THOUGHTS ON PDD

Based on a paper given to the European Association of Avian Veterinarians Aviculture Day by Nigel Harcourt-Brown FRCVS.

This disease has been around in various guises for some years, it has been given various names but all represent the same problem.

• Macaw wasting syndrome/disease
• Neuropathic gastric dilatation syndrome
• Proventricular dilatation syndrome

The disease that has become increasingly common in Psittaciformes over the last decade, but evidence from the USA seems to indicate that it has been around for at least 18 years.

It has been reported in nearly all parrots but macaws and Grey Parrots seem most susceptible, followed by Cockatoos. The other parrots are less commonly or less dramatically affected.

The disease was first described in S. America and is now seen world wide.

Basic Alimentary tract anatomy

• Mouth: does the eating.
• Oesophagus: transfers chewed up food to the crop.
• Crop: food store. No digestion occurs in the crop; food is held until it passes into the digestive 'stomach' which consists of two parts:
• Proventriculus: a reasonably muscular tube like stomach. Acid and the digestive enzyme pepsin are secreted here. The food is sterilised and softened prior to going into the ventriculus: commonly known as the gizzard.
• Gizzard: the main powerhouse of a vegetarian bird's digestive tract. Very muscular walls are harnessed to two horny pads which grind the food, usually with the aid of grit.
• Duodenum: is the first part of the small intestine. Digestion and absorption processes start to take place.
• The rest of the bowel (jejunum, ileum, caecum, rectum, and cloaca) is not very obviously affected by the disease.

Signs of the disease in the bird

Birds of any age may be affected. The major outbreaks may be seen in susceptible collections (i.e. those that have not previously had the disease) and if the virus gets into a nursery of hand reared babies then the effect is appalling. In collections that have the disease the commonest time of infection is at weaning and slightly later. Susceptible adults can also become ill and frequently die.

Initially the signs of the illness are those of a non-specific infection: ill bird, depressed, watery droppings, some regurgitation, maybe some dyspnoea.

Some veterinarians feel that many birds can, at this stage, recover from the disease. Probiotics, broad spectrum antibiotics, and lucky rabbit's feet can all be helpful. A high fibre diet with little seed is also a good idea; pellets may be very useful. It is not possible to make a diagnosis at this stage, therefore these birds are not known to have suffered from the disease. It is likely, but speculative, that most of these birds will rid their body of the virus, but some may remain as symptom free carriers of the disease. It is these birds that when sold may cause further outbreaks.

A proportion of the ill birds succumb to the classic signs of the disease: weight loss, depression, lack of appetite, regurgitation, whole seed in faeces; progressing to very ill, very thin, weak individuals with tremors of the head and body.

In the secondary phase the disease may be suspected if radiography reveals an enlarged proventriculus and gizzard full of seed and occasionally large foreign bodies.

The diagnosis can, at the moment, only be confirmed in the live bird by a crop or proventricular biopsy: small (3-4mm diameter) pieces of tissue are removed from one or both organs under general anaesthetic. It is easier to take crop biopsies. This method of diagnosis can give a false negative result as the pathologist requires some nerve tissue to see the classic changes, It is always possible to fail to obtain nerve in a biopsy so the more taken the better the chances. In some hands this can be as good as 60% diagnostic but this may not be considered satisfactory (tossing a coin is going to be 50% accurate!)

By the later stages of an outbreak of the disease the clinical signs and number of birds affected can be diagnostic by themselves.

Cause

The disease appears to be viral, a virus has recently been cultured from UK cases at the Central Veterinary Laboratory in Weybridge and is being worked on there and in the USA where a virus has also been found, at the moment it isn't known whether these are the same virus. This was made possible by donations of fertile macaw eggs by concerned aviculturists and by a donation from the UK Parrot Society.

Demonstrating that the virus causes the disease requires either infecting susceptible birds such as young Grey Parrots or macaws, or producing a test where a marker will stick to the virus and can then be seen down the microscope as present in diseased cells.

Most outbreaks seem to have started after the introduction of a new bird(s).

There can be a long period between contact and clinical disease: 12 weeks recently in an outbreak but possibly much longer.

Birds are often made worse with a change in diet, especially if placed onto a mainly seed diet.

If sufficient time and funds are available a blood test may be developed.

Vaccination may never be available in the UK as there are too few birds to vaccinate to make the product licensing of a vaccine a financially viable option. It is incredibly expensive to get a product licence for this type of product and sales would not be sufficient!