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Progressive Rod/Cone Degeneration

Progressive Retinal Atrophy (PRA ) refers to a group of inherited diseases that cause loss of sight in many dog breeds. Most forms of PRA are believed to be inherited as simple Mendelian recessives. They differ in their age of onset and histology.  Progressive Rod/Cone Degeneration (prcd) is the form of PRA found in the Australian Cattle Dog (ACD) and in the Australian Stumpy Tail Cattle Dog (ASTCD).

Prcd is known to have caused blindness in Cattle Dogs as young as 3 years old. Age of onset is, however, variable. Some Cattle Dogs do not develop clinical signs of the disease until they are 6 or 7 years old, or even older.

Prcd has been known in ACDs population from early in the breed's history. Old stories have been handed down about "moon-blindness" or "night-blindness" and inability to see in subdued light. These observations are often a sign of prcd. More recently, it become evident that the incidence of prcd was alarmingly high. Because prcd is commonly late in onset, affected animals may parent litters before the disease is diagnosed.

Wooleston Blue Jack, and his ancestors Little Logic and Logic Return are behind all modern ACDs.  Pedigree study suggests that the popularity of this lineage, and the genetic convergence on it, may have contributed to increased incidence of prcd.  It is probable that Little Logic carried the disease.  For example: Glennie Blue Gem, whelped in 1964, was closely line bred to Little Logic.  Her blindness is thought to have been the result of prcd.

Prcd is inherited as an autosomal recessive. This means that an affected dog must have inherited the prcd gene from both parents. A dog that inherits the prcd gene from one parent and the healthy gene from the other will not develop the disease, but can pass the prcd gene on to its offspring. Such a dog is known as a carrier for prcd. A dog which has no copies of the prcd gene can’t (obviously) pass on the disease – such a dog is known as clear for prcd.

Prcd in ACDs attracted the interest of Dr Greg Acland, an Australian veterinary ophthalmologist holding research and academic positions in the USA. In 1996, Dr Acland collected blood samples from over 100 ACDs in the United Kingdom and Netherlands for initial study. Blood samples from ACDs in North America and Australia later enlarged the collection. Dr Acland’s research, carried out at Cornell University, was successful, in 2002, in proving a DNA test that can (a) identify prcd affected ACDs before the disease becomes clinically evident, (b) can determine whether a dog carries the disease (even though it is itself unaffected), and (c) can identify dogs that are completely clear of the disease.  The test became available for ASTCDs in 2004.

More information can be found on the following web sites:


Using OptiGen's DNA test for prcd-PRA


OptiGen Mendelian genetics Definition
Pattern A PP Genetically clear of PRA.
Pattern B Pp Will not become affected by PRA but is very likely to carry the disease and could pass it on to offspring.
Pattern C pp Probably PRA affected.


1. Understand how PRA is inherited


2. Understand which Pattern to Pattern matings produce the lowest PRA incidence


3. Draw a family tree for your own dogs

Add everything you can discover about PRA-affected and PRA-unaffected dogs in the family tree. Then think about which dogs should be DNA tested, as your highest priorities.


4. Minimum testing requirements


Witch Hunting

'Attempts to eradicate heritable disease should not be pursued to the detriment of the breed.'

- H J Hewson-Fruend

It is irresponsible for breeders to ignore heritable diseases, such as PRA. One Australian ophthalmologist has referred to the "moral bankruptcy" of breeders who continue to breed from PRA-affected stock regardless of the implications:

  • increased incidence of the disease in the breed.
  • reduced quality of life for the affected dog when blindness overtakes him.
  • heartbreak to the owners of dogs that are suffering from a progressive disease that cannot be controlled.

In contrast to the breeders who do nothing about PRA, or knowingly breed PRA affected dogs, there are those who will urge that, not only should affected animals be withdrawn from breeding (as soon as the condition is identified) but also their progeny who are immediately identified as carriers (if not affected). This, I suggest, is equally irresponsible.

Rigorous culling has the potential to destroy what is good while attempting to control what is bad. In genetic terms, it may have the effect of eliminating a large bank of valuable genetic material that can never be recovered. There are few pure bred dog populations in any country that can afford large scale loss to the genetic pool.

The softer and less destructive approach is to prefer dogs believed to be at lower risk for a given disease as mates for those known or believed to be at greater risk.

The same approach should be taken with regard to miscoloured ACDS and ASTCDs.  Grossly miscoloured individuals should be culled from breeding programs.  They are contrary to the relevant Breed Standards.  However, the decision as to whether to breed carriers of the b- and e-alleles should be made with regard to whatever other qualities the carrier dogs offer.  But breeders must, in this case, be prepared to implement colour testing of offspring so that the miscolour does not proliferate further through the breed.