The Diseases
Clostridia are a group of anaerobic, spore-forming organisms found in the soil/environment, which produce rapidly fatal disease by the secretion of potent toxins. Conditions such as blackleg, braxy, black disease and the enterotoxaemias, including lamb dysentery, struck and pulpy kidney, are all caused by clostridia (Songer, 1998; Sterne, 1981).
EnterotoxaemiaThere are five distinctive types of C. perfringens (A, B, C, D and E), each of which produces various amounts and permutations of 12 toxins. Disease in sheep is mainly caused by types B (lamb dysentery and haemorrhagic enteritis), C (struck and haemorrhagic enteritis) and D (pulpy kidney), although type A has been held responsible for a fatal haemolitic disease of lambs and the occasional case of gas gangrene in sheep.
The spores of C. perfringens types B, C and D are found in the soil and in faeces of normal animals in areas where the disease is prevalent, as well as in the intestinal contents of infected sheep (Bullen, 1970). Fatal infections occur when conditions alter favourably to allow their rapid multiplication.
Lamb DysenteryLamb dysentery usually affects strong lambs under the age of 2 weeks. The clinical course is seldom longer than a few hours, during which the lamb has abdominal pain, stops sucking, collapses and dies, its faeces being semi-fluid and blood-stained. Occasionally the animal survives a few days and can display central nervous signs due to the development of a focal symmetrical encephalomalacia (Mitchell and Linklater, 1983).
C. perfringens is saccharolytic and can multiply extremely rapidly in the presence of high levels of carbohydrate when oxygen tension is low. Lambs that ingest large quantities of milk are prone to lamb dysentery. Offspring of heavy milking hill breeds with a low fertility are particularly vulnerable (Lewis et al., 1995; Lewis, 1998).
Haemorrhagic EnteritisHaemorrhagic enteritis affects lambs in their first few days of life and is caused by either type B or type C of C. perfringens (Greig, 1975; Niilo, 1988). Death follows a short clinical illness, in which the lamb can shiver, show abdominal pain and pass blood-stained fluid faeces.
StruckStruck is a condition in adult sheep caused by toxins produced by the rapid multiplication of C. perfringens type C in the intestinal contents. Death is sudden and follows a short illness in which the animal might display abdominal pain.
Pulpy KidneyPulpy kidney is a disease which can affect sheep at any age but is most frequent in lambs of 4 - 10 weeks of age and in fattening stock from 6 months to one year of age. It is caused by the rapid multiplication of C. perfringens type D in the small intestines and the subsequent absorption of the epsilon toxin, which is produced by the organisms in the form of a non-toxic prototoxin and converted to a lethal toxin by the action of trypsin (Bullen, 1970).
Pulpy kidney disease is peracute and of short duration, with most cases being found dead. Those found alive show neurological signs and diarrhoea is seen in longer-living cases. Affected animals do not recover.
Sheep changed from a low to a high plane of nutrition may be vulnerable to pulpy kidney disease, as the rumen microbial flora have not adjusted sufficiently rapidly and partly digested food containing carbohydrate passes to the small intestine. This allows C. perfringens to multiply rapidly, producing large amounts of epsilon prototoxin, which is converted to lethal epsilon toxin by the action of trypsin (Buxton and Donachie, 1991).
BraxyBraxy is caused by Clostridium septicum and appears in late autumn and winter. It usually affects lambs born in the previous spring, as older animals appear to develop some immunity to the disease. Clinical disease is sudden and of short duration, with the animals suffering high fever, depression and anorexia. Abdominal pain can be a feature, together with the accumulation of abdominal gas. Recumbency and coma are followed by death within a few hours of the onset of the disease. In the United Kingdom the prevalence of braxy is greatest in Northern Ireland, Wales, Scotland and Northern England. C. septicum survives well in the soil and is often present in the faeces of herbivores. The disease appears to be triggered by the ingestion of frosted food, which seems to produce a favourable microenvironment for C. septicum to invade the tissues and multiply. The disease mainly affects young sheep wintered on hill pastures and old lowland grazing (Buxton and Donachie, 1991). There is evidence that the incidence of the disease is decreasing (Central Veterinary Laboratory, 1995).
Black Disease and Bacillary HaemoglobulinuriaBlack disease is a fatal peracute infection caused by Clostridium oedematiens type B, and bacillary haemoglobulinuria is a rapidly fatal disease caused by C. oedematiens type D. The latter is primarily a disease of cattle and uncommon in sheep. Both are associated with liver damage primarily caused by liver fluke (Bagadi and Sewell, 1973a).
Black disease is characterised by the rapid onset of dullness, followed by an unsteady gait, an inability to move, collapse and quiet death within a few hours of the onset of clinical signs (Bagadi and Sewell, 1973b; Sewell, 1975).
Bacillary haemoglobulinuria is characterised by a sudden high fever and ruminal stasis, with or without apparent abdominal pain. The animal breathes rapidly, has dark red urine, becomes jaundiced and dies within a short time of the onset of clinical signs.
Spores of both C. oedematiens type B and C. oedematiens type D can be found in the soil and in the livers of normal sheep on farms where the disease occurs (Buxton and Donachie, 1991).
BlacklegBlackleg infection is caused by Clostridium chauvoei and commonly follows bruising at handling, shearing, docking, parturition and castration wounds (Wilson and Miles, 1975). Within 48 hours there is a high fever and, if limb muscles are involved, the animal becomes stiff and unwilling to move. Skin discolouration, subcutaneous oedema and gas production may be present, and in cases of blackquarter metritis severe perineal oedema is sometimes seen. Infections of the head may produce marked oedema and even bleeding from the nose (see Malignant Oedema). In cases of gangrenous metritis, associated with parturition, severe perineal oedema is sometimes seen. Death usually follows a period of anorexia, profound depression and prostration.
The spores of C.chauvoei survive well in the soil, and in sheep the majority of cases arise from contamination of the wound (Buxton and Donachie, 1991).
Malignant OedemaMalignant oedema is caused by the infection of wounds with bacilli of the genus Clostridium (C. oedematiens type A; C. chauvoei; C. perfringens; C. sordellii; C. septicum). Clinical signs appear rapidly after infection, and at the site of infection a swelling will develop which will 'pit' on pressure. Gas may be detected as the skin becomes darkened and tenser. A high fever is present and toxaemia develops. The animal dies within 1 - 2 days (Buxton and Donachie, 1991).
The condition occurs as a result of wounds becoming contaminated with dirt containing clostridial spores. Rams are particularly vulnerable, as they often have head wounds as a result of fighting.
TetanusTetanus is caused by the toxin tetanospasmin, released from the spore-forming bacillus Clostridium tetani. The disease occurs more often in lambs than in adults, after spores gain entry to a wound. Germination of spores occurs only if the microenvironment is anaerobic. After germination of the spores within the wound, the C. tetani bacilli proliferate and produce toxin. The toxin is released only after the bacilli become autolysed (Buxton, 1991).
The precise mechanism of action of the tetanus toxin remains unknown. However, it has been shown that the tetanus toxin diffuses out of the site of infection, is taken up in the nerve endings of alpha axons, and migrates up to the alpha motor neurones in the ventral horn of the spinal cord. It has been suggested that the toxin acts at a presynaptic level, causing spinal disinhibition by blocking synaptic inhibition (Buxton, 1991).
The incubation period can be very variable, from 3 days to several months, but most cases occur after about 10 days. At first the animal appears slightly stiff, becomes unwilling to move and develops a fine muscle tremor. The temperature rise is variable (39 - 42° C). The general stiffness of the limbs, head, neck and tail increases after 12 - 24 hours. The animal shows hyperaestesia and repeated spasms. Mastication becomes difficult, due to tetany of the masseter muscle (lockjaw), food is chewed with difficulty, the animal drools saliva and bloat often occurs. There is retention of the urine and constipation. The animal becomes recumbent, with the legs rigidly extended and opistotonos, and the jaws become rigid. The animal usually dies due to respiratory failure 3 - 4 days after the onset of clinical signs. Milder cases, which develop more slowly, can recover over a period of weeks or even months (Aslani et al., 1998).