In recent years, Clostridium difficile isolated from the feces of patients with pseudomembranous enteritis has been shown to produce cytotoxic toxin (toxin B) and enterotoxic toxin (toxin A), the former being an important pathogenic factor in pseudomembranous enteritis. Both of these toxins can cause lethal ileocecal enteritis in hamsters. The toxins can cause increased permeability of the local intestinal mucosal vessel wall, resulting in tissue ischemia and necrosis, and stimulate mucus secretion and the formation of pseudomembranes with inflammatory cells, etc. The positive rate of Clostridium difficile in the stool of healthy people is about 5%, the carriage rate of hospitalized patients is about 13%, and the rate of asymptomatic patients with clonorchiasis is about 8%. In 50% of newborns and 15% to 40% of infants, the bacterium can be isolated in the feces, and even toxin production, but it is not pathogenic.
Clostridium difficile is anaerobic Gram-positive bacteria, about 6-8 × 0.5 μm, the bacterium is large, ovoid, located at the top of the body. In animal experiments, Lactobacillus can reduce the virulence of this bacterium, and other Clostridium difficile can make its virulence strengthen.
After the application of broad-spectrum antibiotics, especially lincomycin, chloramphenicol, aminobenzyl penicillin, hydroxybenzyl penicillin, etc., the normal flora in the intestinal tract is inhibited, so that Clostridium difficile can rapidly multiply and produce toxins and cause the disease. The disease can also occur after surgery, especially after surgery of gastrointestinal cancer, and other patients with serious diseases such as intestinal obstruction, malignant tumor, uremia, diabetes, heart failure, sepsis, etc. In these cases, the general resistance to disease and immunity is extremely low, or the condition requires antibiotic treatment, the internal environment of the body changes, and the intestinal flora is dysregulated, which is conducive to the multiplication of Clostridium difficile and disease.
Clostridium difficile and its toxin are pathogenic factors of the disease, but the potency of the toxin in the feces does not parallel the severity of the disease. This suggests that the toxin is not the only factor affecting the severity of the disease.