Heilsufar

Cotoninn er mjög heilsuhraust tegund en eins og margir aðrir smáhundar þá 

greinist hnéskeljalos stundum í þeim og einnig er gott að fara með 

hundana í augnskoðunog skima eftir augnsjukdómum.

 

Þeir sjúkdómar sem vitað er að greinast stundum í coton eru arfgengir augnsjúkdómar (líkt og allar aðrar tegundir) og hnéskeljalos,

einnig sjúkdómar sem hægt er að DNA testa fyrir líkt og v.willebrant, CMR2. PH1 og DM.

það er hægt að DNA testa fyrir mun fleir sjúkdómum en þeir eru þó ekki sérstaklega þekktir í tegundinni.

Einnig er það í flestum tilfellum að ef hundur er beri fyrir eitthvað að þá sé í lagi að rækta á móti hreinum einstakling, en allt svona þarf að skoða vel og vandlega.

Hér fyrir neðan er fræðsla um sjúkdóma sem geta verið í coton og aðra sjúkdóma sem hægt er að testa fyrir en þekkjast ekki í coton sérstaklega.

Hnéskeljalos 

Luxatingpatella  er einkenni þess að hnéskelin losnar úr lið eða færist úr sínum 

venjulega stað. Hnékslejalos er þekkt í hundum, sérstaklega þó minni hundum,

einkennin koma yfirleitt í ljós frá 4-6 mánaða aldri og alltaf er hægt að staðfesta 

ef um los er að ræða við 12 mánaða aldur. 

 

Hnéskeljalos getur verið ættgengt, en það kemur einnig oft los á hnéskeljar 

eftir hverslags áverka, offitu eða ofhreyfingu ungra hunda. 

Greining á losi fer fram með þreifingu á hnjám, af viðurkenndum dýralækni. 

Ef hnéskeljarnar renna inní liðinn meira en venjulega er ætlast til getur verið um los að ræða. 

 

0 -Hnéskelinni verður ekki hnikað úr grófinni 

1 -Mögulegt er að ýta hnéskelinni úr grófinni, en hún smellur strax aftur á sinn stað 

2-Þegar hnéskelinni er ýtt úr grófinni, liggur hún utan grófarinnar þar til henni er ýttá    sinn stað eða hnéliðurinn réttur 

3 - Hnéskelin liggur að jafnaði utan grófarinnar, en hægt er að ýta henni á sinn stað, þaðan sem hún skreppur á nýjan leik þegar hnéliðurinn beygist 

4 -Hnéskelin er föst utan grófarinnar 

 

það eru ekki til nein DNA próf sem greina hnéskeljalos. 

PRA 

Generalised Progressive Retinal Atrophy (GPRA) er arfgengur augnsjúkdómur

í hundum, þessi sjúkdómur leiðir alltaf til blindu. Í öllum tegundum geturðu 

séð sömu einkenni sjúkdómsins í sýktum hundum, sýktir hundar er náttblindir 

og það er minnkun á getunni til að aðlaga sjónina að dimmri birtu, seinna þegar 

sjúkdómurinn verður ágengari eiga hundarnir erfitt með að aðlaga sjónina að 

dagsbirtu og á endanum verða þeir blindir. Fyrstu merki er óvissu hegðun í þeirra vanalega umhverfi, augasteinarnir verða útvíkkaðir og linsa í auganu verður 

skýjuð og opague / óljós, sem endar sem katarakt.

 

Það eru ekki til nein DNA próf sem geta sagt til um hvort hundur sé sýktur eða 

beri  fyrir PRA.

Það eina sem er hægt að gera er að fara í augnskoðun hjá Hundaræktarfélagi 

Íslands hjá viðurkenndum augnlæknum. 

Hægt er að fá dna test fyrir einni týpu af pra, sem heitir pra-prcd, en eina sem við getum notað í dag til að staðfesta að PRA er ekki í hundi er augnskoðun á hverju dýri fyrir sig. (frekari uppl um PRA-PRCD neðar)

Katarakt 

Katarakt er ljósdeyfni í linsu í auga hunds, valdandi því að hann sé með óskýra 

sjón. Ef kataraktið er smátt í sniðum mun það sennilegast ekki trufla sjón 

hundsins það mikið, en katarakt þarf að fylgjast vel með, því þykkari og breiðari 

þau verða, því líklegra er að það leiði til blindu. Katarakt getur þróast útfrá 

sjúkdómi, elli eða áverka, en arfgengt katarakt er það algengasta. 

 

Fyrstu merki eru yfirleitt ský á augum. Ómeðhöndlað katarakt getur farið á flakk

eða runnið til frá vefnum sem heldur því, valdandi því að það getur flotið til um 

augað og fests og lokað fyrir náttúrulegt flæði vökvar (naturalfluiddrainage.). 

Þetta getur leitt til gláku, sem getur valdið varanlegri blindu. Katarakt geta einnig byrjað að leysast upp með tímanu, vald ansi miklum sársaukafullum bólgum 

í auganum. 

Það eru ekki til nein DNA próf sem geta sagt til um hvort hundur sé sýktur eða 

beri  fyrir gpra. Það eina sem er hægt að gera er að fara í augnskoðun hjá 

Hundaræktarfélagi Íslands hjá viðurkenndum augnlæknum. 

Canine Degenerative Myelopathy (DM): 

Ágengur hrörnunarsjúkdómur sem leggst á mænu eldri hunda. Sjúkdómurinn 

kemur yfirleitt fram í hundum ámilli átta og 14 ára. Fyrstu einkenni eru 

ósamhæfðar hreyfingar (ataxia)í afturfótum (einkenni koma ekki endilega fram 

samtímis í báðum afturfótum) sem lýsa sér með þeim hætti að hundurinn vaggar þegar hann gengur, haltrar eða dregur fæturnar. Eftir því sem sjúkdómurinn 

ágerist verða útlimir veikburða, hundurinn byrjar að stífna upp og á erfitt með að

standa. 

 

Sjúkdómurinn versnar smám saman þar til að hundurinn getur ekki lengur 

gengið. Sjúkdómsgangur getur verið frá sex mánuðum upp í eitt ár þar til að 

hundurinn lamast alveg á afturfótum. Ef sjúkdómurinn heldur áfram að ágerast 

geta hundar farið að missa þvag og hægðir og einkenni komið fram í framfótum.  

 

Því miður er enn enga lækning að finna en sjúkdómurinn veldur þó hundinum 

ekkisársauka. Hægt er að skima fyrir DM með erfðaprófi. 

  

Canine Primary Hyperoxaluria Tegund I (PHI)

Sjaldgæfur og arfgengur sjúkdómur sem snýr að glyoxylate efnaskiptum

í Coton de Tulear. Hyperoxaluria er ástand þar sem þéttni oxalate í þvagi verður mjög há og veldur þar með nýrnaskaða. Primary Hyperoxaluria er sjúkdómur

sem orsakast af stökkbreytingu í geni, sem leiðir af sér offramleiðslu á oxalate í lifur.

 

Til eru þrjár megin tegundir af PH og tengjast allar ákveðnum efnaskiptakvillum. Af þessum þremur er tegund I algengust (í 80% tilvika) og alvarlegust.

Oxalate er lítil sameind sem dýr og men taka upp úr fæðu eða er afurð efnaskipta ákveðinna próteina eða C vítamíns í líkamanum. Oxalate er ekki nýtt né brotið niður í líkamaunum og því skilst það út með þvagi og saur. Í þvagblöðru getur oxalate binst kalsíum og myndað óuppleysanlega kristala (eru aðal orsök nýrnasteina í mannfólki). Steinarnir geta verið í nýrum og þvagblöðru og getur orsakað þvagfærasýkingu (óbeint), þvagteppu og nýrnaskaða og fylgja miklir verkir. Oxalate útfellingar geta myndast í beinum, liðum og beinmerg.

 

Í alvarlegum tilvikum getur sjúkdómurinn leitt af sér blóðskort og blóðflagnafæð. Sjúkdómurinn kemur (skyndilega) fram við þriggja til fjögurra vikna aldur. Einkenninn eru uppköst, lystarleysi, þreyta, minnkuð þvaglát, kviðverkir, blóð í þvagi og síðar dauði. Frá fyrstu einkennum líða um tveir mánuðir þangað til hundurinn deyr (eða er svæfður vegna mikilla veikinda). Í krufningu má ská mikið af oxalate kristöllum í nýrnapíplum og nýrnaberki og á mótum barkar og nýrnamergs? 
 

Canine multifocal retinopathy CMR2

Er arfgengur sjúkdómur í hundum sem hefur áhrif á sjónhimnunna. Sjúkdómurinn tilheyrir hópi arfgengra. The disease belongs to a group of inherited retinal disorders primarily caused by mutations scattered throughout the entire BEST1,

a gene necessary for retinal pigment epithelium (RPE) function. Salient fundus changes are usually present in animals affected with CMR before 4 months of age and are characterized by multifocal areas of retinal which in older dogs progress to multifocal areas of outer retinal atrophy. These multifocal areas of retinal are typically found in both eyes and can appear gray, tan, orange or pink and vary in number, size and location. It seems to be selflimited in most cases, although vision loss has also been described. So far, a specific treatment is not known. 

 

Fjölhæfur sjónukvilla 2 frá hunda er arfur sjúkdómur hjá hundum sem hafa áhrif á sjónu. Sjúkdómurinn tilheyrir hópi arfgengra sjónufarasjúkdóma sem aðallega eru af völdum stökkbreytinga sem dreifðir eru um allt BEST1, gen sem er nauðsynlegt fyrir starfsemi sjónhimnulitunarþekju (RPE). Mikilvægar breytingar á fundus eru venjulega til staðar í dýrum sem hafa áhrif á CMR fyrir 4 mánaða aldur og einkennast af fjölþreyttum sjónhimnu sem hjá eldri hundum fara yfir á fjölþætta svæði ytri sjónhimnu. Þessi fjölþætta svæði sjónhimnu finnast venjulega í báðum augum og geta verið grá, sólbrún, appelsínugul eða bleik og mismunandi eftir fjölda, stærð og staðsetningu. Það virðist vera í flestum tilvikum sjálfstætt, þó að sjónskerðingu hafi einnig verið lýst. 

 

Enn sem komið er er ekki vitað um sérstaka meðferð. 
 

Von Willebrand Disease Type1 (vwd1) 

Von Willebrand disease type 1 (vWD1) is a bleeding disorder of variable severity that results from a quantitative or qualitative defect in von Willebrand factor (vWF). On vascular injury, vWf mediates platelet adhesion to exposed subendothelium and is involved in platelet-to-platelet aggregation.

The disease is the most common hereditary bleeding disorder and it is genetically and clinically heterogeneous. Clinical signs of the disease include spontaneous bleeding from mucosal surfaces and excess blood loss after surgery or trauma. Three clinical types, 1, 2, and 3, have been described. 

Von Willebrand disease type 1 is inherited in a recessive fashion. Bleeding appears to be due to the reduced amount of vWF rather than a qualitative difference. Although Von Willebrand disease type 1 is the most common form of vWD found in most mammals and can cause serious bleeding problems, it is generally less severe than the other 2 types. 

Testing of affected dogs can be done by vWF antigen testing or by coagulation assays, but these procedures yield variable results. This variability makes it difficult for breeders to use this information to eliminate the disease-causing allele from their lines. Thus, it is highly desirable that DNA tests are run to get definitive answers. 

                                      ____________________

Hyperuricosuri (HU)

Lýsir sér þannig að magn þvagsýru í þvagi er of hátt. Þetta getur leitt til myndun 

steina í þvagblöðru og í sumum tilvikum nýrnasteina. Það er hægt að meðhöndla sjúkdóminn með aðgerð en miklar líkur eru á að einkenni komi aftur fram og 

því verður hundurinn að vera á lyfjameðferð út ævina. 

 

Hægt er að skima fyrir (HU) með erfðaprófi. 

Bandera’s Neonatal Ataxia

(also referred to as Bandera’sSyndrome) er arfgengur sjúkdómur sem finnst aðeins í Coton. 

Sjúkdómurinn heitir í höfuðið á hvolpinum sem var nr.2 greindur af sjúkdómnum, sjúkdómurinn lýsir sér í því að erfitt er að samhæfa 

hreyfingar.  

This is due to a mutation in a glutamate receptor gene that affects neurotransmitter levels leading to improper brain signals and impeded movement coordination. Affected puppies can be recognized within the first few weeks as displaying difficulties walking, eating, standing and eliminating. There have been no known adult Cotons affected with Bandera’s Neonatal Ataxia. 

Malignant Hyperthermia(mh) 

Canine malignant hyperthermia (MH) is autosomal dominant inherited disorder of skeletal muscle characterized by hypercarbia, rhabdomyolysis, generalized skeletal muscle contracture, cardiac dysrhythmia, and renal failure that develops on exposure to volatile anesthetics and depolarizing muscle relaxants. When given these agents, MH-susceptible dogs show tachycardia, muscle contractions, hyperthermia, elevated carbon dioxide production, and death if the anesthetic is not discontinued. Malignant hyperthermia is can be triggered in susceptible animals by excitement, apprehension, exercise, or environmental stress. Because of this reason, this disorder is also known as “canine stress syndrome.” 

Canine malignant hyperthermia episodes usually come on unexpectedly and are very serious. If the condition is recognized early enough in an animal under anesthesia, certain measures can be taken in order to be able to save the animal. Some types of anesthesia can be fatal for dogs with malignant hyperthermia gene. This is why it is also important to identify dogs that carry the malognant hyperthermia gene prior to surgical procedures. Unfortunately, regardless of treatment, malignant hyperthermia is usually fatal. Some types of anesthesia can be fatal for dogs with malignant hyperthermia gene. DNA test

 
 

Chondrodystrophy and Chondrodysplasia (CDPA/CDDY, IVDD) 

Chondrodystrophy in dogs is a common trait identified in many dogs’ breeds, characterized by shortened length of the limbs, which is a result of early changes in the structure of growth plates. The short-legged phenotype is known by two names: chondrodystrophy and chondrodysplasia. Chondrodysplasia is also known as canine dwarfism. Word ”chondro” come from cartilage, and ”dysplasia” means an abnormal growth, while word ”dystrophy” means degeneration of the tissue, in this case, of the cartilage. Breeds known for having shorter than normal limbs are: Bulldogs, Corgis, Dachshunds, Bassett Hounds, Pugs, French Bulldogs, 

Pekineses, Lhasa Apsos, Shih Tzus, Beagles and many more. 

Except shorter limbs than normal, other skeletal characteristics of chondrodystrophy include a lower jaw that may protrude further than normal, an unusually short upper jaw, and an over under bit with crooked teeth. Named short-legged breeds are also prone to intervertebral disc disease (IVDD), which impacts health of the affected animal. Based on the histopathological analysis of the short-legged breed puppies, that the short stature is a consequence of the defects in the process where cartilage is replaced with bone in the developing limb, which is known as the endochondral ossification. 

Chondrodysplasia is caused by an FGF4-retrogene insertion in dog chromosome 18. This mutation explains short-legged phenotype in breeds such as Basset Hound, Pembroke Welsh Corgi, Dachshunds, West Highland White Terriers and Scottish Terriers. The mutation is inherited in an autosomal dominant pattern. 

The chondrodystrophy is caused by a second FGF4 retrogene insertion on chromosome 12. This mutation is held responsible also for intervertebral disc disease (IVDD). Dogs in which this mutation has been identified are: Jack Russel Terriers, Dandie Dinmont Terriers, French Bulldogs, Chihuahua, Chinese Crested, Pekingese, Shih Tzu, Havanese, Coton de Tulear, Bishon Frise, Miniature and Toy Puddle, Beagle, Cavalier King Charles Spaniel, English Springer  Spaniel, American Cocker Spaniel, Portuguese Water Dog, Nova Scotia Duck Tolling Retriever or Chesapeake Bay Retriever. Dogs that carry both mutations show a more drastic reduction of leg length. The affected breeds are in particular Basset Hounds, Dachshund, Welsh Corgi and Scottish terriers. 

In breeds where both mutations are present, breeders can benefit from test results to implement breeding strategies to reduce incidence of CDDY, while retaining the short-legged phenotype conferred by CDPA. 

 

Chondrodystrophy (CDDY and IVDD Risk) and Chondrodysplasia (CDPA) 

Shorter legs in dogs are explained by two retrogene insertions of functional fibroblast growth factor 4 (FGF4). FGF4 gene is involved in many biological processes including bone development. 

The first insertion discovered (Parker et al 2009) is an FGF4-retrogene insertion in dog chromosome 18 (FGF4-18). This FGF4-18 insertion explains a short-legged phenotype known as chondrodysplasia (CDPA) in breeds such as Basset Hound, Pembroke Welsh Corgi, Dachshunds, West Highland White Terriers and Scottish Terriers. CDPA inheritance is considered to follow an autosomal dominant mode. 

The Chondrodystrophy (CDDY) mutation was discovered by researchers in the Bannasch Laboratory at the University of California, Davis (Brown et al. 2017) as a second FGF4-retrogene insertion in dog chromosome 12. CDDY includes a short-legged phenotype and abnormal premature degeneration of intervertebral discs leading to susceptibility to Hansen’s type I intervertebral disc disease (IVDD). The intervertebral disc, which sits between vertebrae, is composed of an outer fibrous basket (annulus fibrosus) made of 70% collagen and an inner gel-like layer called the nucleus pulposus. These structures allow for flexibility of the vertebral column. In Chondrodystrophic breeds, premature calcification of the nucleus pulposus at early age (from birth to 1 year of age) results in degeneration of all discs in young dogs. These abnormal discs are predisposed to herniation into the spinal canal where the inflammation, and hemorrhage can cause severe pain and neurological dysfunction (myelopathy) termed Intervertebral Disc Disease or IVDD. IVDD has high mortality rate and high cost of surgical and medical veterinary care. 

CDDY is inherited as a semi-dominant trait for height, meaning that dogs with 2 copies of the mutation are smaller than dogs with only 1 copy. With respect to IVDD, the inheritance follows a dominant mode, meaning that 1 copy of the FGF4-12 mutation is sufficient to cause disc degeneration and predispose dogs to disc herniation. Dogs that have both FGF4-12 and FGF4-18 show a more drastic reduction of leg length. 

The Veterinary Genetics Laboratory offers a combined test for CDDY and CDPA for breeds that have long and short leg phenotypes. Our tests assay for the causal variants, not for linked markers, therefore the genotypes are accurate and not inferred. CDDY and CDPA occur in many breeds. Testing for these mutations can help breeders determine if CDDY is present among breeding stock and to identify dogs at risk for IVDD. In breeds where both mutations are present, breeders can benefit from test results to implement breeding strategies to reduce incidence of CDDY, while retaining the short-legged phenotype conferred by CDPA. 

dna test

Results reported as: 

Chondrodystrophy (CDDY and IVDD Risk) N/N 

No copies of CDDY mutation. 

N/CDDY 

1 copy of CDDY mutation. Dog is at risk for IVDD. Mutation causes leg shortening compared to N/N dogs. When bred to an N/N dog will produce 50% of normal sized puppies and 50% of  puppies at risk for IVDD. 

CDDY/CDDY 

2 copies of CDDY. Dog is at risk for IVDD. Mutation causes leg shortening compared to N/N dogs. Will produce 100% of puppies with shorter legs at risk for IVDD. 

 

Chondrodysplasia (CDPA) 

N/N 

No copies of CDPA mutation. 

N/CDPA 

1 copy of CDPA. Mutation causes leg shortening compared to N/N dogs. 

CDPA/CDPA 

2 copies of CDPA. Mutation causes leg shortening compared to N/N dogs. 

PRA-PRCD

is an eye disorder, which belongs in progressive retinal atrophy group of disorders. Progressive retinal atrophy (PRA) comprises autosomal recessively inherited diseases that lead to degeneration of retinal photoreceptor cells in dogs and other pets. In general, these diseases are characterized by disturbance of dark vision, visual field defects, and abnormalities in the electroretinogram, which can progress to blindness. It appears in both eyes simultaneously. The age of onset and rate of retinal degeneration varies between the different forms of the conditions. Some forms of PRA are common to multiple dog breeds, while others are recognized in just a single breed. PRA appears in most dog breeds, but also in mixed breed dogs. Almost all PRA disorders are recessively inherited, with exceptions of dominant and X-linked PRA inheritance in few breeds, such as Old English Mastiffs, Bullmastiffs, Siberian Husky and Samoyed

upplýsingar um heilsufar fengnar frá 

https://www.divosa.co.uk/health-

https://www.vgl.ucdavis.edu/services/dog/CDDY.php

https://www.gensoldx.com/

http://www.animalabs.com/shop/dogs/inherited-diseases-dogs/chondrodystrophy-chondrodysplasia-canine/

http://www.animalabs.com/shop/dogs/progressive-retinal-atrophy-pra-prcd/

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