Histotoxic enteropathogenic clostridia

• Histotoxic clostridia produce exotoxins that induce local tissue necrosis and systemic effects, resulting in lethality.
• Histotoxic clostridia are present in tissue as latent spores, specifically in muscle and liver.
• Endospores of histotoxic clostridia are widely distributed in the environment and persist for long periods in soil.
• Histotoxic clostridia cause enteropathogenic infections.
• Histotoxic clostridia can cause enteropathogenic infections through both endogenous and exogenous routes.
• In endogenous infections, histotoxic clostridia spores are present in the tissue lumen and tissue injury reduces oxygen levels, leading to spore germination and exotoxins production.
• In exogenous infections, histotoxic clostridia infections occur through infected wounds.
• Enterotoxemia (Type B) is associated with old world diseases (Europe and some regions in Asia), causes lamb dysentery in newborn lambs, and is susceptible to trypsin.
• Immunological aspects of clostridial diseases include circulating antibody to toxins and cellular components determining resistance.
• Clostridium perfringens types A, B, C, D, and E are enterotoxemia (Type A) producing clostridia.
• Clostridium novyi causes Black disease and is associated with Fasciola hepatica (liver parasite).
• Treatment and control of clostridial diseases often involves intravenous penicillin, vaccination of cattle at 3-6 months, vaccination of pregnant ewes 3 weeks prior to parturition, vaccination of lambs during their first year, and change of pasture when cases are first observed.
• Neonatal calves, foals, piglets and lambs worldwide are susceptible to enterotoxemia (Type C), which causes hemorrhagic enteritis, and β-toxin is the principal virulence factor.
• Clostridium produce disease only in defined circumstances.
• Clostridium haemolyticum causes bacillary haemoglobinuria.
• Enterotoxemia (Type A) is characterized by tissue destruction, membrane active toxins and connective tissue toxins, diseases such as outbreaks of gastritis and hemolytic diseases of ruminants, yellow lamb diseases, hemorrhagic enteritis in cattle, horses and infant alpacas, necrotic enteritis in poultry, canine hemorrhagic gastroenteritis, and food poisoning in humans.
• α-toxin, perfringolysin O, and enterotoxins are important toxins in enterotoxemia (Type A).
• Laboratory diagnosis of clostridial diseases includes immunofluorescence of infected tissue smears, sporulated gram positive rods, strict anaerobic conditions, culture medium rich in cysteine and water-soluble vitamins, and detection in tissue or identification in culture can be done by molecular methods (PCR).
• Clostridium present and replicate in the GI tract of enteropathogenic/enterotoxaemia producing clostridia.
• Clostridium perfringens type A, B, C, D, and E are enterotoxemia (Type A) producing clostridia.
• Clostridium produce toxins that can produce local and generalized effects/damage.
• Clostridium chauvoei causes exogenous infection and is associated with infected wounds.
• Diffuse hemorrhagic and necrotizing enteritis is a characteristic of enterotoxemia (Type C).
• β-toxin is the principal virulence factor in enterotoxemia (Type B).
• Clostridium difficile can be isolated using selective medium such as Cycloserine, cefoxitin, and fructose agar (CCFA).
• Clostridium difficile also stimulates the influx of polymorphonuclear cells, the synthesis of prostaglandins, and results in secretion of chloride ions and water, leading to diarrhea.
• Antitoxin, which is orally administered and protective for humans, can be used in the treatment of Clostridium difficile.
• Antitoxin of appropriate type may be given to sick animals and those at risk.
• Alpha toxin produced by Clostridium perfringens interacts with CAMP factor and produce synergistic hemolysis.
• Clostridium sordellii causes fatal myositis and hepatic diseases in ruminants and horses.
• Stormy fermentation and clotting of milk followed by gaseous disruption are signs of enterotoxemia.
• The pathogenesis of Clostridium difficile involves a "trigger" event such as antibiotics, chemotherapy, or disruption of normal flora, which allows C. difficile to adhere to the large intestine and produce toxins.
• Most causes of enterotoxemia are too acute for successful treatment.
• Diarrhea associated with Clostridium difficile responds rapidly to metronidazole, but resistance exists and no vaccines are available.
• Active immunization of dams with two injections of bacterin-toxoid combinations ensures nursling passive protection for the first week.
• In humans, probiotics can be useful in preventing Clostridium difficile diseases.
• Preventive measures include ensuring against overeating and antibiotic treatment can be used in some cases.
• Hand washing by health care personnel is an efficient mechanism for curtailing the spread of Clostridium difficile.
• Clostridium difficile toxins include Toxin A (Tox A or TcdA), which breaks down cytoskeletal components of the affected cell, disrupts the tight junctions between intestinal epithelial cells, and results in cell death.
• Clostridium difficile is a significant cause of diarrheal diseases in humans, including antibiotic-associated diarrhea and pseudomembranous colitis.