<Li> Diarrhea: The prevalence of CF in Europe might be connected with the development of cattle domestication . In this hypothesis, carriers of a single mutant CFTR had some protection from diarrhea caused by lactose intolerance, prior to the appearance of the mutations that created lactose tolerance . </Li> <Li> Tuberculosis: Another possible explanation is that carriers of the gene could have some resistance to TB . This hypothesis is based on the thesis that CFTR gene mutation carriers have insufficient action in one of their enzymes--arylsulphatase - which is necessary for Mycobacterium tuberculosis virulence . As M. tuberculosis would use its host's sources to affect the individual, and due to the lack of enzyme it could not presents its virulence, being a carrier of CFTR mutation could provide resistance against tuberculosis . </Li> <P> CF is supposed to have appeared about 3,000 BC because of migration of peoples, gene mutations, and new conditions in nourishment . Although the entire clinical spectrum of CF was not recognized until the 1930s, certain aspects of CF were identified much earlier . Indeed, literature from Germany and Switzerland in the 18th century warned "Wehe dem Kind, das beim Kuß auf die Stirn salzig schmeckt, es ist verhext und muss bald sterben" or "Woe to the child who tastes salty from a kiss on the brow, for he is cursed and soon must die", recognizing the association between the salt loss in CF and illness . </P> <P> In the 19th century, Carl von Rokitansky described a case of fetal death with meconium peritonitis, a complication of meconium ileus associated with CF . Meconium ileus was first described in 1905 by Karl Landsteiner . In 1936, Guido Fanconi described a connection between celiac disease, cystic fibrosis of the pancreas, and bronchiectasis . </P>

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