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Lethal Acrodermatitis


Lethal Acrodermatitis

Written by T.M Heath - 15th August 1996.

Lethal acrodermatitis is a relatively new disease having only been investigated in the last decade. Lethal acrodermatitis has certain features of a nutritional or infectious disease but since it only occurs in bull terriers it is now suspected to be a genetic disease. It was first recognized in the genetics clinic of the University of Philadelphia (Jezyk and others 1986) and a further two cases studied in West Germany (Trauvetter 1985).
At birth, the lethal acrodermatitis puppy is often the smallest in the litter and looks rather pink as they often lack pigment. The first indication is usually a restless, hungry puppy. Although appearing to suckle well from the dam, test weighing will reveal the puppy is not getting any milk. (Test weigh the pup before it suckles and again after, the difference being the contents of the stomach). The puppy can be fed using a Catac major and teat as the teat is long and will reach the back of the mouth. Within three weeks a size difference will be noticed, the lethal acrodermatitis pup will be markedly smaller than its littermates.

At weaning the puppy will lap successfully at milk but as the meals get more solid, difficulty in mastication and swallowing can be observed. The unusually high arch of the palate causes a problem as food tends to stick to the roof of the mouth. Liquidising the food can help the puppy considerably.

At approximately 6-10 weeks of age, crusted skin lesions can be seen developing between the toes which are distinctly splayed, the footpads are hard and cracked. The foot lesions progress rapidly with the nail bed being involved and the growth of the nails being somewhat distorted. The area of the pads not in direct contact with the floor take on a frond like appearance due to the excessive development of hard skin (keratin) and the feet look deformed. At about the same time, papular or pustular lesions appear around the body orifices, most noticeably on the face and around the eyes. Inflammation of the hair root is most pronounced on the friction areas, eg. elbows and hocks. The third eyelid protrudes and sight can also be affected.

The size difference is very marked and the puppy looks thin and stunted. The puppy tends to stand with its legs splayed and there is a marked problem with co-ordination. Coloured LAD pups will start to lose the colour at about eight weeks of age. eg. a pup born tri-colour will fade to a chocolate colour or fawn.

Diarrhoea can develop early in the disease and this can vary in severity from loose stools to profuse bloody diarrhoea with accompanying dehydration. Respiratory tract infections can be present with mucropurulent nasal discharge. Pneumonia can often be diagnosed by stethoscope or x-ray examination.

Between 4-8 weeks of age the behavior may also be abnormal as the puppy may be aggressive and may even need to be isolated because it is biting its littermates. As the puppy gets older, activity decreases and responses to external stimuli diminishes. They often spend periods staring at objects. The more severely affected, the more the puppy will sleep. The puppy will normally die by fifteen months and the usual cause of death is an intractable respiratory infection.

The condition resembles acrodermatitisenteropatlfica in man and lethal trait A46 in black pied cattle, these are defects in intestinal absorption of zinc (zinc deficiency). High doses of zinc will reverse the clinical signs in humans and calves. However, bull terriers do not respond to zinc therapy, and it is believed there exists in the lethal acrodermatitis puppy some other block to the zinc metabolism.

The incidence of lethal acrodermatitis in British bull terriers is not known. Studies have been instigated in Glasgow University Veterinary School by Mr. Neil McEwan M.R.C.V.S. B.V.M.&S. but to date information is sparse. It is thought that so little is known of f the condition that puppies born with lethal acrodermatitis are being euthanased as deformed, diagnosed as zinc deficiency syndrome, or are dying within a few days of birth without ever being recognized for what they actually are.

Written by T.M. Heath.
Validated by Mr. N. McEwan MRCVS BVM&S. 2nd March 1992


Lethal Acrodermatitis Update

Since the article on lethal acrodermatitis in bull terriers as first published in 1992, quite a lot of progress has been made in the diagnosis and management of the L.A.D. pup.

As with everything, there are different degrees which vary from mildly defected to grossly deformed. A mildly affected L.A.D. pup will often be sold to a pet home as 'the small pup in the litter' but to the experienced eye there is always something not quite right about the pup apart from the size. The gait is usually different as there is nearly always some deformity of the hips, a twist on the femur (thigh bone) and a luxating patella because of this. Operating to correct the patellar luxation is a useless project as the twist on the femur negates the deepening of the trochlear groove (the groove which houses the patella) and could in some cases cause extreme pain in the knee joint. However the L.A.D. pup copes very well with this deformity where there is no surgical intervention but can be considerably helped by giving PLT (predoleucotrophin) - half a tablet am and pm, and they seem to do well on this small dose of painkiller
No matter how mildly or severely the L.A.D. pup is affected, the immune system does not function to optimum level which leaves the L.A.D. pup susceptible to infection, being particularly susceptible to upper respiratory infections. In degree this can vary from mild sniffles to bronchitis and pneumonia. As a prophylactic measure it is advisable to give an antibiotic daily. One ceporex 250mg daily is the drug of choice, as to the best of my knowledge this antibiotic does not give rise to keratoconjunctivitis (dry eye). As a personal preference I also include vitamin B compound giving one tablet daily.

In the average dog, steroids are to be avoided but the L.A.D. pup needs mendrone (4mg daily) and this I have found does improve the quality of life and a deterioration can be observed when the mendrone is withdrawn. One L.A.D. pup I have known lived to six years old and was on steroids all her life with good effect.

The front feet are nearly always affected, with the toes splayed and giving the appearance of being down on the pastens. Almost invariably keratitis develops, (overgrowth of the hard skin of the pads) deforming the feet. This definitely causes problems, being very painful and affecting the dog's ability to walk. The best treatment I have found when keratitis develops is Stockholm tar. There are two methods of application.
  • In milder cases where the condition has been recognized early, the spray version of Stockholm tar can be used preferably sprayed on the tops and undersides of the feet before going out on exercise (being a tar preparation it is not kind to carpets). By the time exercise is over (20-30 minutes) the tar has dried on the foot and the pup can safely be allowed indoors again.
  • Where the keratin growth is more pronounced (1/4 inch) it may be necessary to use the regular Stockholm tar. Spread over the entire foot, pack between the toes with cotton wool, cover the foot with cotton wool and bandage in place with elastoplast. This gives the pup a nice soft cushion to walk on and prevents the tar soaking through onto upholstery. The bandage should be left in place for four days only, then the foot is left uncovered for three days. The treatment should be carried out on a weekly basis until all evidence of the excessive keratin has disappeared.
Skin lesions can also develop on the face, feet and pressure points, eg. elbows and hocks, and these can be treated successfully by cleaning with surgical spirit and applying either Fucidin H or Canastan cream.

The big question remaining is 'What are they like as pets?' - in a word - wonderful!! Given the same socialization and affection as a normal bully they repay with a joy of life that is delightful to see. I am not advocating rearing L.A.D. pups from choice recognized soon after birth I would recommend euthanasia. However, milder affected L.A.D. pups are being sold as pets. Unrecognized by the average vet when the syndrome develops at approximately 12 weeks of age, wrong diagnosis and treatment can be expensive and heartbreaking. People who have them need support and advice on correct medication, feeding and training. It would be extremely difficult for someone who has loved and cared for the pup from 6-8 weeks of age to voluntarily opt for euthanasia, as by this time the personality has developed and the pup is well and truly under the owners skin. It has to be accepted that the life span will be shorter, (approximately 2 years) but a lot of happiness for the pup and the owner can be crammed into that time - but only with help and support from bully breeders who know the condition, accept it's existence and have gone to the trouble of finding out how to improve the L.A.D. pup's quality of life. Unfortunately these are rarely the people who sell them on as pets, so we have to rely on the good old grapevine and offer assistance where needed.

I dont know why these are so tiny but here she is in her pool. if you click on it the picture blows up to full size.


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Hi all
i have just found this post so thought I would reply. I am the owner of Little Lottie the LAD babe who sadly passed to the bridge and is in the pictures posted.

There is now a LAD awareness website which is more updated than the one quoted so if you are interested please take a look.


I do share my life with another LAD suffer Elsa sh eis mildly affected and is now 10 months old, she happilly lives with my Mini Bullies :D




New research is soon to start ,this time to find the gene marker responsible and hopefully,maybe,the mode of inheritance.To HELP..any of you who have a LAD affected bullie,could you e mail me your address and details of your dog,I will be getting packs of sponge swabs and instructions .I need addresses so that as soon as available the testing kits can be sent to you ,and where you will need to mail them to,here in UK.
We will need a minimum of twenty samples from affecteds,and worldwide this should not be too hard to get.
Even if you just know of an affected it would be great if you could alert it`s owner ,so more numbers can be got together.

My E Mail badlesmerebts@aol.com
Thankyou so much.