Clostridial Diseases of Cattle and Sheep Frank Malone Disease Surveillance and Investigation Branch, Veterinary Sciences Division, Department of Agriculture and Rural Development, 43 Beltany Road, Coneywarren, Omagh, Co. Tyrone BT78 5NF, Northern Ireland (Text of a paper presented at the annual meeting of the Association of Veterinary Surgeons Practising in Northern Ireland, Enniskillen, October 2004) Introduction include C. chauvoei, the major cause The Clostridium species affecting of blackleg, and C. novyi type B, which cattle and sheep are large, Gram- causes black disease. positive, rod-shaped, spore-bearing bacteria. Many clostridia are Clostridia which produce enterotoxins saprophytes, which normally grow in C. perfringens species cause soil, water and decomposing plant and enterotoxaemia and enteropathy. animal material. Other species, such Examples include C. perfringens type as C. perfringens, are normal D, which causes pulpy kidney disease inhabitants of the intestines and, after and C. perfringens type B, which the death of the animal, rapidly invade causes lamb dysentery. the blood and tissues playing a major role in decomposing the carcass. There has been an increase in recent These post-mortem invaders must be years in submissions to DARD’s distinguished at post-mortem Veterinary Sciences Division (VSD) of examination from those organisms carcases affected by clostridial causing primary clostridial infections. diseases (Figure 1). Diseases Caused by Pathogenic Neurotrophic Clostridia Clostridia C. tetani Quinn and others (2000) divided the Tetanus occurs sporadically in cattle pathogenic clostridia affecting cattle and sheep of all ages. Tetanus and sheep into the following groups: endospores are present in the neurotrophic clostridia, histotoxic environment and may enter surgical clostridia and clostridia which produce wounds, such as after castration or enterotoxins (Table 1). docking, or traumatised tissues, such as those of the genital tract following Neurotrophic clostridia dystocia. An idiopathic form of C. tetani and C. botulinum produce tetanus also occurs, in which the powerful neurotoxins giving rise to the organism multiplies in the intestinal diseases tetanus and botulism, tract following a dietary imbalance or respectively. change. The incubation period may be from a few days to several weeks. Histotoxic clostridia The clinical presentation of tetanus The exotoxins produced by these includes early stiffness and reluctance clostridia produce local tissue necrosis to move. Bloat, a raised tailhead and and systemic toxaemia. Examples trismus develop and the third eyelid prolapses, particularly when the head recumbent and develops tetanic is moved. In the terminal stages of spasms and opisthotonus. the disease the animal becomes Table 1. Ruminant Diseases Caused by Pathogenic Clostridia (after Quinn and others, 2000) Clostridium Species Disease Neurotoxic clostridia Clostridium tetani Tetanus Clostridium botulinum Botulism Histotoxic clostridia Clostridium chauvoei Blackleg Clostridium septicum Malignant oedema Braxy (sheep) Clostridium novyi type A Big head of rams Clostridium novyi type B Black disease (necrotic hepatitis) Clostridium haemolyticum Bacillary haemoglobinuria (C.novyi type D) Clostridium sordellii Gas gangrene Abomasitis Enterotoxaemia Clostridium perfringens Type B Lamb dysentery (C.welchii) Clostridium perfringens Type C Struck (C.welchii) Clostridium perfringens Type D Pulpy kidney (C.welchii) 250 207 200 18 5 15 0 Cat t le 110 Sheep 10 0 60 55 54 51 50 25 22 19 0 1999 2000 2001 2002 2003 Figure 1. Clostridial diseases of cattle and sheep confirmed post mortem at VSD 2 C. botulinum becomes difficult when the chest or There has been a major increase in diaphragm muscles become paralysed the number of suspected cases of and most affected animals either die botulism in cattle in Northern Ireland in or are euthanased. The clinical signs recent years. Botulism is a neuro- most commonly recorded in recent paralytic disease caused by the toxins cases of bovine botulism in Northern of Clostridium botulinum, which is Ireland are listed in Table 2 (Karina usually fatal. These bacteria are Wrigley, personal communication). commonly found in the environment and will grow in decaying carcasses Botulism does not produce and vegetable matter. There are pathognomonic lesions and therefore seven different types of botulinum cannot be diagnosed by gross port- toxin (types A-G). Type C or D toxins mortem or histopathological cause most cases of botulism in cattle examinations. However, necropsy and as little as 10µg of these toxins may help with differential diagnosis. are lethal to a cow (Gregory and The standard diagnostic test for others, 1996). Type D is the most botulism is the mouse bioassay that is common botulinum toxin type used to detect toxin in faeces or associated with bovine botulism in gastro-intestinal contents of affected Northern Ireland. animals. Botulism can affect cattle of all ages. Outbreaks of botulism in Northern If large amounts of toxin have been Ireland have been reported in cattle ingested the animal may be found grazing pasture on which poultry litter dead without showing signs of illness. had been spread (McIlroy and others, However, signs of illness usually 1987) and in cattle fed ensiled poultry become apparent within 24 hours to 7 litter (McLoughlin and others, 1988). days of ingesting botulinum toxin. The Recent outbreaks of bovine botulism main clinical feature is lack of muscle in Northern Ireland have been tone resulting in progressive muscle reported where broiler poultry litter weakness. had been spread on pasture, used as bedding in cattle houses or stacked on In the early stages of the disease, the farm adjacent or close to pasture affected cattle may stagger about, where cattle were grazing. The have hind leg stiffness and be presence of the carcases of birds that reluctant to move. They occasionally have died during production is become aggressive and may attempt regarded as the likely source of to charge people in close proximity. botulinum toxins. Scavengers may Muscle weakness usually affects the gain access to this material after it has hindquarters first before progressing been stacked outside or spread on to the forequarters, head and neck. pasture. It is speculated that even Affected animals may be found lying small fragments of carcasses on their chest with the head turned transferred onto pasture or silage by towards the flank (similar to cows with scavenger animals, such as foxes, "milk fever"). A few cattle may dogs or crows, can pose a risk to develop paralysis of the tongue grazing cattle. muscles resulting in inability to chew or swallow, drooling of saliva or, less commonly, protrusion of the tongue from the mouth. Breathing eventually Table 2. Clinical signs of bovine or hay is to be harvested, in the same botulism recorded on 30 Northern year. This is because fragments of Ireland farms carcases may persist on pasture for a considerable time. If poultry litter must Clinical signs Number of be spread, it should be deep-ploughed farms into arable ground. If this is not an (n=30) option and litter must be disposed off Progressive flaccid 29 by spreading on pasture, cattle should paralysis not have access to the treated fields Lateral recumbency 29 for at least several months. However, Sternal recumbency 27 there is no guarantee that the treated Difficulty rising 16 fields would then be safe for cattle and Ataxia 12 it is important to remember that Posterior weakness 5 scavenger animals and birds to Tongue paralysis 6 neighbouring fields may transport Difficulty in 6 fragments of carcases on pasture. swallowing/excessive salivation Vaccination may protect cattle grazing Lethargy 5 potentially contaminated pasture. Aggression 3 Spreading poultry litter on a windy day Staring eyes 2 may also pose a risk of contaminating adjacent fields. Any animal or bird carcases, or portions of carcases, Careful disposal of animal or bird visible on pasture or in cattle houses, carcases and poultry litter is should be promptly removed. Even necessary to minimise the risk of small fragments of carcases may be botulism to cattle. Poultry carcases dangerous to cattle and should be should be promptly removed from the disposed of by incineration or chicken house and disposed of by rendering. In any case, it is an incineration, or rendering (as required offence to leave carcases or part by EU Regulation No. 1774/2002). carcasses on any land, and any Following removal of the broiler crop, person discovered so doing may be all poultry house doors should be kept prosecuted. closed until the litter is removed. The litter should not be removed from the No vaccine is available under general house until it can be loaded directly licence in the UK for the protection of onto covered vehicles or immediately cattle against botulism. However, a covered. At no time should it be vaccine against types C and D accessible to dogs, foxes, crows or botulism is available under “special other scavengers that may carry treatment authorisation” (STA) from carcases onto adjacent pasture or into the Veterinary Medicines Directorate cattle housing. Washings from poultry (VMD). A recent survey by VSD staff houses and yards should be collected of veterinary surgeons that have used in tanks rather than be allowed to flow this vaccine in Northern Ireland onto adjacent land. indicates that it is effective in controlling botulism in cattle. The results of investigations by VSD Veterinary surgeons who wish to staff suggest that poultry litter should consider vaccination of clients' herds not be spread on agricultural land that may apply to the VMD for an STA to is to be grazed, or from which silage obtain and use this vaccine. It is 4 important to remember that two doses following signs of systemic toxaemia: of vaccine are required at an interval dyspnoea, recumbency and coma. of 4-6 weeks. Cattle receiving only one dose are not fully protected. At post-mortem examination lesions are principally found in the large The risk to humans from cases of muscle masses of the fore- and botulism in cattle appears remote.