PLL in Miniature Bull Terriers: Clear, Carrier, Affected

The short answer. Primary lens luxation (PLL) is an inherited, painful eye disease. The lens slips out of place, and the result can be glaucoma and blindness. In miniature bull terriers it's caused by a known mutation in the ADAMTS17 gene, and a single DNA test tells you a dog's status for life.

A clear (N/N) dog won't develop PLL from this mutation and can't pass it on. A carrier (N/PLL) has one copy, carries a low but real risk, and can pass it on. An affected (PLL/PLL) dog is at high risk. Breeding a carrier to a clear dog produces no affected puppies. Breeding two carriers is expected to produce about 25% affected.

PLL is the one inherited problem in the breed where the genetics are fully understood, and that works in your favour as a buyer. With the right document in front of you, you can know before you pay whether a puppy can be affected. This guide explains the disease, the test, the results and the maths, and ends with a checklist for verifying a PLL certificate.

What PLL is and why it matters

Inside the eye, the lens is held in place behind the pupil by a ring of fine fibres called zonular ligaments. In PLL those fibres weaken and break down. The lens then partly slips (subluxation) or falls fully out of position (luxation), as the OFA explains.

If the lens moves forward into the front chamber of the eye, "glaucoma and loss of vision can quickly result", according to The Royal Kennel Club. The UC Davis Veterinary Genetics Laboratory calls it "a painful inherited eye disorder".

When it appears. The sources give slightly different age ranges, but all put it in adulthood, long after a puppy has gone to its new home:

UC Davis VGL: typically 3 to 8 years, and both eyes aren't necessarily affected at the same time.
The Royal Kennel Club: clinical signs "can be detectable at 20 months", with complete luxation typically at 3 to 8 years.
OFA: most commonly 3 to 6 years across the affected breeds, often in both eyes.

So a puppy's eyes look perfect at 8 weeks whatever its genotype. The only way to know its risk in advance is the DNA test, on the puppy or on both parents.

The gene behind it: ADAMTS17

In 2010, a research team including the University of Missouri found the cause. It's a single-letter change at a splice site of the ADAMTS17 gene (c.1473+1 G>A), which makes the cell skip part of the gene when building the protein (Farias et al., Investigative Ophthalmology & Visual Science, 2010). The mutation was significantly associated with PLL in three breeds: miniature bull terriers, Lancashire heelers and Jack Russell terriers.

A follow-up study in 2011 found the same mutation in PLL-affected dogs of 14 more breeds (Gould et al., Veterinary Ophthalmology, 2011). It also measured how common the mutation was in the mini bull. The authors estimated a mutation frequency of 0.27 to 0.39 in the breed, corresponding to 7.3 to 15.2% PLL-affected dogs. That estimate predates more than a decade of widespread testing, so it doesn't describe today's population. It does explain why breed clubs made the test a priority.

PLL is inherited as an autosomal recessive trait. Every dog has two copies of the gene, one from each parent. A dog needs two mutated copies to be affected, and each parent passes on one of its two copies at random.

Clear, carrier, affected: what each result means

Labs write results in slightly different ways, but they all describe the same three genotypes:

Result	Also written as	Risk of developing PLL	What it can pass to puppies
Clear	N/N, Normal, Normal/Clear	None from this mutation. VGL: "will not have primary lens luxation"	Only the normal copy
Carrier	N/PLL, Carrier/Low risk	Low but not zero (see below)	Either copy, 50/50 per puppy
Affected	PLL/PLL, Affected/High risk	High. VGL: "will have or are at risk of developing" PLL; OFA: usually between 4 and 8 years	Only the mutated copy

How risky is it to be a carrier?

This is the question buyers ask most, and the honest answer is that the sources word it differently:

UC Davis VGL: carriers "are at slight risk of developing primary lens luxation". Dogs with one copy "most frequently show no sign of the disease but can, on occasion, develop PLL".
OFA: a carrier "has a slight (5-10%) risk of developing Primary Lens Luxation".
MBTCA (US breed club): carriers "have an extremely low risk".
Gould et al. 2011: found "an increased risk of PLL associated with heterozygosity", suggesting that "carriers carry a low risk".

Put together: a carrier puppy is much less likely to develop PLL than an affected one, but its risk is higher than a clear puppy's. The Royal Kennel Club's own page describes one copy as causing "no signs of the disease", so you'll also see simpler wording in some places. If you're choosing between puppies, a clear puppy is the lowest-risk option. A carrier pet from an honest breeder isn't a disaster, but you should know which one you're buying.

Pairing table: parent A × parent B → expected puppies

Because the trait is autosomal recessive, you can work out what a litter can inherit from the two parents' results alone. These are standard Mendelian probabilities per puppy, and each puppy is an independent draw.

Parent A	Parent B	Clear (N/N)	Carrier (N/PLL)	Affected (PLL/PLL)
Clear	Clear	100%	0%	0%
Clear	Carrier	50%	50%	0%
Clear	Affected	0%	100%	0%
Carrier	Carrier	25%	50%	25%
Carrier	Affected	0%	50%	50%
Affected	Affected	0%	0%	100%

Assumes the parents' results are genuine and belong to the actual sire and dam.

Carrier × carrier: each puppy independently has a 25% chance of being clear, 50% of being a carrier and 25% of being affected. The UC Davis VGL states that such matings "are predicted to produce 25% primary lens luxation-affected puppies".

A worked example: why "25%" understates the problem

Say two carriers are mated and produce six puppies. Each puppy has a 75% chance of not being affected. The chance that none of the six is affected is 0.75⁶ ≈ 0.18, so the chance that at least one puppy in the litter is affected is about 82%.

That's why carrier × carrier matings are avoided. It's also why the pairing matters more to you than either parent's result on its own.

Can a PLL carrier be bred?

Yes. The table shows that a carrier bred to a clear dog can't produce affected puppies. Breeders sometimes keep carriers with other qualities in a breeding programme, as long as every mate is DNA-clear. What matters to you as a buyer is the other parent's result. If one parent is a carrier and the other has no PLL result at all, you can't rule out affected puppies.

"Clear by parentage": when it's valid and when to ask for the dog's own test

Sometimes a puppy is described as "clear by parentage" or "hereditary clear". It hasn't been tested itself, but both of its parents are DNA-clear. The genetics support this. A clear parent can only pass on the normal copy, as the VGL puts it: N/N dogs "cannot transmit this variant to their offspring". So two clear parents can only produce clear puppies.

The weak point is identity, not genetics. The claim only holds if:

both parents have their own DNA certificates. A parent that is itself only "clear by parentage" adds another link that has to be right;
each certificate carries the microchip number of the dog you're told is the sire or dam;
the sire is really the sire. With a stud dog or a kennel with several males, that depends on honest records.

For a pet puppy from two parents with verifiable certificates, parentage-based clear status is a reasonable basis to buy. If you plan to breed from the dog, or if either parent's paperwork is weak, a DNA test on the puppy itself settles it. The test works at any age, and VGL's standard sample is a cheek swab.

Warning signs in an adult dog

This section is for owners, whatever their dog's result. Lens luxation can also happen secondary to other eye problems such as inflammation, cataracts, glaucoma, cancer or trauma.

Signs described by the OFA and The Royal Kennel Club include:

a red, painful or teary eye;
a hazy or cloudy look to the eye;
signs of reduced vision in one or both eyes.

Treat these as urgent and see a vet the same day. The OFA notes that uveitis and glaucoma are "painful and potentially blinding diseases if not identified and treated early", and that if lens luxation is detected early, surgical removal of the lens can be beneficial. A veterinary ophthalmologist is the specialist for this. In the US the American College of Veterinary Ophthalmologists lists board-certified specialists.

How to check a PLL certificate

A PLL result is one of the easiest health claims to fake, because it's just a word on a page. Before you rely on one, go through this checklist:

Named laboratory. The certificate comes from a genetics lab (for example UC Davis VGL, or the lab behind the OFA's test), not from the breeder or a generic template.
The dog's microchip number on the certificate. The Royal Kennel Club won't record a DNA certificate unless it carries the microchip or tattoo number plus the registered name or number. Hold every certificate to that standard.
Microchip scanned live. On a video call, ask the breeder to scan the parent dog and show you the reader's display. Compare the digits with the certificate.
The test named correctly. PLL / primary lens luxation, ADAMTS17. A clinical eye exam is useful, but it isn't a PLL DNA result.
A public database where one exists. For OFA-registered dogs, search the OFA database. For dogs on the UK register, use The Royal Kennel Club's Health Test Results Finder or its published list of PLL-tested miniature bull terriers.
Direct confirmation otherwise. For dogs registered elsewhere, contact the lab named on the certificate, quote the case or certificate number, and ask it to confirm the result.

If a breeder can't give you a lab name, won't show the microchip, or sends a certificate that looks edited, stop. Our guide on how to spot fake paperwork covers the wider patterns. PLL is one of several screenings worth asking about. The others are in our guide to other health tests for mini bulls.

Every breeding dog of ours has a PLL lab report. Ask for it before you commit.

On the video call we'll show you the laboratory's certificate for both parents, scan their microchips on camera, and send you copies to check yourself. Nothing is paid before that.

Request the lab report

On our homepage we say our parents are DNA-tested for primary lens luxation, with the laboratory's own report available to you. This page is the explanation behind that sentence.

Frequently asked questions

What does PLL clear mean in a miniature bull terrier?

PLL clear (N/N) means the dog carries two normal copies of the ADAMTS17 gene. According to the UC Davis Veterinary Genetics Laboratory, it will not develop primary lens luxation from this mutation and cannot pass the variant on to its puppies.

Is a PLL carrier puppy a bad choice?

Not necessarily. A carrier (N/PLL) has one mutated copy. Sources describe its own risk as slight or low (the OFA gives 5-10%), much lower than an affected dog's but higher than a clear dog's. If you plan to breed, it must only be mated to a DNA-clear dog.

What happens if you breed two PLL carriers?

Each puppy has a 25% chance of being affected, 50% of being a carrier and 25% of being clear. In a litter of six, the chance that at least one puppy is affected is about 82%, which is why responsible breeders avoid carrier × carrier matings.

At what age do miniature bull terriers get PLL?

Typically in adulthood. UC Davis VGL and The Royal Kennel Club give 3 to 8 years for complete luxation, and the OFA says most commonly 3 to 6 years across affected breeds. The Royal Kennel Club notes clinical signs can be detectable from about 20 months.

Can PLL be treated?

PLL itself is not reversed by treatment, but the OFA notes that if lens luxation is detected early, surgical removal of the lens can be beneficial, and medication can relieve the inflammation and glaucoma it causes. Any painful, red or cloudy eye needs a vet the same day.

Is a puppy from two PLL clear parents guaranteed clear?

Genetically yes, because a clear parent can only pass on the normal copy. The guarantee is only as good as the paperwork, though: both parents need their own lab certificates with matching microchip numbers, and the stated sire must be the real sire. A DNA test on the puppy removes any doubt.

Medical disclaimer. This article is general information about an inherited eye disease and its DNA test, compiled from the sources linked above. It is not veterinary advice. Any dog with a painful, red or cloudy eye should be seen by a vet urgently, whatever its DNA result.

Sources

UC Davis Veterinary Genetics Laboratory, Primary Lens Luxation (genotype interpretation, inheritance, carrier × carrier outcome, breeds).
Orthopedic Foundation for Animals, Primary Lens Luxation (description, age of onset, result definitions).
The Royal Kennel Club, DNA test PLL and DNA testing (certificate identification requirements).
Miniature Bull Terrier Club of America, Health Issues.
Farias FH et al. (2010). An ADAMTS17 splice donor site mutation in dogs with primary lens luxation. Investigative Ophthalmology & Visual Science 51(9):4716-21. PubMed 20375329.
Gould D et al. (2011). ADAMTS17 mutation associated with primary lens luxation is widespread among breeds. Veterinary Ophthalmology 14(6):378-84. PubMed 22050825.
OMIA, Lens luxation in dogs (OMIA 000588-9615).

Primary Lens Luxation (PLL) in Miniature Bull Terriers, Explained