This is shared with permission of Heather Powell from the UK.
Hi, I’ve recently joined the forum and have been reading the postings on CPL with interest. I don’t own an affected horse, but was partly responsible for the study at UCDavis into using combined decongestive therapy (CDT) with horses with CPL. In conventional human medicine, CDT is the treatment for lymphoedema. A paper on the study has been accepted for publication, so hopefully the results will be more widely available soon. My involvement in the study has raised some questions for me and I would welcome any thoughts about them, and perhaps I can contribute information on some of the points raised in the forum. If, in doing so, I make some errors about the breed, or inadvertently offend anyone, I apologise in advance!
Clearly there is a fair amount of confusion and lack of accurate information about CPL which is not surprising, as the lymphatic system has been difficult to visualise and examine, and it ‘s only recently that advances in this field have started to change this. In the horse, there is a real lack of knowledge, and many of our established horse care practices which affect the lymphatic system are based on traditional assumptions, not fact based research. Although horses appear to be prone to lymphoedema it is frequently not recognised and not treated as such.
Lymphoedema is caused by an inability of the lymphatic system to function adequately. One if it’s major roles is to remove excess fluid from the tissues. Fluid and nutrient carrying protein molecules, oxygen etc are constantly leaving the tiny blood capillaries and entering the ‘interstitium’ which surrounds the cells, to feed them. This fluid is then removed by the lymphatic system – it doesn’t return to the local blood vessels as used to be thought – and also the ‘carrier’ protein molecules. These molecules also attract more water, so if they aren’t removed, swelling - oedema develops. With time the protein also changes, leading to the firm-hard tissue which develops with equine lymphoedema.
Lymphoedemas can be divided into ‘primary lymphoedema’ which is congenital, though often not showing symptoms immediately, and may also be hereditary, and ‘secondary lymphoedemas’ in which a previously healthy system is damaged by injury etc. Sometimes an oedema will develop because the system is asked to remove too much at once, e.g. following trauma, however it is still functioning normally and removing the proteins, and eventually the swelling resolves. This isn’t lymphoedema, though if it goes on long enough it may result in some damage and exhaustion to the system and lead to a ‘combined lymphoedema’ which may result in serious damage to the skin. It’s also possible that following trauma an apparently secondary lymphoedema develops in a system with primary lymphoedema which up to that trigger point was asymptomatic.
It is suggested that an important reason why lymphoedema is seen often in horses is that they have evolved as creatures almost constantly on the move. The lymphatic system responds to movement, and particularly that of the horse, and in it’s distal leg this is the major factor stimulating the system. Our modern methods of restricting horses for stabling etc take away this vital requirement, and whilst horses with healthy systems can cope, others do not, perhaps because they were born with fewer lymph vessels or ones with functional anomalies. These horses with latent primary lymphoedema typically develop filled legs/stock up when forced to be immobile, but because this oedema often disappears with movement it’s dismissed as harmless. However the condition does gradually worsen and there is growing suspicion that these horses are more likely to develop lymphangitis in later life. Interestingly, research has shown that using stable bandages/wraps on these horses stops the flow of lymph, leaving metabolic wastes stagnating in the tissues, and may contribute to this deterioration. Lymphangitis can also result in a permanent swelling, which again is (secondary) lymphoedema. There is very little tissue between the skin and the lymphatic vessels in the distal leg, so it’s not surprising that bacteria which gain entry can easily cause infection there.
There is a mesh of tiny lymphatic vessels lying just under the skin, which is where lymphoedema appears. The lymphatic system is part of the immune defences which have to deal with any infestation or infection which attacks the skin and also the inflammation caused by this. With lymphoedema a vicious cycle can develop, it damages the immunity of the skin, greatly increasing the risk of infection, which in turn causes inflammation which stressed the damaged lymphatic system.
As I’m sure you all know, CPL was discovered through research conducted in Belgium and UCDavis into ‘therapy resistant pastern dermatitis’ which had been found in some breeds of draft horses. In the process of this it was discovered that there was an underlying vascular issue, lymphoedema, and that the skin problems were secondary to this. Further work suggests that CPL is caused by deficiencies in elastin, a protein essential to the healthy functioning of the lymphatic system and many other tissues. If this is true it follows that CPL is a specific form of lymphoedema, not to be confused with others which affect horses. There is incidentally, an article still present on the internet, on research at UCDavis into therapy resistant pastern dermatitis. This is work that preceded the discovery that it is a form of lymphoedema, and should be read as such, it is the same condition that’s being described, not an alternative one. I do think it’s continued availability has caused some confusion.
One of the difficulties with CPL is that it apparently affects horses with heavy feather, and is initially not spotted because the lesions it produces are not visible under this. The oedema in affected limbs is initially soft, and will depress rather like soft butter, but unless this is being specifically looked for is easily missed. Fibrous folds developing in the pastern area, which are caused by changes in the protein molecules, are often the first changes felt, but, at least in the UK, are frequently dismissed as scar tissue from mite infestation. This, apart from an overall lack of awareness, may be one of the reasons why CPL isn’t spotted during purchasing vettings. Unless a horse is familiar from birth, it’s history may be unknown. Scrupulous attention to hygiene and skin care does seem to be very helpful in slowing down the development of skin lesions in CPL, but again it can be difficult to know if a previous owner has attended to this, and to what extent it may affect appearance in an individual horse.
As far as I am aware, there is no easy biological test to show that a horse has CPL. During the research which identified it, skin biopsies were taken, my understanding is that this isn’t something the researchers would routinely recommend because they have to be relatively deep to reach the layer of tissue containing the lymphatic vessels, however it was this necessary process which crucially identified a vascular problem. They now suggest that the symptoms of CPL – recurrent infections and inflammation, lower leg enlargement and development of thick skin folds and nodules - are sufficient to identify the condition. They have never said that the ELISA test is diagnostic for CPL, only that it may indicate the presence of the condition, because it identifies abnormality in the body’s elastin, and it should be born in mind that other conditions also elicit a positive reaction, including diabetes and lymphoedema per se because this itself damages elastin. The emphasis now is on finding genetic markers for the disease, and although the ones for common lymphoedemas in people proved negative in horses, there appears to be some progress being made in Germany.
During the study we found that some horses had mites, although initially there was no sign of these, and their care had been excellent, and we suspected that the warmth of the compression bandages we were applying had encouraged them to become active. The recommendation to their owners was to treat them regularly regardless of signs of presence, with ivermectin or similar, and to use topical fipronil (unless pregnant or with foal). ‘Frontline’ is one brand of fipronil, but I believe that, at least here, others are available. Some people have suggested that there may be products for cattle which work the same way, though I’m not personally familiar with these. It’s really essential that this gets right down to the upper layers of the skin where the mites live, and from experience of using it with clipped legs I would imagine this would be very difficult, if not impossible, through dense feather.
One of the difficulties with treating CPL is that an obvious response must be to clip the legs and remove the feather, indeed it is difficult to imagine this not being done. However I do understand that this is a very thorny issue for breed enthusiasts. From across the Atlantic, the most striking feature about the American Gypsy Horse is the remarkable quantity of hair carried by some horses and the importance attached to this. The official recognition of the ‘Gypsy Horse’ in the UK is very recent and I understand owing to the enthusiasm for the breed in the States, although as a type within the equine population here it is common though traditionally with more emphasis on its ability to perform a function than its appearance. Another striking characteristic is the popularity of black and white animals in the US, and how closely bred many of these horses appear to be. Sorry if I’ve offended anyone, from ‘outside’ that’s just how it looks.
Does this relate to the impression that CPL may be hereditary? Again, the large draft horses in which it’s been identified often share common blood lines, having almost become extinct in the previous century. Over the last hundred years they have also changed significantly, and looking at early pictures of Clydesdales and Belgians, it is striking how little feather they have. But then they were still working animals, and excessive feather would have been a hindrance. But this does raise a question as to whether copious feather exacerbates CPL by providing a perfect environment for asociated skin problems, or whether there may be a genetic link between the two. And, if a genetic marker were found for CPL, would owners of horses with it refrain from breeding them? The answer may seem obvious, but talking to draft horse owners here I’m not so sure, and I suspect that some horses from valuable bloodlines will continue to be used for breeding, with the explanation that CPL really is ‘just’ pastern dermatitis.
Overbreeding has been mentioned, and sending horses from the UK to Europe for slaughter. My understanding is that there is a tradition of breeding these horses for this purpose, along with others, to supply the horsemeat trade and that there is also an established market for their skins, so their export and slaughter isn’t necessarily due to overbreeding. Transport of live horses abroad for the meat market is a big issue in the UK.
One thing that does concern me is people’s fear that CPL will kill their horses. On the Davis website it has been compared to elephantiasis nostras verrucosa in people. This is an old term for the skin conditions which can develop with severe untreated lymphoedema, it’s not how the condition starts out. These days, at least in the Western world, there is no reason why this should happen, unless a long standing lymphoedema is untreated. Even then, using combined decongestive therapy, there is a lot that can be done to improve a sufferer’s health. Lymphoedema itself is not life threatening, the danger comes with the infections that can easily take hold, and again the risk if this is greatly reduced with proper treatment. In horses there is also the possibility of mechanical lameness caused by the presence of fibrotic tissue interfering with joints, and the possibility of it damaging tendons etc. In the Davis study we were able to quickly improve the movement in affected horses. With all lymphoedemas, the sooner treatment is started, the better the results.
I’m not sure what’s meant by ‘scratches’, not a UK term, but it seems to cover a number of conditions. With CPL it is very important to find out what's causing infection and inflammation in the legs as they need different treatments. For example we are advised to lift the scabs caused by Dermatophilus congolensis, but it’s so obvious that we must be sure that this is what we’re dealing with before doing so, as if it’s something else, opening skin in affected horses is an invitation to inflammation and infection. it may seem so obvious, but proper diagnosis is essential. It’s very important to remember that the skin of horses with lymphoedema is fragile, and disturbed by it. Lymphoedema dries the skin out, encouraging the uppermost layers to lift and make infestation easier, so it’s important to keep it supple and flexible, using a non greasy hypoallergenic moisturiser if necessary. Some owners have become concerned about ‘greasy’ areas on their horses legs, and their significance, again, these are a sign of the overall disturbance to the skin. It’s essential not to use anything severe on the skin, including volatile oils (e.g. tea tree), or to scrub it.
If there is an unpleasant smell present, this isn’t caused by the lymphoedema, which doesn’t smell, but probably indicates the presence of bacteria or fungus.
There are no dietary recommendations for people with lymphoedema, except to eat well and not get overweight. I have heard that supplements in safe amounts of omega 3 and vitamin c may help maintain good skin health in affected horses, but this is anecdotal and not researched. It does make sense to give a feed balancer in case essential nutrients are otherwise missing.
I realise this has become very long! I would like to add something about lymphoedemous conditions which may resemble CPL and about it’s treatment with combined decongestive therapy and whether there are ways to adapt this successfully to meet the needs of Gypsy Horses with CPL, but this had better be another post.