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PUBLIC RELEASE DATE:
7-Jan-2014

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Contact: Andrew Thompson
andrew@landesbioscience.com
Landes Bioscience

Special focus issue on sepsis

A special issue on sepsis has been released by the publisher Landes Bioscience (Austin, TX USA). The articles contained in this special issue of the journal Virulence have been authored by world-class investigators and provide new insights into both the pathogen-related factors and the host defense mechanisms that lead to septic shock and contribute to its resolution or fatal outcome.

Sepsis, or septic shock, is an excessive inflammatory response in answer to a serious infection, most commonly by bacteria, but also fungi, viruses, and parasites. Different microbial components, such as bacterial lipopolysaccharide (LPS), endotoxins, or exotoxins can cause the typical septic inflammatory cascade. The condition can continue even after the infection that caused it is gone. It is a significant cause of morbidity and mortality worldwide. Characteristics of sepsis are massive release of proinflammatory cytokines resulting in tissue damage, an uncontrolled reduction in blood-pressure, multiple organ failure, and death. Sepsis can originate anywhere microbes can gain entry to the body, common sites including the genitourinary tract, the liver and its bile ducts, the gastrointestinal tract, and the lungs. The condition is often life-threatening, especially in people with a weakened immune system or other medical issues.

Dr. Steven Opal from Alpert Medical School of Brown University (Pawtucket, RI USA) has worked with the editorial team of Virulence to organize this special issue on sepsis. Over 20 papers in this issue discuss many different aspects of sepsis and septic shock, such as epidemiology of severe sepsis (Sachin Yende), gender differences in sepsis (Irshad Chaudry), systemic inflammatory response syndrome (Robert Balk), the PIRO model (John Marshall), host innate immune responses to sepsis (Willem Joost Wieringa), the changing immune system in sepsis (Jonathan Boomer), pathogenesis of bacteremia (Eirini Christaki), role of mitochondrial dysfunction in sepsis-induced multi-organ failure (Mervyn Singer), pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock (Daniel De Backer), an alternate pathophysiologic paradigm of sepsis and septic shock—implications for optimizing antimicrobial therapy (Anand Kumar), meningococcal disease and the complement system (Lisa Lewis and Sanjay Ram), contribution of group A streptococcal virulence determinants to the pathogenesis of sepsis (Shiranee Sriskandan), the complex link between influenza and severe sepsis (Diana Florescu), animal models of sepsis (Mitchell Fink), invasive candidiasis as a cause of sepsis (Thierry Calandra), neonatal sepsis (James Padbury), pediatric sepsis (Adrienne Randolph), clinical controversies in the management of patients with severe sepsis (Simon Finfer), clinical impact of multidrug-resistant gram-negative bacilli in the management of septic shock (Aurora Pop-Vicas), bacterial toxins in sepsis (Girish Ramachandran), anti-endotoxin vaccines (Alan Cross), bacteriophage therapy (Xavier Wittebole), rapid diagnosis of sepsis (Konrad Reinhart), and severe sepsis and septic shock—management and performance improvement (Christa Schorr).

In an accompanying editorial, Dr. Opal highlights the importance of this collection of review articles, providing a detailed summary of the current knowledge and science of septic shock research, extending from the molecular to the population level. He writes, "Septic shock continues to pose formidable challenges for emergency room physicians, critical care specialists, surgeons, and infectious disease clinicians alike in caring for these critically ill patients. Early recognition of sepsis and improved therapies to manage the multi-organ dysfunction that frequently follows sepsis pathophysiology remain major unmet medical needs."

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To view all articles in the special issue, visit the following link: http://www.landesbioscience.com/journals/virulence/toc/volume/5/issue/1/



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