Research Progress on the pathogenic mechanism of Streptococcus suis 2

Streptococcus suis (S.suis) is an important zoonotic pathogen that can cause many diseases in pigs, such as sepsis, arthritis, endocarditis, and meningitis, of which meningitis is the most serious. There are 35 serotypes, and serotype two is the most virulent. At the same time, Streptococcus suis serotype 2(SS2) can also infect humans, causing severe public health problems. Although SS2 has attracted significant attention worldwide, the research on its pathogenesis is still limited. The adhesion of pathogenic bacteria to the surface of host cells or tissues and its subsequent invasion and diffusion are the critical steps of pathogenic bacteria. Moreover, the interaction between pathogen and host is involved in these processes. Therefore, to study the pathogenic mechanism of pathogenic bacteria is to study the interaction between pathogenic bacteria and host. This paper described several common virulence factors, such as CPS, SLY, MRP, EF, SAO, Srt, FBPS, SadP, and Eno. Under the actions of virulence factors, SS2 adheres and colonizes to the mucosal and epithelial surface of host cells. Then SS2 invades into deeper tissues and bloodstream. If SS2 in the blood does not cause fatal sepsis, It can go to the third stage. The third stage is to cross the BBB and access the CNS and ultimately causes meningitis. During pathogenesis, SS2 interacts with multiple host cells, such as neutrophils, macrophages, epithelial cells, and microvascular endothelial cells to evade the innate or adaptive immunity of the host.

Polymorphonuclear Cells Show Features of Dysfunctional Activation During Fatal Sepsis

Sepsis and septic shock remain leading causes of morbidity and mortality for patients in the intensive care unit. During the early phase, immune cells produce various cytokines leading to prompt activation of the immune system. Polymorphonuclear leukocytes (PMNs) respond to different signals producing inflammatory factors and executing their antimicrobial mechanisms, resulting in the engulfment and elimination of invading pathogens. However, excessive activation caused by various inflammatory signals produced during sepsis progression can lead to the alteration of PMN signaling and subsequent defects in their functionality. Here, we analyzed samples from 34 patients in septic shock, focusing on PMNs gene expression and proteome changes associated with septic shock. We revealed that, compared to those patients who survived longer than five days, PMNs from patients who had fulminant sepsis were characterized by a dysfunctional hyper-activation, show altered metabolism, and recent exit from the cell cycle and signs of cellular lifespan. We believe that this multi-omics approach, although limited, pinpoints the alterations in PMNs’ functionality, which may be rescued by targeted treatments.

Lung Abscess with a Refractory Bronchopleural Fistula Saved from Potentially Fatal Sepsis by Omentoplasty and Extracorporeal Membrane Oxygenation

Controlling air leaks during thoracic drainage in patients with lung abscesses caused by bronchopleural fistulas is challenging. To reduce the occurrence of air leaks, positive pressure ventilation should be avoided whenever possible. A 69-year-old man presented with a 10-day history of gradually worsening chest pain. He had lost consciousness and was brought to the emergency room. His SpO2 was approximately 70%, and his systolic blood pressure was approximately 60 mmHg. Chest radiography and computed tomography revealed findings suggestive of a right pyothorax. Therefore, thoracic drainage was performed. However, the patient’s respiratory status did not improve, and his circulatory status could not be maintained. Therefore, extracorporeal membrane oxygenation was introduced after the improvement in circulation by noradrenaline and fluid resuscitation, resulting in adequate oxygenation and ventilation without the use of high-pressure ventilator settings. Subsequently, omentoplasty for a refractory bronchopleural fistula was successfully performed, and the air leak was cured without recurrence of the lung abscess.

Role of Interventional Radiology in the Management of Acute Cholangitis

Acute cholangitis presents with a wide severity spectrum and can rapidly deteriorate from local infection to multiorgan failure and fatal sepsis. The pathophysiology, diagnosis, and general management principles will be discussed in this review article. The focus of this article will be on the role of biliary drainage performed by interventional radiology to manage acute cholangitis. There are specific scenarios where percutaneous drainage should be preferred over endoscopic drainage. Percutaneous transhepatic and transjejunal biliary drainage are both options available to interventional radiology. Additionally, interventional radiology is now able to manage these patients beyond providing acute biliary drainage including cholangioplasty, stenting, and percutaneous cholangioscopy/biopsy.

Draft Genome Sequence of Methicillin-Resistant Staphylococcus aureus Harboring Staphylococcal Cassette Chromosome mec Type IX, Isolated from a Fatal Bacteremic Pneumonia Case

Here, we report the whole-genome sequence of a methicillin-resistant Staphylococcus aureus strain harboring staphylococcal cassette chromosome mec (SCC mec ) type IX, isolated from a fatal sepsis case. Genomic analysis revealed that the isolate was sequence type 9 and spa type t3446, carrying multiple antimicrobial-resistant genes comprising mecA , blaZ , aac(6′)-aph(2″) , aadD , ant(6)-Ia , lsa (E), dfrG , tet (M), fexA , and lnu (B).

A Narrative Review of the W, X, Y, E, and NG of Meningococcal Disease: Emerging Capsular Groups, Pathotypes, and Global Control

Neisseria meningitidis, carried in the human nasopharynx asymptomatically by ~10% of the population, remains a leading cause of meningitis and rapidly fatal sepsis, usually in otherwise healthy individuals. The epidemiology of invasive meningococcal disease (IMD) varies substantially by geography and over time and is now influenced by meningococcal vaccines and in 2020–2021 by COVID-19 pandemic containment measures. While 12 capsular groups, defined by capsular polysaccharide structures, can be expressed by N. meningitidis, groups A, B, and C historically caused most IMD. However, the use of mono-, bi-, and quadrivalent-polysaccharide-conjugate vaccines, the introduction of protein-based vaccines for group B, natural disease fluctuations, new drugs (e.g., eculizumab) that increase meningococcal susceptibility, changing transmission dynamics and meningococcal evolution are impacting the incidence of the capsular groups causing IMD. While the ability to spread and cause illness vary considerably, capsular groups W, X, and Y now cause significant IMD. In addition, group E and nongroupable meningococci have appeared as a cause of invasive disease, and a nongroupable N. meningitidis pathotype of the hypervirulent clonal complex 11 is causing sexually transmitted urethritis cases and outbreaks. Carriage and IMD of the previously “minor” N. meningitidis are reviewed and the need for polyvalent meningococcal vaccines emphasized.

Dynamic changes in human single cell transcriptional signatures during fatal sepsis

Systemic infections, especially in patients with chronic diseases, result in sepsis: an explosive, uncoordinated immune response that can lead to multisystem organ failure with a high mortality rate. Sepsis survivors and non-survivors oftentimes have similar clinical phenotypes or sepsis biomarker expression upon diagnosis, suggesting that the dynamics of sepsis in the critical early stage may have an impact on these opposite outcomes. To investigate this, we designed a within-subject study of patients with systemic gram-negative bacterial sepsis with surviving and fatal outcomes and performed single-cell transcriptomic analyses of peripheral blood mononuclear cells (PBMC) collected during the critical period between sepsis recognition and 6 hours. We observed that the largest sepsis-induced expression changes over time in surviving versus fatal sepsis were in CD14+ monocytes, including gene signatures previously reported for sepsis outcomes. We further identify changes in the metabolic pathways of both monocytes and platelets, the emergence of erythroid precursors, and T cell exhaustion signatures, with the most extreme differences occurring between the non-sepsis control and the sepsis non-survivor. Our single-cell observations are consistent with trends from public datasets but also reveal specific effects in individual immune cell populations, which change within hours. In conclusion, this pilot study provides the first single-cell results with a repeated measures design in sepsis to analyze the temporal changes in the immune cell population behavior in surviving or fatal sepsis. These findings indicate that tracking temporal expression changes in specific cell-types could lead to more accurate predictions of sepsis outcomes. We also identify molecular pathways that could be therapeutically controlled to improve the sepsis trajectory toward better outcomes.Summary sentenceSingle cell transcriptomics of peripheral blood mononuclear cells in surviving and fatal sepsis reveal inflammatory and metabolic pathways that change within hours of sepsis recognition.

Draft Genome Sequence of Invasive Salmonella enterica Serovar Cannstatt Harboring mcr-1.1, Isolated from a Fatal Sepsis Case

ABSTRACT Here, we report the whole-genome sequence of multidrug-resistant Salmonella enterica serovar Cannstatt harboring mcr-1.1, isolated from a fatal sepsis case. Genomic analysis revealed that the isolate was sequence type 2390 carrying mcr-1.1, blaCTX-M-14, aac(3)IId, aac(6′)Iaa, floR, qnrS1, sul2, tetA, and tetM. Three Inc plasmids were observed, including the IncX4 plasmid containing mcr-1.1.