Hereditary equine regional derma astenia o più comunemente conosciuta come hyperelastosis cutis.
Chiedo venia,ma questa volta sono io che vi chiedo se sapete qualche cosa su questa patologia...Ho trovato questa malattia girando sui siti in inglese (stavo facendo una ricerca sulle malattie genetiche legate a certe linee di sangue quarter ) e sinceramente è la prima volta che ne sento parlare anche se a tutti gli effetti esiste dal 1971...Io (mea culpa) non macino benissimo l'inglese...e da quello che ho capito è una malattia legata al collagene.Lo strato di pelle superiore non si "lega"con gli strati più profondi,e quando il cavallo si ferisce,non solo non guarisce...ma può letteralmente scoiarsi.

Grazie per l'aiuto

Cosa vuoi sapere esattamente?
Ho trovato qualcosa su Google, dice che la linea QH é quella di Poco Bueno (il 95% di cavalli affetti studiati dalla Mississippi University discende da lui da entrambi i genitori, il restante 5% da linee strettamente collegate a Poco Bueno).

La malattia funziona come dici tu: mancanza di adesione del derma causato da un difetto di collagene. Poiché gli strati della pelle non sono uniti bene tra di loro, si possono separare. A seguito di traumi (che possono anche solo essere l'avere la sella addosso) lo strato di pelle piu esterno si separa da quello sotto, o in certi casi si puó staccare del tutto. Per questo un cavallo affetto puó fare solo vita da animale da giardino. La malattia é incurabile.

Il gene che causa la malattia é recessivo quindi entrambi i genitori devono esserne portatori perché il puledro ne possa essere a sua volta affetto (al contrario ad esempio della hyperkalemic periodic paralysis (HYPP) della linea Impressive in cui il gene é dominante e basta un genitore portatore per la potenziale trasmissione ai figli).

Il fatto che stia diventando piú comune dipende dall'inbreeding col sangue di Doc O'Lena (discendente di Poco Bueno). Mi sembra che si tratti soprattutto di cavalli da cutting.

http://www.bringinglighttohypp.org/HERDA.html

Oh cielo ho visto delle foto orribili.

Sembra una cosa orribile questa malattia. C'era il resoconto di un signore che aveva un puledrino di 4 mesi che un giorno in paddock si é preso un piccolo tronco sulla schiena, giocando. Nel giro di un'ora, un'area di pelle molto piú grande dell'area del piccolo pezzo di legno che lo aveva toccato era caduta, lasciando scoperti i muscoli. Nel giro di pochi giorni é morto.

La maggior parte dei casi si scopre intorno ai 2 anni quando viene messa la sella la prima volta ai puledri e la pelle si stacca In altri casi il "trauma" che fa staccare la pelle puó essere una semplice rotolata in paddock!

In casi estremi, la pelle si stacca da sola, partendo dalla schiena e scendendo giú, e il cavallo muore davvero scoiato vivo Credo che sia una delle malattie piú orribili che abbia mai sentito.

Ah, sopra ho tradotto/riassunto da quel link (accademico). Guardando su altri siti ho scoperto che sono ricercatori della Cornell & Mississippi ad aver avanzato questa teoria per primi, ma la questione della "colpa" di Poco Bueno é "scottante", e non accettata da tutti. Lo dico per completezza

Grazie mille Pascal.Gentilissima come sempre!
Tu ne avevi mai sentito parlare?io sinceramente sono rimasta sconvolta...Se per caso non riesco a capire qualche cosa posso postare qua,e sperare in un tuo aiuto o in quello della tua dolce metà???(prometto che non vi rifilerò papiri interi)
Grazie ancora.
Un bacio e un abbraccio

Certo! Posta pure qui, magari interessa anche ad altri. Se non hai un'urgenza incredibile vanno bene anche papiri interi

No, io non ne avevo mai sentito parlare di questa malattia e ne sono rimasta sconvolta. Lí per lí, leggendo dei muscoli "a vista", credevo che il risultato fosse simile alle foto che ti mandaii anni fa, ricordi? Peró a vedere le foto pubblicate su Internet questa sembra diversa. Prima di staccarsi, la pelle si rigonfia in un modo orribile e spropositato, proprio come se ci fossero dei tunnel di aria tra due strati di pelle.

Che brutta cosa, e poveri, poveri cavalli.

Stammi bene

Mamma mia che malattia orribile ... sembra quasi fantascienza .... anche se purtroppo è reale ...

Si...mi ricordo molto bene( )Ho avuto il tuo stesso pensiero,e non solo io...ma anche un'altra persona a cui avevo mostrato le tue foto.Mi è capitato di vedere in un trottatore una cosa del genere.Si era riempido d'aria dopo che l'asta del sulky gli era entrata sottopelle nell'ascella o nella spalla(non ricordo bene) dopo un'incidente.. ho provato ad associare la cosa per rendermi conto di quanto può soffrire una bestia con una simile patologia...dire che mi vengono i brividi è poco....
Grazie ancora...guarda che ti prendo in parola!!!

Sí Elly, é davvero il termine giusto...

Red, davvero, posta qualsiasi cosa che vuoi tradotta (almeno riappari un po' sul forum! )

Quello che vorrei sapere io é l'incidenza di questa malattia....é relativamente comune? Quei ricercatori hanno studiato 1500 cavalli, mi sembra un numero abbastanza elevato, ma non ho termini di paragone...

Non lo so Pascal...piacerebbe anche a me capire questa cosa...Anche perchè una delle cavalle che ho avuto era imparentata con poco bueno...ma non ha mai avuto problemi..
Poi come ti ripeto,è una cosa di cui non avevo mai sentito parlare..è anche per questo che ho voluto chiedere qua...per saperne qualche cosa di più...ma ho paura che la risposta non sarà così facile da trovare....non so in quanti conoscano questa patologia...forse quelli della monta western...aspetto e spero

Uhm, teoricamente potrebbe essere portatrice, e trasmettere il gene ai figli.

La Mississippi University nel mio primo link si diceva disposta ad analizzare pedigree di qualsiasi cavallo discendente da Poco Bueno e che si voleva far accoppiare.

Se trovate altre v prego postate

la cavalla di una mia amica è discendente di Poco Bueno ma non so se è "portatrice sana"...ha avuto anche vari puledri però tutti sani.

Per l'Herda, il rischio (alto) c'é se il padre é anche lui discendente da Poco Bueno. Devono esserlo entrambi i genitori.

Pascal,ho guardato e riguardato in internet...ma gli articoli sono molto simili fra loro (uff...)...
Ne ho scelti due fra tanti.te li posto...quando hai tempo.(sottolineo)..e voglia.....
Bacio bacio



Hyperelastosis Cutis or HERDA
By Michael Lowder, DVM, MS

Hyperelastosis cutis (HC), a genetic disorder, has come to light recently. Also referred to as Hereditary Equine Regional Dermal Asthenia (HERDA), the condition is most commonly reported in Quarter Horses but was reported in an Arabian-cross horse in 1984.
In diseased horses, there is a lack of adhesion within the dermis (the deep layers of the skin) due to a collagen defect. These skin layers separate with trauma.
A number of great horses were obtained by designed breeding programs and not by chance. It is not uncommon in these breeding programs to breed related horses. As the relationship of the horses becomes closer, we frequently get the highly desirable traits that we are breeding for but we also, just as frequently get, the undesirable ones.
this is the case with HERDA. The condition has been reported to be common in some families of cutting Quarter horses and its occurrence is solely due to in-breeding.
Dr. Ann Rashmir, associate professor of surgery and head of the Hyperelastosis Cutis Research Program at Mississippi State University, and Dr. Nena Winand, a geneticist and assistant professor in the Department of Molecular Medicine at Cornell University, have identified the sire line linked to the condition known as HERDA.
Previously described as hyperelastosis cutis, HERDA is the more accurate description as it is not excessive elastic fibers that cause the problem. Instead, researchers agree that the loss of dermal strength is due to dysfunctional collagen bundles within the dermis resulting in loss of strength and durability of the skin.
To fully understand the condition, we must first have a basic understanding of some breeding terms.
" Inbreeding
• Production of offspring from parents more closely related than the average of the population. Inbreeding increases the proportion of homozygous gene pairs and decreases the proportion of heterozygous gene pairs. Undesirable recessive genes are facilitated by inbreeding.
" Linebreeding
• This is a form of inbreeding where an attempt is made to concentrate the inheritance of a specific ancestor.
" Outbreeding
• This is breeding of horses less (or not) related than the average of the population.
" Homozygous
• The state of having the same genetics for a given characteristic.
" Heterozygous
• The state of having different genetics for a given characteristic.
" Dominant
• Exerting a ruling or controlling influence. Capable of expression when carried by only one of the parents.
" Recessive
• Incapable of expression unless the responsible gene is carried by both parents. In cases of homozygous dominant gene defects, the trait is often self-limiting because of culling or death. While HERDA is not due to a dominant gene, it is self-limiting in homozygous horses because most affected horses are euthanized due to non-healing traumatic skin wounds.
Now let's do some basic genetics. This genetic defect is believed to be homozygous recessive. What does this mean? In order to get an affected foal, you must breed an affected mare (carrier) to an affected stallion (carrier). In genetics, a trait is usually assigned some letter. Capital letters stand for a dominant gene and lower case letters are assigned to a recessive gene. We will use an 'N' for a normal gene and a 'h' for the HERDA gene.
In the above example, all of the horses are normal with 50% of the offspring having the chance of carrying the defective gene. It is important that we understand that the 50% carrier is for each breeding. Thus, we could breed this pair 10 or 20 times and never get a carrier but we would have a 50% chance on each breeding.
If we breed a heterozygous carrier (Nh) horse to another heterozygous (Nh) horse, our chance for an affected offspring would change.
In this case, you would have a 25% chance of getting a normal offspring, 50% chance of getting a carrier horse and 25% chance of getting an affected horse. Again, this is for each breeding. From a book standpoint of breeding 100 horses, 25 would be normal, 50 carriers and 25 affected. However, in reality, we may breed this pair of horses a number of times and never get an affected offspring. If we breed a heterozygous carrier (Nh) to a homozygous affected horse (hh), the percentages change again.
In this case we have a 100% chance of getting a carrier or affected horse. If we bred a normal horse to an affected horse, our chances change again.
In this case 100% of the offspring are carriers and no affected horses are produced. This would be an unusual cross as most horses with HERDA rarely perform, and most breeders only want to breed horses with proven performance records.
Most affected horses usually show signs of the disease when they begin training. The rigors of training and the weight of the saddle and rider start the cycle of skin damage, which becomes apparent usually on the horse's back. The condition becomes noticeable as seromas (fluid accumulation under the skin) and hematomas (blood accumulation under the skin) form; skin becomes loose and, in most cases, open wounds develop and sloughing of the skin occurs.
In summary, it is important to recognize this genetic defect but it is also just as important to understand your chances of obtaining an affected foal. Prevention is as simple as not breeding related horses.



e questo...

Approximately 100 Quarter Horse stallion owners have received, or will receive, a telephone message from Ann Rashmir, DVM, MS, Dipl. ACVS, associate professor of surgery and head of the Hyperelastosis Cutis (HC) Research Program at Mississippi State University, that contains unwelcome news. The message is that the stallion is a carrier of the recessive gene that causes HC, also known as hereditary equine regional dermal asthenia (HERDA).
Being a recipient of that information, says Steven Hanson, a Billings, Mont., attorney as well as a cutting horse exhibitor and breeder, just might serve to place a special responsibility on the stallion owner to reveal to mare owners that the stallion is a carrier.
Rashmir says she has no immediate plans to make the names of the known carrier stallions public.
"I think it is only fair that the owners should be informed first," she said. "They shouldn't have to read about it in a publication. My hope is that they will then make this information available to persons planning to breed mares to their stallion or stallions."
The stallions known to be carriers are those which have sired an HC-affected offspring. Siring even one HC offspring is proof that the stallion is a carrier, says Rashmir.
Rashmir and Nena Winand, DVM, PhD, a geneticist and assistant professor in the Department of Molecular Medicine at Cornell University, announced earlier that 100% of the horses they have studied which are afflicted with HC trace through both sire and dam to Poco Bueno or his immediate relatives--Poco Bueno's sire, King, and Poco Bueno's full brother, Old Granddad. Rashmir and Winand are collaborators on HC research.
What is HC?
When a horse has HC, there is a lack of adhesion within the dermis, the deep layer of skin, due to a collagen defect. Collagen serves as a form of glue that holds the skin layers together. In horses with HC, the "glue" is inferior and the skin layers separate. When the horse is ridden under saddle or suffers trauma to the skin, the outer layer often splits or separates from the deeper layer, or it can tear off completely. It rarely heals without disfiguring scars. New damaged areas arise continuously, sometimes without obvious trauma. Click here to see images of HC/HERDA.
The condition has manifested itself more frequently in cutting horses, but other disciplines are not immune, with cases showing up in reiners and pleasure horses which trace back to Poco Bueno.
Because the condition is caused by a recessive gene, it means that both sire and dam must possess the gene before an offspring of the two will be afflicted. Even when both sire and dam possess the gene, the disease will not necessarily be manifested. Under the laws of genetics, if a carrier is bred to a carrier, 25% of the offspring will have HC, 25% will not be afflicted or be carriers (they'll be genetically normal), and 50% will become carriers but not be afflicted.
One of the reasons that HC rears its head more often in cutting horse circles than any other, it is theorized, is that one of the most popular lines traces back to Poco Bueno through Doc O'Lena and Dry Doc and their dam, Poco Lena, a daughter of Poco Bueno. Both Doc O'Lena and Dry Doc are proven carriers of the recessive HC gene. Through the years, cutting horse breeders have tended to utilize the Doc O'Lena and Dry Doc bloodlines on both sides of the pedigree--breeding cousins to cousins. In essence, they have created a gene pool of carriers.
"It isn't the horse's fault," says Rashmir. "The problem revolves around the way we have bred them. Carriers have been bred to carriers. Breeders have a responsibility to avoid doing this if they know that stallion and mare are indeed carriers."
This does not mean, she says, that one should avoid the Poco Bueno bloodline when establishing a breeding program.
"If you owned Poco Bueno and knew that he had a genetic flaw, would you have stopped using him as a breeding stallion?" she asked rhetorically. "Not at all. He was a wonderful athlete and a great progenitor, but you would have, or should have, worked around the problem by avoiding inbreeding. It's the same with many of his descendants. They are great athletes and even if they are carriers, it has no effect on their performance capability. Simply having the recessive gene produces no harm to that individual. The problem arises when carrier is bred to carrier, setting the stage for HC to be manifested."
The American Quarter Horse Association (AQHA) is funding research at the University of California, Davis, aimed at finding a genetic marker for the disease. Researchers say they are two to three years away from being able to identify the recessive gene.
AQHA also has funded research at Mississippi State where Rashmir and associates are attempting to establish a protocol for dealing with afflicted horses. While the disease is a death sentence for many, Rashmir said, there has been some progress in developing ways to mitigate the effects of HC. Some afflicted horses, she said, have been able to perform in at least a limited manner.
Owners of Carrier Stallions
What are the legal ramifications when a stallion owner knows that his horse is a carrier? Is he/she bound to disclose that information to mare owners?
We asked attorney Hanson to respond to that question. Here, in part, is what he had to say:
"Because apparently there is no method yet developed to test through tissue biopsy for carrier status in breeding stock, at present the only known method of determining whether a mare or stallion is a carrier, if not themselves affected, is to confirm the existence of the condition in affected offspring. The production of an affected offspring means that both sire and dam are carriers.
"That begs the question of whether the stallion owner should make disclosure once he has knowledge of his sire's carrier status," continued Hanson. "If a mare owner has a known carrier, or a mare with known carrier ancestors, he can avoid producing an affected foal by mating the mare with a non-carrier stallion; but if the mare owner is unaware of a prospective sire's carrier status, and the owner of the stallion does not disclose the stallion's genetic flaw, does the mare owner have a legally enforceable cause of action against the stallion owner in the event the resulting offspring is affected with HC?
"Normally, saying nothing stands a better chance of avoiding legal liability than saying the wrong thing; i.e., speaking falsely or in a manner that misleads," added Hanson. "When dealing with fraud or misrepresentation, however, silence may be construed as actionable.
"Fraud and misrepresentation, as causes of action against the speaker, are usually associated with contract cases where the damaged party was either intentionally or negligently induced to enter into an agreement and then later discovered, to his detriment, that the other party had misrepresented or falsely stated a material fact upon which the damaged party had justifiably relied," Hanson explained. "The other party could even be held liable for damages, whether or not he intended to actually cause harm to the innocent party, if by saying nothing he covered up a fact that is construed as information that would be material to the unsuspecting party in making a breeding decision.
"The courts in such cases give consideration to numerous factors, or elements of proof, and of course each case will be decided on its own merits," he added. "In general, it may be said, however, that failure to disclose a known defect in the quality of the goods which are the subject of the contract could indeed be a basis for an award of damages against the silent non-disclosing party to the contract.
"In the end, even though it may have an adverse impact in the form of reduced breeding fee sales, owners of stallions which are known HC carriers may be placing themselves in legal jeopardy if they fail to make disclosure of the existence of the genetic defect in their breeding sires," Hanson stated. "The duty to disclose may also extend to sellers of young horses which have not exhibited the outward manifestations of HC, but which are the offspring of known carriers."
Hanson has personal experience with HC, although inadvertently. It is a story that is being told here because it demonstrates the insidious manner in which HC can surface.
Hanson purchased a promising son of the late Shorty Lena--tracing back to Poco Bueno through Doc O'Lena and Poco Lena. Wondering if the young horse was stallion material, Hanson offered to breed the stallion, free of charge, to a mare owned by a friend. At the time, Hanson and the mare owner knew little about HC. The mare's granddam, traced directly to Poco Bueno through a grandparent and a great-grandparent.
The mare, bred to Hanson's stallion, produced what appeared to be a quality filly. Before reaching one year of age, however, she manifested clinical signs of HC. A biopsy was sent to Mississippi State University. The diagnosis was hyperelastosis cutis.
Hanson did not face any major decisions as to how to handle the situation because, before learning that the stallion was a carrier, he had decided that standing a stud wasn't for him and the horse was gelded. The mare owner had not paid a breeding fee, so there were no damages from that aspect.
Hanson concluded his remarks on legal obligation involving HC carriers thusly: "The duty to disclose, or lack thereof, presents a moral as well as a legal dilemma. Ethicists may argue the question at length, but in the final analysis, each owner of a known carrier stallion will settle that debate for himself in his own mental wrestling match.
As to the legal question, persons suffering damage in consequence of misrepresentation by silence are urged to seek the advice of an attorney who can render an opinion after consideration of all the facts and the law of the state which has jurisdiction over the parties and the subject matter of the breeding contract," concluded Hanson.
While there are approximately 100 known carrier stallions, they are only the tip of the iceberg, said both Rashmir and Winand. They fear that there are a great many others which have either sired affected offspring or which have the potential to do so.
Cutting horse trainer James Johnson of Casper, Wyo., purchased a quality two-year-old prospect from a breeder. The horse's lineage traced back to Poco Bueno through Doc O'Lena. Johnson took the horse to his ranch and turned it out in a pasture with some other horses. One day he noticed the colt had what appeared to be a slight tear in the skin on his neck. Johnson surmised that a young Longhorn bull in the same pasture might have been responsible. The wound was treated, but it didn't heal. Later, it appeared to heal, but lesions opened in other parts of the colt's body. Veterinarians were called in and specialists were consulted. Although no biopsy was taken, the conclusion was that the young horse was afflicted with hyperelastosis cutis.
"It was awful," Johnson said. "He just never healed."
The veterinarians said there was nothing further they could do and the youngster was put down.
The next question is this: Will knowing that a stallion is a carrier dissuade mare owners from breeding to him when the mare might also be a carrier? The answer is sometimes yes, sometimes no. One breeder, who requested anonymity, said he is willing to take his chances breeding carrier to carrier because the bloodlines with which he is involved are producing winners in the cutting pen. He has the financial means to take the risk.
There is another side to the coin. One breeder who feels she has suffered a damaging financial loss due to HC is Cindy Lyles of Haslet, Texas. She bred her mare and did an embryo transfer. When flushed, the mare produced two viable embryos and each was implanted in a surrogate mare. Two foals were born. Both of them demonstrated outward signs of HC early in their lives. Further analyses, including biopsies, proved they were afflicted. Lyles has donated the two colts to the HC research herd at Mississippi State University.
The woman estimates that she has invested $17,000 in the breeding fee, embryo transfers, and veterinary bills. Both sides of the pedigree trace back to Poco Bueno through Doc O'Lena.
Until a genetic test is established that will determine carrier status, the horse owner is left with guesswork in many cases when Poco Bueno bloodlines are involved. As an assist, Rashmir has offered to analyze pedigrees and provide information concerning the odds of a particular mating producing a foal with HC. The charge for an eight-generation pedigree analysis is $25 with the proceeds going directly to the Mississippi State University HC research fund.
Rashmir also has advised stallion and mare owners to include a provision concerning HC in their breeding contracts in case a foal is affected.

Ho tradotto il primo, l'ho fatto un po' troppo velocemente forse ma ci sono alcune cose che non mi tornano a proposito della genetica...non che io ne capisca qualcosa, di genetica, peró.
Comunque questo é quello che dice:

Hyperelastosis Cutis (HC) or HERDA
di Michael Lowder, DVM, MS

La HC, una malattia genetica, é stata scoperta recentemente. Viene anche chiamata Astenia equina regionale della pelle ereditaria (acronimo in inglese: HERDA) e riguarda soprattutto Quarter Horses, anche se nel 1984 c'é stato un caso che coinvolse un incrocio arabo.
Nei cavalli affetti, si ha una mancanza di adesione all'interno del derma (lo strato profondo della pelle) a causa di un difetto di collagene. Gli strati di pelle si separano a seguito di traumi.
Diversi cavalli importanti nacquero a seguito di programmi allevatoriali ben specifici, e non per incroci naturali. Non é raro, in questi programmi allevatoriali, di incrociare cavalli imparentati tra di loro. Con l'andare avanti di questi incroci sempre piú stretti, si ottengono sia i tratti, molto desiderabili, per ottenere i quali si é lavorato, sia, con la stessa frequenza, i tratti meno desiderabili.
Questo é il caso dell'HERDA. La malattia si é rivelata diffusa in certe famiglie di QH da cutting, e la sua apparizione é esclusivamente dovuta all'inbreeding.
Dr. Ann Rashmir, professore associato di chirurgia e a capo del Programma per la Ricerca sull'HERDA della Mississippi State University, e Dr. Nena Winand, geneticista e assistente professore nel Dipartimento di Medicina Molecolare della Cornell University, hanno identificato lo stallone la cui linea é collegata alla malattia conosciuta come HERDA.
In precedenza chiamata hyperelastosis cutis, HERDA é una definizione piú accurata, poiché non é un'eccessiva elasticitá della pelle che causa il problema. Al contrario, i ricercatori sono d'accordo nel dire che la perdita di forza da parte del derma é causata da una disfunzione dei legami di collagene all'interno del derma, il che risulta in perdita di forza e durevolezza della pelle. Per capire bene la malattia, dobbiamo avere una conoscenza basica dei termini allevatoriali.
" Inbreeding
• La produzione di figli da genitori che sono piú strettamente imparentati che la media della popolazione. L'inbreeding aumenta la percentuale di geni omozigoti e diminuisce la percentuale di geni eterozigoti. Geni recessivi indesiderabili vengono facilitati dall'inbreeding.
" Linebreeding
• Una forma di inbreeding dove si tenta di concentrare l'ereditá di un progenitore specifico.
" Outbreeding
• La produzione di cavalli da genitori non imparentati o meno imparentati che la media della popolazione.
" Omozigota
• L'avere la stessa genetica per un dato carattere
" Eterozigota
• L'avere diversa genetica per un dato carattere
" Dominante
• Gene che esercita una influenza dominante, o di controllo. In grado di esprimersi quando portato da un solo genitore.
" Recessivo
• Gene che non é in grado di esprimersi, a meno che non sia portato da entrambi i genitori.
Nel caso di difetti di un gene omozigota dominante, il carattere spesso si esaurisce per abbattimento o morte. Sebbene l'HERDA non sia causata da un gene dominante, si limita comunque in cavalli omozigoti perché la maggior parte dei cavalli affetti sono abbattuti, a causa di inguaribili ferite traumatiche alla pelle.
Adesso passiamo alla genetica di base. Questo difetto genetico si pensa che sia recessivo omozigota. Cosa significa questo? Al fine di avere un puledro affetto, bisogna incrociare una cavalla affetta (portatrice) con uno stallone affetto (portatore). Nella genetica, di solito si assegna una lettera a ogni carattere. Le maiuscole stanno per geni dominanti, le minuscole per geni recessivi. Noi useremo una N per un gene normale e una h per il gene dell'HERDA.
Nell'esempio sopra [quale? N.d.S.], tutti i cavalli sono normali con il 50% dei figli che possono portare il gene difettoso. E' importante ricordare che la percentuale 50% si intende per ogni incrocio. Quindi, possiamo incrociare questa coppia 10 o 20 volte, e non avere mai un portatore, ma con ogni incrocio c'é la possibilitá del 50% di avere un portatore.
Se incrociamo un portatore eterozigota (Nh) a un altro Nh, la percentuale di avere figli sani cambierebbe, In questo caso, ci sarebbe il 25% di probabilitá che i figli siano normali, 50% che siano portatori, 25% che siano affetti.Di nuovo, questo si intende per ogni incrocio. Incrociando 100 cavalli, 25 sarebbero normali, 50 portatori, 25 affetti. In realtá, potremmo incrociare questi cavalli diverse volte e non avere mai un cavallo affetto.
Se noi incrociamo un portatore eterozigota (Nh) a un cavallo affetto omozigota (hh), le probabilitá cambiano di nuovo.
In questo caso abbiamo la certezza al 100% di ottenere un portatore o un affetto.
Se incrociamo un cavallo normale a uno affetto, le probabilita cambiano di nuovo.
In questo caso, 100% dei figli saranno portatori, ma nessuno affetto. Questo peró sarebbe un incrocio raro perché di solito si incrociano cavalli che competono e raramente i cavalli affetti da HERDA possono competere.
Di solito, cavalli affetti mostrano segni della malattia quando iniziano l'addestramento. Il rigore dell'addestramento e il peso della sella e del cavaliere di solito fanno iniziare il ciclo del danno alla pelle, che di solito é visibile sulla schiena del cavallo. La malattia diventa visibile come seromi (accumulo di liquido sottopelle) o ematomi (accumulo di sangue sottopelle); la pelle si separa e, nella maggior parte dei casi, si sviluppano ferite aperte e la pelle cade.
In conclusione, é importante saper riconoscere questo difetto genetico ma é altrettanto importante capire quali sono le vostre possibilitá di ottenere un puledro affetto. La prevenzione é semplicissima, basta non incrociare cavalli imparentati.