| First Published in: | The Journal of Small Animal Practice, December 1993, Vol. 34 592-593 |
It makes for an interesting
commentary on the veterinary profession that two veterinarians, resident in
the same Australian city, should choose the JSAP for communication of their
ideas on Feline Lower Urinary Tract Disease (FLUTD). Associate Professor, ADJ
Watson (1993) draws attention to the crystalluria finding in normal cats thus
making the point that correlation does not imply causation. Osborne and others
(1989) cast further doubt on the causative role of crystalluria by pointing
out that most FLUTD patients have neither uroliths nor plugs.
Osborne and others (1992) postulated a unifying hypothesis that linked infection-induced
inflammation, crystalluria and concomitant inflammation/crystalluria in the
aetiopathogenesis of the disease. Watson (1993) calculated that 76.2% of FLUTD
cases in Osborne and others' (1989) study were of unknown aetiology. It should
be borne in mind that the bacteria, viruses and uroliths implicated as causal
agents in the minority of cases (23.8%) may have occupied a lesser contributory
role in the disease process or existed as co-incidental findings.
Now I am aware that leaping to conclusions on 100% correlation of observed signs
can be equally misleading. However, all cats presenting with FLUTD at our clinic
have all suffered variable degrees of periodontal disease and all were fed on
processed food. This has been the common finding for all cases of miliary dermatitis,
inflammatory bowel disease (Tam, 1986) and plasma cell pododermatitis diagnosed
at our clinic. In a number of cases we have confirmed the diagnosis histopathologically.
(Muller, Scott and Kirk, 1983) Whilst we have not been at liberty to biopsy
the bladder and urethra of FLUTD clinical cases, we believe that the inflammatory
infiltrates would share characteristics of the other cases mentioned.
A 'Cybernetic Hypothesis of Periodontal Disease in Mammalian Carnivores' (Lonsdale
- unpublished, 1992) was formulated to explain and predict this generalised
class of diseases characterised by immune cell infiltrates. This postulates
inter alia a species survival mechanism for preservation of the gene pool. Cats
at the margin which do not eat their quota of natural food do not maintain effective
physical cleansing of the oral cavity. (Colyer, 1947) Addy, Slayne and Wade
(1992) comment that conditions suitable for the growth of anaerobes exist in
plaque after three to four days undisturbed maturation. The mature plaque flora
is extraordinarily complex and may contain up to 325 different species. The
bacteria/host reaction manifests as periodontal disease (Harvey, 1993) Within
the 'Cybernetic Hypothesis' it is further postulated that a cascade of hypo-,
hyper- and auto-immune responses will be triggered. In the natural state this
would create a further competitive disadvantage culminating in the loss of the
individual and thus, protection of the well-fed members of the group.
Approaching the proposition from the other side, we assume that cats well fed
on natural food will not develop periodontal disease, miliary dermatitis, IBD,
FLUTD or plasma cell pododermatitis. To date this prediction has held true for
the small number of cats surveyed. Professor Watson asks, 'For some well designed
studies to examine critically the role of diet changes in treatment and prevention
of the common forms of FLUTD.' I believe that our studies need only be expanded
to provide the numerical 'proof' on a range of diseases. Elucidation of the
pathways should then proceed as a logical process.
In the meantime, the cornerstone of our treatment for many cat diseases is dentistry
followed by institution of a more natural diet. (Colyer, 1947, Lonsdale, 1993)
Providing raw meaty bones, in the form of chicken, quail, rabbit or fish, comprise
at least 90% of the diet ongoing oral health prevails. Corticosteroids and antibiotics
still have a place in the initial treatment of oral and associated diseases,
but long term or intermittent use is a rarity.