One of the most important relationships that infection preventionists can cultivate is with their institution's epidemiologist. It's a partnership that is equally appreciated by the epidemiologist who shares the objective of good patient outcomes. It's an alliance that dates back to 1985, when the SENIC Project provided scientific evidence that infection control programs with qualified IPs and hospital epidemiologists could prevent nearly one-third of healthcare-associated infections (HAIs).
Bacteria that cause ulcers in humans undergo accelerated evolution during the initial stages of infection, allowing them to evade the immune system, according to new research by an international team of researchers including Penn State scientists. The study shows, for the first time, and in real-time, the interplay between the human immune system and invading bacteria that allows the bacteria to counter the immune response by quickly evolving. A paper describing the research is published in the June 13, 2014 issue of the journal Nature Communications.
An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, have identified the genes encoding a molecule that famously defines Group A Streptococcus (strep), a pathogenic bacterial species responsible for more than 700 million infections worldwide each year.
The human body is comprised of roughly 10 times more bacterial cells than human cells. In healthy people, these bacteria are typically harmless and often helpful, keeping disease-causing microbes at bay. But, when disturbances knock these bacterial populations out of balance, illnesses can arise. Periodontitis, a severe form of gum disease, is one example. In a new study, University of Pennsylvania researchers show that bacteria responsible for many cases of periodontitis cause this imbalance, known as dysbiosis, with a sophisticated, two-prong manipulation of the human immune system.