Adult intestinal toxemia botulism (ITB) is a rare illness that can be fatal if not recognized. ITB can occur when botulinum neurotoxin-producing clostridia colonize the intestine. Underlying intestinal abnormalities associated with dysbiosis are likely a prerequisite for colonization. Dysbiosis seems necessary for spore germination and neurotoxin production. Botulism neurotoxins are the most lethal poisons known and are classified into 7 serotypes: A through G. The clinical presentation consists of cranial nerve abnormalities and descending flaccid paralysis. Prompt recognition and treatment with botulism antitoxin and supportive measures is often successful, but delayed recognition can be fatal. In this study, we present a case of a 40-year-old woman with Crohn's disease who developed ITB. This is the first case in literature to report adult intestinal botulism from Clostridium botulinum producing toxin B and F in the same patient.

Clostridium botulinum causes infant and adult intestinal botulism by colonizing in the intestine and producing botulinum neurotoxin (BoNT). Antimicrobial agents are not currently used for treatment due to the potential facilitation of BoNT production and bacterial cell lysis, which releases toxins into the intestinal lumen. In this study, we analyzed effects of four antibiotics on the viability of and BoNT production by four C. botulinum group I strains. Our results indicate that metronidazole rapidly reduced their viability without enhancing BoNT production. Antibiotics with these properties may promote elimination of C. botulinum from the intestines while maintaining low levels of BoNT.

Intoxication with botulinum neurotoxin can occur through various routes. Foodborne botulism results after consumption of food in which botulinum neurotoxin-producing clostridia (i.e., Clostridium botulinum or strains of Clostridiumbutyricum type E or Clostridiumbaratii type F) have replicated and produced botulinum neurotoxin. Infection of a wound with C. botulinum and in situ production of botulinum neurotoxin leads to wound botulism. Colonization of the intestine by neurotoxigenic clostridia, with consequent production of botulinum toxin in the intestine, leads to intestinal toxemia botulism. When this occurs in an infant, it is referred to as infant botulism, whereas in adults or children over 1 year of age, it is intestinal colonization botulism. Predisposing factors for intestinal colonization in children or adults include previous bowel or gastric surgery, anatomical bowel abnormalities, Crohn's disease, inflammatory bowel disease, antimicrobial therapy, or foodborne botulism. Intestinal colonization botulism is confirmed by detection of botulinum toxin in serum and/or stool, or isolation of neurotoxigenic clostridia from the stool, without finding a toxic food. Shedding of neurotoxigenic clostridia in the stool may occur for a period of several weeks. Adult intestinal botulism occurs as isolated cases, and may go undiagnosed, contributing to the low reported incidence of this rare disease.

The cholinergic heat-labile neurotoxin produced by Clostridium species is primarily responsible for the clinical manifestations of botulism. The classic phenotypic presentation of botulism consists of subacute descending flaccid paralysis with intact sensory function. Traditionally, it is classified into 3 main forms (foodborne, wound-related, and infantile) on the basis of primary site of toxin entry into the human nervous system. Toxemia is the common pathophysiology in all forms of botulism. Adult intestinal toxemia botulism is an extremely rare form of the disease with pathogenesis similar to that of infant-type botulism. Symptomatic adults usually have an anatomic abnormality in the gastrointestinal tract leading to changes in normal gut flora. The current case is an addition to the growing literature on this unusual clinical variant of botulism.

Diseases triggered by microorganisms can be controlled by vaccines, which need neutralizing antigens. Hence, it is very crucial to identify extremely efficient immunogens for immune prevention. Botulism, a fatal neuroparalytic disease, is caused by botulinum neurotoxins produced by the anaerobic, Gram-positive spore-forming bacteria, Clostridium botulinum. Food-borne botulism and iatrogenic botulism are caused by botulinum toxin. Wound botulism, infant botulism, and adult intestinal botulism are caused by primarily C. botulinum followed by secondary intoxication. To identify protective antigens, whole cell proteome of C. botulinum type B was separated by two-dimensional gel electrophoresis. 2-D gel of whole cell proteins was probed with hyper immune sera of whole cell proteins of C. botulinum types A, E, and F. Six cross immunoreactive proteins were identified. These immunoreactive proteins will be further tested for developing vaccines and serodiagnostic markers against botulism.