Fatal 1918 pneumonia case complicated by erythrocyte sickling.
Ontology highlight
ABSTRACT:
SUBMITTER: Sheng ZM
PROVIDER: S-EPMC3294594 | biostudies-literature | 2010 Dec
REPOSITORIES: biostudies-literature
Publications
Fatal 1918 pneumonia case complicated by erythrocyte sickling.
Sheng Zong-Mei ZM Chertow Daniel S DS Morens David M DM Taubenberger Jeffery K JK
Emerging infectious diseases 20101201 12
Similar Datasets
Project description:A 74-year-old man with no co-morbidities presented to hospital with a 3-day history of diarrhoea and vomiting. He met the modified Duke's criteria for definite infective endocarditis and was immediately started on an intravenous antibiotic. Over Days 1-9, he developed renal failure. On Day 10, he was transferred to a tertiary hospital for mitral valve replacement. However, he tested positive for SARS-CoV-2 on arrival at the tertiary hospital, which delayed his surgery. He underwent bi-weekly nasopharyngeal swabs for SARS-CoV-2 with a plan to operate as soon as he tested negative, or as soon as his incubation period for COVID-19 pneumonia had elapsed. Unfortunately, he died on Day 31 from acute respiratory distress syndrome secondary to COVID-19 pneumonia. We describe the challenges in deciding on the optimal timing for valve replacement. We conclude by suggesting that earlier valve replacement may result in better outcomes.
| S-EPMC8713583 | biostudies-literature
Project description:IntroductionNF is a life-threatening infection and progressive disease resulting in widespread fulminant tissue destruction. It is rarely caused by Group B Streptococcus pneumonia. Early management with surgical removal of devitalized tissue and urgent antibiotic administration are key therapies.AimThe aim of this report is to highlight the importance of atypical microorganisms seen in NF.MethodA case presentation and cohort summary of reported NF cases secondary to SPN from the year 2011 to 2020.ResultsWe report the case of a 67-year-old male, not on immune-suppressive medications, admitted to our intensive care unit with septic shock and multiorgan failure secondary to left leg NF following a 3-week history of cactus prick with an SPN bacteraemia and LRINEC score of 5 on admission. He required multiple surgical debridements and was commenced on appropriate antibiotics. Despite continuous vasopressor supportive therapy, high flux CRRT, and IVIG, our patient died after an 8-day inpatient stay. A 10-year review showed only 5 reported GBSPn NF cases with an associated mortality rate of 40%.ConclusionA high clinical suspicion of SPN infections in NF is required to avoid high mortality with early diagnosis and targeted anti-microbial therapy. Severity scores may not align with clinical severity.
| S-EPMC9216318 | biostudies-literature
Project description:Sickle cell disease is induced by a mutation that converts normal adult hemoglobin to sickle hemoglobin (HbS) and engenders intracellular polymerization of deoxy-HbS and erythrocyte sickling. Development of anti-sickling therapies requires quantitative understanding of HbS polymerization kinetics under organ-specific conditions, which are difficult to assess with existing experimental techniques. Thus, we developed a kinetic model based on the classical nucleation theory to examine the effectiveness of potential anti-sickling drug candidates. We validated this model by comparing its predictability against prior in vivo and in vitro experimental results. We used the model to quantify the efficacy of sickling inhibitors and obtain results consistent with recent screening assays. Global sensitivity analysis on the kinetic parameters in the model revealed that the solubility, nucleation rate prefactor, and oxygen affinity are quantities that dictate HbS polymerization. This finding provides quantitative guidelines for the discovery of intracellular processes to be targeted by sickling inhibitors.
| S-EPMC6703859 | biostudies-literature
Project description:BackgroundAlthough the prevalence of pneumoconiosis has been decreasing due to improvements in working conditions and regular health examinations, occupational hygiene measures are still being established. Plasterers encounter a number of hazardous materials that may be inhaled in the absence of sufficient protection.Case presentationA 64-year-old man who plastered without any dust protection for more than 40 years was referred to our hospital with suspected interstitial pneumonia. Mixed dust pneumoconiosis and an unusual interstitial pneumonia (UIP) pattern with fibroblastic foci were diagnosed by video-assisted thoracoscopic surgery, and an elemental analysis detected elements included in plaster work materials. Despite the cessation of plaster work and administration of nintedanib, the patient developed advanced respiratory failure.ConclusionPlasterers are at an increased risk of pneumoconiosis and may have a poor prognosis when complicated by the UIP pattern. Thorough dust protection and careful monitoring are needed.
| S-EPMC6323823 | biostudies-literature
Project description:Small molecules that increase the oxygen affinity of human hemoglobin may reduce sickling of red blood cells in patients with sickle cell disease. We screened 38,700 compounds using small molecule microarrays and identified 427 molecules that bind to hemoglobin. We developed a high-throughput assay for evaluating the ability of the 427 small molecules to modulate the oxygen affinity of hemoglobin. We identified a novel allosteric effector of hemoglobin, di(5-(2,3-dihydro-1,4-benzodioxin-2-yl)-4H-1,2,4-triazol-3-yl)disulfide (TD-1). TD-1 induced a greater increase in oxygen affinity of human hemoglobin in solution and in red blood cells than did 5-hydroxymethyl-2-furfural (5-HMF), N-ethylmaleimide (NEM), or diformamidine disulfide. The three-dimensional structure of hemoglobin complexed with TD-1 revealed that monomeric units of TD-1 bound covalently to β-Cys93 and β-Cys112, as well as noncovalently to the central water cavity of the hemoglobin tetramer. The binding of TD-1 to hemoglobin stabilized the relaxed state (R3-state) of hemoglobin. TD-1 increased the oxygen affinity of sickle hemoglobin and inhibited in vitro hypoxia-induced sickling of red blood cells in patients with sickle cell disease without causing hemolysis. Our study indicates that TD-1 represents a novel lead molecule for the treatment of patients with sickle cell disease.
| S-EPMC4205001 | biostudies-literature
Project description:BackgroundAcute pericarditis generally follows a mild clinical course and is rarely fatal. Coronary vein involvement is rarely reported.Case summaryWe report an autopsy case of cardiac tamponade from idiopathic myopericarditis due to coronary venous perforation under the triple antithrombotic therapy. A 69-year-old man was admitted to our hospital with abnormal findings on electrocardiography, bloody pericardial effusion, and mild elevation of troponin I. Oral anti-inflammatories were started and the patient followed a benign course. However, on hospital Day 5, he suddenly suffered cardiogenic shock with pulseless electric activity due to cardiac tamponade under the combination use of the dual antiplatelet drugs and an anticoagulant drug. He died despite intense medical treatment. Autopsy revealed cardiac tamponade caused by perforation in the coronary venous wall. To the best of our knowledge, this is the first description of fatal myopericarditis as a complication of coronary venous perforation.DiscussionThe aetiology and mechanism remain unknown; however, we should take care for this rare complication in patients with acute myopericarditis and bloody effusion under the triple antithrombotic therapy.
| S-EPMC8188861 | biostudies-literature
Project description:Background: Cerebral infarction is a rare neurological complication of Kawasaki disease (KD) and occurs in the acute or subacute stage. There have been no reported cases of late-onset fatal cerebral infarction presenting over 1 year after the onset of KD. Case Presentation: A 5-month-old male patient with KD received timely intravenous immunoglobulin therapy; however, extensive coronary artery aneurysms (CAA) and coronary artery thrombosis (CAT) developed 1 month later. Anticoagulation and thrombolytic agents were suggested, but the child's parents refused. Fifteen months after KD onset, an attack of syncope left him with left hemiplegia; brain computerized tomography (CT) scans revealed cerebral infarction of the right basal ganglion without hemorrhage. Magnetic resonance angiography (MRA) revealed severe stenosis of the right middle cerebral artery, and a series of tests were performed to exclude other causes of cerebral infarction. Considering the cerebral infarction and CAT, combination therapy with urokinase and low-molecular-weight heparin (LMWH) was initiated within 24 h of syncope onset, together with oral aspirin and clopidogrel. Five days later, his clinical symptoms partially regressed and he was discharged. Unfortunately, 5 days after discharge, his clinical condition suddenly deteriorated. Repeat brain CT showed hemorrhagic stroke involving the entire left cerebral area, in addition to the previous cerebral infarction in the right basal ganglion, with obvious secondary cerebral swelling and edema, which might have been caused by previous thrombolysis. Severe cerebral hernias developed quickly. Regrettably, the patient's parents abandoned treatment because of economic factors and unfavorable prognosis, and he died soon after. Conclusions: Cerebral infarction and cerebral artery stenosis can develop late, even 1 year after the onset of KD. Pediatricians should be aware of the possibility of cerebrovascular involvement in addition to cardiac complications during long-term follow-up of KD patients. Prompt anticoagulation therapy and regular neuroimaging evaluation are essential for the management of patients with KD with giant CAA and/or CAT.
| S-EPMC8170391 | biostudies-literature
Project description:Sickle cell disease (SCD) results from a hemoglobin (Hb) mutation βGlu6 → βVal6 that changes normal Hb (HbA) into sickle Hb (HbS). Under hypoxia, HbS polymerizes into rigid fibers, causing red blood cells (RBCs) to sickle; leading to numerous adverse pathological effects. The RBC sickling is made worse by the low oxygen (O2) affinity of HbS, due to elevated intra-RBC concentrations of the natural Hb effector, 2,3-diphosphoglycerate. This has prompted the development of Hb modifiers, such as aromatic aldehydes, with the intent of increasing Hb affinity for O2 with subsequent prevention of RBC sickling. One such molecule, Voxelotor was recently approved by U.S. FDA to treat SCD. Here we report results of a novel aromatic aldehyde, VZHE-039, that mimics both the O2-dependent and O2-independent antisickling properties of fetal hemoglobin. The latter mechanism of action-as elucidated through crystallographic and biological studies-is likely due to disruption of key intermolecular contacts necessary for stable HbS polymer formation. This dual antisickling mechanism, in addition to VZHE-039 metabolic stability, has translated into significantly enhanced and sustained pharmacologic activities. Finally, VZHE-039 showed no significant inhibition of several CYPs, demonstrated efficient RBC partitioning and high membrane permeability, and is not an efflux transporter (P-gp) substrate.
| S-EPMC7679387 | biostudies-literature
Project description:BackgroundThere is a growing interest in Klebsiella variicola as a causative pathogen in humans, though its clinical features and the impact of co-infection or secondary infection with COVID-19 remain unknown.Case presentationA 71-year-old man presented with fever, altered mental status and generalized weakness and was admitted to ICU due to severe COVID-19 pneumonia. He was newly diagnosed with type II diabetes mellitus upon admission. On hospital day 3, his respiratory status deteriorated, requiring invasive mechanical ventilation. On hospital day 10, superimposed bacterial pneumonia was suspected and subsequently, broad-spectrum antibiotics were administered for the associated bloodstream infection. On hospital day 13, despite administration of active antibiotics and appropriate source control, he decompensated and died. The causative organism isolated from blood cultures was initially reported as K. pneumoniae, but it was identified as K. variicola by a genetic analysis. A representative isolate (FUJ01370) had a novel multilocus sequence typing allelic profile (gapA-infB-mdh-pgi-phoE-rpoB-tonB: 16-24-21-27-52-17-152), to which sequence type 5794 was assigned (GenBank assembly accession: GCA_019042755.1).ConclusionsWe report a fatal case of respiratory and bloodstream infection due to K. variicola complicating severe COVID-19. Co-infection or secondary infection of K. variicola in COVID-19 is likely under-recognized and can be fulminant as in this case.
| S-EPMC10052270 | biostudies-literature
Project description:BackgroundBacillus cereus is a gram-positive rod bacterium that is responsible for food poisoning. It is naturally widely distributed, and thus often contaminates cultures. Although it is rarely considered responsible, it can cause serious infections under certain conditions. However, lethal infections, especially in immunocompetent patients, are rare.Case presentationA healthy 60-year-old man developed community-acquired B. cereus pneumonia and alveolar hemorrhage unveiled by abrupt chest pain and hemoptysis with no other advance symptoms. B. cereus induced silent alveolar destruction without any local or systemic inflammatory response. Although the lesion resembled lung anthrax, there was no evidence of Bacillus anthracis toxin.ConclusionsSome isolates of B. cereus can cause anthrax-like fulminant necrotizing pneumonia in immunocompetent patients. If this type of B. cereus were used as a means of bioterrorism, it may be quite difficult to recognize as bioterrorism. We should keep B. cereus in mind as a potential pathogen of fulminant human infectious disease.
| S-EPMC6391836 | biostudies-literature