Lemierre Syndrome is a condition that appears to have been overlooked in recent decades in clinical practice, often resulting in death or long-lasting sequelae when left undetected and untreated. Typically, it occurs following an upper respiratory tract infection, often stemming from tonsillitis, leading to thrombosis of the internal jugular vein and subsequent multiple septic emboli. Here, we present a case a 46-year-old patient with the clinical presentation of pneumogenic sepsis. Remarkably, we were able to diagnose the simultaneous presence of chronic pulmonary aspergillosis and Lemierre syndrome.

Background: Immune responses to seasonal endemic coronaviruses might have a pivotal role in protection against SARS-CoV-2. Those SARS-CoV-2-crossreactive T cells were recently described in immunocompetent individuals. Still, data on cross-reactive humoral and cellular immunity in kidney transplant recipients is currently lacking. Methods: The preexisting, crossreactive antibody, B, and T cell immune responses against SARS-CoV-2 in unexposed adults with kidney transplantation (Tx, n=14) and without (non-Tx, n=12) sampled before the pandemic were compared with 22 convalescent COVID-19 patients (Cp) applying ELISA and flow cytometry. Results: In both unexposed groups SARS-CoV-2 IgG antibodies were not detectable. Memory B cells binding spike (S) protein SARS-CoV-2 were detected in unexposed individuals (64% Tx, 50% non-Tx) and higher frequencies after infection (80% Cp). The numbers of SARS-CoV-2-reactive T cells were comparable between Tx and non-Tx. Of note, SARS-CoV-2-reactive follicular T helper (Tfh) cells were present in 61% of the unexposed cohort in both, Tx and non-Tx. Conclusions: Cross-reactive memory B and T cells against SARS-CoV-2 exist also in transplanted adults suggesting a primed adaptive immunity. The impact on disease course may depend on the concomitant immunosuppressive drugs.

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Aims Patients with cardiac disease are considered high risk for poor outcomes following hospitalization with COVID-19. The primary aim of this study was to evaluate heterogeneity in associations between various heart disease subtypes and in-hospital mortality. Methods and results We used data from the CAPACITY-COVID registry and LEOSS study. Multivariable Poisson regression models were fitted to assess the association between different types of pre-existing heart disease and in-hospital mortality. A total of 16 511 patients with COVID-19 were included (21.1% aged 66-75 years; 40.2% female) and 31.5% had a history of heart disease. Patients with heart disease were older, predominantly male, and often had other comorbid conditions when compared with those without. Mortality was higher in patients with cardiac disease (29.7%; n= 1545 vs. 15.9%; n= 1797). However, following multivariable adjustment, this difference was not significant [adjusted risk ratio (aRR) 1.08, 95% confidence interval (CI) 1.02-1.15; P = 0.12 (corrected for multiple testing)]. Associations with in-hospital mortality by heart disease subtypes differed considerably, with the strongest association for heart failure (aRR 1.19, 95% CI 1.10-1.30; P <0.018) particularly for severe (New York Heart Association class III/IV) heart failure (aRR 1.41, 95% CI 1.20-1.64; P < 0.018). None of the other heart disease subtypes, including ischaemic heart disease, remained significant after multivariable adjustment. Serious cardiac complications were diagnosed in <1% of patients. Conclusion Considerable heterogeneity exists in the strength of association between heart disease subtypes and in-hospital mortality. Of all patients with heart disease, those with heart failure are at greatest risk of death when hospitalized with COVID-19. Serious cardiac complications are rare during hospitalization. [GRAPHICS] .

AbstractAimsPatients with cardiac disease are considered high risk for poor outcomes following hospitalization with COVID-19. The primary aim of this study was to evaluate heterogeneity in associations between various heart disease subtypes and in-hospital mortality.Method and resultsWe used data from the CAPACITY-COVID registry and LEOSS study. Multivariable Poisson regression models were fitted to assess the association between different types of pre-existent heart disease and in-hospital mortality. 16,511 patients with COVID-19 were included (21.1% aged 66 – 75 years; 40.2% female) and 31.5% had a history of heart disease. Patients with heart disease were older, predominantly male and often had other comorbid conditions when compared to those without. Mortality was higher in patients with cardiac disease (29.7%; n=1545 versus 15.9%; n=1797). However, following multivariable adjustment this difference was not significant (adjusted risk ratio (aRR) 1.08 [95% CI 1.02 – 1.15; p-value 0.12 (corrected for multiple testing)]). Associations with in-hospital mortality by heart disease subtypes differed considerably, with the strongest association for heart failure aRR (1.19 [1.10 – 1.30]; p-value <0.018) particularly for severe NYHA III/IV) heart failure (aRR 1.41 [95% CI 1.20 – 1.64; p-value <0.018]. None of the other heart disease subtypes, including ischemic heart disease, remained significant after multivariable adjustment. Serious cardiac complications were diagnosed in <1% of patients.ConclusionConsiderable heterogeneity exists in the strength of association between heart disease subtypes and in-hospital mortality. Of all patients with heart disease, those with heart failure are at greatest risk of death when hospitalized with COVID-19. Serious cardiac complications are rare.

Introduction Since the early SARS-CoV-2 pandemic, cancer patients have been assumed to be at higher risk for severe COVID-19. Here, we present an analysis of cancer patients from the LEOSS (Lean European Open Survey on SARS-CoV-2 Infected Patients) registry to determine whether cancer patients are at higher risk. Patients and methods We retrospectively analyzed a cohort of 435 cancer patients and 2636 non-cancer patients with confirmed SARS-CoV-2 infection, enrolled between March 16 and August 31, 2020. Data on socio-demographics, comorbidities, cancer-related features and infection course were collected. Age-, sex- and comorbidity-adjusted analysis was performed. Primary endpoint was COVID-19-related mortality. Results In total, 435 cancer patients were included in our analysis. Commonest age category was 76–85 years (36.5%), and 40.5% were female. Solid tumors were seen in 59% and lymphoma and leukemia in 17.5% and 11% of patients. Of these, 54% had an active malignancy, and 22% had recently received anti-cancer treatments. At detection of SARS-CoV-2, the majority (62.5%) presented with mild symptoms. Progression to severe COVID-19 was seen in 55% and ICU admission in 27.5%. COVID-19-related mortality rate was 22.5%. Male sex, advanced age, and active malignancy were associated with higher death rates. Comparing cancer and non-cancer patients, age distribution and comorbidity differed significantly, as did mortality (14% vs 22.5%, p value < 0.001). After adjustments for other risk factors, mortality was comparable. Conclusion Comparing cancer and non-cancer patients, outcome of COVID-19 was comparable after adjusting for age, sex, and comorbidity. However, our results emphasize that cancer patients as a group are at higher risk due to advanced age and pre-existing conditions.

Infections in immunosuppressed patients represent a particular challenge in the diagnostics and treatment. They often present with atypical and particularly severe courses, for which rapid diagnostics and treatment are decisive for treatment success. Opportunistic infections with human herpes viruses occur not only more frequently in immunocompromised patients compared to healthy people but also represent a special challenge. In the treatment of immunosuppressed patients, e.g. with human immunodeficiency virus infections and patients with solid organ transplantations, infections with herpes simplex virus, varicella zoster virus, Epstein-Barr virus and cytomegalovirus are particularly important. The symtoms are very variable, ranging from asymptomatic detection of viremia to vital life-threatening organ manifestations. This review article describes the most important clinical presentations of these opportunistic infections. Furthermore, the diagnostic, therapeutic and prophylactic strategies for human herpes viruses are summarized.

Abstract Background and Aims B cell activating factor (BAFF) is a cytokine which drives B cell survival and maturation. Several studies have shown that elevated BAFF levels in renal transplant patients are associated with increased risk for the development of donor specific antibodies and antibody mediated rejection. It was the aim of this study to investigate neutrophils as cellular source of BAFF in renal transplant patients. Method Neutrophils (NT) were freshly isolated from whole blood of healthy controls (HC) and renal transplant patients (RTX). After isolation, purity of neutrophils was usually above 98%. Neutrophils were stimulated with LPS or TNFα in presence of Granulocyte-colony stimulating factor (GCSF) or Granulocyte macrophage colony-stimulating factor (GMCSF). In selected conditions, FK506 or rapamycin was added. Supernatants were harvested after 20 hours of culture and BAFF levels were determined by ELISA. Results GCSF/TNFα and GCSF/LPS were the most potent stimuli leading to BAFF secretion of NT in HC (403 ±64 pg/ml and 421 ±69 pg/ml). NT derived RTX showed similar capacity to secrete BAFF as compared to HC (GCSF/TNFα: 515 ±31 pg/ml and GCSF/LPS: 539.4 ±36 pg/ml). Treatment of cultures with rapamycin reduced BAFF levels (515 ±100 pg/ml vs. 348 ±27 pg/ml, p<0.001). Treatment with FK506 was less efficacious (515 ±31 pg/ml vs. 465 ±31 pg/ml, p=0.01). Conclusion NT may enhance of B cell maturation and survival via BAFF. BAFF-secretion by NT can be suppressed with mTOR inhibitors. In renal transplantation, NT might promote formation of allo-antibodies and drive antibody mediated rejection.

Die autosomal-dominante polyzystische Nierenerkrankung („autosomal dominantpolycystic kidneydisease“,ADPKD) ist mit einer Inzidenz von etwa 1:1000 eine der häufigsten Erberkrankungen beim Menschen. Autosomal-dominant vererbt werden Mutationen des PKD1oderPKD2-Gens,welche für die Proteine Polycystin-1 bzw. Polycystin-2 kodieren. Diese Proteine sind unter physiologischen Bedingungen in der Zellmembran lokalisiert. Ein Verlust führt zu der für die Erkrankung charakteristischen Zystenbildung. Mit Zunahme der Anzahl und der Größe der Zysten geht ein chronisch-progredienter Verlust der Nierenfunktion einher. Nachdem eine vermehrte Expression von Aquaporin-1und -2-Kanälen in den Zysten identifiziert worden war, zeigte der pharmakologische Einsatz des 2015 zugelassenen Vasopressin-2Antagonisten Tolvaptan erstmalig eine signifikante Reduktion des Nierenfunktionsverlusts [3, 4, 4]. Die durch die ADH(antidiuretisches Hormon)-Hemmung vermittelte Polyurie mit bis zu 7 l täglich führt zu der zum Teil schlechten subjektiven Therapieverträglichkeit. Auch ein Transaminasenanstieg erfordert eineTherapiebeendigung [2, 3]. Ein alternativer, vielversprechender Ansatz auf der Suche nach weiteren Therapieoptionen über das detaillierte Verständnis der veränderten Signalwege in der ADPKD scheint die Hemmung des JAK(Januskinase, „just another kinase“)STAT(Signaltransduktoren und Aktivatoren der Transkription)-Signalwegs zu sein. Entsprechende pharmakologische Interventionen reduzierten in ersten Untersuchungen die Zystenbildung sowie das Zystenvolumen und führten zu einer geringeren Einschränkung der glomerulären Filtrationsrate (GFR; [1, 2, 5]).

Results of recent studies in renal transplant recipients indicated an adjunct role of mTOR kinase activity in pharmacodynamic drug monitoring used for the dosage adjustment of calcineurin inhibitors (CNI) and mammalian target of rapamycin inhibitors (mTORi) used also as immunosuppressive therapy also in lung transplant recipients. Due to immunosuppression these patients are at risk for cytomegalovirus (CMV) reactivation. CMV replication is dependent on the activity of the mammalian target of rapamycin (mTOR) pathway. Therefore, it was studied whether mTOR activity (indicated by the phosphorylation status of p70S6 in T-cells) is associated with CMV reactivation in patients and whether this could be used for therapeutic monitoring of the immunosuppression.