing a barrier in forensic investigations. Methods: In this study, we report the presence of RNA of SARS CoV-2 by real time RT-PCR, in nasopharyngeal swabs collected after death from two groups of bodies – one who died due to COVID-19 and the other who died due to other diagnoses. A prospective study on 199 corpses, who had tested positive for COVID-19 ante-mortem, was conducted at a tertiary care center. RNA testing was conducted at different time intervals (T1-T5). Results: 112(56.3%) died primarily due to COVID-19 and 87(43.7%) died due to other diagnoses. 144(72.4%) were male and 55(27.6%) were female. A total of 115 (57.8%) tested positive for COVID-19 after death at different time points. The mean age was 50.7±18.9 years and the length of hospitalization ranged from 1-50 days with a mean of 9.2±7.6 days. Realtime RT-PCR positivity of SARS CoV-2 RNA decreases with time. Conclusion: We observed that real time RT-PCR positivity, indicating viral RNA detection, decreases with time. Therefore, it is advisable to follow appropriate COVID-19 precautions to carry out scientific studies, medico-legal investigations and mortuary services on suspected/confirmed COVID-19 corpses.

3.
J Clin Endocrinol Metab ; 2022 Oct 19.
Article in English | MEDLINE | ID: covidwho-2079596

ABSTRACT

CONTEXT: Infection by SARS-CoV-2 may be associated with testicular dysfunction that could affect male fertility. OBJECTIVE: Testicles of fatal COVID-19 cases were investigated to detect virus in tissue and to evaluate histopathological and transcriptomic changes. METHODS: Three groups were compared: a. uninfected controls (subjects dying of trauma or sudden cardiac death; n = 10); b. subjects dying of COVID-19 (virus-negative in testes; n = 15); c. subjects dying of COVID-19 (virus-positive in testes; n = 9). SARS-CoV-2 genome and nucleocapsid antigen were probed using RT-PCR, in situ hybridization, immunohistochemistry (IHC). Infiltrating leukocytes were typed by IHC. mRNA transcripts of immune-related and testis-specific genes were quantified using the nCounter method. RESULTS: SARS-CoV-2 was detected in testis tissue of 9/24 (37%) COVID-19 cases accompanied by scattered T-cell and macrophage infiltrates. Size of testicles and counts of spermatogenic cells were not significantly different among groups. Analysis of mRNA transcripts showed that in virus-positive testes immune processes were activated (interferon-alpha and -gamma pathways). By contrast, transcription of 12 testis-specific genes was downregulated, independently of virus positivity in tissue. By IHC, expression of the luteinizing hormone/choriogonadotropin receptor was enhanced in virus-positive compared to virus-negative testicles, while expression of receptors for androgens and the follicle-stimulating hormone were not significantly different among groups. CONCLUSION: In lethal COVID-19 cases, infection of testicular cells is not uncommon. Viral infection associates with activation of interferon pathways and downregulation of testis-specific genes involved in spermatogenesis. Due to the exceedingly high numbers of infected people in the pandemic, the impact of virus on fertility should be further investigated.

4.
Ann Clin Lab Sci ; 52(5): 831-837, 2022 Sep.
Article in English | MEDLINE | ID: covidwho-2073089

ABSTRACT

Tuberculosis (TB) and SARS-CoV-2 (COVID-19) are two important infectious diseases causing morbidity and mortality worldwide. Active TB infection can stimulate host immune responses and together with COVID-19, may lead to cytokine storm and immune dysregulation leading to multi-organ failure. We present a rare case of both miliary tuberculosis and SARS-CoV-2 co-infection in an infant who was a 6-month-old previously healthy term boy. He had persistent cough and congestion, became severely ill, and was brought to the emergency department. He was found to be COVID-19 positive by PCR test. Laboratory studies showed pancytopenia, elevated inflammatory markers, and an abnormal coagulation profile with coagulopathy. He developed strokes, severe sepsis, and electrolyte abnormalities, and declined rapidly within 6 days. Autopsy examination showed multifocal micro-abscesses in multiple organs, which on microscopic examination showed necrotic foci teeming with Mycobacteria and were culture positive for M. tuberculosis Neuropathological examination showed infarction in the right middle and posterior cerebral artery territories. This patient helps illuminate some immunological and pathological aspects of two co-occurring infectious diseases and the susceptibility for the development of fatal complications with SARS-CoV-2 infection in the pediatric population.


Subject(s)
COVID-19 , Mycobacterium tuberculosis , Tuberculosis, Miliary , Child , Male , Humans , Infant , Tuberculosis, Miliary/complications , Tuberculosis, Miliary/diagnosis , Tuberculosis, Miliary/pathology , COVID-19/complications , SARS-CoV-2 , Electrolytes
5.
Vaccines (Basel) ; 10(10)2022 Oct 01.
Article in English | MEDLINE | ID: covidwho-2066613

ABSTRACT

The current report presents the case of a 76-year-old man with Parkinson's disease (PD) who died three weeks after receiving his third COVID-19 vaccination. The patient was first vaccinated in May 2021 with the ChAdOx1 nCov-19 vector vaccine, followed by two doses of the BNT162b2 mRNA vaccine in July and December 2021. The family of the deceased requested an autopsy due to ambiguous clinical signs before death. PD was confirmed by post-mortem examinations. Furthermore, signs of aspiration pneumonia and systemic arteriosclerosis were evident. However, histopathological analyses of the brain uncovered previously unsuspected findings, including acute vasculitis (predominantly lymphocytic) as well as multifocal necrotizing encephalitis of unknown etiology with pronounced inflammation including glial and lymphocytic reaction. In the heart, signs of chronic cardiomyopathy as well as mild acute lympho-histiocytic myocarditis and vasculitis were present. Although there was no history of COVID-19 for this patient, immunohistochemistry for SARS-CoV-2 antigens (spike and nucleocapsid proteins) was performed. Surprisingly, only spike protein but no nucleocapsid protein could be detected within the foci of inflammation in both the brain and the heart, particularly in the endothelial cells of small blood vessels. Since no nucleocapsid protein could be detected, the presence of spike protein must be ascribed to vaccination rather than to viral infection. The findings corroborate previous reports of encephalitis and myocarditis caused by gene-based COVID-19 vaccines.

6.
Open Neurology Journal ; 16 (no pagination), 2022.
Article in English | EMBASE | ID: covidwho-2065269

ABSTRACT

Objective: After the outbreak of the global pandemic caused by SARS-CoV-2 infection at the end of the year 2019, it took one year to start vaccinatioagainst this infection with products from various manufacturers. As of November 2021, more than 8 billion vaccine doses against COVID-19 havbeen administered, which is essentially linked to a spike in adverse events reports following these vaccinations, including a number of neurologicaadverse events. Case Report: We report a case of a 71-year-old patient with lethal fulminant onset of Guillain-Barre syndrome after the second dose of mRNA vaccintozinameran. This is, to our best knowledge, the first case report of this adverse event supported by autopsy and histological examination. Thpatient presented with progressive ascending weakness and paresthesia, with typical cytoalbuminologic dissociation in cerebrospinal fluid ansevere motoric and sensitive axonal-demyelinating polyneuropathy on electromyography. The patient's history and complex diagnostic workup dinot reveal any other possible causative factors. The patient did not respond to the treatment with intravenous immunoglobulins and died 10 daylater due to aspiration bronchopneumonia as a complication of respiratory muscles paralysis. Conclusion(s): Most of the reported adverse reactions following COVID-19 vaccination include mild or moderate events noticed in the post-vaccination periodhowever, reports of possible lethal outcomes are no exception. Still, the overall incidence of GBS after vaccination does not significantly exceed itincidence in the general population. Each such report should be carefully examined by a team of specialists to prevent overestimation of lethaadverse events linked to vaccinations, especially in fatalities that happen in the post-vaccination period. Copyright © 2022 Mosna et al.

7.
Medicina (Kaunas) ; 58(10)2022 Sep 29.
Article in English | MEDLINE | ID: covidwho-2066245

ABSTRACT

We report the case of a 34-year-old male patient, a bodybuilding trainer and user of anabolic androgenic steroids (AASs) for 16 years. He was found in cardio-respiratory arrest in his home. By performing a medico-legal autopsy, a severe form of COVID-19, aortic atherosclerotic plaques, and an old myocardial infarction was found. The SARS-CoV-2 RT-PCR test on necroptic lung fragments was positive, with a B.1.258 genetic line. The histopathological examinations showed microthrombi with endothelitis in the cerebral tissue, massive pulmonary edema, diffuse alveolar damage grade 1, pulmonary thromboembolism, hepatic peliosis, and severe nesidioblastosis. The immunohistochemical examinations showed SARS-CoV-2 positive in the myocardium, lung, kidneys, and pancreas. ACE-2 receptor was positive in the same organs, but also in the spleen and liver. HLA alleles A*03, A*25, B*18, B*35, C*04, C*12, DRB1*04, DRB1*15, DQB1*03, DQB1*06 were also identified. In conclusion, death was due to a genetic predisposition, a long-term abuse of AASs that favored the development of a pluriorganic pathological tissue terrain, and recent consumption of AASs, which influenced the immune system at the time of infection.


Subject(s)
COVID-19 , Male , Humans , Adult , Autopsy , SARS-CoV-2 , Testosterone Congeners , Steroids
8.
Int J Mol Sci ; 23(19)2022 Oct 01.
Article in English | MEDLINE | ID: covidwho-2066135

ABSTRACT

Sudden death is defined as the unexpected death of a healthy person that occurs within the first hour of the onset of symptoms or within 24 h of the victim being last seen alive. In some of these cases, rare deleterious variants of genes associated with inherited cardiac disorders can provide a highly probable explanation for the fatal event. We report the case of a 21-year-old obese woman who lost consciousness suddenly in a public place and was pronounced dead after hospital admission. Clinical autopsy showed an inconclusive gross examination, while in the histopathological analysis an eosinophilic inflammatory focus and interstitial fibrosis in the sino-atrial node were found. Molecular autopsy revealed an intronic variant in the KCNQ1 gene (c.683 + 5G > A), classified as likely pathogenic for long QT syndrome according to the guidelines provided by the American College of Medical Genetics and Genomics. Therefore, there were many anomalies that could have played a role in the causation of the sudden death, such as the extreme obesity, the cardiac anomalies and the KNCQ1 variant. This case depicts the difficult interpretation of rare cardiac structural abnormalities in subjects carrying rare variants responsible for inherited arrhythmic disorders and the challenge for the forensic pathologist to make causal inferences in the determinism of the unexpected decease.


Subject(s)
Long QT Syndrome , Sinoatrial Node , Adult , Autopsy , Death, Sudden, Cardiac/etiology , Death, Sudden, Cardiac/pathology , Female , Humans , KCNQ1 Potassium Channel , Long QT Syndrome/complications , Long QT Syndrome/genetics , Sinoatrial Node/pathology , Young Adult
9.
Histopathology ; 81:13-14, 2022.
Article in English | Academic Search Complete | ID: covidwho-2063713

ABSTRACT

Increasing Traumatic Brain Injury Incidence during COVID-19 Pandemic in the Emergency Department of Cipto Mangunkusumo National General Hospital-A National Referral Hospital in Indonesia. Incidence of methamphetamine use in homicide victims - a retrospective study L Tan SP 1 sp , L Stephenson SP 2 sp , R Byard SP 3 sp SP I 1 i sp I Adelaide Medical School, The University of Adelaide, Adelaide, South Australia, Australia;i SP I 2 i sp I School of Biomedicine, The University of Adelaide, Adelaide, South Australia, Australia;and i SP I 3 i sp I Forensic Science South Australia, Adelaide i B Background: b Methamphetamine use is increasing in the Australian community. B Result: b There was a decrease in admission rate due to TBI during COVID-19 pandemic compared with the previous year (135 (54.9%) vs 111 (45.1%)). [Extracted from the article] Copyright of Histopathology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)

10.
American Journal of Transplantation ; 22(Supplement 3):598-599, 2022.
Article in English | EMBASE | ID: covidwho-2063361

ABSTRACT

Purpose: Therapies for COVID-19 in immunocompromised (IC) patients (pts), including transplant (tx) pts, are limited. We describe our experience with ALVR109, an allogeneic, partially HLA-matched T-cell product, given through emergency investigational new drug (eIND) application to 4 consecutive IC pts with protracted COVID-19. Method(s): To measure SARS-CoV-2 viral loads, SARS-2 RNA was quantified by RT-PCR (N gene) in plasma and saliva. ALVR109 was manufactured for Allovir at Baylor College of Medicine. Result(s): Between May and October 2021, ALVR109 was given to 4 IC pts with COVID-19 (details in Table 1). 2 pts had lymphoma (1 post auto-tx) and 2 had lung tx. All pts had SARS-CoV-2 RNA detected in plasma (viremia) in the weeks leading up to ALVR109 administration. Infusions (20-40 million cells (MC) per dose) were well-tolerated with no adverse events. Prior to ALVR109, pts 1 and 3 had progressive COVID-19 and ongoing SARS-CoV-2 viremia despite monoclonal antibodies (mABs) and remdesivir. Following ALVR109 administration both patients had a decrease in viremia with marked clinical improvement in pt 1, but both eventually died from their underlying disease. Viral loads (plasma/saliva) and functional scores for pt 1 are shown in the figure. Autopsy of pt 3 showed no evidence of SARS-CoV-2 infection by lung in-situ hybridization (ISH). Pts 2 and 4 received ALVR109 as adjunctive therapy to mABs and remdesivir;viremia continued to decline following ALVR109 and both pts survived and were discharged home. Conclusion(s): This initial experience suggests a potential role of ALVR109 in the treatment of IC and tx pts with COVID-19. SARS-CoV-2-specific T-cells appear to be safe and may control viremia in IC pts. Larger studies are needed to confirm this observation, define the best candidates for ALVR109, and determine optimal timing of administration. (Table Presented).

11.
Chest ; 162(4):A877, 2022.
Article in English | EMBASE | ID: covidwho-2060716

ABSTRACT

SESSION TITLE: Critical Care Infections SESSION TYPE: Case Reports PRESENTED ON: 10/19/2022 09:15 am - 10:15 am INTRODUCTION: Francisella tularensis is a zoonotic disease by an aerobic, gram negative coccobacillus. It is transmitted by exposure to infected animal or vectors in individuals who landscape or camp. Common symptoms are fever, chills, anorexia, and headache. Abdominal tularemia can present with abdominal pain, emesis, diarrhea, and rarely intestinal ulceration and hemorrhage. It is treated with aminoglycosides, fluoroquinolones and tetracycline. CASE PRESENTATION: 38-year-old male presented with fever, cough, anorexia, and black stool for 5 days. Patient worked as a landscaper. He has no pets, travel history or sick contacts. He does not take any medications at home. Physical exam was significant for sinus tachycardia and rhonchi of right upper lobe. Significant labs include WBC of 9.8 with 41% bands, hemoglobin 15.5, sodium 125, procalcitonin 27.3, and lactic acid 1.8. COVID-19, MRSA, Legionella and Pneumococcal urine antigen were negative. CTA chest revealed mass-like opacity in right upper lobe with multiple bilateral pulmonary nodules. Lower respiratory culture showed Candida albicans. Patient was empirically started on ceftriaxone and azithromycin. He was transferred to intensive care for worsening respiratory status and was placed on non-invasive ventilation on hospital day 1. Antibiotics were broadened to ceftaroline and levofloxacin due to suspicion of tularemia. Amphotericin B was added. Labs for Histoplasma, Blastomyces, TB, Leptospira, and HIV were negative. Patient then suffered a cardiac arrest on hospital day 2 after having large brown secretions pouring from his mouth. Cardiopulmonary resuscitation was initiated and patient was intubated and started on vasopressors with return of spontaneous circulation. Massive blood transfusion protocol was initiated. Emergent bedside upper endoscopy showed large blood clot adherent to duodenal ulcer. Interventional radiology planned on performing gastric duodenal artery embolization. However, patient suffered two more cardiac arrest with resuscitation efforts terminated per family request. Karius Digital Culture later was positive for Francisella tularensis. Autopsy revealed diffuse alveolar hemorrhage, hilar lymphadenopathy, and perforated duodenal ulceration with large adherent clot. DISCUSSION: Gastrointestinal tularemia is rare and usually from drinking contaminated water or oral inoculation of bacteria. Intestinal tract involvement can present with mesenteric lymphadenopathy and ulcerative lesions resulting in gastrointestinal bleeding with case fatality rate of 50%. Even though this is noted in the literature, to our knowledge no case reports have been published. CONCLUSIONS: Careful history taking and early identification of risk factors are important when severe tularemia infection is suspected such as in individuals with extensive outdoor activities. Treatment should be empirically initiated in high risk patients. Reference #1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585636/ Reference #2: https://casereports.bmj.com/content/2017/bcr-2017-22125. Reference #3: Altman GB, Wachs JE. Tularemia: A pathogen in nature and a biological weapon. Aaohn Journal. 2002 Aug;50(8):373-9. DISCLOSURES: No relevant relationships by Maria Haider Baig

12.
Chest ; 162(4):A854, 2022.
Article in English | EMBASE | ID: covidwho-2060707

ABSTRACT

SESSION TITLE: Drug-Induced and Associated Critical Care Cases Posters 2 SESSION TYPE: Case Report Posters PRESENTED ON: 10/19/2022 12:45 pm - 01:45 pm INTRODUCTION: Drug-induced hepatotoxicity is a well-known occurrence from a variety of different medications. However, phenobarbital (PHB) induced hepatotoxicity has not been well studied, and acute liver injury from PHB even less so. In this case, although our patient had many reasons to develop acute liver failure, including alcohol and toluene exposure, timing and investigations seem to point to PHB being responsible. CASE PRESENTATION: Patient is a 39 y.o male with past medical history significant for hepatitis A and B, hyperlipidemia and alcohol abuse who was found unresponsive by EMS after friends reported witnessing patient drinking alcohol and sniffing paint thinner. Patient remained unresponsive on arrival and was intubated and transferred to the MICU. Patient was afebrile with BP 100/55 and otherwise normal vital signs. Significant labs on presentation included a WBC of 8.15, CO2 of 16, lactic acid of 3.6 and mildly elevated transaminases (ALT: 59, AST: 48). Urine toxicology was positive for marijuana. EKG, chest x-ray and CT Head without contrast unremarkable. COVID negative. Video EEG was negative except for generalized slowing. On hospital day 3, patient was increasingly agitated, at which point phenobarbital was started due to concerns for alcohol withdrawal. Hepatic function panel the following mornings showed significant increases in transaminases (ALT: 972 and 5,746, AST: 790 and 4,805) and total bilirubin (6.8 and 11.4), and mild increase in alkaline phosphatase (112 and 125), respectively. Hepatitis panel, acetaminophen level and salicylate level were unremarkable. RUQ ultrasound was also negative for pathology. Gastroenterology was consulted, who recommended starting NAC protocol. Phenobarbital was discontinued. Hepatic function panel the following morning showed significant improvement. Liver transplant was considered, however LFTs continued to downtrend and remainder of hospital course was unremarkable. DISCUSSION: PHB is an anticonvulsant developed primarily for seizure management. However its use has expanded to alcohol withdrawal and even sedative withdrawal. Studies have demonstrated in vitro liver toxicity as well as idiosyncratic reactions and acute liver failure in children (1) (2), with minimal documentation in adults. And while there has even been histological analysis with linkage of chronic phenobarbital use to hepatic necrosis and granulomatous formation (3), there has been minimal documentation regarding acute liver failure in an adults taking phenobarbital. CONCLUSIONS: In conclusion, it is clear that phenobarbital played a significant role in this patient's liver injury and may need to be considered in future episodes of acute liver injury with unclear etiology. Reference #1: Li AM, Nelson EA, Hon EK, Cheng FW, Chan DF, Sin NC, Ma KC, Cheung KL, Fok TF. Hepatic failure in a child with anti-epileptic hypersensitivity syndrome. J Paediatr Child Health. 2005 Apr;41(4):218-20. doi: 10.1111/j.1440-1754.2005.00591.x. PMID: 15813878;PMCID: PMC7166358. Reference #2: Roberts EA, Spielberg SP, Goldbach M, Phillips MJ. Phenobarbital hepatotoxicity in an 8-month-old infant. J Hepatol. 1990 Mar;10(2):235-9. doi: 10.1016/0168-8278(90)90058-y. PMID: 2332596. Reference #3: Di Mizio Di Mizio, G., Gambardella, A., Labate, A., Perna, A., Ricci, P., & Quattrone, (2007). Hepatonecrosis and cholangitis related to long-term phenobarbital therapy: An autopsy report of two patients. Seizure, 16(7), 653–656. https://doi.org/10.1016/j.seizure.2007.05.008 DISCLOSURES: No relevant relationships by Zachary Banbury No relevant relationships by Michael Basir No relevant relationships by Inessa Bronshteyn No relevant relationships by Kyle Foster No relevant relationships by Anna-Belle Robertson

13.
Chest ; 162(4):A755, 2022.
Article in English | EMBASE | ID: covidwho-2060683

ABSTRACT

SESSION TITLE: COVID-19 Co-Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Human cytomegalovirus (CMV) is a herpesvirus with a high prevalence that causes latent disease in immunocompetent hosts. It is an important opportunistic infection with a variety of clinical manifestations, including pneumonia, in immunocompromised patients.[1] CASE PRESENTATION: A 45-year-old man with no past medical history presented with fever and dyspnea and was positive for coronavirus disease 2019 (COVID-19). He developed acute respiratory distress syndrome (ARDS) and was intubated 13 days after presentation, but developed refractory hypoxemia requiring veno-venous extracorporeal membrane oxygenation (ECMO) (cannulated 16 days after presentation). He received a 5-day course of remdesivir and 10 days of dexamethasone 6 mg daily. His course was complicated by acute renal failure requiring continuous renal replacement therapy, septic shock due to a pseudomonal ventilator-associated pneumonia, right ventricular failure, heparin induced thrombocytopenia, and right pneumothorax requiring chest tube thoracostomy. After 4 weeks of ECMO there was lung recovery with ECMO sweep gases <1L/minute, improved radiographic appearance and tidal volumes, and decannulation was anticipated. However, he subsequently developed profound shock of unknown etiology with a rapid worsening of his lung function requiring increased ECMO support. Care was withdrawn at ECMO day 46 due to multiorgan failure. Pathology of his lungs at autopsy showed prominent intranuclear viral inclusions and positive immunohistochemistry in alveolar macrophages consistent with a diagnosis of CMV pneumonia. DISCUSSION: While CMV typically causes latent disease it can reactivate in the setting of immunosuppression and/or critical illness.[1] Patients with severe COVID-19 frequently are treated with immunosuppressive therapies, such as corticosteroids, anti-interluekin-6 therapies, and JAK inhibitors. Due to this immunosuppression, opportunistic infections have been reported in these patients.[2] It can be difficult to differentiate COVID-19 pneumonia from other respiratory infections based on imaging and lab studies alone, especially in patients with prolonged mechanical ventilation and with severe parenchymal disease requiring ECMO support. Little is known about the incidence of CMV and COVID-19 coinfection. There are several cases of biopsy-proven CMV pneumonia in immunocompromised critically ill patients with COVID-19, but this is the first reported case in an immunocompetent patient. CONCLUSIONS: This case highlights the need to maintain a high degree of suspicion for CMV pneumonia in patients with severe COVID-19 pneumonia who receive immunosuppressive therapies. While the diagnosis was made at autopsy in this case, it may be possible to arrive at an earlier diagnosis with CMV polymerase chain reaction (PCR) assays sent from the serum and bronchoalveolar lavage (as lung biopsies are usually impractical in ARDS). Reference #1: de la Hoz RE, Stephens G, Sherlock C. Diagnosis and treatment approaches of CMV infections in adult patients. J Clin Virol. 2002 Aug;25 Suppl 2:S1-12. doi: 10.1016/s1386-6532(02)00091-4. PMID: 12361752. Reference #2: Abdoli A, Falahi S, Kenarkoohi A. COVID-19-associated opportunistic infections: a snapshot on the current reports [published online ahead of print, 2021 Aug 23]. Clin Exp Med. 2021;1-20. doi:10.1007/s10238-021-00751-7 DISCLOSURES: No relevant relationships by Nancy Law No relevant relationships by Mazen Odish No relevant relationships by Robert Owens No relevant relationships by Travis Pollema No relevant relationships by Alyssa Self No relevant relationships by Cassia yi

14.
Chest ; 162(4):A623-A624, 2022.
Article in English | EMBASE | ID: covidwho-2060649

ABSTRACT

SESSION TITLE: Unusual Pneumonias SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/19/2022 12:45 pm - 1:45 pm INTRODUCTION: Invasive pulmonary aspergillosis (IPA) commonly occurs in the setting of immunosuppression. Underlying lung disease is a well-known risk factor for IPA;however, interstitial lung disease (ILD) has not been recognized as a risk factor for IPA[1]. CASE PRESENTATION: A 40-year-old male with a history of a failed kidney transplant now on hemodialysis (HD), Juvenile Rheumatoid Arthritis, Mixed Connective Tissue Disease, Aspergilloma led to right lower lobectomy a year ago, COVID-19 infection three months ago, chronic lung disease (CLD) thought to be due to Nonspecific interstitial pneumonia (NSIP) presented with dyspnea. He had several hospitalizations for respiratory failure needing intubation or NIPPV, broad-spectrum antibiotics, steroids, and HD with improved respiratory status, eventually discharged. Bronchoalveolar lavage fluid culture grew aspergillus terreus but was negative for Pneumocystis (PCP), bacteria, acid-fast bacilli, and Nocardia. The transbronchial biopsies showed mixed inflammatory type and fungal forms in one specimen. Additionally, the initially negative galactomannan converted into a serial rise in galactomannan (>3.75 Index) along with a rise in beta d-glucan (>500 pg/ml). Unfortunately, he had gaps in antifungals and was readmitted similarly. Micafungin was added for dual fungal coverage and was planned for surgical lung biopsy to characterize ILD further once his respiratory status allows. DISCUSSION: He has multiple risk factors for developing IPA, such as high-dose steroids for ILD and recent COVID infection. Initially, respiratory failure was thought to be due to exacerbation of ILD, and suspicion for IPA was low because of lack of neutropenia, negative fungal biomarkers, lack of classic findings on lung imaging, and in-hospital clinical improvement with steroids. However, the eventual course of recurrent respiratory failure while on high-dose steroids, along with gaps in antifungal therapy and continued growth of Aspergillus, made IPA the most likely diagnosis. For IPA, the mainstay of treatment is both adequate antifungal therapy and reduction in immunosuppression to the extent possible[2];however, it is unclear if his underlying ILD can tolerate steroid taper. He will need a lung transplant after adequately treating IPA. CONCLUSIONS: There are no current guidelines on simultaneously treating IPA and NSIP. It is challenging to balance reduction in immunosuppression as tolerated for ILD and concurrently maintain antifungal therapy. During this patient's hospitalization, there have been considerations of using a steroid-sparing agent for his suspected NSIP, however, in the setting of active infection, its benefit is debatable.[3] Reference #1: Matsuyama H, Miyoshi S, Sugino K, et al. Fatal Invasive Pulmonary Aspergillosis Associated with Nonspecific Interstitial Pneumonia: An Autopsy Case Report. Intern Med. 2018;57(24):3619-3624. doi:10.2169/internalmedicine.1144-18 Reference #2: Thomas F. Patterson, George R. Thompson, III, David W. Denning, Jay A. Fishman, Susan Hadley, Raoul Herbrecht, Dimitrios P. Kontoyiannis, Kieren A. Marr, Vicki A. Morrison, M. Hong Nguyen, Brahm H. Segal, William J. Steinbach, David A. Stevens, Thomas J. Walsh, John R. Wingard, Jo-Anne H. Young, John E. Bennett, Practice Guidelines for the Diagnosis and Management of Aspergillosis: 2016 Update by the Infectious Diseases Society of America, Clinical Infectious Diseases, Volume 63, Issue 4, 15 August 2016, Pages e1–e60, https://doi.org/10.1093/cid/ciw326 Reference #3: Mezger, M., Wozniok, I., Blockhaus, C., Kurzai, O., Hebart, H., Einsele, H., & Loeffler, J. (2008). Impact of mycophenolic acid on the functionality of human polymorphonuclear neutrophils and dendritic cells during interaction with Aspergillus fumigatus. Antimicrobial agents and chemotherapy, 52(7), 2644–2646. https://doi.org/10.1128/AAC.01618-07 DISCLOSURES: No relevant relationships by Nasir Alhamdan No relevant relati nships by Parth Jamindar No relevant relationships by Harshitha Mergey Devender No relevant relationships by Abira Usman No relevant relationships by Vishruth Vyata

15.
Chest ; 162(4):A553, 2022.
Article in English | EMBASE | ID: covidwho-2060629

ABSTRACT

SESSION TITLE: Critical Care Presentations of TB SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 12:25 pm - 01:25 pm INTRODUCTION: We present a case of tuberculous pericarditis and cardiac tamponade due to suspected sequela of SARS-Coronavirus 19 (COVID-19) infection. It is important for clinicians to include tuberculosis (TB) in the differential diagnoses for patients presenting with presumptive viral pericarditis and tamponade. CASE PRESENTATION: A 52-year-old Hispanic man with chronic kidney disease not on hemodialysis was admitted with shortness of breath, fluid overload, hypoxemia and concern for uremic pericarditis. The patient tested positive for COVID-19 to which the symptoms were initially attributed, and he was treated with steroids, remdesevir, tocilizumab and hemodialysis. The patient incidentally had a positive QuantiFERON gold test obtained before initiating hemodialysis. On day 60 of hospitalization, the clinical exam abruptly deteriorated with stuporous mentation, hypotension, and cool skin. Bedside point of care echocardiography revealed a new large circumferential pericardial effusion with right ventricular diastolic collapse and increased respiratory variation in peak E-wave mitral inflow velocity consistent with tamponade physiology. Emergent pericardiocentesis was performed, and hemodynamic instability resolved immediately after aspiration of 750 milliliters of frank pus. Empiric antibiotics were initially given for pyogenic pericarditis. When the pericardial fluid later tested positive for acid-fast bacilli and adenosine deaminase, anti-TB therapy was started. The hospitalization was further complicated by septic shock and cardiac arrest. Though found to have a re-accumulated pericardial effusion on bedside ultrasound peri-arrest, there was no tamponade physiology (suggestive of at least a partial response to the TB treatment in the setting of overall poor underlying reserve). DISCUSSION: The coexistence of COVID-19 and tuberculous pericarditis with tamponade has been reported to date in one other case to our knowledge. COVID-19 with massive pericardial tamponade is rare and a careful diagnostic approach involving multi-modality imaging with bedside echocardiogram is invaluable in the evaluation and treatment of obstructive shock. In this case, we hypothesize that the COVID-19 infection may have led to re-activation of latent TB despite treatment of COVID-19 with corticosteroids (which are an adjunct tuberculostatic treatment in patients with tuberculous pericarditis). Tuberculous pericarditis with tamponade is a relatively uncommon manifestation of extrapulmonary TB and is a major cause of cardiovascular death and morbidity. Even with aggressive antituberculosis therapy, 30-60% of patients may need surgical pericardiectomy for constrictive pericarditis. CONCLUSIONS: This case highlights the need to consider possibility of concomitant viral and TB pericarditis in the diagnostic differential for tamponade. More histopathologic or post-mortem examinations of COVID-19 pericarditis cases are needed. Reference #1: Asif T, Kassab K, Iskander F, Alyousef T. Acute pericarditis and cardiac tamponade in a patient with COVID19: a therapeutic challenge. Eur J Case Rep Intern Med. 2020 May 6;7(6):001701. Reference #2: Barrett et al. Increase in disseminated TB during the COVID19 pandemic. Int J Tuberc Lung Dis. 2021 Feb 1;25(2):160-166. Reference #3: Wong SW, Ng J. K.X., Chia YW. Tuberculous pericarditis with tamponade diagnosed concomittantly with COVID19: a case report. Eur Heart J Case Rep. 2020 Dec 28;5(1):ytaa491. eCollection 2021 Jan. DISCLOSURES: No relevant relationships by Jaskiran Khosa No relevant relationships by Walter Klein No relevant relationships by Amy Tran No relevant relationships by Michael Ulrich

16.
Int J Environ Res Public Health ; 19(18)2022 Sep 17.
Article in English | MEDLINE | ID: covidwho-2055245

ABSTRACT

Autopsy examination, the gold standard for defining causes of death, is often difficult to apply in certain health care settings, especially in developing countries. The COVID-19 pandemic and its associated difficulties in terms of implementing autopsy examinations have made the need for alternative means of determining causes of death even more evident. One of the most interesting alternatives to the conventional autopsy is the verbal autopsy, a tool that originated in Africa and Asia in the 1950s and consists of a structured interview with the deceased's family members concerning the symptoms manifested by the person and the circumstances of death. In the early 1990s, the first doubts emerged about the validity of verbal autopsies, especially about the real reliability of the cause of death identified through this tool. The objective of the review was to identify studies that had assayed the validity of verbal autopsies through a rigorous comparison of the results that emerged from it with the results of conventional autopsies. When starting from an initial pool of 256 articles, only 2 articles were selected for final review. These are the only two original research articles in which a verbal autopsy validation process was performed by employing the full diagnostic autopsy as the gold standard. The two papers reached opposite conclusions, one suggesting adequate validity of verbal autopsy in defining the cause of death and the other casting serious doubts on the real applicability of this tool. Verbal autopsy undoubtedly has extraordinary potential, especially in the area of health and demographic surveillance, even considering the implementation that could result from the use of artificial intelligence and deep learning. However, at present, there appears to be a lack of solid data to support the robust reliability of this tool in defining causes of death.


Subject(s)
Artificial Intelligence , COVID-19 , Autopsy/methods , Cause of Death , Delivery of Health Care , Humans , Pandemics , Reproducibility of Results
17.
Front Cardiovasc Med ; 9: 970045, 2022.
Article in English | MEDLINE | ID: covidwho-2055000

ABSTRACT

We report findings in a 34-year-old female patient who presented with fulminant myocarditis 8 days after receiving the first dose of the ZF2001 RBD-subunit vaccine against coronavirus disease 2019 (COVID-19). Autopsy showed severe interstitial myocarditis, including multiple patchy infiltrations of lymphocytes and monocytes in the myocardium of the left and right ventricular walls associated with myocyte degeneration and necrosis. This report highlights the details of clinical presentations and autopsy findings of myocarditis after ZF2001 (RBD-subunit vaccine) vaccination. The correlation between vaccination and death due to myocarditis is discussed.

18.
Revista Cubana de Medicina Militar ; 51(2), 2022.
Article in Spanish | Scopus | ID: covidwho-2044866

ABSTRACT

Introduction: A case of a patient who died from COVID-19 is presented, which the authors consider to be the prototype of most of those who died from this condition, which was performed at autopsy. Objective: Disseminate the experiences in the study of the autopsy of this type of patients and contribute to its application in clinical and scientific practice. Clinical case: A 78-year-old male patient is presented, with arterial hypertension, diabetes mellitus and obesity, who began with cough, fever, runny nose, who was admitted with a diagnosis of COVID-19, progressed to severity and died 10 days later. of his admittance. The fundamental elements of the clinical history, the diagnoses of causes of death pre-mortem and post-mortem are presented. Autopsy diagnoses and quality assessment results of clinical cause of death diagnoses are specified. Conclusions: The experiences of the study of this autopsy as a prototype, reaffirm the damage caused by SARS-CoV-2 and contribute to the knowledge of this field. © 2022, Editorial Ciencias Medicas. All rights reserved.

19.
Infektsionnye Bolezni ; 20(2):16-22, 2022.
Article in Russian | EMBASE | ID: covidwho-2044282

ABSTRACT

New coronavirus infection (COVID-19) is highly contagious viral disease caused by SARS-CoV-2 leading to the pandemic. The autopsy of COVID-19 patients often showed features of previous brain diseases including neurodegeneration, previous strokes, demyelinating diseases and atherosclerosis. Patients with acute cerebrovascular accidents and severe COVID-19 had higher numbers of lethality in comparison to non-severe course of infection without cerebrovascular accidents. A comparative analysis of morphological changes in lungs of deceased patients who died in different periods of first clinical symptoms is to be conducted. Objective. Description of pathomorphological changes in deceased patients during the period of reconvalescence. Patients and methods. The analysis of 15 fatal cases which took place in Botkin Hospital with the diagnosis of ischemic stroke and new coronavirus infection in the previous 2-4 months has been held. Macro and microscope examination of brain, lungs, brachiocephalic arteries, kidneys and liver has been carried out. Results. All patients had morphological features of ischemic damage of grey matter in the brain. Beside necrosis of neurocytes with diffuse infiltration in the grey matter, hematoxylin cycles were found, in some cases they were placed in a perivascular way in choroid plexus. Also 5 patients suffered a myocardial infarction up to 3 days. 10 patients had structures disorganisation in areas of lung parenchyma with hystoacrchitectonic changes because of the fibrosis. Alveoli in some places collaborated mostly with single airway clearance. The fact that most patients had lung hemosiderosis can prove coronavirus infection suffered earlier with microcirculatory bed damage. Conclusion. Thus, morphological changes seen in the period of reconvalescence of COVID-19 is a result of pathomorphosis of changes described earlier for acute period of coronavirus infection and affect not only lungs, but also other organs and tissues. This proves systematic characteristic of the infection.

20.
Journal of Neuromuscular Diseases ; 9:S35, 2022.
Article in English | EMBASE | ID: covidwho-2043374

ABSTRACT

The COVID-19 pandemic caused by infection by SARS-CoV-2 has been associated with several neuromuscular disorders including various inflammatory neuropathies (e.g., Guillain-Barre syndrome) and myopathies (e.g., rhabdomyolysis, myositis). Temporal associations however do not imply causality. In this lecture, Dr. Amato will review the literature regarding to neuromuscular complications associated with SARS-CoV-2 infection. There are conflicting studies but if SARS-CoV-2 infection indeed causes GBS it is likely quite rare (probably < 1 case per 100000 infection). Less is known about other infl ammatory neuropathies (mononeuritis, plexitis, or CIDP). Larger epidemiological studies are needed to better define the causality. Elevated serum creatine kinase and myalgias are common in hospitalized patients with COVID-19 and in some myositis has been demonstrated on muscle biopsy. Furthermore, autopsy series have shown myositis and neuritis in patients who died from COVID-19 though virus has not been demonstrated in muscle or peripheral nerve. The inflammation is primarily felt to be due to cytokine release and not direct viral invasion of muscle or nerve. Finally, many affected patients have lingering symptoms (Long COVID) or Post-Acute Sequelae of COVID-19 (PASC) that often include neuromuscular symptoms (fatigue, weakness, lightheadedness, sensory loss and pain) that are of unclear nature.

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