SARS-CoV-2 and Its Bacterial Co- or Super-Infections Synergize to Trigger COVID-19 Autoimmune Cardiopathies.

Autoimmune cardiopathies (AC) following COVID-19 and vaccination against SARS-CoV-2 occur at significant rates but are of unknown etiology. This study investigated the possible roles of viral and bacterial mimicry, as well as viral-bacterial co-infections, as possible inducers of COVID-19 AC using proteomic methods and enzyme-linked immunoadsorption assays. BLAST and LALIGN results of this study demonstrate that SARS-CoV-2 shares a significantly greater number of high quality similarities to some cardiac protein compared with other viruses; that bacteria such as Streptococci, Staphylococci and Enterococci also display very significant similarities to cardiac proteins but to a different set than SARS-CoV-2; that the importance of these similarities is largely validated by ELISA experiments demonstrating that polyclonal antibodies against SARS-CoV-2 and COVID-19-associated bacteria recognize cardiac proteins with high affinity; that to account for the range of cardiac proteins targeted by autoantibodies in COVID-19-associated autoimmune myocarditis, both viral and bacterial triggers are probably required; that the targets of the viral and bacterial antibodies are often molecularly complementary antigens such as actin and myosin, laminin and collagen, or creatine kinase and pyruvate kinase, that are known to bind to each other; and that the corresponding viral and bacterial antibodies recognizing these complementary antigens also bind to each other with high affinity as if they have an idiotype-anti-idiotype relationship. These results suggest that AC results from SARS-CoV-2 infections or vaccination complicated by bacterial infections. Vaccination against some of these bacterial infections, such as Streptococci and Haemophilus, may therefore decrease AC risk, as may the appropriate and timely use of antibiotics among COVID-19 patients and careful screening of vaccinees for signs of infection such as fever, diarrhea, infected wounds, gum disease, etc.

Clostridia and Enteroviruses as Synergistic Triggers of Type 1 Diabetes Mellitus.

What triggers type 1 diabetes mellitus (T1DM)? One common assumption is that triggers are individual microbes that mimic autoantibody targets such as insulin (INS). However, most microbes highly associated with T1DM pathogenesis, such as coxsackieviruses (COX), lack INS mimicry and have failed to induce T1DM in animal models. Using proteomic similarity search techniques, we found that COX actually mimicked the INS receptor (INSR). Clostridia were the best mimics of INS. Clostridia antibodies cross-reacted with INS in ELISA experiments, confirming mimicry. COX antibodies cross-reacted with INSR. Clostridia antibodies further bound to COX antibodies as idiotype-anti-idiotype pairs conserving INS-INSR complementarity. Ultraviolet spectrometry studies demonstrated that INS-like Clostridia peptides bound to INSR-like COX peptides. These complementary peptides were also recognized as antigens by T cell receptor sequences derived from T1DM patients. Finally, most sera from T1DM patients bound strongly to inactivated Clostridium sporogenes, while most sera from healthy individuals did not; T1DM sera also exhibited evidence of anti-idiotype antibodies against idiotypic INS, glutamic acid decarboxylase, and protein tyrosine phosphatase non-receptor (islet antigen-2) antibodies. These results suggest that T1DM is triggered by combined enterovirus-Clostridium (and possibly combined Epstein-Barr-virus-Streptococcal) infections, and the probable rate of such co-infections approximates the rate of new T1DM diagnoses.

Burnout of Support Personnel in the Cardiac Catheterization Laboratory.

Background: Healthcare professionals experience stressors in the workplace, putting them at elevated risk for burnout. The cardiac catheterization lab is a dynamic environment with high-acuity patients; however, little has been published investigating burnout syndrome among healthcare workers. The aim of the study was to identify the prevalence, demographic, and workload factors, which contribute to burnout syndrome among this population. Methods: This is a multicenter cross-sectional study assessing burnout with the Maslach Burnout Inventory (MBI) among registered nurses and registered cardiac invasive specialists working in the catheterization/electrophysiology lab and cardiac observation unit at four hospital centers in the metro Detroit area. Results: Of the 48 participants, 69% (n = 33) were female. The overall prevalence of burnout syndrome was 33% (n = 16). Significantly more males experienced burnout than females (P < 0.05). Of the participants experiencing burnout, a greater proportion worked in the catheterization lab compared to the cardiac observation unit (93.8% vs. 6.3%). Burned-out participants worked on average more day shifts, ST-segment elevation myocardial infarction (STEMI) call shifts, and extended day shifts per month compared to those not experiencing burnout. The rate of burnout was significantly higher for individuals reporting increased stress during the pandemic (69% vs. 18%, P < 0.05). Conclusions: Registered nurses and registered cardiac invasive specialists working in the cardiac catheterization or electrophysiology lab experience elevated levels of burnout. Greater attention should be placed in identifying and optimizing workplace variables which contribute to burnout among this population.