Clostridium tetani of Clostridium Infections
Tetanus arises from a neurotoxin produced by when spores of C. tetani germinate after gaining access to the wounds. The disease may develop after penetrating trauma, chronic skin ulcers, infections about the umbilical stump of newborn (neonatal tetanus), obstetric procedures (postabortal tetanus), and infected injection sites in IVDA. Unlike botulism, only one antigenic type of toxin is involved and therefore an effective montypic toxoid is available. C. tetani is a strict anaerobe without a capsule. Its spherical terminal spores give a characteristic “drumstick” appearance. It is found in the soil and faeces of farm and domestic animals. In humans, the faecal carrier rate is low (0-25%) suggesting that the organism’s presence is transient.
Most cases arises from small puncture wounds or lacerations. The infection remains localised to the site of entry. Access of tetanus spores to open wounds does not necessarily result in disease, especially in clean wounds where the oxygen supply is good and germination is inhibited. In necrotic or infected wounds, anaerobic conditions will permit germination. The incubation period ranges from several days to many weeks. The usual form of the disease is characterised by sever painful spasms and rigidity of voluntary muscles. Spasms of the pharyngeal muscles causes dysphagia and death may result from paralysis of respiratory muscles.
The diagnosis of tetanus is usually based on clinical findings alone. However, attempts should be made to culture C. tetani from all suspicious lesions. The organism can only be cultured from infective focus in 30% of cases. Antitoxin should be promptly administered in all cases of suspected tetanus. It is ineffective when the toxin is already fixed in the CNS. Tetanus immune globulin (TIG) prepared from persons who have been hyperimmunised with tetanus toxoid has supplanted conventional equine antitoxin. Careful debridement of the lesion and removal of foreign bodies should be carried out after TIG had been given. Penicillin should also be administered to prevent the germination of spores and further bacterial multiplication. Intensive supportive measures should be given.
Because spores of C. tetani are so widely distributed, the only effective way to control tetanus is by prophylactic immunisation. Tetanus toxoid is usually given as part of DPT. Whenever a previously immunised individual sustains a potentially dangerous wound, a booster dose of toxoid should be given. Non-immunised individuals should be given TIG.
A variety of species of clostridium are associated with invasive infection in humans i.e. C. perfringens, novyi, septicum, histolyticum, tertium, bifermentans, sporogenes. They are not highly pathogenic when introduced into healthy tissues; but in the presence of tissue injury, in particular damaged muscle, they can cause a rapidly progressive devastating infection characterised by the accumulation of gas and the extensive destruction of muscle and connective tissue. Pathogenesis is due to the production of various toxins with necrotising, haemolytic or other destructive properties.
There are three types of clostridial wound infection: wound contamination, anaerobic cellulitis, and true myonecrosis (gas gangrene). 80 to 90% of isolations of C. perfringens from hospital represent wound contamination which does not herald invasive infection. Anaerobic cellutitis is a clostridial infection that does not involve the muscle and is much less aggressive than gas gangrene. Germination occurs in damaged tissue where damage to the blood supply has reduced the supply of oxygen. The vegetative bacilli multiply and anaerobic cellulitis develops after several days. The marked gas formation is detectable by the resulting crepitus. Gas gangrene is an intensively aggressive highly lethal infection, primary of muscle. After the germination of clostridial spores in the injured muscle, bacterial multiplication and toxin production occur. A self-perpetuating cycle of progressive tissue injury ensue. The onset of the disease is sudden, usually following an onset of 6 to 72 hours after injury or abdominal surgery. Of the six clostridial species capable of producing gas gangrene, C. perfringens account for the majority of cases.
C. perfringens is present in the genital tract of 5% of women. After septic abortion, it may invade the uterine wall, producing extensive necrosis, high fever, and shock. Severe bacteraemia characteristically occurs. Bacteraemia caused by C. perfringens or other species occasionally occur in other debilitated patients e.g. leukaemia, other cancers, GI bleeding etc. Bacteraemia occur in 15% of patients with gas gangrene.
C. difficile had been found in 25% of cases of moderate diarrhoea resulting from treatment with antibiotics, especially clindamycin, ampicilllin, or cephalosporins. In the more severe reaction known as pseudomembranous collitis, C. difficile is found in 95% of cases. This occasionally fatal illness is characterised by diarrhoea, multiple small colonic plaques, and toxic megacolon. The antibiotic selects for overgrowth of organsism that produce a heat-labile toxin; faecal extracts from these patients are cytotoxic in cell culture. The enterotoxicity of C. difficile is due to two toxins; toxin A, and toxin B.
C. perfringens is a common organism frequently found in excreta from humans and animals and in raw meats, poultry and other foods, including dehydrated products. It can survive heat and dehydration by means of spores that remain dormant in food, soil, and dust. Illness occurs after eating food contaminated with large numbers of C. Perfringens grown from spores: the spores had been activated by heat shock. The enterotoxin is only produced during sporalation and not during vegetative growth. Multiplication of bacteria take place during long slow cooking and warm storage of food in the kitchen or canteen. Cooked meat, poultry, fish, stews, pies, and gravies are excellent media for growth at temperatures up to 50oC. There is little growth below 15oC. The spores of some strains of C. Perfringens can withstand long hours of boiling. The organism may be isolated in large numbers from boiled, stewed, steamed, braised, or even roasted foods, particularly those cooked in bulk and stored unrefrigerated for a few hours.
Symptoms occur 8 to 22 hours after consumption of the contaminated food. They include abdominal pain, profuse diarrhoea, and nausea, but rarely vomiting. Symptoms may continue for 12 to 48 hours. The symptoms occur as a result of an enterotoxin produced by a large number of ingested organisms. An effective amount of toxin is not usually formed in the food before it is eaten. There are 5 types of C. Perfringens (A to E) classified according to the various toxins they produce. Only two of these produce the enterotoxin which cause gastroenteritis: type A is the more common agent of food poisoning whereas type C is responsible for a more serious but rare condition known as enteritis necroticans.