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Aim: In ENT (Ear, Nose and Throat) treatment units, medical devices for examination are commonly stored on open trays. The aim of this study is to investigate whether open storage is a relevant cause for microbiological contamination of ENT instruments during a working day. Methods: Qualitative and quantitative tests, such as imprints and swabs, were performed on the instruments and the surfaces of the treatment units in an ENT outpatient clinic at the beginning and at the end of consultation hours. The microbiological analysis of the samples focused on potential pathogens, e.g., or , bacteria of skin and oral microbiota, as well as the number of colony forming units (CFU). The samples were collected at three distinct ENT treatment units over five working days.Results: The samples taken at the beginning of consultation hours showed a low number of CFU and no pathogens. Overall, 5% of the instruments were contaminated with bacteria of skin microbiota. At the end of a working day, this rate increased significantly to 17.5% (p

Background: The arising challenges over endoscope reprocessing quality proposes to look for possibilities to measure and control the process of endoscope reprocessing.Aim: The goal of this study was to evaluate the feasibility of monitoring endoscope reprocessing with an adenosine triphosphate (ATP) based bioluminescence system.Methods: 60 samples of eight gastroscopes have been assessed from routine clinical use in a major university hospital in Germany. Endoscopes have been assessed with an ATP system and microbial cultures at different timepoints during the reprocessing. Findings: After the bedside flush the mean ATP level in relative light units (RLU) was 19,437 RLU, after the manual cleaning 667 RLU and after the automated endoscope reprocessor (AER) 227 RLU. After the manual cleaning the mean total viable count (TVC) per endoscope was 15.3 CFU/10 ml, and after the AER 5.7 CFU/10 ml. Our results show that there are reprocessing cycles which are not able to clean a patient used endoscope.Conclusion: Our data suggest that monitoring of flexible endoscope with ATP can identify a number of different influence factors, like the endoscope condition and the endoscopic procedure, or especially the quality of the bedside flush and manual cleaning before the AER. More process control is one option to identify and improve influence factors to finally increase the overall reprocessing quality, best of all by different methods. ATP measurement seems to be a valid technique that allows an immediate repeat of the manual cleaning if the ATP results after manual cleaning exceed the established cutoff of 200 RLU.

Background: Infective endocarditis (IE) poses a significant health risk, especially in patients with prosthetic heart valves. Despite advances in treatment, mortality rates remain high. This study aims to investigate the antibacterial properties of a copper titanium dioxide (4× Cu‐TiO2) coating on cardiovascular implants against Staphylococcus aureus, a common causative agent of IE. Methods: Titanium oxide carriers functionalized with copper ions were employed as an antibacterial coating for heart and vascular prostheses. The coating's antibacterial efficacy was assessed using S. aureus ATCC 29213. Microscopic evaluations were conducted on both biological and artificial materials. Antibacterial activity was qualitatively assessed via a modified disc diffusion method and quantitatively measured through colony counts in NaCl suspensions. Results: The coating process was successfully applied to all tested cardiovascular prosthetic materials. Qualitative assessments of antibacterial effectiveness revealed an absence of bacterial growth in the area directly beneath the coated valve. Quantitative evaluations showed a significant reduction in bacterial colonization on coated mechanical valves, with 2.95 × 104 CFU per valve, compared to 1.91 × 105 CFU in control valves. Conclusions: The 4× Cu‐TiO2 coating demonstrated promising antibacterial properties against S. aureus, suggesting its potential as an effective strategy for reducing the risk of bacterial colonization of cardiovascular implants. Further studies are needed to assess the longevity of the coating and its efficacy against other pathogens. [ABSTRACT FROM AUTHOR]

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which causes coronavirus disease (COVID-19), is characterized by severe respiratory distress, fever, and cough. High death rates, especially in older persons and [...]

Influenza A virus (IAV) can cause severe respiratory infection leading to significant global morbidity and mortality through seasonal epidemics. Likewise, the constantly increasing number of cancer diseases is a growing problem. Nevertheless, the understanding of the mutual interactions of the immune responses between cancer and infection is still very vague. Therefore, it is important to understand the immunological cross talk between cancer and IAV infection. In several preclinical mouse models of cancer, including melanoma and colorectal cancer, we observed that IAV infection in the lung significantly decreased the tumour burden. Concomitantly, tumour-specific CD8+ T-cells are strongly activated upon infection, both in the tumour tissue and in the lung. CD8+ T-cell depletion during infection reverses the reduced tumour growth. Interestingly, IAV infection orchestrated the migration of tumour-specific CD8+ T-cells from the tumour into the infected lung. Blocking the migration of CD8+ T-cells prevented the anti-tumoural effect. Thus, our findings show that viral respiratory infection has significant impact on the anti-tumour CD8+ T-cell response, which will significantly improve our understanding of the immunological cross talk between cancer and infection. Author summary: The Influenza A virus (IAV) causes severe respiratory infections during seasonal outbreaks, while the rising incidence of cancer presents a growing health concern, yet our understanding of the interactions between immune responses to infection and cancer is still unclear. Therefore, we aimed to decipher the immunological cross talk between cancer and IAV infection. Using preclinical mouse models of melanoma and colorectal cancer, we made intriguing observations. IAV infection in the lung led to a significant reduction in tumour growth. Additionally, the infection activated tumour-specific CD8+ T-cells, crucial components of the immune system's cancer-fighting ability, both in the lung and tumour tissue. Remarkably, when CD8+ T-cells were depleted during infection, the tumour growth reduction was reversed. It appears that IAV infection orchestrates the migration of tumour-specific CD8+ T cells from the tumour into the infected lung, since blocking migration abolished the antitumor effect. These findings shed light on the significant impact of viral respiratory infection on the anti-tumour CD8+ T-cell response, advancing our understanding of the intricate interplay between cancer and infection. Such insights hold promise for tackling these complex health challenges more effectively. [ABSTRACT FROM AUTHOR]

Broad-spectrum antibiotics are widely used with patients in intensive care units (ICUs), many of whom develop hospital- acquired infections with Pseudomonas aeruginosa. Although preceding antimicrobial therapy is known as a major risk factor for P. aeruginosa-induced pneumonia, the underlying mechanisms remain incompletely understood. Here we demonstrate that depletion of the resident microbiota by broad-spectrum antibiotic treatment inhibited TLR-dependent production of a proliferation-inducing ligand (APRIL), resulting in a secondary IgA deficiency in the lung in mice and human ICU patients. Microbiota-dependent local IgA contributed to early antibacterial defense against P. aeruginosa. Consequently, P. aeruginosa-binding IgA purified from lamina propria culture or IgA hybridomas enhanced resistance of antibiotic-treated mice to P. aeruginosa infection after transnasal substitute. Our study provides a mechanistic explanation for the welldocumented risk of P. aeruginosa infection following antimicrobial therapy, and we propose local administration of IgA as a novel prophylactic strategy., Introduction National and international point-prevalence studies show that 64%-71% of all patients in intensive care units (ICUs) receive antibiotics (1, 2) and up to 10%-51% suffer from hospital-acquired infections (HAIs) [...]

Neuropilin-1 (Nrp-1) expression on CD8+ T cells has been identified in tumor-infiltrating lymphocytes and in persistent murine gamma-herpes virus infections, where it interferes with the development of long-lived memory T cell responses. In parasitic and acute viral infections, the role of Nrp-1 expression on CD8+ T cells remains unclear. Here, we demonstrate a strong induction of Nrp-1 expression on CD8+ T cells in Plasmodium berghei ANKA (PbA)-infected mice that correlated with neurological deficits of experimental cerebral malaria (ECM). Likewise, the frequency of Nrp-1+CD8+ T cells was significantly elevated and correlated with liver damage in the acute phase of lymphocytic choriomeningitis virus (LCMV) infection. Transcriptomic and flow cytometric analyses revealed a highly activated phenotype of Nrp-1+CD8+ T cells from infected mice. Correspondingly, in vitro experiments showed rapid induction of Nrp-1 expression on CD8+ T cells after stimulation in conjunction with increased expression of activation-associated molecules. Strikingly, T cell-specific Nrp-1 ablation resulted in reduced numbers of activated T cells in the brain of PbA-infected mice as well as in spleen and liver of LCMV-infected mice and alleviated the severity of ECM and LCMV-induced liver pathology. Mechanistically, we identified reduced blood-brain barrier leakage associated with reduced parasite sequestration in the brain of PbA-infected mice with T cell-specific Nrp-1 deficiency. In conclusion, Nrp-1 expression on CD8+ T cells represents a very early activation marker that exacerbates deleterious CD8+ T cell responses during both, parasitic PbA and acute LCMV infections. Author summary: Malaria is caused by the parasite Plasmodium and remains one of the most life threatening infectious diseases worldwide. In 2021, WHO reported 247 million malaria cases and more than 600,000 deaths. In this study, we infect mice with Plasmodium berghei ANKA (PbA), a scientific model of experimental cerebral malaria (ECM), which affects the brain and is often fatal. During infection, CD8+ T cells are known to invade the brain and contribute to brain damage and inflammation through their activated and cytotoxic potential. We investigate whether T cell-expressed Neuropilin-1 (Nrp-1), a co-receptor for semaphorin and vascular endothelial growth factor (VEGF) known to play a role in immune cell activation and migration, has an impact on ECM manifestation. The results of our study demonstrate that Nrp-1 is associated with increased T cell activation and significantly aggravates the severity of ECM. Importantly, our results are also applicable to other CD8+ T cell-induced immunopathologies as we show similar effects during lymphocytic choriomeningitis virus (LCMV) infection. Together, this implies that Nrp-1 may be an early prognostic marker and blockade of Nrp-1 could be a promising target to control exacerbated T cell responses in different diseases. [ABSTRACT FROM AUTHOR]