ABSTRACT
Secondary bacterial infection is one of the important risk factors for the development of severe course and death in COVID-19. The rational choice of antibacterial therapy is based on the data of microbiological monitoring of pathogens of healthcare-associated infections. The aim of the study is to determine the main options for antibiotic therapy of Acinetobacter baumannii bloodstream infection in COVID-19 patients. Material and methods. A retrospective, single-centre, uncontrolled study of the incidence of A. baumannii bacteremia in COVID-19 patients treated at the City Clinical Hospital No. 52 in Moscow from October 2020 to September 2021 was performed. For each strain of A. baumannii sensitivity to the main antibacterial agents was determined. Genetic determinants of antibiotic resistance were studied by real-time multiplex polymerase chain reaction. The main therapeutic options for A. baumannii bloodstream infection were analyzed. Results and discussion. Bloodstream infections were diagnosed in 4.7% of hospitalized patients with COVID-19 (758/16 047). Gram-negative bacteria were the causative agents of bloodstream infections in 76% of cases. A. baumannii were isolated from the blood of 143 patients (0.89%). Detection of the pathogen in the blood of COVID-19 patients was associated with severe and extremely severe course of the disease. Most of the strains (93%) were isolated in the intensive care unit. The A. baumannii strains studied were carbapenem-resistant (CRAb) and phenotypically belonged to the XDR class. According to a PCR study, A. baumannii strains were producers of oxacillinases OXA-23, OXA-40, and OXA-51. Conclusion. The circulation of A. baumannii CRAb in intensive care units makes empiric therapy based on carbapenems irrational and ineffective. For the etiotropic therapy of A. baumannii bloodstream infection it is recommended to use combined antibiotic therapy regimens with the inclusion of polymyxin B and sulbactam.Copyright © Eco-Vector, 2022.
ABSTRACT
Pseudomonas aeruginosa can cause severe nosocomial infections and sepsis, especially in immunocompromised comorbid patients. The purpose of the study was to assess the frequency, clinical course, and the possibility of antimicrobial therapy for bloodstream infections caused by P. aeruginosa in patients with COVID-19. Material and methods. A retrospective single-center uncontrolled study was performed from October 1, 2020 to September 31, 2021 on the basis of a temporary infectious diseases hospital for patients with COVID-19 at the City Clinical Hospital No. 52, Moscow. During the analyzed period, 16 047 patients were admitted to the infectious diseases hospital. The study included 46 patients over 18 years of age with a diagnosis of COVID-19 confirmed by PCR RNA SARS-CoV-2 nasopharyngeal swab (U 07.1) and/or computed tomography (CT) of the lungs (U 07.2). Statistical data processing was carried out using the BioStat, 2009 program (AnalystSoft, USA). Results and discussion. P. aeruginosa has been isolated from the blood of 0.29% of patients with COVID-19. In the structure of bacteremia, P. aeruginosa accounted for 6.1%. In 87% of cases, pathogens were isolated from the blood of patients in the ICU. Most strains are classified as XDR phenotypes - 74% and MDR - 21.7%. The sensitivity of hospital strains of P. aeruginosa was: to colistin - 97%, to amikacin - 39.1%, meropenem - 32.6%. All patients had concomitant diseases: cardiovascular (60%), oncological (27.5%), diabetes mellitus (20%), obesity (22.5%) and others. In 47.5% of cases (19/40), the cause of bloodstream infections was ventilator-associated pneumonia. The mortality rate among patients with COVID-19 with P. aeruginosa bacteremia is 80%. Conclusion. The wide distribution of multidrug-resistant strains of P. aeruginosa limits the number of therapeutic options. In severe bloodstream infections caused by P. aeruginosa XDR, combined antibiotic therapy regimens with the inclusion of polymyxin B are advisable.Copyright © 2022 Tomsk Polytechnic University, Publishing House. All rights reserved.
ABSTRACT
Pseudomonas aeruginosa can cause severe nosocomial infections and sepsis, especially in immunocompromised comorbid patients. The purpose of the study was to assess the frequency, clinical course, and the possibility of antimicrobial therapy for bloodstream infections caused by P. aeruginosa in patients with COVID-19. Material and methods. A retrospective single-center uncontrolled study was performed from October 1, 2020 to September 31, 2021 on the basis of a temporary infectious diseases hospital for patients with COVID-19 at the City Clinical Hospital No. 52, Moscow. During the analyzed period, 16 047 patients were admitted to the infectious diseases hospital. The study included 46 patients over 18 years of age with a diagnosis of COVID-19 confirmed by PCR RNA SARS-CoV-2 nasopharyngeal swab (U 07.1) and/or computed tomography (CT) of the lungs (U 07.2). Statistical data processing was carried out using the BioStat, 2009 program (AnalystSoft, USA). Results and discussion. P. aeruginosa has been isolated from the blood of 0.29% of patients with COVID-19. In the structure of bacteremia, P. aeruginosa accounted for 6.1%. In 87% of cases, pathogens were isolated from the blood of patients in the ICU. Most strains are classified as XDR phenotypes – 74% and MDR – 21.7%. The sensitivity of hospital strains of P. aeruginosa was: to colistin – 97%, to amikacin – 39.1%, meropenem – 32.6%. All patients had concomitant diseases: cardiovascular (60%), oncological (27.5%), diabetes mellitus (20%), obesity (22.5%) and others. In 47.5% of cases (19/40), the cause of bloodstream infections was ventilator-associated pneumonia. The mortality rate among patients with COVID-19 with P. aeruginosa bacteremia is 80%. Conclusion. The wide distribution of multidrug-resistant strains of P. aeruginosa limits the number of therapeutic options. In severe bloodstream infections caused by P. aeruginosa XDR, combined antibiotic therapy regimens with the inclusion of polymyxin B are advisable. © 2022 Tomsk Polytechnic University, Publishing House. All rights reserved.
ABSTRACT
Secondary bacterial infection is one of the important risk factors for the development of severe course and death in COVID-19. The rational choice of antibacterial therapy is based on the data of microbiological monitoring of pathogens of healthcare-associated infections. The aim of the study is to determine the main options for antibiotic therapy of Acinetobacter baumannii bloodstream infection in COVID-19 patients. Material and methods. A retrospective, single-centre, uncontrolled study of the incidence of A. baumannii bacteremia in COVID-19 patients treated at the City Clinical Hospital No. 52 in Moscow from October 2020 to September 2021 was performed. For each strain of A. baumannii sensitivity to the main antibacterial agents was determined. Genetic determinants of antibiotic resistance were studied by real-time multiplex polymerase chain reaction. The main therapeutic options for A. baumannii bloodstream infection were analyzed. Results and discussion. Bloodstream infections were diagnosed in 4.7% of hospitalized patients with COVID-19 (758/16 047). Gram-negative bacteria were the causative agents of bloodstream infections in 76% of cases. A. baumannii were isolated from the blood of 143 patients (0.89%). Detection of the pathogen in the blood of COVID-19 patients was associated with severe and extremely severe course of the disease. Most of the strains (93%) were isolated in the intensive care unit. The A. baumannii strains studied were carbapenem-resistant (CRAb) and phenotypically belonged to the XDR class. According to a PCR study, A. baumannii strains were producers of oxacillinases OXA-23, OXA-40, and OXA-51. Conclusion. The circulation of A. baumannii CRAb in intensive care units makes empiric therapy based on carbapenems irrational and ineffective. For the etiotropic therapy of A. baumannii bloodstream infection it is recommended to use combined antibiotic therapy regimens with the inclusion of polymyxin B and sulbactam. © Eco-Vector, 2022.
ABSTRACT
Coronavirus infection caused by the SARS-CoV-2 virus is a multifaceted disease due to generalized vascular endothelial damage. Endothelial damage also underlies COVID-associated coagulopathy. The paper presents a case of coagulopathy causing myocardial infarction in a 43-year-old patient with no history of coronary disease. We have reviewed the available literature for the pathophysiological rationale of the assumed possibility of coronary thrombosis resulting from coagulopathy with the intact intima of the coronary arteries. Conclusion. The present observation of coronary thrombosis with radiographically intact coronary artery intima confirms the important role of coronavirus infection in triggering endothelial dysfunction. Currently, the most effective strategy for this type of coronary lesions is the use of anticoagulants and antiplatelet agents along with ECG, echocardiography and troponin level monitoring. Copyright © 2022, V.A. Negovsky Research Institute of General Reanimatology. All rights reserved.
ABSTRACT
Pneumonia is a serious complication of the new coronavirus infection, also known as COVID-19. Patients if risk groups who require ICU care and mechanical ventilation are at the highest risk to develop lung fibrosis. This review analyzes the use of cytostatic agents such as cyclophosphamide with his proven efficacy against lung fibrosis of various etiologies and considers its potential effectiveness in the treatment of post-Covid pulmonary fibrosis.
ABSTRACT
Pregnant women occupy a special place in the incidence structure of the new coronavirus infection COVID -19. Taking into account the likelihood of a more severe course of acute respiratory syndrome (ARDS) in this group, it is worth remembering the possibility of timely use of veno-venous extracorporeal membrane oxygenation (IV ECMO) in order to correct life-threatening hypoxia. At the Lapino Clinical Hospital, a cesarean section was successfully performed in a 37-year-old female patient at 20–21 weeks of gestation against the background of IV ECMO with further decannulation and discharge from the hospital. © 2021 Sklifosovsky Research Institute for Emergency Medicine. All rights reserved.
ABSTRACT
Background : Coagulopathy is among the most alarming drivers of COVID-19-induced pathology. COVID-19 can result in blockade of the microvasculature in the lungs with microthrombi. While most of the studies concern COVID-19 impact on plasma coagulation, platelet dysfunction has been reported as well. However, the mechanism of platelet malfunctioning in COVID-19 has not been described yet. Aims : To determine the mechanism of COVID-19 induced platelet disfunction. Methods : 46 patients with confirmed COVID-19 (11 non-ICU, 26 ICU, and 9 ECMO) and 26 healthy volunteers were studied (independent ethics committee of NMRC PHOI No 3/2020). Citrated whole blood samples were diluted in Tyrode's buffer and activated by collagen and TRAP-6. Platelets of healthy donors were additionally washed and pre-treated by 0.5 nM of thrombin. Samples were analyzed using BC Navios flow cytometer. Additionally, light transmission aggregometry (AP-2110 SOLAR) of citrated platelet-rich plasma (PRP) with TRAP-6 and fucoidan as activators was conducted. Results : Platelet forward scattering parameter (FSC-A) for COVID-19 patients was significantly increased compared to healthy donors. This parameter reversibly correlated with mild thrombocytopenia observed in some patients. The amount of Annexin-V positive platelets was increased in all patients as well. Relative CD42b and CD62p binding upon activation were decreased, being statistically different in non-ICU and ICU patients. Both of the parameters also correlated to CRP concentration in patient blood plasma. Platelet aggregation was reduced as well. Altogether, platelets demonstrated refractoriness resembling desensitization of receptors. To prove this hypothesis, we performed thrombin pre-treatment of healthy donor platelets, which resulted in a phenotype resembling the COVID-19. Conclusions : Platelets of COVID-19 patients demonstrate refractoriness to activation through PAR1 receptor, probably because of a previous activation with thrombin in circulation. Together with their increased size and fraction of necrotic platelets, this suggests that in COVID-19 platelets encounter thrombin in circulation.
ABSTRACT
Materials and methods: a prospective non-randomized pilot multicenter study of the informativeness and clinical significance of hemostasis laboratory tests in 1210 patients with COVID-19 in disease course, including favorable and unfavorable outcomes, was performed. Hemostasis was assessed using clotting tests and D-dimer concentration, thromboelastography (TEG) and thrombodynamics (TD). Results: comparison of COVID-19 laboratory parameters and clinical picture showed that 75% of patients have pronounced activation of the plasma coagulation system upon admission to the hospital. Hypercoagulation is recorded in all tests, reaching a maximum in patients with subtotal (CT-3) and total (CT-4) lung lesion and/or resuscitation patients with a clinical picture of pulmonary embolism and unfavorable outcome. Low molecular weight heparins (LMWH) in a standard dosage leads to suppression of the initial hypercoagulable syndrome in more than half of the patients (from 75 to 31%). All patients without LMWH laboratory effect developed thrombotic complications. For clotting tests, insufficient sensitivity to changes in hemostasis against the background of LMWH was revealed. The D-dimer test effectively correlates with the severity and outcomes of COVID-19, but is not suitable for the control of heparin therapy, which is associated with the effect of lysis of existing blood clots and the lack of response to a decrease in the coagulation activity of patients. Methods of thromboelastography and thrombodynamics effectively record a decrease in the activity of the coagulation system and can be used to control heparin therapy. The correlation coefficient between the methods was 0,77. The dynamic indices of D-dimers, TEG and TD in severe patients and, especially, in patients with fatal outcomes revealed the greatest sensitivity to the control of heparin therapy in the Thrombodynamics test, which allows, along with thrombosis, to record hypercoagulable states and the risk of bleeding, which are the outcome of thrombohemorrhagic syndrome in patients with COVID-19. Материалы и методы исследования: проведено проспективное открытое нерандомизированное пилотное многоцентровое исследование информативности и клинической значимости лабораторных тестов гемостаза у 1210 пациентов с COVID-19 в динамике заболевания, включая благоприятные и неблагоприятные исходы. Оценку гемостаза проводили с использованием клоттинговых тестов и концентрации D-димера, тромбоэластографии (ТЭГ) и тромбодинамики (ТД). Результаты: при сопоставлении лабораторных показателей и клинической картины COVID-19 показано, что у 75% больных при поступлении в стационар наблюдается выраженная активация плазменной системы свертывания. Гиперкоагуляция фиксируется по всем тестам, достигая максимума у больных с субтотальным (КТ-3) и тотальным (КТ-4) поражением легких и/или реанимационных больных с клинической картиной тромбоэмболии легочной артерии и неблагоприятным исходом. Назначение низкомолекулярных гепаринов (НМГ) в стандартной дозировке приводит к подавлению исходного гиперкоагуляционного синдрома более чем у половины больных (с 75 до 31%). Все пациенты без лабораторного эффекта НМГ развили тромботические осложнения. Для клоттинговых тестов выявлена недостаточная чувствительность к изменениям гемостаза на фоне НМГ. Тест на D-димер эффективно коррелирует с тяжестью и исходами COVID-19, но непригоден для контроля гепаринотерапии, что связано с эффектом лизиса существующих тромбов и отсутствием ответа на снижение коагуляционной активности больных. Методы ТЭГ и ТД эффективно регистрируют снижение активности свертывающей системы и могут использоваться для контроля гепаринотерапии. Коэффициент корреляции между методами составил 0,77. Заключение: динамические индексы D-димеров, ТЭГ и ТД у тяжелых больных и особенно у пациентов с летальными исходами выявили наибольшую чувствительность к контролю гепаринотерапии у теста ТД, что позволяет наряду с тромбозами фиксировать гиперкоагуляционные состояния и риск кровотечений - исходы тромбогеморрагического синдрома у больных с COVID-19.