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Genetic aganglionic megacolon in rats is a condition resulting from lack of, or failure of, the enteric ganglion cells to develop in the myenteric plexus of the rectosigmoid area of the large intestine (colon). The result is reduced, or complete lack of, peristaltic movement or defecation reflex in the large intestine, and the inability to move fecal material through the colon.
Acquired megacolon is any pathology that obstructs intestinal contents and prevents movement that results in extreme distention of the colon.
Genetic aganglionic megacolon in rats is a congenital condition similar to Hirschsprung’s disease (in humans), lethal white foal syndrome (in horses), piebald related megacolon (in mice), and some types of Waardenburg syndrome (in humans).
In genetic megacolon the autonomic nerve ganglions of the smooth muscle of the colon are absent. It can involve either a limited segment or the entire colon. The affected segment is narrowed, contains strictures, and is permanently contracted. The bowel proximal to that segment is both hypertrophied and dilated. Normal internal relaxation of the sphincter muscle that occurs with rectal distention is absent, and instead of having the sphincter relax, it contracts. As stool fails to pass, and dilatation of the bowel results, abdominal distention occurs. This increased pressure of the bowel, and resistance to stretching of the rectal wall, results in blood flow being decreased in that area, as well as, deterioration of the mucosal barrier. Because the stool is not able to move through the bowel, stasis occurs and bacterial growth lead to enterocolitis and a resulting sepsis.
Genetic megacolon occurs as a result of faulty neural crest cell development in the embryo stage. The defects in the neural crest-derived melanocytes, which cause white spotting, and the defects in the peripheral neurons, which result in the lack of ganglia in the digestive tract, occur on the same migration path.
Thus, you will often see genetic megacolon in BEW (black-eyed white), husky, blazed, split-capped, tei-colored, odd-eyed, and other “high white” lines of rats. The same relationship occurs in a certain type of Waardenburg syndrome in humans where there is either odd-eyes or a white patch of hair or pigment accompanying the digestive involvement. Lethal white foal syndrome in horses occurs in the overo types (white or mostly white) and causes death from megacolon within a few hours or days of birth.
The method of inheritance does not follow typical genetic disposition and there are several gene variations. The genes responsible seem to involve polygenetic (multifactorial) modes of inheritance. Multifactorial inheritance virtually makes it impossible to predict the outcome of breeding rats that are, or appear to be, at high-risk for megacolon. It has been noted that multifactorial modes of inheritance involving megacolon have a “slight” risk. In cases where the megacolon is severe and/or there are multiple siblings affected then the inheritance is thought to increase.
Megacolon can be either early or late (delayed) onset.
With early onset megacolon the signs will usually begin to show as soon as the baby begins eating solid food (around 2 weeks) although sometimes it is not apparent there is a problem till they are 3 or 4 weeks old. Some babies will show a distinct failure to thrive even though they are eating well. This occurs due to the lack of proper absorption of nutrients in the damaged digestive tract. Early onset signs such as bloating, diarrhea, and severe constipation typify the quick advancement of the disease. It is recommended to consider euthanasia rather than to let the disease follow its ultimate lethal course.
Late, or delayed, onset megacolon appears to have the same genetic origin as early onset and is seen in the same lines as early onset. It may be a milder form of the disease, but unfortunately it does progress in severity until it becomes lethal. Often the first sign of delayed onset megacolon is shown by the baby rat’s failure to thrive. Gastrointestinal problems may not become apparent until the rat is 2-5 months old. At that time you may see bloating, diarrhea, constipation, or alternating bouts of diarrhea and constipation. Stools passed may be hard, fibrous, foul smelling, dry, oversized, oddly shaped, blunt on the ends, and have blood or mucus in or between them.
Late onset can also be even more delayed, sometimes not becoming symptomatic until the rat has reached a later age of 4-10 months. With no early warning signs of a problem (such as failure to thrive, unusual stools, or chronic diarrhea) the very late onset type may often be too far advanced, by the time the owner notices a problem, to treat.
Abdominal distention with absence of stool in rectum.
On radiologic exam, gas and fluid filled loops can be visualized.
May present with enterocolitis, reflected as diarrhea containing blood, dehydration, perforation, pericolic abscess, and septicemia.
Rats that survive past weaning and infancy require lifetime treatment. Quality of life can be maintained, though lifespan may be shorter. In larger mammals surgery can be performed which removed the parts of the colon that are damaged. This is not an option for pet rats at this time.
Providing additional fluids by offering fruits such as cantaloupe and watermelon slices, to your rat, encourages necessary fluid intake.
Enemas with mineral oil may be of help with dry stool passage.
Enemas using mild liquid soap (e.g., Ivory).
Note: It is not recommended that saline be used; since the possibility of shock exists from excessive water absorption of isotonic saline. It is also not recommended to use hypertonic phosphate solutions as they may cause tetany (muscle spasms, severe cramping, twitching) with the change to Na concentrations in the venous system following absorption.
The use of the following medications have been found to be helpful when used in conjunction with the above treatment:
Posted on June 25, 2003, 10:04,
Last updated on January 8, 2013, 17:56