Thiamin deficiency in cats and dogs associated with feeding meat preserved with sulphur dioxide VP STUDDERT and R H LABUC Veterinary Clinical Centre, University of Melbourne, Werribee, Victoria 3030
SUMMARY: Thiamin deficiency was diagnosed in cats and dogs being fed fresh minced meat, which contained sulphur dioxide as a preservative and less than 0.5 mg/kg thiamin. Thiamin in the meat and in added dietary ingredients, including a supplementary vitamin mixture, was destroyed by the sulphur dioxide. Aust Vet J 68: 54-57
Introduction Numerous reuorts of thiamin deficiency in cats and, less frequently, dogs exist in the literature. In- these, the dietary deficiency was attributed to destruction of thiamin by heat during cooking or processing (Loew et all970; Read et all977; Baggs et a1 1978) or by thiaminase-containing fish (Smith and Proutt 1944; Jubb et a1 1956; Houston and Hulland 1988). Sulphites are capable of destroying thiamin in food (WHO 1962), but only one brief communication in veterinary literature reports sulphur dioxide (SO,) being associated with clinical thiamin deficiency in animals (Toepfer 1974). Veterinary textbooks of clinical nutrition (Edney 1987; Layis et a1 1987), internal medicine (O’Donnell and Hayes 1987; Greene and Braund 1989) and neurology (Chrisman 1982; deLahunta 1983) fail to include sulphites as a cause of thiamin deficiency, possibly because preserved fresh pet meat is not commonly used in many countries. In this report, naturally occurring thiamin deficiency in cats and dogs fed fresh meat preserved with SO2 is described. Materials and Methods Case Reports Cases of thiamin deficiency in cats and dogs presented to the University of Melbourne Veterinary Clinic and Hospital were investigated to determine the dietary history and source of the deficiency. Post-Mortem Examination Lesions, characteristic of thiamin deficiency (Jubb et a1 1956), were focal, bilaterally symmetrical haemorrhagic necrosis in periventricular grey matter involving consistently and, most severely, the caudal colliculi, but often vestibular, lateral geniculate, oculomotor, cuneate and red nuclei and, irregularly, other nuclei. Sulphur Dioxide a n d Thiamin Assays Meat samples submitted with the clinical cases were qualitatively tested for the presence of SO, using filter paper strips impregnated with malachite green, a modification of the procedure described by Horowitz (1980). Three samples of fresh minced pet meat, obtained from 3 different pet shops in the Melbourne metropolitan area, 2 cans of a commercial canned cat food, and 2 mixtures of pet meat and the canned cat food were submitted for SO, and thiamin analysis*.
Results Case Histories Case I: A shelter housing approximately 200 cats reported a syndrome of depression, pupillary dilatation and ataxia (referred to as ‘wobbles’), which occasionally progressed to seizures and death and had been observed in resident cats for several years. Numbers affected varied from less than one per month to 40 with 4 deaths in a 10-month period. There was no consistency in age, sex or duration of stay at the shelter in the affected cats. Postmortem examination of an affected cat showed gross and
histopathological lesions in the brain characteristic of thiamin deficiency. Cats in the shelter were fed a diet of fresh minced pet meat and canned cat food?, approximately 1:1, which was mixed by hand 0.5 to 2 h before feeding. The meat, either ox cheek or kangaroo, was delivered by a pet meat supplier twice weekly and refrigerated until used. Following the post-mortem findings, the same diet was fortified with dried brewer’s yeast powder, but cats with similar signs continued to be observed. Shelter personnel then began treating affected cats with an injection of thiamin$ as soon as signs were noted and there was a rapid clinical improvement. No further deaths were reported.
Case 2: A 4-year-old male German shepherd dog was presented for post-mortem examination. The dog had a 48 h history of forelimb extension and seizures before dying despite veterinary treatment, which was symptomatic only, as thiamin deficiency was not suspected. Histopathological lesions in the brain, consistent with thiamin deficiency, were found. The dog had been fed only fresh pet mince for the previous 6 w. The meat was obtained from a local pet shop, where the product, chopped beef with a visibly high fat content, was referred to as puppy mince. Case 3: A 4-year-old male English springer spaniel was presented with a history of weight loss for one week and vomiting, ataxia, hyperaesthesia, particularly on extension of the neck, proprioceptive deficits and seizures for 48 h. At the time of examination, the dog was dull and hyporesponsive to stimuli. Two days later the owner’s other dog, a 4-year-old female English springer spaniel, developed a similar ataxia. Both dogs had been fed a diet based on fresh pet meat with added vegetables and table scraps for a long period, but in the 3 w prior to the onset of signs in the first dog, only the pet meat had been given. Both dogs showed a rapid improvement and resolution of clinical signs following parenteral treatment with thiamin§. Case 4: In a 4 w period, 6 Bouvier des Flandres, 5 females and one male, in a kennel with 65 dogs of 5 different breeds, showed acute signs of hindlimb ataxia and paraplegia or quadriplegia progressing to paralysis with extensor rigidity. Three of the clinically affected dogs, euthanased within 2 d of the onset of signs, were submitted for post-mortem examination. Histopathological lesions in the brain, characteristic of thiamin deficiency, were found in 2 dogs, one of which also had focal degenerative lesions in the myocardium. An affected surviving dog with paraparesis showed some knuckling with absent placing, hopping and stretch reflexes, and slow pedal withdrawal reflexes in the hindlimbs. This dog, and 2 others less severely affected, were treated parenterally with thiamin.§ This dog showed a slow improvement, becoming ambulatory within 7 d. Three months later, the owner reported
t Whiskas Mixed Fish@,Uncle Ben’sof Australia, Wodonga, Victoria 3690 $ B-Calm@,Ilium Veterinary Products, Smithfield,New South Wales
2164
0 Thiabex injection, Coopers Veterinary Products, Silverwater, New * Dairy Technical Services Ltd, North Melbourne, Victoria 3051 54
South Wales 2141 Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
TABLE 2 Thiamin requirements of cats and dogs
TABLE 1 Sulphur dioxide and thiamin concentrations in pet foods Sample No. 1
Content
raw minced beef (for human consumption) fresh pet meat (case 4) 2 3 fresh beef pet mince 4 beef mince2 5 kangaroo pet mince3 6 canned chicken and turkey cat food4 7 canned tuna cat food4 8 mixtures of samples 5 & 6 mixtures of samples 3 & 7 9 plus 0.104 mg thiamin6 10-21 12 knackery samples7
Sulphur dioxide Thiamin mgk3 mglkg 0.81 ND
ND 420 1480 860 1100
(0.5
( 10
1 .o
(10 610
2.5 0.5
560 0-4078 (mean 1194)
( 0.5 ( 0.5
0.5 ND
N D not done 1 Thomas and Corden 1977 2 Bonnie Vita Plus cat and kitten mince, vacuum pack, Clinkat (Australia) Pty Ltd, Thomastown, Victoria 3 Bonnie minced ’roo, vacuum pack, Clinkat (Australia) Pty Ltd, Thomastown, Victoria 4 Whiskas, Uncle Ben’s of Australia, Wodonga, Victoria 5 approximately 1:l by volume 6 Vetzyme tablets, Philips Yeast Products Ltd, London 7 from 8 establishments
near complete recovery but a slight hindlimb ataxia was still detectable. There was more rapid improvement in the less affected dogs. All dogs in the kennel had been fed a diet based on horse meat obtained from a local knackery with added breakfast-type cereals, lucerne meal, limestone and rendering residue. A sample of the meat was found to contain 420 mg S02/kg(Table 1). After the diagnosis was made, all unaffected dogs were treated parenterally with thiamin and the meat source was changed t s one reportedly not using SO, preservatives. No other dogs were affected.
Sulphur Dioxide a n d Thiamin Analyses All representative meat samples submitted with the 4 cases and the 3 samples purchased from pet shops showed the presence of SO, in the qualitative test using malachite green. The results of quantitative analyses for thiamin and SO2in purchased meat, canned food and meat fed in Case 4 are shown in Table 1. Discussion Clinical signs of thiamin deficiency in cats and dogs have been described previously (Everett 1944; Read and Harrington 1981). They occur in 3 stages during which inappetence, loss of weight, vomiting and neurological abnormalities, particularly pupillary dilatation, ataxia and terminal seizures, develop. Read and Harrington (1981) grouped the terminal signs observed in dogs into a neurological syndrome, with ataxia, paraparesis, extensor rigidity, vestibular signs and seizures, and a sudden death syndrome caused by acute cardiac failure. In the cases described, there were clinical signs consistent with thiamin deficiency and response to parenteral treatment with thiamin. In 3 cases, brain lesions characteristic of thiamin deficiency were found on post-mortem examination of at least one affected animal. In each case, there was a history of a diet based predominantly or exclusively on fresh pet meat. A clinical diagnosis can be established on history and clinical signs (Lewis eta/ 1987) and by response to treatment with thiamin (O’Donnell and Hayes 1987). Laboratory confirmation was not available to show reduced blood thiamin and erythrocyte transketolase and elevated blood pyruvate and lactate levels (Read and Harrington 1982). Focal myocardial degeneration associated with thiamin deficiency, as found in Case 4, has been described in several species (Sullivan 1985). Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
Cat mglkg diet (dry matter) pglkg body weight/day adult growth mg/lOOO kcal *
5’ 100s: 308s: 1.on
Dog 17
209 549 0.39
National Research Council 1978
t Lewis et a/ 1987 $ Kallfelz 1989
5 National Research Council 1985 1 National Research Council 1986 Meat has important nutritional deficiencies, especially of calcium, iodine and vitamins A and D, but it normally contains thiamin (Table 1) adequate to meet the requirements of dogs and cats (Table 2). Lean pork and organ meats such as heart, brain, liver and kidney are especially good sources of thiamin. However, thiamin is heat-labile and cooking or processing can result in losses of 40 to 50% (McDowell 1989). A variety of sulphiting agents, including SO, and several inorganic sulphites, are used to preserve food, particularly meat, fresh fruits and vegetables and dried fruit. They extend the storage life of meat by slightly delaying spoilage but mask the signs without preventing putrefaction (WHO 1962). The odour and red colour of fresh meat is retained longer following treatment with sodium metabisulphite, reportedly by inhibiting the oxidation of myoglobin to metmyoglobin (Krol and Moerman 1959), but this fails to explain the restoration of redness to discoloured, spoiled meat which is possible with the same treatment. In untreated meat, a putrid odour develops when bacterial counts reach about 100 million per gram, whereas in meat treated with SOz,a weaker, less objectionable odour is not detectable until the bacterial population reaches about 500 million per gram (Christian 1963). Bacteria are more susceptible to the biocidal and biostatic effects of SO2 than moulds and yeasts, and gram-positive organisms are more resistant than gram-negatives (Lueck 1980). In the absence of sulphites, spoilage of sausage meat is dominated by gram-negative rods, but in the presence of sulphite, only gram-positive rods are found (Dyett and Shelley 1966; Banks and Board 1981). Salmonellae are particularly sensitive to the effects of SO,. Roberts and Boag (1 975) suggest the preservative is effective against their growth even if they are not destroyed. Little is known concerning the effects of sulphites on spores (Wedzicha 1984). Thiamin is subject to cleavage by sulphites, including SO,, into constituent pyrimidine and thiazole compounds, thereby rendering it inactive. In experimental diets, SO, can be used to specifically destroy thiamin without damaging other nutrients (Williams et all935). The rate is accelerated in aqueous solution and with increased temperature (Joslyn and Leichter 1967). The extent of destruction of thiamin in sulphited meat increases linearly with increasing SO, content, so that 400 and 1000 mg S O J k g depletes thiamin content by 55% and 95% respectively, with the loss occurring essentially within the first hour after addition (Hermus 1969). The World Health Organization recommends that human foods serving as significant sources of thiamin, such as meat, cereal grains, dairy products and nuts, should not be treated with sulphites (WHO 1962). It also recommends that sulphite preservatives not be used on meat, because they can lead to deception regarding freshness and possible injury from the consumption of tainted meat. The principle toxic effects of sulphites in food are the result of destruction of thiamin. Large doses are required to cause gastrointestinal irritation in humans, rabbits, rats and dogs (Allen and Brook 1971). Sulphites in food have also been associated with anaphylactoid reactions in humans (Stevenson and Simon 1981). The use of SO, in meat for human consumption is prohibited in the European Economic Community (Wilson 198l ) , and limited to sausage meat at a maximum of 500 mg/kg 55
in Australia (National Health and Medical Research Council 1987) and 450 mg/kg in the United Kingdom (Jukes 1984). Analysis of pet meat being fed to dogs in Case 4, 3 samples of purchased pet mince and 12 samples from 8 knackeries in Victoria supplying the pet met trade in 1983 to 1984, showed that sulphites are commonly used to preserve fresh pet meat (Table 1). Only 1 of 16 samples failed to contain SO,, and 10 (63%) had levels up to 8 times higher than those allowed in meat for human consumption. Although an unpleasant, metallic flavour is detectable by humans in foods treated with SO,, which limits the amounts used (Allen and Brook 1971), dogs and cats do not appear to discriminate against treated meat, even those samples containing high levels. For preservation of pet meat, the usual source of SO, is sodium metabisulphite, applied to the meat as a powder or by soaking in an aqueous solution at the knackery (Department of Agriculture, Victoria, unpublished report 1985). There are no regulations controlling the level of SO, in pet meat in Victoria and the wide range of levels found suggest no standard is followed. As found in the 2 samples of canned cat food analysed (Table l), commercial pet foods formulated to meet the nutritional requirements of dogs and cats (National Research Council 1985, 1986) contain adequate levels of thiamin, even after losses associated with processing and storage occur. Although the diet of cats in Case 1 was approximately 50% canned cat food, the remainder was pet mince preserved with SO,. Analyses of samples 8 and 9 showed that mixing these ingredients approximately 1 h before feeding, as was the practice in Case 1, not only reduced the concentration of thiamin, but also permitted SO, destruction of the thiamin contributed by the canned food in sample 9. In both samples, the level of SO, was approximately half that present in the pet meat, reflecting that 1:l dilution with canned cat food, which contained neglible amounts. For the same reason, the thiamin content of the mixture in sample 8 was 50% of that in the canned food, but in sample 9 it was reduced by 80070, indicating destruction had occurred. The extent of thiamin loss would be dependent on the original levels of SO, and thiamin, how long the ingredients were mixed before feeding, the composition of other ingredients which might form inactive complexes with the SO, (Abalaka 1980) and factors influencing the rate of reaction such as pH and temperature (Joslyn and Leichter 1967). Under similar circumstances, a nutritionally adequate diet containing raw, thiaminase-containing fish pieces was responsible for thiamin deficiency in foxes in the original report of Chastek paralysis (Green 1936). In Case 1, the addition of dried brewer’s yeast, a very rich source of thiamin, which contains 95.2 mg thiamidkg (McDowell 1989), to the diet containing pet meat was ineffective in preventing the occurrence of clinical signs of thiamin deficiency, probably due to destruction by SO,. The pet mince product fortified with vitamins and minerals by the manufacturer (sample 4) was also deficient in thiamin (Table 1). This may have been due to destruction by SO, in the meat and/or the effects of mineral sulphates in the pre-mix used (Verbeeck 1975). The addition of crushed vitamin tablets to the food (sample 9), as commonly recommended on product labels, also failed to raise the level of thiamin in the mixed diet to meet requirements. Assuming an average caloric value of 2.6 kcal/g for raw beef (Thomas and Corden 1977), the thiamin levels found in the SO, preserved pet meats (Table 1) were less than 19% of the 1.0 mg/1000 kcal recommended for cats (National Research Council 1986) and less than 64% of the 0.3 mg/1000 kcal recommended for dogs (National Research Council 1985). The actual deficit cannot be calculated because the levels fell below the minimum detected in the analytical methods used. Thiamin requirements are influenced by both physiological and dietary factors (National Research Council 1985). They are increased during pregnancy, lactation and growth. Because thiamin is specifically involved in carbohydrate metabolism, the requirement is raised when the dietary carbohydrate is increased relative to other energy-supplying components. The thiaminsparing effect of protein and fat has been recognised (McDowell 1989), and the high meat diets fed to cats and dogs in the cases 56
described were probably protective of the low thiamin levels present. Only a small percentage of the cats and dogs in Cases I and 4 showed clinical signs of thiamin deficiency when fed the deficient diet. Because thiamin is not stored in the body to any extent (McDowell 1989), anorexia from any cause can precipitate deficiency, particularly in cats, because of their high requirement for the vitamin. Various disease conditions, including parasitism, diarrhoea and malabsorption, as well as stress, all of which were possible in the cats in Case 1, can increase the requirement and result in variation between animals. A similar sporadic occurrence was seen in a specific-pathogen-free cat colony with over 100 cats receiving the same processed, thiamin-deficient diet (Baggs et a1 1978). In Case 4, the 6 affected dogs were of the same breed, leaving 59 dogs of 4 other breeds clinically normal during the period before the diet was changed. This might suggest a breed variation in thiamin requirements. Sulphur dioxide is undoubtedly useful in enhancing the storage life and acceptability of pet meat, which is at greater risk of spoilage than human meat because of the conditions under which it is produced, stored and, in some cases, transported, but its use creates other health hazards for cats and dogs. As well as masking the signs of spoilage and bacterial contamination, which misleads the purchaser and increases the risk of food poisoning, the destruction of thiamin by SO, leads to a serious, life-threatening nutritional deficiency. The inclusion of SO,-preserved pet meat destroys thiamin in an otherwise nutritionally adequate diet, and additional thiamin, whether added by the manufacturer or by the owner as a vitamin supplement in the food, may be unsuccessful in correcting the deficiency and preventing clinical disease. The extent of the deficiency may not be clinically apparent. Subclinical thiamin deficiency has been proposed as a cause of poor growth in young sheep (Thomas 1986). It must be assumed that fresh pet meat will contain SO,. If it is fed, other sources of thiamin should be included in the diet, but not mixed with the pet meat. Green et a1 (1942) observed that feeding fresh fish and a diet containing adequate thiamin on different days was successful in preventing the occurrence of thiamin deficiency in foxes. This is a possible regime for using SO,-preserved pet meat in cats and dogs. Food laws limit, or prohibit, the use of SO, in human foods; yet because human diets are usually varied, the effects of thiamin destruction by sulphites in certain preserved foods would be expected to be less severe in humans than in dogs or cats, which may be fed the treated meat exclusively. The introduction of regulations controlling the use of SO, in pet meat may be effective in preventing the range of clinical and subclinical disease that can result from indiscriminate use of the preservative.
Acknowledgments Drs RW Mitten and RM Kerlin are thanked for their assistance.
References Abalaka JA (1980) - Microbios 29: 15 Allen RJL and Brook M (1971)- Effectsof SulphurDioxidein Animals and Man, In Proc Third Int Cong Food Scr Ech. Washington, p799 Baggs RB, deLahunta A and Averill DR (1978) Lab Anim Sci 28: 323 Banks JG and Board RG (1981) - J Appl Bact 51: 9 Chrisman C (1982) - Problems in Small Animal Neurology, Lea and Febiger, Philadelphia Christian J H B (1963) - CSIRO Food Pres Quart 23: 30 deLahunta A (1983) - Veterinary Neuroanatomy and Clinical Nuerology, 2nd edition, Saunders, Philadelphia Dyett EJ and Shelley D (1966) - J Appl Bact 2 9 439 Edney ATB (1987) - Dog and Cat Nutrition, Pergamon, Oxford Everett GM (1944) - A m J Physiol 141: 439 Greene CE and Braund KG (1989) - In Textbook of Veterinary Internal Medicine, 3rd edition, edited by Ettinger SJ, Saunders, Philadelphia, p615 Green RG (1936) - Minn Wild1 Dis Invest 2: 106 Green RG, Carlson WE and Evans CA (1942) - J Nutrition 23: 165 Hermus RJJ (1969) - Inf J Vit Res 3 9 175 Horwitz W (1980) - OfficialMethods of Analysis, Association of Official Analytical Chemists, Washington, DC, p340 ~
Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
Houston DM and Hulland TJ (1988) - Can Vet J 2 9 383 Joslyn MA and Leichter J (1967) - J Nutrition 96: 89 Jubb KV, Saunders LZ and Coates HV (1956) - J Comp Path 66: 217 Jukes DJ (1984) -Food Legislation ofthe UK, Butterworths, London, p70 Kallfelz FA (1989) - In Current Veterinary Therapy X , edited by Kirk RW, Saunders, Philadelphia, p1352 Krol B and Moerman P C (1959) - Conserva 8:1, cited in Chemistry of Sulphur Dioxide in Foods, Wedzicha BL (1984), Elsevier Applied Science, London, p303 Lewis LD, Morris MJ and Hand MS (1987) - Small Animal Clinical Nutrition III, Mark Morris Associates, Topeka, Kansas Loew FM, Martin CL, Dunlop RH, Mapletoft RJ and Smith SI (1970) - Can Vet J 11: 109 Lueck E (1980) - Antimicrobial Food Additives, Springer-Verlag, Berlin, cited in Chemistry of SulphurDioxide in Foods, Wedzicha BL (1984), Elsevier Applied Science, London, p262 McDowell LR (1989) - Vitamins in Animal Nutrition, Academic Press, San Diego National Health and Medical Research Council (1987) - FoodStandard Code, Australian Government Publishing Service, Canberra, p160 National Research Council (1978) - Nutrient Requirements of Cats, National Academy Press, Washington, DC National Research Council (1985) - Nutrient Requirements of Dogs, National Academy Press, Washington, DC National Research Council (1986) - Nutrient Requirements of Cats, National Academy Press, Washington, DC O’Donnell JA and Hayes KC (1987) - In Diseasesof the Cat, Voli, edited by Holzworth J, Saunders, Philadelphia, p29 Read DH, Jolly RD and Alley MR (1977) - Vet Pathol 1 4 103 Read DH and Harrington DD (1981) - Am J Vet Res 42: 984 Read D H and Harrington DD (1982) - Am J Vet Res 43: 1258 Roberts D and Boag K (1975) - J Hygiene (Cambridge) 15: 173 Smith DC and Proutt LM (1944) - Proc Soc Exp Biol Med 56: 1 Stevenson DD and Simon RA (1981) - J Allergy Clin Immunol68: 26 Sullivan ND (1985) - In Pathology of Domestic Animals, 3rd edition, Jubb KV, Kennedy P C and Palmer N, Academic Press, San Diego, p256 Thomas KW (1986) - vet Res Comm 1 0 125 Thomas S and Corden M (1977) - Metric Tables of Composition of Australian Foods, Australian Goverment Publishing Service, Canberra, PI4 Toepfer SA (1974) - Aust Vet Pract 4(2): 76 Verbeeck J (1975) - Feedstuffs47(36):4,45, cited in Vitamins in Animal Nutrition, McDowell LR (1989), Academic Press, San Diego, p181 Wedzicha BL (1984) - Chemistry of Sulphur Dioxide in Foods, Elsevier Applied Science, London WHO (1962) - World Health Org Tech Rep Ser 28: 96 Williams RR, Waterman RE, Keresztesy JC and Buchman ER (1935)= J Am Chem SOC57: 536 Wilson NRP (1981) - Meat andMeat Products, Applied Science, London, PI21
(Accepted for publication 25 September 1990)
ANNOTATION
Semi-automated slaughtering and dressing of cattle Slaughtering animals is a slow, arduous, messy and dangerous occupation. The hazards to abattoir workers are reflected in the industry’s annual $330 million workers’ compensation and related payouts. The CSIRO Division of Food Processing recognised that alternative slaughtering and dressing technologies could lead to more efficient and safe working conditions, and that major gains in productivity could be achieved through some degree of automation. Beginning in 1974 a group at the Division’s Meat Research Laboratory in Cannon Hill, Queensland dissected the slaughtering system. They split the key processes into what are termed modules, then looked at how to automate each module and best integrate it into the complete process.
Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
The Australian Meat and Livestock Research and Development Corporation has supported the project with the aim of cutting meat-processing costs by at least 30%. That aim is close to realisation. The group hopes that two fully functional commercial plants will be operating by the end of 1990. The new automated processing system, known as Fututech, represents a radical departure from conventional meat-processing techniques. It offers considerable cost savings, reduced stress on animals and hence a better-quality meat, and a significant improvement in the working environment. At the core of Fututech is a ‘programmable logic controller’ (PLC) that oversees the whole process through seven ‘slave’ PLCs running the 10 modules involved in the process. The first module deals with the lead-up, capture, stunning, and spinal inactivation of the animal, followed by bleeding. Animals are led singly down a sloping race along a moving footway. A central ridge separates the legs until the animal is finally comfortably suspended with legs dangling down. The head is contacted just behind the ears and a 120-voltpulse of electricity induces an electroplectic fit that renders it paininsensitive. A second electric shock is used to stop all involutary muscle activity, including the heart. An air-knife with two opposing serrated blades (to make sure the wound stays open) then severs the main artery above the heart to bleed the animal. The process is over within a few seconds. The carcase is towed out of the area and enters the hornremoval module. After the horns have been cut off the carcase is tipped onto its side and then rolled onto its back onto one of a series of cradles mounted on a moving work conveyor. On this cradle many of the remaining manual tasks are performed, with slaughtermen preparing the carcase for the automatic hideremoval and evisceration modules. An overhead conveyor system then transports the carcase through the other modules, tilting it through the range of positions demanded during processing. For example, during pelvic-bone cutting - necessary to allow the viscera to slide out easily - the animal is positioned head-down at 30” to the horizontal to avoid contact between blade and internal organs. When the time comes for viscera ejection, the position is reversed - the animal is held head-up at 30” to the horizontal - so the ejection arm can push the contents out between the hind limbs. Human involvement is necessary during the process - overseeing the action, cleaning up the details, and generally making sure that everything is as it should be - but advanced robotics dominate the scene. Viscera-ejector arms, hide-pullers, knives and saws are controlled by the slave PLCs and are guided in their tasks by various sensors - photo-optic or ultrasonic or magnetic. The Fututech commercial prototypes can process a beast to a split carcase in the same time as a medium-size conventional processing plant. In doing so labour requirements are vastly reduced. The Fututech prototype is currently designed to process 600 animals a day and is continually being refined. The facility is currently set up to handle cattle of 220-800 kg body weight, and another aim is to adapt the process so it can handle smaller animals, particularly sheep. CSIRO has signed an agreement with FMC (Australia) Ltd to commercialise the Fututech semi-automated slaughtering equipment. FMC is a Melbourne-based engineering group with international experience in the abattoir industry. Fututech is claimed to be the greatest advance in meatprocessing technology this century. (Adapted from Rural Research 147, Winter 1990, pages 26-28 with acknowledgment to CSIRO Division of Food Processing). AK Sutherland
57
SUMMARY: Thiamin deficiency was diagnosed in cats and dogs being fed fresh minced meat, which contained sulphur dioxide as a preservative and less than 0.5 mg/kg thiamin. Thiamin in the meat and in added dietary ingredients, including a supplementary vitamin mixture, was destroyed by the sulphur dioxide. Aust Vet J 68: 54-57
Introduction Numerous reuorts of thiamin deficiency in cats and, less frequently, dogs exist in the literature. In- these, the dietary deficiency was attributed to destruction of thiamin by heat during cooking or processing (Loew et all970; Read et all977; Baggs et a1 1978) or by thiaminase-containing fish (Smith and Proutt 1944; Jubb et a1 1956; Houston and Hulland 1988). Sulphites are capable of destroying thiamin in food (WHO 1962), but only one brief communication in veterinary literature reports sulphur dioxide (SO,) being associated with clinical thiamin deficiency in animals (Toepfer 1974). Veterinary textbooks of clinical nutrition (Edney 1987; Layis et a1 1987), internal medicine (O’Donnell and Hayes 1987; Greene and Braund 1989) and neurology (Chrisman 1982; deLahunta 1983) fail to include sulphites as a cause of thiamin deficiency, possibly because preserved fresh pet meat is not commonly used in many countries. In this report, naturally occurring thiamin deficiency in cats and dogs fed fresh meat preserved with SO2 is described. Materials and Methods Case Reports Cases of thiamin deficiency in cats and dogs presented to the University of Melbourne Veterinary Clinic and Hospital were investigated to determine the dietary history and source of the deficiency. Post-Mortem Examination Lesions, characteristic of thiamin deficiency (Jubb et a1 1956), were focal, bilaterally symmetrical haemorrhagic necrosis in periventricular grey matter involving consistently and, most severely, the caudal colliculi, but often vestibular, lateral geniculate, oculomotor, cuneate and red nuclei and, irregularly, other nuclei. Sulphur Dioxide a n d Thiamin Assays Meat samples submitted with the clinical cases were qualitatively tested for the presence of SO, using filter paper strips impregnated with malachite green, a modification of the procedure described by Horowitz (1980). Three samples of fresh minced pet meat, obtained from 3 different pet shops in the Melbourne metropolitan area, 2 cans of a commercial canned cat food, and 2 mixtures of pet meat and the canned cat food were submitted for SO, and thiamin analysis*.
Results Case Histories Case I: A shelter housing approximately 200 cats reported a syndrome of depression, pupillary dilatation and ataxia (referred to as ‘wobbles’), which occasionally progressed to seizures and death and had been observed in resident cats for several years. Numbers affected varied from less than one per month to 40 with 4 deaths in a 10-month period. There was no consistency in age, sex or duration of stay at the shelter in the affected cats. Postmortem examination of an affected cat showed gross and
histopathological lesions in the brain characteristic of thiamin deficiency. Cats in the shelter were fed a diet of fresh minced pet meat and canned cat food?, approximately 1:1, which was mixed by hand 0.5 to 2 h before feeding. The meat, either ox cheek or kangaroo, was delivered by a pet meat supplier twice weekly and refrigerated until used. Following the post-mortem findings, the same diet was fortified with dried brewer’s yeast powder, but cats with similar signs continued to be observed. Shelter personnel then began treating affected cats with an injection of thiamin$ as soon as signs were noted and there was a rapid clinical improvement. No further deaths were reported.
Case 2: A 4-year-old male German shepherd dog was presented for post-mortem examination. The dog had a 48 h history of forelimb extension and seizures before dying despite veterinary treatment, which was symptomatic only, as thiamin deficiency was not suspected. Histopathological lesions in the brain, consistent with thiamin deficiency, were found. The dog had been fed only fresh pet mince for the previous 6 w. The meat was obtained from a local pet shop, where the product, chopped beef with a visibly high fat content, was referred to as puppy mince. Case 3: A 4-year-old male English springer spaniel was presented with a history of weight loss for one week and vomiting, ataxia, hyperaesthesia, particularly on extension of the neck, proprioceptive deficits and seizures for 48 h. At the time of examination, the dog was dull and hyporesponsive to stimuli. Two days later the owner’s other dog, a 4-year-old female English springer spaniel, developed a similar ataxia. Both dogs had been fed a diet based on fresh pet meat with added vegetables and table scraps for a long period, but in the 3 w prior to the onset of signs in the first dog, only the pet meat had been given. Both dogs showed a rapid improvement and resolution of clinical signs following parenteral treatment with thiamin§. Case 4: In a 4 w period, 6 Bouvier des Flandres, 5 females and one male, in a kennel with 65 dogs of 5 different breeds, showed acute signs of hindlimb ataxia and paraplegia or quadriplegia progressing to paralysis with extensor rigidity. Three of the clinically affected dogs, euthanased within 2 d of the onset of signs, were submitted for post-mortem examination. Histopathological lesions in the brain, characteristic of thiamin deficiency, were found in 2 dogs, one of which also had focal degenerative lesions in the myocardium. An affected surviving dog with paraparesis showed some knuckling with absent placing, hopping and stretch reflexes, and slow pedal withdrawal reflexes in the hindlimbs. This dog, and 2 others less severely affected, were treated parenterally with thiamin.§ This dog showed a slow improvement, becoming ambulatory within 7 d. Three months later, the owner reported
t Whiskas Mixed Fish@,Uncle Ben’sof Australia, Wodonga, Victoria 3690 $ B-Calm@,Ilium Veterinary Products, Smithfield,New South Wales
2164
0 Thiabex injection, Coopers Veterinary Products, Silverwater, New * Dairy Technical Services Ltd, North Melbourne, Victoria 3051 54
South Wales 2141 Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
TABLE 2 Thiamin requirements of cats and dogs
TABLE 1 Sulphur dioxide and thiamin concentrations in pet foods Sample No. 1
Content
raw minced beef (for human consumption) fresh pet meat (case 4) 2 3 fresh beef pet mince 4 beef mince2 5 kangaroo pet mince3 6 canned chicken and turkey cat food4 7 canned tuna cat food4 8 mixtures of samples 5 & 6 mixtures of samples 3 & 7 9 plus 0.104 mg thiamin6 10-21 12 knackery samples7
Sulphur dioxide Thiamin mgk3 mglkg 0.81 ND
ND 420 1480 860 1100
(0.5
( 10
1 .o
(10 610
2.5 0.5
560 0-4078 (mean 1194)
( 0.5 ( 0.5
0.5 ND
N D not done 1 Thomas and Corden 1977 2 Bonnie Vita Plus cat and kitten mince, vacuum pack, Clinkat (Australia) Pty Ltd, Thomastown, Victoria 3 Bonnie minced ’roo, vacuum pack, Clinkat (Australia) Pty Ltd, Thomastown, Victoria 4 Whiskas, Uncle Ben’s of Australia, Wodonga, Victoria 5 approximately 1:l by volume 6 Vetzyme tablets, Philips Yeast Products Ltd, London 7 from 8 establishments
near complete recovery but a slight hindlimb ataxia was still detectable. There was more rapid improvement in the less affected dogs. All dogs in the kennel had been fed a diet based on horse meat obtained from a local knackery with added breakfast-type cereals, lucerne meal, limestone and rendering residue. A sample of the meat was found to contain 420 mg S02/kg(Table 1). After the diagnosis was made, all unaffected dogs were treated parenterally with thiamin and the meat source was changed t s one reportedly not using SO, preservatives. No other dogs were affected.
Sulphur Dioxide a n d Thiamin Analyses All representative meat samples submitted with the 4 cases and the 3 samples purchased from pet shops showed the presence of SO, in the qualitative test using malachite green. The results of quantitative analyses for thiamin and SO2in purchased meat, canned food and meat fed in Case 4 are shown in Table 1. Discussion Clinical signs of thiamin deficiency in cats and dogs have been described previously (Everett 1944; Read and Harrington 1981). They occur in 3 stages during which inappetence, loss of weight, vomiting and neurological abnormalities, particularly pupillary dilatation, ataxia and terminal seizures, develop. Read and Harrington (1981) grouped the terminal signs observed in dogs into a neurological syndrome, with ataxia, paraparesis, extensor rigidity, vestibular signs and seizures, and a sudden death syndrome caused by acute cardiac failure. In the cases described, there were clinical signs consistent with thiamin deficiency and response to parenteral treatment with thiamin. In 3 cases, brain lesions characteristic of thiamin deficiency were found on post-mortem examination of at least one affected animal. In each case, there was a history of a diet based predominantly or exclusively on fresh pet meat. A clinical diagnosis can be established on history and clinical signs (Lewis eta/ 1987) and by response to treatment with thiamin (O’Donnell and Hayes 1987). Laboratory confirmation was not available to show reduced blood thiamin and erythrocyte transketolase and elevated blood pyruvate and lactate levels (Read and Harrington 1982). Focal myocardial degeneration associated with thiamin deficiency, as found in Case 4, has been described in several species (Sullivan 1985). Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
Cat mglkg diet (dry matter) pglkg body weight/day adult growth mg/lOOO kcal *
5’ 100s: 308s: 1.on
Dog 17
209 549 0.39
National Research Council 1978
t Lewis et a/ 1987 $ Kallfelz 1989
5 National Research Council 1985 1 National Research Council 1986 Meat has important nutritional deficiencies, especially of calcium, iodine and vitamins A and D, but it normally contains thiamin (Table 1) adequate to meet the requirements of dogs and cats (Table 2). Lean pork and organ meats such as heart, brain, liver and kidney are especially good sources of thiamin. However, thiamin is heat-labile and cooking or processing can result in losses of 40 to 50% (McDowell 1989). A variety of sulphiting agents, including SO, and several inorganic sulphites, are used to preserve food, particularly meat, fresh fruits and vegetables and dried fruit. They extend the storage life of meat by slightly delaying spoilage but mask the signs without preventing putrefaction (WHO 1962). The odour and red colour of fresh meat is retained longer following treatment with sodium metabisulphite, reportedly by inhibiting the oxidation of myoglobin to metmyoglobin (Krol and Moerman 1959), but this fails to explain the restoration of redness to discoloured, spoiled meat which is possible with the same treatment. In untreated meat, a putrid odour develops when bacterial counts reach about 100 million per gram, whereas in meat treated with SOz,a weaker, less objectionable odour is not detectable until the bacterial population reaches about 500 million per gram (Christian 1963). Bacteria are more susceptible to the biocidal and biostatic effects of SO2 than moulds and yeasts, and gram-positive organisms are more resistant than gram-negatives (Lueck 1980). In the absence of sulphites, spoilage of sausage meat is dominated by gram-negative rods, but in the presence of sulphite, only gram-positive rods are found (Dyett and Shelley 1966; Banks and Board 1981). Salmonellae are particularly sensitive to the effects of SO,. Roberts and Boag (1 975) suggest the preservative is effective against their growth even if they are not destroyed. Little is known concerning the effects of sulphites on spores (Wedzicha 1984). Thiamin is subject to cleavage by sulphites, including SO,, into constituent pyrimidine and thiazole compounds, thereby rendering it inactive. In experimental diets, SO, can be used to specifically destroy thiamin without damaging other nutrients (Williams et all935). The rate is accelerated in aqueous solution and with increased temperature (Joslyn and Leichter 1967). The extent of destruction of thiamin in sulphited meat increases linearly with increasing SO, content, so that 400 and 1000 mg S O J k g depletes thiamin content by 55% and 95% respectively, with the loss occurring essentially within the first hour after addition (Hermus 1969). The World Health Organization recommends that human foods serving as significant sources of thiamin, such as meat, cereal grains, dairy products and nuts, should not be treated with sulphites (WHO 1962). It also recommends that sulphite preservatives not be used on meat, because they can lead to deception regarding freshness and possible injury from the consumption of tainted meat. The principle toxic effects of sulphites in food are the result of destruction of thiamin. Large doses are required to cause gastrointestinal irritation in humans, rabbits, rats and dogs (Allen and Brook 1971). Sulphites in food have also been associated with anaphylactoid reactions in humans (Stevenson and Simon 1981). The use of SO, in meat for human consumption is prohibited in the European Economic Community (Wilson 198l ) , and limited to sausage meat at a maximum of 500 mg/kg 55
in Australia (National Health and Medical Research Council 1987) and 450 mg/kg in the United Kingdom (Jukes 1984). Analysis of pet meat being fed to dogs in Case 4, 3 samples of purchased pet mince and 12 samples from 8 knackeries in Victoria supplying the pet met trade in 1983 to 1984, showed that sulphites are commonly used to preserve fresh pet meat (Table 1). Only 1 of 16 samples failed to contain SO,, and 10 (63%) had levels up to 8 times higher than those allowed in meat for human consumption. Although an unpleasant, metallic flavour is detectable by humans in foods treated with SO,, which limits the amounts used (Allen and Brook 1971), dogs and cats do not appear to discriminate against treated meat, even those samples containing high levels. For preservation of pet meat, the usual source of SO, is sodium metabisulphite, applied to the meat as a powder or by soaking in an aqueous solution at the knackery (Department of Agriculture, Victoria, unpublished report 1985). There are no regulations controlling the level of SO, in pet meat in Victoria and the wide range of levels found suggest no standard is followed. As found in the 2 samples of canned cat food analysed (Table l), commercial pet foods formulated to meet the nutritional requirements of dogs and cats (National Research Council 1985, 1986) contain adequate levels of thiamin, even after losses associated with processing and storage occur. Although the diet of cats in Case 1 was approximately 50% canned cat food, the remainder was pet mince preserved with SO,. Analyses of samples 8 and 9 showed that mixing these ingredients approximately 1 h before feeding, as was the practice in Case 1, not only reduced the concentration of thiamin, but also permitted SO, destruction of the thiamin contributed by the canned food in sample 9. In both samples, the level of SO, was approximately half that present in the pet meat, reflecting that 1:l dilution with canned cat food, which contained neglible amounts. For the same reason, the thiamin content of the mixture in sample 8 was 50% of that in the canned food, but in sample 9 it was reduced by 80070, indicating destruction had occurred. The extent of thiamin loss would be dependent on the original levels of SO, and thiamin, how long the ingredients were mixed before feeding, the composition of other ingredients which might form inactive complexes with the SO, (Abalaka 1980) and factors influencing the rate of reaction such as pH and temperature (Joslyn and Leichter 1967). Under similar circumstances, a nutritionally adequate diet containing raw, thiaminase-containing fish pieces was responsible for thiamin deficiency in foxes in the original report of Chastek paralysis (Green 1936). In Case 1, the addition of dried brewer’s yeast, a very rich source of thiamin, which contains 95.2 mg thiamidkg (McDowell 1989), to the diet containing pet meat was ineffective in preventing the occurrence of clinical signs of thiamin deficiency, probably due to destruction by SO,. The pet mince product fortified with vitamins and minerals by the manufacturer (sample 4) was also deficient in thiamin (Table 1). This may have been due to destruction by SO, in the meat and/or the effects of mineral sulphates in the pre-mix used (Verbeeck 1975). The addition of crushed vitamin tablets to the food (sample 9), as commonly recommended on product labels, also failed to raise the level of thiamin in the mixed diet to meet requirements. Assuming an average caloric value of 2.6 kcal/g for raw beef (Thomas and Corden 1977), the thiamin levels found in the SO, preserved pet meats (Table 1) were less than 19% of the 1.0 mg/1000 kcal recommended for cats (National Research Council 1986) and less than 64% of the 0.3 mg/1000 kcal recommended for dogs (National Research Council 1985). The actual deficit cannot be calculated because the levels fell below the minimum detected in the analytical methods used. Thiamin requirements are influenced by both physiological and dietary factors (National Research Council 1985). They are increased during pregnancy, lactation and growth. Because thiamin is specifically involved in carbohydrate metabolism, the requirement is raised when the dietary carbohydrate is increased relative to other energy-supplying components. The thiaminsparing effect of protein and fat has been recognised (McDowell 1989), and the high meat diets fed to cats and dogs in the cases 56
described were probably protective of the low thiamin levels present. Only a small percentage of the cats and dogs in Cases I and 4 showed clinical signs of thiamin deficiency when fed the deficient diet. Because thiamin is not stored in the body to any extent (McDowell 1989), anorexia from any cause can precipitate deficiency, particularly in cats, because of their high requirement for the vitamin. Various disease conditions, including parasitism, diarrhoea and malabsorption, as well as stress, all of which were possible in the cats in Case 1, can increase the requirement and result in variation between animals. A similar sporadic occurrence was seen in a specific-pathogen-free cat colony with over 100 cats receiving the same processed, thiamin-deficient diet (Baggs et a1 1978). In Case 4, the 6 affected dogs were of the same breed, leaving 59 dogs of 4 other breeds clinically normal during the period before the diet was changed. This might suggest a breed variation in thiamin requirements. Sulphur dioxide is undoubtedly useful in enhancing the storage life and acceptability of pet meat, which is at greater risk of spoilage than human meat because of the conditions under which it is produced, stored and, in some cases, transported, but its use creates other health hazards for cats and dogs. As well as masking the signs of spoilage and bacterial contamination, which misleads the purchaser and increases the risk of food poisoning, the destruction of thiamin by SO, leads to a serious, life-threatening nutritional deficiency. The inclusion of SO,-preserved pet meat destroys thiamin in an otherwise nutritionally adequate diet, and additional thiamin, whether added by the manufacturer or by the owner as a vitamin supplement in the food, may be unsuccessful in correcting the deficiency and preventing clinical disease. The extent of the deficiency may not be clinically apparent. Subclinical thiamin deficiency has been proposed as a cause of poor growth in young sheep (Thomas 1986). It must be assumed that fresh pet meat will contain SO,. If it is fed, other sources of thiamin should be included in the diet, but not mixed with the pet meat. Green et a1 (1942) observed that feeding fresh fish and a diet containing adequate thiamin on different days was successful in preventing the occurrence of thiamin deficiency in foxes. This is a possible regime for using SO,-preserved pet meat in cats and dogs. Food laws limit, or prohibit, the use of SO, in human foods; yet because human diets are usually varied, the effects of thiamin destruction by sulphites in certain preserved foods would be expected to be less severe in humans than in dogs or cats, which may be fed the treated meat exclusively. The introduction of regulations controlling the use of SO, in pet meat may be effective in preventing the range of clinical and subclinical disease that can result from indiscriminate use of the preservative.
Acknowledgments Drs RW Mitten and RM Kerlin are thanked for their assistance.
References Abalaka JA (1980) - Microbios 29: 15 Allen RJL and Brook M (1971)- Effectsof SulphurDioxidein Animals and Man, In Proc Third Int Cong Food Scr Ech. Washington, p799 Baggs RB, deLahunta A and Averill DR (1978) Lab Anim Sci 28: 323 Banks JG and Board RG (1981) - J Appl Bact 51: 9 Chrisman C (1982) - Problems in Small Animal Neurology, Lea and Febiger, Philadelphia Christian J H B (1963) - CSIRO Food Pres Quart 23: 30 deLahunta A (1983) - Veterinary Neuroanatomy and Clinical Nuerology, 2nd edition, Saunders, Philadelphia Dyett EJ and Shelley D (1966) - J Appl Bact 2 9 439 Edney ATB (1987) - Dog and Cat Nutrition, Pergamon, Oxford Everett GM (1944) - A m J Physiol 141: 439 Greene CE and Braund KG (1989) - In Textbook of Veterinary Internal Medicine, 3rd edition, edited by Ettinger SJ, Saunders, Philadelphia, p615 Green RG (1936) - Minn Wild1 Dis Invest 2: 106 Green RG, Carlson WE and Evans CA (1942) - J Nutrition 23: 165 Hermus RJJ (1969) - Inf J Vit Res 3 9 175 Horwitz W (1980) - OfficialMethods of Analysis, Association of Official Analytical Chemists, Washington, DC, p340 ~
Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
Houston DM and Hulland TJ (1988) - Can Vet J 2 9 383 Joslyn MA and Leichter J (1967) - J Nutrition 96: 89 Jubb KV, Saunders LZ and Coates HV (1956) - J Comp Path 66: 217 Jukes DJ (1984) -Food Legislation ofthe UK, Butterworths, London, p70 Kallfelz FA (1989) - In Current Veterinary Therapy X , edited by Kirk RW, Saunders, Philadelphia, p1352 Krol B and Moerman P C (1959) - Conserva 8:1, cited in Chemistry of Sulphur Dioxide in Foods, Wedzicha BL (1984), Elsevier Applied Science, London, p303 Lewis LD, Morris MJ and Hand MS (1987) - Small Animal Clinical Nutrition III, Mark Morris Associates, Topeka, Kansas Loew FM, Martin CL, Dunlop RH, Mapletoft RJ and Smith SI (1970) - Can Vet J 11: 109 Lueck E (1980) - Antimicrobial Food Additives, Springer-Verlag, Berlin, cited in Chemistry of SulphurDioxide in Foods, Wedzicha BL (1984), Elsevier Applied Science, London, p262 McDowell LR (1989) - Vitamins in Animal Nutrition, Academic Press, San Diego National Health and Medical Research Council (1987) - FoodStandard Code, Australian Government Publishing Service, Canberra, p160 National Research Council (1978) - Nutrient Requirements of Cats, National Academy Press, Washington, DC National Research Council (1985) - Nutrient Requirements of Dogs, National Academy Press, Washington, DC National Research Council (1986) - Nutrient Requirements of Cats, National Academy Press, Washington, DC O’Donnell JA and Hayes KC (1987) - In Diseasesof the Cat, Voli, edited by Holzworth J, Saunders, Philadelphia, p29 Read DH, Jolly RD and Alley MR (1977) - Vet Pathol 1 4 103 Read DH and Harrington DD (1981) - Am J Vet Res 42: 984 Read D H and Harrington DD (1982) - Am J Vet Res 43: 1258 Roberts D and Boag K (1975) - J Hygiene (Cambridge) 15: 173 Smith DC and Proutt LM (1944) - Proc Soc Exp Biol Med 56: 1 Stevenson DD and Simon RA (1981) - J Allergy Clin Immunol68: 26 Sullivan ND (1985) - In Pathology of Domestic Animals, 3rd edition, Jubb KV, Kennedy P C and Palmer N, Academic Press, San Diego, p256 Thomas KW (1986) - vet Res Comm 1 0 125 Thomas S and Corden M (1977) - Metric Tables of Composition of Australian Foods, Australian Goverment Publishing Service, Canberra, PI4 Toepfer SA (1974) - Aust Vet Pract 4(2): 76 Verbeeck J (1975) - Feedstuffs47(36):4,45, cited in Vitamins in Animal Nutrition, McDowell LR (1989), Academic Press, San Diego, p181 Wedzicha BL (1984) - Chemistry of Sulphur Dioxide in Foods, Elsevier Applied Science, London WHO (1962) - World Health Org Tech Rep Ser 28: 96 Williams RR, Waterman RE, Keresztesy JC and Buchman ER (1935)= J Am Chem SOC57: 536 Wilson NRP (1981) - Meat andMeat Products, Applied Science, London, PI21
(Accepted for publication 25 September 1990)
ANNOTATION
Semi-automated slaughtering and dressing of cattle Slaughtering animals is a slow, arduous, messy and dangerous occupation. The hazards to abattoir workers are reflected in the industry’s annual $330 million workers’ compensation and related payouts. The CSIRO Division of Food Processing recognised that alternative slaughtering and dressing technologies could lead to more efficient and safe working conditions, and that major gains in productivity could be achieved through some degree of automation. Beginning in 1974 a group at the Division’s Meat Research Laboratory in Cannon Hill, Queensland dissected the slaughtering system. They split the key processes into what are termed modules, then looked at how to automate each module and best integrate it into the complete process.
Australian Veterinary Journal, Vol. 68, No. 2, February, 1991
The Australian Meat and Livestock Research and Development Corporation has supported the project with the aim of cutting meat-processing costs by at least 30%. That aim is close to realisation. The group hopes that two fully functional commercial plants will be operating by the end of 1990. The new automated processing system, known as Fututech, represents a radical departure from conventional meat-processing techniques. It offers considerable cost savings, reduced stress on animals and hence a better-quality meat, and a significant improvement in the working environment. At the core of Fututech is a ‘programmable logic controller’ (PLC) that oversees the whole process through seven ‘slave’ PLCs running the 10 modules involved in the process. The first module deals with the lead-up, capture, stunning, and spinal inactivation of the animal, followed by bleeding. Animals are led singly down a sloping race along a moving footway. A central ridge separates the legs until the animal is finally comfortably suspended with legs dangling down. The head is contacted just behind the ears and a 120-voltpulse of electricity induces an electroplectic fit that renders it paininsensitive. A second electric shock is used to stop all involutary muscle activity, including the heart. An air-knife with two opposing serrated blades (to make sure the wound stays open) then severs the main artery above the heart to bleed the animal. The process is over within a few seconds. The carcase is towed out of the area and enters the hornremoval module. After the horns have been cut off the carcase is tipped onto its side and then rolled onto its back onto one of a series of cradles mounted on a moving work conveyor. On this cradle many of the remaining manual tasks are performed, with slaughtermen preparing the carcase for the automatic hideremoval and evisceration modules. An overhead conveyor system then transports the carcase through the other modules, tilting it through the range of positions demanded during processing. For example, during pelvic-bone cutting - necessary to allow the viscera to slide out easily - the animal is positioned head-down at 30” to the horizontal to avoid contact between blade and internal organs. When the time comes for viscera ejection, the position is reversed - the animal is held head-up at 30” to the horizontal - so the ejection arm can push the contents out between the hind limbs. Human involvement is necessary during the process - overseeing the action, cleaning up the details, and generally making sure that everything is as it should be - but advanced robotics dominate the scene. Viscera-ejector arms, hide-pullers, knives and saws are controlled by the slave PLCs and are guided in their tasks by various sensors - photo-optic or ultrasonic or magnetic. The Fututech commercial prototypes can process a beast to a split carcase in the same time as a medium-size conventional processing plant. In doing so labour requirements are vastly reduced. The Fututech prototype is currently designed to process 600 animals a day and is continually being refined. The facility is currently set up to handle cattle of 220-800 kg body weight, and another aim is to adapt the process so it can handle smaller animals, particularly sheep. CSIRO has signed an agreement with FMC (Australia) Ltd to commercialise the Fututech semi-automated slaughtering equipment. FMC is a Melbourne-based engineering group with international experience in the abattoir industry. Fututech is claimed to be the greatest advance in meatprocessing technology this century. (Adapted from Rural Research 147, Winter 1990, pages 26-28 with acknowledgment to CSIRO Division of Food Processing). AK Sutherland
57
