Hvad betyder "Ryd"?
Dyret bærer ikke mutationen. Det vil ikke udvikle sygdommen og vil ikke give det videre.
Hund Achromatopsia Type 3 i tysk korthåret pointer (PRAcd)
The DNA test for Achromatopsia Type 3 (PRAcd) in German Shorthaired Pointers is essential for responsible breeding. This genetic screening identifies carriers of the PRAcd mutation, which causes progressive vision loss and color blindness in affected dogs. Early detection through DNA testing helps breeders prevent passing this hereditary condition to future generations. By using the PRAcd test, owners can ensure healthier litters and maintain the breed’s overall well-being. Regular testing supports informed breeding decisions and promotes the longevity of German Shorthaired Pointers. Protect your dog’s vision and contribute to breed health with the Achromatopsia Type 3 DNA test.
Forkortelse: PRAcd
Analyseret mutation: CNGB3 c.784G>A
Arv: Autosomal recessiv
Akronym
PRAcd
Observeret frekvens
Klinisk sværhedsgrad
Klinisk klassificering
Øjensygdomme
Analyseret mutation
CNGB3 c.784G>A
p.(D262N)
p.(D262N)
Arvemåde
Autosomal recessiv
Testresumé:
The DNA test for Achromatopsia Type 3 (PRAcd) in German Shorthaired Pointers helps identify carriers and affected dogs. This inherited condition causes complete color blindness and vision problems. Early testing allows breeders to make informed decisions to reduce the risk of passing the disorder. By screening breeding dogs, the prevalence of PRAcd can be minimized in future generations. Responsible breeding ensures healthier dogs with better quality of life.
Tilgængelig fra pakken: Basic
Denne DNA-test er inkluderet fra vores pakke Basic — og er også en del af pakkerne Basic, Standard, Advanced, Complete.
Se DNA-testpakker →Vælg den flok, der passer bedst til din avls- eller sundhedsstrategi for dine dyr.
Understanding Achromatopsia Type 3 in German Shorthaired Pointers
Achromatopsia Type 3, also known as Progressive Retinal Atrophy with complete color blindness (PRAcd), is a hereditary condition that affects the vision of German Shorthaired Pointers. This genetic disorder results from mutations in specific genes that are crucial for the proper functioning of photoreceptor cells in the retina, leading to vision impairment over time.
Symptoms of Achromatopsia Type 3
Dogs affected by Achromatopsia Type 3 typically exhibit symptoms such as a lack of color vision, difficulty seeing in bright light, and potential night blindness. Owners may notice that their dogs have trouble navigating their environment, particularly in brightly lit areas, as their ability to perceive colors is significantly diminished.
Genetic Basis of the Condition
This condition is inherited in an autosomal recessive manner, meaning that both copies of the gene must be mutated for the dog to express the disease. Carriers, which have one normal and one mutated gene, do not show symptoms but can pass the condition to their offspring. Identifying carriers through DNA testing is essential for responsible breeding practices, as it helps prevent the propagation of the condition in future generations.
Impact on Quality of Life
While Achromatopsia Type 3 can lead to significant visual impairment, many dogs adapt well to their condition. Owners can assist by providing a safe environment and ensuring that their pets are comfortable in low-light conditions or areas with bright lighting. Understanding the limitations of their dog's vision allows owners to make necessary adjustments to enhance their pet's quality of life.
Management and Care
Managing a dog with Achromatopsia Type 3 primarily involves environmental modifications rather than medical interventions. Owners should ensure that their living space is free from obstacles that could pose a danger, as affected dogs may not respond to visual cues in the same way as their sighted counterparts. Regular veterinary check-ups are also advised to monitor the dog's overall eye health and address any other potential issues that may arise.
Konklusion
Achromatopsia Type 3 in German Shorthaired Pointers is a serious genetic condition that affects visual perception. Understanding the symptoms, genetic basis, and management strategies is crucial for owners and breeders alike. Through responsible breeding and proper care, the impact of this condition on affected dogs can be alleviated, allowing them to lead fulfilling lives despite their visual challenges.
Racen anerkendt til testen: Achromatopsia Type 3 i tysk korthåret pointer (PRAcd)
- German Shorthaired Pointer
🧬 Interpretation of genotypes PRAcd
Genotype
Status
🟡 N/N
Ikke-transportør - Ingen risiko
🟡 N/PRAcd
Transportør - Ingen risiko
❌ PRAcd/PRAcd
Berørt - i fare
FAQ: forstå fortolkningen
Er en "Carrier" seriøs?
Nej. Dyret er generelt sundt, men kan overføre mutationen til dens afkom.
Hvad hvis et dyr er "påvirket"?
Den bærer to muterede kopier. Kliniske tegn forventes afhængig af sygdommen. Det skal ikke avles.
Hvorfor er der forskel på mand/kvinde?
Nogle sygdomme er kønsbundne, så deres udtryk varierer afhængigt af dyrs køn.
Forudsig afkom
N/N (ikke-transportor)
N/PRAcd (Transportør)
PRAcd/PRAcd (Påvirket)
Ofte stillede spørgsmål om DNA-test
Hvad opdager denne DNA-test?
This DNA test detects the mutation associated with Achromatopsia Type 3 In German Shorthaired Pointer (PRAcd) in order to identify clear, carrier, or at-risk animals.
Hvorfor teste et avlsdyr?
DNA-test hjælper opdrættere med at planlægge sikrere parringer og reducerer risikoen for at overføre mutationen til afkom.
Hvad er arvemetoden for denne test?
Den nedarvede tilstand, der er rapporteret for denne test, er autosomal recessiv.
Hvilken mutation analyseres i denne test?
This test analyses the mutation CNGB3 c.784G>A.
Er et bærende dyr nødvendigvis påvirket?
Ikke nødvendigvis. Fortolkningen afhænger af arvemønsteret og den resulterende genotype.
Referencer
Sidjanin Duska J, Lowe Jennifer K, McElwee John L, Milne Bruce S, Phippen Taryn M, Sargan David R, Aguirre Gustavo D, Acland Gregory M, Ostrander Elaine A. Canine CNGB3 mutations establish cone degeneration as orthologous to the human achromatopsia locus ACHM3. Hum Mol Genet. 2002 Aug 1;11(16):1823-33. doi: 10.1093/hmg/11.16.1823.