I think this would be connected to missing enzymes called protease. These enzymes digest dietary proteins. I posted a great deal of information on the association to these missing enzymes and MS on this thread. general-discussion-f1/topic22806.html
Researchers have already determined that in animals a lack of protease leads to the proliferation of C. perfringens. For instance, the following information states that ingestion of a protein-rich diet in a protease-deficient intestinal tract allows for "rapid growth" of C. perfringens. Pathogenic bacteria, such as C. perfringens, feed and proliferate on the undigested protein fragments.
Managing Clostridial Diseases in Cattle
Sheila M. McGuirk, DVM, PhD
"Possible risk factors for calves... Ingestion of C. perfringens in the first few days of colostrum feeding...Ingestion of protein-rich diet in a protease-deficient intestinal tract allows rapid growth of C. perfringens organisms"
The following information from Wiki states that trypsin (trypsin is a protease) shortages in the digestive system of experimental animals has been used to "induce" Clostridium perfringens.
"Clostridium perfringens beta toxin one of the four major lethal toxins produced by Clostridium perfringens Type B and Type C strains...C. perfringens beta toxin is susceptible to breakdown by proteolytic enzymes, particularly trypsin. Beta toxin is therefore highly lethal to infant mammals because of trypsin inhibitors present in the colostrum...It is primarily fatal to animals 1–3 days old, whose digestive enzymes may not be sufficiently active to break down beta toxin. It has been experimentally shown that trypsin may normally break down beta toxin and trypsin shortages in the digestive system of experimental animals has been used to induce type C disease."http://en.wikipedia.org/wiki/Clostridiu ... beta_toxin
So, as we can see, pathogenic organisms such as C. perfringens would proliferate in the absence of protease.