Most Clostridium infections arise from endogenous sources. That is, many of the Clostridium species that are associated with disease in humans are part of the normal intestinal microflora, which is true of Clostridioides difficile. Clostridium difficile was reclassified in 2016 to Clostridioides difficile. Clostridium species were grouped together due to broad phenotypical similarities like being anaerobic, gram-positive, spore-forming rods. Now with molecular testing, it has been determined that C. difficile does not truly fit in with this group. Instead, C. difficile should be in a new genus Peptoclostridium within the family Peptostreptococcaceae. But C. difficile is such a prominent name with many commercial products, that it would be a huge financial undertaking to completely rename it. Thus, Clostridioides was born to separate C. difficile from the other Clostridium species, but to allow it to keep the familiar "C. diff" nomenclature.2
The organism was originally isolated in 1935 as a component of the normal intestinal flora of healthy newborns. It was dubbed "difficile" because the organism grows slowly and is difficult to culture. Early investigators also noted that the organism produced a potent toxin, but the relationship between C. difficile antibiotic-associated diarrhea (AAD) and pseudomembranous colitis (PMC) was not elucidated until the 1970s. PMC is an inflammatory disease of the colon caused by toxins of C. difficile.
Normal intestinal flora is an important factor in the host response to an infectious microorganism. Resistance to intestinal infection is significantly reduced when there is a decrease in the normal flora as a result of antibiotic treatment. The most common manifestation of this decreased host resistance is the development of PMC.
