Until November 1994, with the exception of BSE and scrapie, none of the other TSEs were notifiable. On the other hand, the Government believe that most cases of TSE have been reported to Agriculture Departments and epidemiological investigations have been carried out where possible. With respect to exotic ruminants, risk of infection was primarily associated with consumption of feed, often produced for cattle, which contained meat and bone meal (MBM). With respect to exotic felines and domestic cats, the risk was considered to be associated with consumption of central nervous system tissue which could legally be fed to them until it was banned in September 1990.

No cases of TSE have been found confirmed in canines, although a case of spongiform encephalopathy in a Norwegian dog showing a spongiform change in the brain is under investigation. This is not yet confirmed and speculation about its origin delayed until results are available.

Hound studies
>
> This largely started after it was found that dogs were being reported with
a
> spongiform encephalopathy and ataxia. The condition seemed to take place
in
> older dogs and was being reported from various parts of the UK. There was
> never any proof that it was caused by a TSE. One of the most difficult
> prblems to get around in all this was the outbreak of the disease that was
> seen in a large pack of game dogs. It was as if all the animals developed
> the disease concurrently..as would be expected if an infection was
involved.
> The animals were not very young and no specific infective cause or toxic
> cause was found.
>
> The documents below became clear during the Phillips Inquiry and represent
> documents passed around in the UK Ministry of Agriculture and Central
> Veterinary Laboratory:
> http://www.bseinquiry.gov.uk/files/yb/1991/10/18001001.pdf
> http://www.bseinquiry.gov.uk/files/yb/1993/12/06001001.pdf
> From these various documents:
>
> 37.Putative TSE in hounds - work started 1990 -(see para 41)
>
> Robert Higgins, a Veterinary Investigation Officer at Thirsk,
> had been working on a hound survey in 1990. Gerald Wells
> and I myself received histological sections from this survey
> along with the accompanying letter (YB90/11.28/1.1) dated
> November 1990. This letter details spongiform changes found
> in brains from hunt hounds failing to keep up with the rest of
> the pack, along with the results of SAF extractions from
> fresh brain material from these same animals. SAFs were not
> found in brains unless spongiform changes were also present.
> The spongiform changes were not pathognomonic (ie.
> conclusive proof) for prion disease, as they were atypical,
> being largely present in white matter rather than grey matter in
> the brain and spinal cord. However, Tony Scott, then head of
> electron microscopy work on TSEs, had no doubt that these
> SAFs were genuine and that these hounds therefore must have
> had a scrapie-like disease. I reviewed all the sections
> myself (original notes appended) and although the pathology
> was not typical, I could not exclude the possibility that this was
> a scrapie-like disorder, as white matter vacuolation is seen
> in TSEs and Wallerian degeneration was also present in the
> white matter of the hounds, another feature of scrapie.
>
> 38. Terry Singletary reviewed the literature on hound neuropathology, and
> discovered that micrographs and descriptive neuropathology from
> papers on 'hound ataxia' mirrored those in material from
> Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had
> done much of this work, and I obtained original sections
> from hound ataxia cases from him. This enabled me provisionally to
> conclude that Robert Higgins had in all probability detected
> hound ataxia, but also that hound ataxia itself was possibly a
> TSE. Gerald Wells confirmed in 'blind' examination of single
> restricted microscopic fields that there was no distinction
> between the white matter vacuolation present in BSE and
> scrapie cases, and that occurring in hound ataxia and the hound
> survey cases.
>
> 39.Hound ataxia had reportedly been occurring since the 1930's,
> and a known risk factor for its development was the feeding
> to hounds of downer cows, and particularly bovine offal.
> Circumstantial evidence suggests that bovine offal may also be
> causal in FSE, and TME in mink. Despite the inconclusive
> nature of the neuropathology, it was clearly evident that this
> putative canine spongiform encephalopathy merited further
> investigation.
>
> 40.The inconclusive results in hounds were never confirmed,
> nor was the link with hound ataxia pursued. I telephoned Robert
> Higgins six years after he first sent the slides to CVL.
> I was informed that despite his submitting a yearly report to the
> CVO including the suggestion that the hound work be continued,
> no further work had been done since 1991. This was
> surprising, to say the very least.
>
> 41.The hound work could have provided valuable evidence
> that a scrapie-like agent may have been present in cattle offal long
> before the BSE epidemic was recognised. The MAFF hound
> survey remains unpublished. Histopathological support to various other
> published
> MAFF experiments
>
> 42.These included neuropathological examination of material
> from experiments studying the attempted transmission of BSE to
> chickens and pigs (CVL 1991) and to mice (RVC 1994).
>
> http://www.bseinquiry.gov.uk/files/ws/s067.pdf
> nothing to offer scientifically;
> http://www.bseinquiry.gov.uk/files/yb/1991/10/17001001.pdf
> maddogs and Englishman
> http://www.bseinquiry.gov.uk/files/yb/1990/11/28001001.pdf
>
> Editorial: Things are really not as clear with dogs and TSE as you might
> think. The first thing was that the MAFF in the UK decided to do no
> scientific work investigating the cases (e.g. by inoculating them into
> animals), and that they were really not happy about discussing this with
the
> public. I was contacted by an Member of the UK Parliament in 1994
> concerning the possibility that a series of dogs near Doncaster had gone
> down with a similar condition that sounded very similar to BSE. The
animals
> were roughly the same age, and had been fed collectively by the owner.
The
> other main possibility was that the condition was due to a poisoning
element
> present in the food. A second group was in contact in around 1995 in
which
> the animals were considered to have been poisoned with heavy metals but no
> proof (or even investigation) seems to have taken place. This
determination
> by MAFF not to carry out any studies of inoculating BSE into dogs was
indeed
> strange at the time. The reason for this being so odd is that dogs are
> commonly available for experimental animals and it would be looked on as
> being a low cost experiment. However politically it is always extremely
bad
> to do experiments with loveable domestic dogs by inoculating them with a
> disease that could, to some degree be blamed on the incompitence of the
> government of the time.