FELINE DYSAUTONOMIA (KEY-GASKELL SYNDROME) STUDY GROUP

WHAT IS FELINE DYSAUTONOMIA?

FD is a disease of domestic cats characterised by extensive degeneration of the autonomic nervous system. This causes a variety of clinical signs characterised by regurgitation, constipation, dilated pupils that are unresponsive to light, prolapsed third eyelids, and reduced tear secretion. Clinical signs usually develop over a matter of days and less than a third of affected cats survive (Refs 6,7).

FD was first reported in 1982 in the UK but has now been reported sporadically from the USA, the United Arab Emirates, New Zealand, and countries throughout Europe. FD appears to be one of a group of primary dysautonomias affecting dogs, hares, rabbits, and horses (equine grass sickness [EGS]). These diseases have very similar clinical signs and underlying pathological changes (Ref 8).

With the exception of canine dysautonomia, which has largely been reported from the mid-western USA (Ref 1), the vast majority of animals with dysautonomia have been reported in Britain.

After over twenty years of dysautonomia in cats and dogs, and almost a century of EGS, the causes of this group of diseases remains unknown. The study group involves Vale Referrals, University of Glasgow Veterinary School, and University of Edinburgh’s Department of Medical Microbiology.

WHAT ARE THE AIMS OF THE STUDY GROUP?

1. To raise awareness of this disease amongst veterinary surgeons
2. To provide information that will help vets confirm the diagnosis
3. To provide information that will help vets treat this condition
4. To monitor the incidence of the disease in Britain
5. To investigate the causes of this disease

DISEASE INCIDENCE

Many FD cases were reported in Britain during the early 1980’s (Ref 6,7). Towards the end of the decade, the number of cases and the disease severity appeared to decline (Ref 2).

During the 1990’s a few cases were reported in pet cats and a large outbreak occurred in a closed research cat colony (Ref 9). In 2001 an outbreak occurred in a closed colony of pet cats in Scotland (Ref 3). Our investigations suggest the current incidence of FD in Britain remains low (between 1 in 20,000 and 1 in 50,000 cats per year).

CLINICAL SIGNS

The onset of clinical signs varies from a few hours to several weeks. Prodromal signs (serous oculo-nasal discharge or diarrhoea) have been reported. Some common clinical signs such as constipation, prolapsed third eyelids, and dry mouth are very non-specific i.e. they are also seen in many other diseases. Others such as reduced tear secretion, mydriasis (dilated pupils), regurgitation and megaoesophagus are more specific to FD. It is generally the finding of multiple clinical signs in the same cat that suggest a diagnosis of FD.

Dilated pupils, prolapsed third eyelids, reduced lacrimal secretions, regurgitation, and constipation were seen in over 75% of pre-1984 cases (Ref 6,7). Each of these signs occurred in less than 60% of cases between 1984 and 1987 suggesting that the clinical severity of FD may have reduced (Ref 2). This trend has not been supported by more recently reported cases (Ref 3,9).

DIAGNOSIS

Definitive diagnosis currently requires histopathological examination of autonomic ganglia. Samples for this process can only be obtained at post-mortem after cats have died. The coeliacomesenteric ganglion may be the easiest ganglion to identify. However it often proves difficult to identify this at post-mortem resulting in a failure to confirm a suspected diagnosis. Attached is a powerpoint or pdf file demonstrating how to obtain the necessary samples at post-mortem. We would also recommend the submission of sections of small intestine. Right Click on the links to download the files, they have the same content.

A clinical scoring system has been developed for ante mortem diagnosis (Ref 8). The ideas on which this scoring system are based are sound but we do not currently know how sensitive and specific it is for FD. In order to fully evaluate a suspected case of FD you MUST note heart rate, pupillary light response, anal reflex, proprioceptive responses and perform Schirmer tear tests in both eyes. Thoracic radiography to demonstrate megaoesophagus is also strongly recommended in all cases. This should ideally be obtained with the cat unsedated as sedation itself can cause megaoesophagus. If megaoesophagus is not visible on plain radiographs a barium swallow should be performed as this significantly improves detection. In addition to megaoeosphagus, thoracic radiographs may demonstrate if aspiration pneumonia has occurred. Ocular pharmacological tests of denervation hypersensitivity should also be performed.

Other tests that may be beneficial include abdominal radiography, which may demonstrate delayed gastric emptying and distension of the urinary bladder or colon. Fluoroscopic assessment of oesophageal motility may be beneficial and may detect subclinical disease in in-contact cats (Ref 3). Additional tests employed in past cases include detection of reduced plasma or urine catecholamine levels or response to intradermal histamine (Ref 8).

Routine haematology, serum biochemistry, and virology are only useful in identifying concurrent conditions. Differential diagnoses are few in cats with multiple cardinal clinical signs. A caudal equina lesion could cause multiple similar caudal symptoms. In less severe grades there are multiple differential diagnosis e.g. causes of regurgitation or pupillary dilation alone.