Readings Newsletter
Become a Readings Member to make your shopping experience even easier.
Sign in or sign up for free!
You’re not far away from qualifying for FREE standard shipping within Australia
You’ve qualified for FREE standard shipping within Australia
The cart is loading…
This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Jean-Claude Rambaud The place occupied today in basic and clinical research by intestinal disease related to Clostridium difficile is such that it is hard to remember that this range of disorders was completely identified only in 1977-1978, even though pieces of the puzzle had been identified much earlier. A brief historical review of the discovery of the enteropathogenicity of C. difficile in man might thus be useful. The bacterium was described in 1935 in the stools of infants, using the name Bacillus difficilis [7]. Until 1977, the microorganism, renamed C. difficile, considered to be of endogenous origin, was isolated only in rare cases of abscess or infection, most often unrelated to the digestive tract. Its role in genito-urinary infections [6] was not confirmed. However, the frequency of infant healthy carriers was recognized from the outset [7, 13]. Pseudo-membranous colitis (PMC) was described in 1883 following a gastroenterostomy. Many cases of this condition were published subsequently before the antibiotic era, describing various risk factors [4]. However the disease began to flourish only with the increasingly wide use of antibiotics. Antibiotic associated PMC was first described as an enterocolitis, though with little pathological evidence. It was principally related to the use of chloramphenicol and tetracyclines and attributed to proliferation of Staphylococcus au reus [11], a concept strengthened by the spectacular therapeutic action of vancomycin.
$9.00 standard shipping within Australia
FREE standard shipping within Australia for orders over $100.00
Express & International shipping calculated at checkout
This title is printed to order. This book may have been self-published. If so, we cannot guarantee the quality of the content. In the main most books will have gone through the editing process however some may not. We therefore suggest that you be aware of this before ordering this book. If in doubt check either the author or publisher’s details as we are unable to accept any returns unless they are faulty. Please contact us if you have any questions.
Jean-Claude Rambaud The place occupied today in basic and clinical research by intestinal disease related to Clostridium difficile is such that it is hard to remember that this range of disorders was completely identified only in 1977-1978, even though pieces of the puzzle had been identified much earlier. A brief historical review of the discovery of the enteropathogenicity of C. difficile in man might thus be useful. The bacterium was described in 1935 in the stools of infants, using the name Bacillus difficilis [7]. Until 1977, the microorganism, renamed C. difficile, considered to be of endogenous origin, was isolated only in rare cases of abscess or infection, most often unrelated to the digestive tract. Its role in genito-urinary infections [6] was not confirmed. However, the frequency of infant healthy carriers was recognized from the outset [7, 13]. Pseudo-membranous colitis (PMC) was described in 1883 following a gastroenterostomy. Many cases of this condition were published subsequently before the antibiotic era, describing various risk factors [4]. However the disease began to flourish only with the increasingly wide use of antibiotics. Antibiotic associated PMC was first described as an enterocolitis, though with little pathological evidence. It was principally related to the use of chloramphenicol and tetracyclines and attributed to proliferation of Staphylococcus au reus [11], a concept strengthened by the spectacular therapeutic action of vancomycin.