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The Invisible Enemy in Iraq
By creating the most heroic and efficient means of saving lives in the history of warfare, the Pentagon had accidentally invented a machine for accelerating bacterial evolution and was airlifting the pathogens halfway around the world.
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Since OPERATION Iraqi Freedom began in 2003, more than 700 US soldiers have been infected or colonized with Acinetobacter baumannii. A significant number of additional cases have been found in the Canadian and British armed forces, and among wounded Iraqi civilians. The Armed Forces Institute of Pathology has recorded seven deaths caused by the bacteria in US hospitals along the evacuation chain. Four were unlucky civilians who picked up the bug at Walter Reed Army Medical Center in Washington, DC, while undergoing treatment for other life-threatening conditions. Another was a 63-year-old woman, also chronically ill, who shared a ward at Landstuhl with infected coalition troops.
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Nevertheless, the bug makes an unlikely candidate for the next mass plague. It preys exclusively on the weakest of the weak and the sickest of the sick, slipping into the body through open wounds, catheters, and breathing tubes. Colonization poses no threat to people who aren't already ill, but colonized health care workers and hospital visitors can carry the bacteria into neighboring wards and other medical facilities. Epidemiologist Roberta Carey at the Centers for Disease Control and Prevention calls acinetobacter the Rodney Dangerfield of microorganisms: "It doesn't get a lot of respect because it's not out there bumping off normal, healthy people." But lately the bacteria has been getting its due, because it is rapidly evolving resistance to all of the antibiotics that used to keep it in check.
...strains of acinetobacter are emerging now that are immune to every known remedy. Multidrug - resistant pathogens are an epidemiologist's nightmare - reminders of the dark ages when millions of people died every year of runaway infections...
And they're spreading fast. A major outbreak in Chicago two years ago infected 81 patients, killing at least 14. Arizona health officials tracked more than 200 infections in state hospitals early last year. Doctors at Vanderbilt University Medical Center in Tennessee used to see an infection or two every year; now it's one or more a month. "These bacteria are developing very, very quickly," says CDC epidemiologist Arjun Srinivasan, who has been consulting with the DOD about the military outbreak. "The bad news is that we're many years away from having new drugs to treat them. It should be a call to arms."
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Nevertheless, the bug makes an unlikely candidate for the next mass plague. It preys exclusively on the weakest of the weak and the sickest of the sick, slipping into the body through open wounds, catheters, and breathing tubes. Colonization poses no threat to people who aren't already ill, but colonized health care workers and hospital visitors can carry the bacteria into neighboring wards and other medical facilities. Epidemiologist Roberta Carey at the Centers for Disease Control and Prevention calls acinetobacter the Rodney Dangerfield of microorganisms: "It doesn't get a lot of respect because it's not out there bumping off normal, healthy people." But lately the bacteria has been getting its due, because it is rapidly evolving resistance to all of the antibiotics that used to keep it in check.
Genes Linked to Autoimmune Diseases
The immune system is what keeps most people's bodies healthy and free of disease, but for as many as 23 million Americans, it is a cause of disease, too. In autoimmune disorders, the system goes haywire, mistaking the body's own tissues for foreign invaders and destroying them. Drugs for these conditions, which include type 1 diabetes, multiple sclerosis and lupus, have been elusive. But on Sunday, scientists are reporting in the journal Nature that they have found a set of 30 genes that go awry in autoimmune disorders - and that could be potential targets for cures.
...scientists discovered the "brain" of the regulatory T cells, or the gene that tells them how to do their job. This is a gene called Foxp3.
And these are the 30 genes, the ones that aren't following the proper directions. So you think this dysfunction is the basis not just for one disorder, but a whole host of autoimmune diseases?
Marson: Yes, regulatory T cells appear to be key in preventing type 1 diabetes, lupus, multiple sclerosis, rheumatoid arthritis, and inflammatory bowel disease, as well as autoimmune thyroid disorders. Dysregulation of the genes controlling those cells could contribute to a wide range of autoimmune conditions.