Docstoc

Thiamine deficiency in dogs due to the feeding of sulphite

Document Sample
Thiamine deficiency in dogs due to the feeding of sulphite Powered By Docstoc
					Australian College of Veterinary Scientists – Science Week 2005 – Small Animal Medicine Chapter meeting

       Thiamine deficiency in dogs due to the feeding of sulphite preserved meat
                                                 M Singh
                   Veterinary Specialist Centre, PO Box 307, North Ryde, NSW, 2113

    Thiamine is a water soluble B vitamin (B1) required for the metabolism of carbohydrates and
   energy production.1 It is minimally stored in the body and must be consistently obtained from the
   environment or synthesised. Thiamine in its phosphorylated form (thiamine diphosphate) is an
   essential cofactor for the function of the tricarboxylic acid (TCA) cycle and the pentose
   phosphate pathway. These pathways are the major sources of neuronal energy production.1 The
   TCA cycle is also important in the synthesis of gamma aminobutyric acid (GABA), an inhibitory
   neurotransmitter in the CNS.1 In the absence of supply, clinical signs of deficiency develop
   quickly.2 Cessation of oxidative metabolism in the central nervous system forces the brain into
   anaerobic metabolism, which results in a build up of lactic acid. Bilaterally symmetrical
   haemorrhage and necrosis of the grey matter (which has a higher metabolic rate than white
   matter) occurs.2
    Reports of thiamine deficiency are sporadic in the veterinary literature. Affected species have
   included ruminants,2 horses,2 cats,4, 5 mink,6 seals7 and foxes.6 The aetiology of thiamine
   deficiency varies between monogastrics and ruminants. Thiamine is synthetised by the normal
   bacterial flora in the rumen and caecum of herbivores. Thiamine deficiency only occurs in these
   species when alterations in the ruminal flora precipitate cessation of thiamine production. Causes
   of thiamine deficiency in carnivores include the ingestion of fish high in thiaminase,7, 8
   inactivation of thiamine by cooking or processing5 and the addition of sulphur dioxide or sulphite
   preservatives to meat.4, 5 These include preservatives 220, 221, 223, 224, 225 and 228. Sulphating
   agents delay spoilage by inhibiting the oxidation of myoglobin into metmyoglobin, decreasing
   odour and preserving the red colour of meat.9 These agents also increase the shelf life and
   palatability of cooked meat. Thiamine is cleaved by sulphites into its inactive constituent
   compounds, pyrimidine and thiazole.9 When sulphite preserved meat is fed alone or at the same
   time as a thiamine source (for example commercial pet food), the thiamine in all the food is
   cleaved and a thiamine deficient state can result. The extent of thiamine destruction increases
   linearly with the amount of sulphur dioxide in the meat. A level of 400 mg of sulphur dioxide/kg
   depletes thiamine by 55% and 1000 mg/kg depletes it by 95%.
    The feeding of sulphite treated meat to pets on a regular basis may lead to potentially fatal
   thiamine deficiency, however the danger does not appear to be widely recognised by pet owners
   or veterinarians. A 6-year-old female entire Golden Retriever, a 4-year-old female spayed
   Maltese Terrier and three 7-week-old American Staffordshire Terrier puppies were diagnosed
   with thiamine deficiency caused by feeding sulphite treated meat. The Golden Retriever
   presented with a history of inappetence, weight loss and vomiting which rapidly progressed to
   signs of multifocal intracranial disease including mental dullness, paresis, seizures, spontaneous
   nystagmus and strabismus. Thiamine pyrophosphate effect was elevated at 58% and magnetic
   resonance imaging revealed bilaterally symmetrical hyper-intensity of the caudate nucleus and
   rostral colliculi. The dog recovered with thiamine supplementation. The Maltese Terrier and the
   three American Staffordshire Terrier puppies also presented with rapidly progressive multifocal
   central nervous system signs including ataxia, paresis, increased muscle tone, seizures,
   nystagmus and exophthalmos. The 4-year-old dog made a rapid recovery with thiamine
   supplementation. Euthanasia and necropsy of a puppy revealed malacia of multiple brainstem
   nuclei and oedema of the cerebral cortex. These findings were consistent with thiamine
   deficiency.

                                                     30
Australian College of Veterinary Scientists – Science Week 2005 – Small Animal Medicine Chapter meeting

    The diagnosis of thiamine deficiency can be difficult antemortem. The clinical signs of thiamine
   deficiency in dogs have been described by Read and Harrington3 who induced thiamine
   deficiency experimentally in young Beagle dogs by feeding a thiamine deficient diet. Three
   stages were observed: i) a short phase of suboptimal growth (18 +/- 7.9 days), ii) an intermediate
   phase of inappetence, weight loss and copraphagia (58 +/- 37 days) and iii) a terminal short phase
   of neurological signs characterised by anorexia, emesis, central nervous system depression,
   paresis, ataxia, torticollis, circling, exophthalmos, convulsions and death. Some dogs died
   suddenly without recognition of the early phases. Thiamine deficiency is more commonly
   recognised in the cat.4, 5 As well as inappetence and vomiting, clinical signs commonly
   recognised in this species include nystagmus, dilated, poorly responsive pupils, cervical
   ventroflexion, tetraparesis, mental depression and death.4. 5
    In thiamine deficiency, other diagnostic tests such has haematological, biochemical and
   cerebrospinal fluid analysis are generally unremarkable. A thorough dietary history is important
   in the diagnosis. Fresh meat manufactured for pet consumption and cooked, non- refrigerated pet
   food rolls have often been shown to be high in sulphite preservatives.9, 10 No requirements
   currently exist to identify the use or concentration of sulphite preservatives in meat for pet
   consumption. Sulphites are permitted as food additives for human consumption in some
   processed meats (such as sausages) but are prohibited in most others. Maximum permitted
   concentrations exist for processed foods and these must be labelled.4
    There are several approaches to the biochemical evaluation of vitamin status, none of which are
   widely available. The absolute concentration or co-enzyme form can be measured on plasma or
   whole blood. The validity of this method depends on the assumption that circulating
   concentrations reflect chronic intake and tissue concentrations.11 Functional tests for vitamin
   status depends on biological effects. They are a more sensitive index of absolute vitamin
   concentrations and are more widely used.11 The most commonly used test for thiamine deficiency
   in humans is the measurement of erythrocyte transketolase activity.12 The activity of
   transketolase decreases significantly in the early stages of thiamine deficiency and can be
   monitored in red blood cells. Transketolase activity can be restored by the addition of thiamine
   pyrophosphate in vitro.12 This finding provided the basis of the clinical test for marginal thiamine
   deficiency used commonly in humans, the thiamine pyrophosphate (TPP) effect.12 This test is
   carried out on haemolysed red blood cells. Results are expressed as TPP effect (%), which
   represents the amount of stimulated enzyme activity resulting from the addition of thiamine to the
   red cell haemolysates. An increased TPP effect is proportional to the degree of thiamine
   deficiency.7 This procedure has been used for more than 20 years to measure thiamine deficiency
   in humans. The normal range is 2 to 20%. It is assumed that abnormalities in red blood cell
   transketolase also reflect similar changes in the brain enzyme. Although this assumption seems
   reasonable, little supportive evidence exists.
    The ‘TPP effect’ has not been widely used in animals. Read and Harrington13 used it as an
   indirect supporter of thiamine deficiency when experimentally induced in young Beagle dogs.
   They found the ‘TPP effect’ on erythrocyte transketolase to increase to a mean terminal value of
   64%, indicating a thiamine deficient state. The controls were stable at a mean of 11%. They also
   found a reduction in erythrocyte transketolase activity and increased concentrations of blood and
   cerebrospinal fluid lactate and pyruvate. Because of the decreased activity of thiamine dependent
   enzymes, the intermediate metabolites of the TCA cycle and anaerobic metabolism (pyruvate and
   lactate respectively) accumulate in the blood.
    Thiamine deficiency is a not a common disease of dogs and is easily prevented, however we are
   continuing to recognise it on a regular basis at our veterinary hospital. Veterinarians must assume
   that fresh pet meat and non-refrigerated cooked pet food rolls will contain sulphite preservatives
   and should be aware of the health risks to dogs and cats. It is recommended that a balanced
                                                     31
Australian College of Veterinary Scientists – Science Week 2005 – Small Animal Medicine Chapter meeting

   commercial pet food be substituted for these foods. If fresh meat must be fed, meat purchased for
   human consumption is preservative free. Response to treatment with thiamine is good if
   recognised and treated early.

   References
      1. Stryer L. Biochemistry. 2nd edn. WH Freeman, San Francisco, 1981: 333-342.
      2. Oliver JE, Hoerlein BF, Mayhew IG. Veterinary Neurology. Saunders, Philadelphia,
          1987: 271-272.
      3. Read DH, Harrington DD. Experimentally induced thiamine deficiency in beagle dogs:
          clinical observations. Am J Vet Res 1981; 42: 984-991.
      4. Steele RJS. Thiamine deficiency in a cat associated with the preservation of ‘pet meat’
          with sulphur dioxide. Aust Vet J 1997; 75: 719-721.
      5. Davidson MG. Thiamine deficiency in a colony of cats. Vet Rec 1992; 130: 94-97.
      6. Okada HM, Chihaya Y, Mitsukawa K. Thiamine deficiency encephalopathy in foxes and
          mink. Vet Pathol 1987; 24: 180-182.
      7. Geraci JR. Thiamine deficiency in seals and recommendations for its prevention. J Am
          Vet Med Assoc 1974; 165: 801-803.
      8. Houston DM, Hulland TJ. Thiamine deficiency in a team of sled dogs. Can Vet J 1988;
          29: 383-385.
      9. Studdert VP, Labuc RH. Thiamin deficiency in cats and dogs associated with feeding
          meat preserved with sulphur dioxide. Aust Vet J 1991; 68: 54-57.
      10. Malik R, Sibraa D. Thiamine deficiency due to suphur dioxide preservative in ‘pet meat’
          – a case of déjà vu. Aust Vet J (in press).
      11. Garosi LS, Dennis R, Platt SR et al. Thiamine deficiency in a dog: clinical,
          clinicopathological and magnetic resonance imaging findings. J Vet Intern Med 2003; 17:
          719-723.
      12. Rooprai HK, Pratt OE, Shaw GK, Thompson AD. Thiamine pyrophosphate and
          normalized erythrocyte transketolase activity ratio in Wernicke-Korsakoff patients and
          acute alcoholics undergoing detoxification. Alcohol Alcohol 1996; 31: 493-501.
      13. Read DH, Harrington DD. Experimentally induced thiamine deficiency in beagle dogs:
          clinicopathologic findings. Am J Vet Res 1982; 43: 1258-1267.




                                                     32

				
DOCUMENT INFO
Shared By:
Categories:
Stats:
views:59
posted:4/17/2010
language:English
pages:3
Description: Thiamine deficiency in dogs due to the feeding of sulphite ...