Several years ago, one of my colleagues died tragically from a laboratory-acquired Yersinia pestis infection. A description of his illness and of postmortem investigations coordinated by the CDC has recently been published (1). My colleague had been working with a strain of Y. pestis that was thought to be non-pathogenic because of a defect in its iron-acquiring ability. Postmortem studies showed that he had markedly elevated serum iron and other indices of iron overload. Genetic testing revealed that he was homozygous for the C282Y hemochromatosis mutation, although he was not aware of having hemochromatosis and had never had any symptoms of this disease. Hemochromatosis is known to increase the risk of infection by other Yersinia species, including Y. enterocolitica and Y. pseudotuberculosis, which are impaired in their ability to acquire iron from infected hosts (2). The CDC report suggested that my colleague’s hemochromatosis-induced iron overload might have increased the virulence of this attenuated Y. pestis strain. buy propecia online https://infoblobuy.com/propecia.html no prescription
Eugene Weinberg and others have studied the molecular mechanisms of our evolved iron-withholding defenses and have documented the importance of these defenses in protecting us against pathogens (3). The reduced serum iron seen in patients with infectious diseases is now recognized as an adaptation that decreases the virulence of these diseases, and the dangers of giving iron to patients with infections are well known. Unfortunately, however, the other side of this relationship—that even sub-clinical defects in iron withholding, due to hemochromatosis or other causes, can increase susceptibility to infection—is not widely appreciated. A greater awareness and understanding of the clinical relevance of our iron-withholding defenses should lead to improved medical practice.
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1. Fatal laboratory-acquired infection with an attenuated Yersinia pestis strain—Chicago, Illinois, 2009. MMWR 60(7), 201–5, 2011.
2. Khan FA, Fisher MA, Khakis RA. Association of hemochromatosis with infectious diseases: Expanding spectrum. Int J Infect Dis 11(6):482–7, 2007.
3. Weinberg ED. Iron availability and infection. Biochim Biophys Acta 1790(7):600–5, 2009. buy proair online https://infoblobuy.com/proair.html no prescription
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Interesting post… but can anyone comment?
The hemochromatosis that contributed to this fate has been credited with protecting people from strains of plague that circulate in the wild. Sharon Moalem, an evolutionary biologist and author of “Survival of the Sickest,” posited that the disorder shifts iron from certain white blood cells, where it is typically sought by the plague bacterium.
I value the article post.Really thank you! Will read on…
Do you have some new findings to it? Was the connection confirmed or … ? Could there be also other link with the disposition, was your friend recessive or dominant? It really sounds a bit strange to me… I would have the similar question as Marcus, if you could comment it, thank you. I have never heard it vice versa, even the cases with the ferrum in the serum (or bound) which attracts any bacteria (not only pathogens). I would appreciate any new comments on the topic, thank you!
My colleague’s illness and death were reported last year in the New England Journal of Medicine: Frank, K.M., et al., Investigation of a Researcher’s Death Due to Septicemic Plague, N Engl J Med 364(26):2563-64. I am aware of Sharon Moalem’s proposal that hemochromatosis-associated alleles spread because they conferred resistance to Yersinia pestis but I don’t know any evidence that supports this hypothesis. Iron overload increases the virulence of many infections, including infections caused by attenuated strains of Y. pestis in mice and in monkeys. Despite Moalem’s suggestion, there is no reason to believe that the iron overload associated with hemochromatosis would not also enhance the virulence of Y. pestis infections.