PET FOODS’ INSIDIOUS CONSEQUENCES PART 3

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FOUL MOUTH AIDS – A DIETARY DISEASE

The following paper was published in the Post Graduate Committee in Veterinary Science’s Control and Therapy Series.

Raw Meaty Bones Promote Health Control and Therapy No. 3323

The raw versus processed food debate became obstipated. A stand-off occurred across the philosophical and scientific divide with little new material being exchanged and certainly no movement of personnel between the camps.

The methodological incompatibility of the two factions were as the inhabitants of Lilliput to those of Brobdingnag.

With the emergence of some recent information, the latter day Gulliver can catch a glimpse of the rich new areas of inquiry waiting to be explored.

The Zubrycki silky terriers represent just such a case. From November ’85 to August ’91, Tuffy and Blossom were presented at the surgery on numerous occasions. Often with vexatious non-specific illness/lethargy/dermatitis.

A recurrent complaint was that Tuffy had attacks of the ‘scurries’. Variously determined to be hyperventilation or bouts of mad anxiety. Several theories and treatments were proposed by ourselves but to no avail.

On 6/8/91, at time of annual vaccination, it was determined we should be entirely resolute in our dealings. The owners were persuaded to adopt a thorough approach to flea control, and the dogs were booked in for radical dentistry. Previously our advice to give an occasional raw bone had been overlooked. Now we insisted that a raw meaty bone should be a staple of the diet.

The WCC of 12/8/91 were:

Tuffy Blossom Normals
Tot.WBC 5.1 5.2 6.0-14.0
Differential WCC (absolutes)
Neut. 3.4 4.0 4.1-9.4
Lymph 1.5 0.8 0.9-3.6
Mono. 0.1 0.2 0.2-1.0
Eos. 0.2 0.3 0.1-1.2

Several times, in the intervening weeks, I met Mrs. Zubrycki in the street. Each time she remarked on the lack of ‘scurrying’ attacks, much improved skin, vitality and breath. On 17/6/92 she was persuaded to bring the dogs back for follow up and blood test. The results are reprinted below.

Tuffy Blossom Normals
Tot.WBC 8.5 8.2 6.0-14.0
Neut. 4.8 5.9 4.1-9.4
Lymph 2.7 1.7 0.9-3.6
Mono. 0.4 0.4 0.2-1.0
Eos. 0.5 0.2 0.1-1.2

Some gingivitis and tartar accumulation was evident where opposing teeth had been removed, but otherwise the mouth was healthy.

Comment A number of explanations could be postulated to explain the findings. My rude hunch is that just like the millions of other process food fed dogs, the sequence of events is as follows.

Traumatic gingivitis of teething and plaque-induced gingivitis of normal living becomes exacerbated by calcification of plaque. All of the former remaining unchecked by nature’s cleaning, polishing, washing action at feeding sessions.

During the canine evolutionary phase there would have been no pressure to cope with chronic mouth lesions.

The modern dog protected from heat, cold, starvation and predation has to withstand the affront of a mouthful of gram negative bacteria and toxins.

Ill-equipped for the task, the bone marrow suffers toxic suppression and a concomitant bacteraemia compounds the problem. The whole noxious mess occasionally punctuated by dramatic demonstrable disease entities, (septic arthritis, endocardiosis, nephritis). More usually characterized by suboptimal health of an insidious nature running parallel with the aging process and confused with the same.

This paper has now been expanded into a survey of the first eight dentistry cases presented at our clinic with a low white cell count and low RBC.

Not all animals had RCC’s performed as initial investigation was for WBC changes. The animals were not objectively assessed for dehydration. Tess Abson had complete laboratory profile and heartworm, microfillaria and serology testing. She was noticeably dehydrated and thus would provide erroneously high base readings at first presentation. She subsequently gained 20% in weight with a presumed corresponding increase in total circulating erythrocytes. Accordingly adjustment should be made for her minus 3% RCC change in value.

Changes in RCC varied from minus 3% to 46% increase. Average 28%. WBC counts varied from 37 to 150 % increase. Average 78%. Neutrophil counts varied from 0 to 170% increase. Average 77% Lymphocyte counts varied from 8 to 136% increase. Average 72%

By completing dental extractions/scaling prior to the change of diet could only serve to accelerate improvement of those severely affected. It is acknowledged that diet alone can bring about improvements in oral hygiene and thereby health. ‘This test confirms the feasibility of preventing the accumulation of dental calculus in experimental beagle dogs by regular feeding of oxtails’. (Brown and Park, 1968) ‘Her dental hygiene and lack of dragon breath is a joy to behold. She enjoys her six kilometer walk everyday on her tiny little legs and has a new zest for life.’ (Consultant, obstetrician and gynecologist commenting on dietary change for elderly terrier).

Results of owner observations were arguably more valuable than the scientific parameters. Owners living in close association with their pets are able to make value judgments which mostly depend on behavioral changes.

Eg. “Didn’t know X was sick”. “Like a kitten again”. “Stopped the strange behavior pattern”. “Could not sleep was up all night, now sleeps soundly.”

These subjective assessments add support for the ‘Cybernetic Hypothesis’ which predicts that dogs and cats which do not receive the ‘wash, scrub and polish’ of natural feeding will suffer a foul mouth and severe health consequences.

Four cases were initially presented for annual vaccinations. These were perceived as ‘normal’ by their owners. The figures are tabulated here.

RCC(x10^12/L) WBC(x10^9/L)
Before dentistry After dentistry Before dentistry After dentistry
Case 1 6.00 7.10 5.10 8.50
Case 2 5.60 7.40 5.20 8.20
Case 3 5.27 7.68 4.90 7.80
Case 4 6.03 8.83 5.70 8.00
Average 5.72 7.75 5.22 8.10

The average RCC increase was 35% and the average WCC increase was 55%.

Sources of Error

That every animal tested showed such a dramatic improvement in blood values and general health is remarkable given that a number of interactive factors would be expected to create errors.

a. Elderly patients addicted to processed foods are not good candidates for diet change. Owner compliance was often in question.
b. Once established periodontal disease can be expected to persist albeit at a reduced level, even after extensive dental work.
c. If the observed changes in blood parameters and health were triggered by chronic periodontal disease the withdrawal of the stimulus would not necessarily result in abatement of the clinical condition.
d. Other preexisting pathology could be expected to exert an influence on blood values and perceived health status.

Laboratory Tests

The reference range referred to by ourselves originated from Macquarie Vetnostics in Sydney. Dr B Duff states: ‘Our reference ranges were derived from approximately 100 animals presenting at Sydney general practices in 1986. Veterinarians submitted blood according to a recommended protocol. The animals were selected as being ‘clinically normal’ as opposed to animals specifically raised for the purpose of biomedical research.’ No comment could be made on the diet and oral health of the survey sample.

Veterinary Pathology Services’ Dr Bill Vernau states: ‘Our reference range was derived from 40 dogs and 40 cats between 1989 and 1991. These animals were accessed via veterinary clinics. They had to be ‘healthy’ animals more than one year of age presented for vaccinations etc.’ Dr Vernau could not comment on diet and dental status but the animals were supposedly ‘healthy’ and did not require dental ‘prophylaxis’.

Comparable ranges published in Kirk’s “Current Veterinary Therapy No. 11” derived from the University of Guelph between 1989 to 1991. ‘There was a mix of mongrels and pure-breds. All were vaccinated against distemper and hepatitis and treated for parasites. They were fed a balanced commercial diet (Hills Science Diet, wet and dry). Dogs were held in a preconditioning unit four to six weeks prior to testing. All dogs were healthy and Dr Lumsden states that, ‘none had periodontal disease’. Cats had a similar protocol, age ranges six to twenty-four months.’

MVS VPS GUELPH
Dogs Cats Dogs Cats Dogs Cats
RCC (x1012/L) 5.00-8.00 5.50-10.0 5.5-8.5 5.5-10.0 5.6-8.5 5-10
WBC (x109/L) 6.0-14.0 6-16 6.0-17.0 5.5-19.0 6.1-17.4 5.5-15.4
Neut. (x109/L) 4.1-9.4 3.8-10.1 4.0-12.0 2.0-13.0 3.9-12.0 2.5-12.5
Lymph (x109/L) 0.9-3.6 1.6-7.0 0.9-5.0 0.9-7.0 0.8-3.6 1.5-7
Mono (x109/L) 0.2-1.0 0.1-0.6 0.1-0.6 0.1-0.4 0.1-1.8 0.0-0.85
Eos. (x109/L) 0.1-1.2 0.2-1.4 0.1-0.5 0.1-0.8 0.0-1.9 0.0-0.75

We did have concerns and pathologists are the first to admit the fallibility of single tests and the interpretations arising. When a patient (Tess Abson) shows a blood profile within the reference range although 20% underweight and chronically ill one must question the validity of the reference range. When the patient subsequently glows with relative health (for a twelve year old with a mammary carcinoma, cardiopathy, hepatopathy and no teeth in the upper jaw) but the pathologist comments on several perceived problems, then we have serious cause for alarm.

General practitioner awareness of periodontal disease scarcely existed in 1986 when Macquarie Vetnostics Services obtained their results. Things have not progressed greatly since that time. One must be suspicious of the oral hygiene claims for the sample populations used by Veterinary Pathology Services and the University of Guelph. Dr Lumsden’s comment that the laboratory animals did not have periodontal disease is at variance with: ‘Dr Dan Carey of the Iams Corporation maintained that animals on canned food would require six monthly prophylactics. Dr Jo Wills, Scientific Affairs Manager – Waltham, expressed as a point of pride that their research animals received six monthly prophylactics to resolve/control dental health problems.’ (Lonsdale, 1992 – Unpublished)

The conclusion must be drawn that reference ranges have been established utilizing periodontal disease-affected animals. It is therefore likely that the reference ranges are too wide. At the low end chronic disease affected animals suffering Acquired Immune Deficiency are designated as ‘within normal limits’.

This survey did not look at animals through all stages of life and periodontal disease, however basic pathological principles tell us that during inflammatory phases of the disease the cellular counts could rise and accordingly falsely extend the reference range upwards.

Similar remarks appear to apply for erythrocyte counts. Although within the laboratory reference range four of the six animals tested appeared to have suffered relative anemia in conjunction with their periodontal disease.

The summation of these effects is that: artificial diets and periodontal disease have been factored into the ‘normal’ reference ranges.

Part of paper (submitted for publication, Lonsdale, 1993)

FELINE EOSINOPHILIC GRANULOMA DISEASE COMPLEX

‘Feline Eosinophilic GRANULOMA Disease Complex. Control and Therapy Nol 3271

The severity of the lip and tongue lesions in Ming Hobbs the 7 year old de-sexed female cat cause me to reproduce the Anapath histology report in full.

Microscopic Description

Lip: The biopsy shows a large ulcer in the skin covered by a thick necrotic crust containing numerous large colonies of bacterial cocci. There are heavy infiltrates of eosinophils throughout the granulating ulcer bed and underlying dermis.
Tongue: The large yellow nodule is an area of reactive lymphoid follicle formation, interspersed with mixed inflammatory cell infiltrates including numerous eosinophils, mast cells and plasma cells. The smaller lesions show areas of granulating ulceration with extensive eosinophilic inflammation and superficial necrosis and bacterial infection.

Final Anatomic Diagnosis

  1. Multifocal severe ulcerative eosinophilic dermatitis and glossitis with superficial bacterial infection.
  2. Focal moderate lymphoid hyperplasia with interspersed eosinophilic inflammation, tongue.

Comment

The lesions on the lip and tongue are consistent with eosinophilic granulomas, each with significant secondary superficial bacterial infection. One of the nodules in the jar labeled “tongue” was an area of lymphoid hyperplasia, probably in response to the chronic inflammation and infection in the mouth. Many cats with eosinophilic granuloma-type lesions have underlying hypersensitivity problems (food allergy, atopy etc.)

The treatment on 28.04.92:

  • Debridement of tongue
  • Dental overhaul
  • Long acting penicillin, Dexamethasone I.M.
  • 10 mg Depopred intra-lip lesion
  • 5 mg Megestrol Acetate every 2nd day for 2 weeks

The diet was changed to include a raw chicken wing or ox tail or similar every day. At 28.05.92 Ming is thoroughly enjoying the new diet and the mouth lesions are totally healed.

Comment

Never before have I insisted on a total dietary change nor have I seen such a rapid recovery. It will take me years to accumulate a series of such cases. If other practitioners try this approach we can quickly determine if there is a diet, periodontal disease, eosinophilic granuloma nexus.’

The above was the first of a series. In the mild cases we now dispense with the usual Megestrol Acetate and corticosteroids and treat with dental and dietary change alone. Rather than see these signs as part of a single disease, we consider it to be part of a larger immune system disease complex of which milary dermatitis, FLUTD, lymphocytic histiocytic enteritis, plasma cell pododermatitis etc are examples. Deposition of any or all of the following are the main histological findings: Eosinophils, histiocytes, lymphocytes, neutrophils, monocytes and plasma cells.

PLASMA CELL PODODERMATITIS OF CATS

‘Plasma Cell Pododermatitis of Cats Control and Therapy No. 3270

The extensive feeding of processed food and the equally extensive prevalence of periodontal disease has come under scrutiny. Recently I have dealt with two cases of an obscure nature. The absence of raw bones, or presence of periodontal disease seems to be implicated somewhere in the pathogenesis.

Muller, Kirk and Scott state that “The cause of Plasma Cell Pododermatitis is unknown. Hyper gammaglobulinaemia, lymphocytosis and the histopathologic findings suggest an immunologic basis. The therapy of choice is not clear”.

Case 1
07.91 Toby, 4 year old de-sexed male. Clinical findings pododermatitis, and as with any 4 y.o. cat on processed food, moderate to severe periodontal disease. Treatment consisted of dental overhaul, post op. course of amoxycillin. A raw chicken wing to be included in diet daily. Histopathology confirmed the diagnosis.
Case 2
01.92 Alf, 7 year old de-sexed male. Findings and treatment same as for Toby. Histopath not performed. In both cases the ulceration healed in about 7 days. The pads have remained soft but otherwise there has been no relapse up to the time of writing.
Comment
The beauty of these cases is that with a change of diet the condition was reversible. Such an expedient is not available to us in a host of end stage auto immune conditions, nephritis, cardiomyopathy etc.
Nevertheless, I believe it is diet and diet-induced periodontal disease which is the trigger. Assuming this to be so, then we are under a dual obligation.
  • To advise and continue to remind our clients of the need for daily raw bones before irreversible disease sets in.
  • Conduct controlled studies to elucidate the precise mechanisms.’

We are pursuing this research and our findings to date suggest that cats with severe periodontal disease will have a variable range and population of inflammatory cells in their foot pads.

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