OTHER CLOSTRIDIAL DISEASES IN WILDLIFE
ALEKSIJA NEIMANIS
Department of Pathology and Wildlife Diseases, National Veterinary Institute, Uppsala, Sweden
Reports of disease in wildlife caused by other clostridial species are uncommon.
Their toxins target different organ systems: enterotoxaemia (C. perfringens), muscle, superficial soft tissue and systemic toxaemia (C. chauvoei, C. novyi, C. septicum, C. perfringens), and the nervous system (C. tetani). Like C. botulinum, they grow and produce toxin under appropriate conditions, but this occurs i n vivo. With the exception of enterotoxaemia caused by C. perfringens, disease tends to occur in individual wild animals rather than causing large epizootics. Although most reports of these diseases in wildlife come from areas outside of Europe, they are briefly summarized here because these clostridial species are ubiquitous.CLOSTRIDIUM PERFRINGENS - NECROTIC ENTERITIS
Clostridium perfringens causes acute ulcerative, haemorrhagic and necrotizing enteritis in birds.
This bacterium is found in soil and in the gastrointestinal tracts of animals. Types A-E have been described based on the combination of exotoxins produced by the bacterium. In wildlife, types A and C are most significant. Type A produces only alpha toxin, and type C produces alpha and beta toxin.
This disease was first described in wild waterfowl in Florida, USA. In Europe, 155 ducks were reported to have died from C. perfringens enterotoxaemia in 1981 and 1982 in the lower Rhine region, Germany(51). More recently, 30 whooper swans (Cyngus cyngus) in East Anglia, UK died in November 2003 after a dry summer and wintering birds had been supplemented with wheat(52). A review of earlier records revealed six other suspected incidents involving 65 whooper swans and 14 mute swans (Cyngus olor). In five of six incidents, supplemental wheat had been provided.
Several incidents were associated with environmental change such as temporary changes to local aquatic habitat. Incidents occurred between November and January. The largest epizootics (hundreds of birds) of necrotic enteritis recorded occurred during autumn months in migrating wild geese in western Canada(53). Other free-ranging species affected in isolated, suspected outbreaks of necrotic enteritis include western bluebirds (Sialia mexicana) and a greater sage grouse ( Centrocercus urophasianus) in western USA(54,55), crows ( Corvus macrorhynchos) in Japan(56) and lorikeets (Trichoglossus spp.) in Australia1-57). Necrotizing enteritis associated with C. perfringens type A was the most common cause of death in captive capercaillies (Tetrao urogallus) in Norway(58).Necrotic enteritis occurs when intestinal conditions favour proliferation and toxin production of C. perfringens. Disease has been associated with sudden dietary changes such as those encountered during migration, trypsin inhibitors in feed, gut stasis, stress and intestinal parasit- ism(53). In migrating geese in western Canada, these authors hypothesized that a sudden shift in diet to carbohydrate- rich grains containing trypsin inhibitors allowed C. perf- ringens to colonize the intestine. Supplemental wheat provided to swans in the UK coupled with environmental stressors may have helped to initiate disease.
Toxigenic C. perfringens colonize tips of intestinal villi, where they produce and secrete alpha and beta toxins. Alpha toxin is a lecithinase and causes necrosis, and beta toxin paralyses the intestine. Damage to the intestinal mucosa leads to necrosis and ulceration and further invasion of bacteria. Beta toxins are inactivated by proteases such as trypsin, so dietary trypsin inhibitors permit active toxin to persist in the intestine and exert its effect. Gross and microscopic changes are characterized by ulceration, haemorrhage and necrosis in the intestine.
Watery, often blood-stained content and fibrin casts are frequently seen in intestines grossly. In geese from western Canada, whole grain and legumes were found in the upper digestive tract and in a few cases undigested grain was seen throughout the intestine(53). Lesions tend to be more common in the mid and distal intestine, but can involve the entire intestine and even colon(52). Birds generally are in good nutritional condition. Overgrowth of large Gram-positive rods is seen in the damaged intestine microscopically. Lesions start at the tips of villi, but may progress transmurally. Fibrin thrombi and infiltration by heterophils are also often seen. The liver may be haemorrhagic and friable or may show multifocal necrosis, as observed in 28% of affected captive capercaillies(58).Birds typically are found dead, but clinical signs have occasionally been described; affected geese had reduced alertness and were unable to fly(53), swans were described as ‘drowsy and wobbly'(52) and lorikeets showed general malaise and had diarrhoea(57).
Standard diagnostic techniques employ anaerobic bacterial culture followed by typing of C. perfringens using laboratory animal bioassays, immunoassays (e.g. immunofluorescence or ELISA) or molecular techniques (PCR). Because C. perfringens is a normal inhabitant of the gut and proliferates in decaying carcasses, it can be difficult to definitively diagnose enterotoxaemia. Characteristic gross and microscopic lesions and evidence of bacterial toxi- genicity should accompany a positive culture before necrotic enteritis caused by C.perfringens is diagnosed as cause of death.
OTHER CLOSTRIDIA
Clostridial myonecrosis and malignant oedema (also called gas gangrene) from C. chauvoei, C. novyi, C. septicum and/ or C. perfringens result from deep wounds contaminated with bacterial spores. In an appropriate localized anaerobic environment, spores germinate and produce toxin in vivo that is absorbed systemically.
Clostridial myonecrosis has been reported in various captive and free - ranging mammals, but these incidents generally have been sequelae to injections or darting during capture and handling. Naturally occurring wounds from intraspecific aggression or accidental trauma could result in similar disease.Tetanus is caused by a neurotoxin produced by C. tetani. Spores present in the environment gain access to the body via wounds and germinate if favourable anaerobic conditions exist. The neurotoxin produced acts on the central nervous system at presynaptic sites ofspinal motor neurons. Blockage of the inhibitory mediators gamma-amino butyric acid and glycine cause uncontrolled muscle stimulation, resulting in localized or generalized hypertonia of skeletal muscles with accompanying spasms or contractions. Tetanus has been documented in a free-ranging grey squirrel ( Sciurius carolinensis) in Canada with severe trauma to the foot from a leg-hold trap(59), and a presumptive case of tetanus was reported in a free- ranging hippopotamus (Hippopotamus amphibius) with skin lacerations in South Africa(60). There are no published reports of tetanus in European wildlife.
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