* Congenital or aganglionic megacolon * Medication * Acquired megacolon, of which there are several possible causes: * Idiopathic megacolon * Toxic megacolon * Megacolon secondary to infection * Clostridium difficile * Trypanosoma cruzi<unk><unk>  * Pheochromocytoma, possibly secondary to its presenting constipation. * Other neurologic, systemic and metabolic<unk> s Aganglionic megacolon Also called Hirschsprung's<unk> , it is a congenital disorder of the colon in which nerve cells of the myenteric plexus in its walls, also known as ganglion cells, are absent. It is a rare disorder (1:5 000), with prevalence among males being four times that of females. Hirschsprung's<unk>  develops in the fetus during the early stages of pregnancy. A genetic predisposition to Hirschsprung's<unk>  has been linked to chromosome 13 where a missense mutation at an ultraconserved region impairs functionality of the W276C receptor. Seven other genes seem to be implicated, however. If untreated, the patient can develop enterocolitis. Medication Risperidone, an anti-psychotic medication, can result in megacolon. Toxic megacolon Toxic megacolon is mainly seen in ulcerative colitis and pseudomembranous colitis, two chronic inflammations of the colon (and occasionally, in the other type of inflammatory bowel<unk> , Crohn's<unk> . Its mechanism is incompletely understood. It is probably due to excessive production of nitric oxide, at least in ulcerative colitis. The prevalence is about the same for both sexes. In patients with HIV/AIDS, cytomegalovirus (CMV) colitis is the leading cause of toxic megacolon and emergency laparotomy. CMV may also increase the risk of toxic megacolon in non-HIV/AIDS patients with IBD.<unk><unk>  Megacolon can be associated with<unk><unk> . In Central and South America, the most common incidence of chronic megacolon is that observed in about 20% of patients affected with<unk><unk> .<unk>  is caused by Trypanosoma cruzi, a flagellate protozoan transmitted by the feces of a hematophagous insect, the assassin bug, when it feeds.<unk>  can also be acquired congenitally, through blood transfusion or organ transplant, and rarely through contaminated food (for example garapa). There are several theories on how megacolon (and also megaesophagus) develops in<unk><unk> . The Austrian-Brazilian physician and pathologist Fritz Köberle was the first to propose the neurogenic hypothesis based on the documented destruction of the myenteric plexus in the walls of the intestinal tracts of<unk>  patients. In this, the destruction of the autonomic nervous system innervation of the colon leads to a loss of the normal smooth muscle tone of the wall and subsequent gradual dilation. His research proved that, by extensively quantifying the number of neurons of the autonomic nervous system in the Auerbach's plexus, that: # neurons were strongly reduced all over the digestive tract; # megacolon appeared only when there was a reduction of over 80% of the number of neurons # these pathologies appeared as a result of the disruption of the neurally integrated control of peristalsis (muscular annular contraction) in those parts where a strong force is necessary to impel the luminal bolus of feces # idiopathic megacolon and<unk>  megacolon appear to have the same cause, namely the degeneration of the myenteric plexus. Why T. cruzi causes the destruction, however, remains to be determined. There is evidence for the presence of specific neurotoxins as well as a disorderly immune system reaction.
complications of Chagas disease
complications of Shigellosis
complications of West Nile fever
complications of Schistosomiasis
complications of Yellow fever
complications of Okamoto syndrome
complications of Amoebiasis
complications of Campylobacteriosis