Pet-Specific Care for the Veterinary Team

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A practical guide to identifying risks in veterinary patients and tailoring their care accordingly Pet-specific care refers to a practice philosophy that seeks to proactively provide veterinary care to animals throughout their lives, aiming to keep pets healthy and treat them effectively when disease occurs. 
 offers a practical guide for putting the principles of pet-specific care into action. Using this approach, the veterinary team will identify risks to an individual animal, based on their particular circumstances, and respond to these risks with a program of prevention, early detection, and treatment to improve health outcomes in pets and the satisfaction of their owners. The book combines information on medicine and management, presenting specific guidelines for appropriate medical interventions and material on how to improve the financial health of a veterinary practice in the process. Comprehensive in scope, and with expert contributors from around the world, the book covers pet-specific care prospects, hereditary and non-hereditary considerations, customer service implications, hospital and hospital team roles, and practice management aspects of pet-specific care. It also reviews specific risk factors and explains how to use these factors to determine an action plan for veterinary care. This important book: 
Offers clinical guidance for accurately assessing risks for each patient Shows how to tailor veterinary care to address a patient’s specific risk factors Emphasizes prevention, early detection, and treatment Improves treatment outcomes and provides solutions to keep pets healthy and well Written for veterinarians, technicians and nurses, managers, and customer service representatives, 
 offers a hands-on guide to taking a veterinary practice to the next level of care.

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Most veterinary practices believe that clients should receive selection counseling before they purchase a pet, but most practices do not offer this important service.

Clients who select an appropriate pet are less likely to relinquish it, and are more prepared for the likely care the pet will need.

Discussing issues proactively allows the team to be regarded as advocates; when such counseling is not provided and problems ensue, the practice can sometimes appear adversarial (you never warned me about that).

Most selection counseling can be performed by the nonveterinary team and it can be a great bonding experience even without veterinary involvement.

It is better for veterinary teams to be involved preemptively in the selection process rather than complain about the results when they are not involved.

MISCELLANEOUS References 1 1 Ackerman LJ 2011 The Genetic Connection - фото 184MISCELLANEOUS

References

1 1 Ackerman, L.J. (2011). The Genetic Connection, 2e. Lakewood, CO: AAHA Press.

2 2 Landsberg, G., Hunthausen, W., and Ackerman, L. (2013). Behavior Problems of the Dog and Cat, 3e. Edinburgh: Elsevier.

Recommended Reading

1 American Animal Hospital Association‐American Veterinary Medical Association Preventive Health Guidelines Task Force (2011). J. Am. Vet. Med. Assoc. 239 (5): 625–629.

2 Ackerman, L. (2020). Proactive Pet Parenting: Anticipating pet health problems before they happen. Problem Free Publishing.

3 Fivecoat‐Campbell, K. (2020). Adoption marketing. Marketing to the new adopters of shelter and rescue animals. AAHA Trends 36 (2): 51–55.

4 Partners for Healthy Pets: www.partnersforhealthypets.org

3.11 Integrating Genotypic and Phenotypic Testing

Lowell Ackerman, DVM, DACVD, MBA, MPA, CVA, MRCVS

Global Consultant, Author, and Lecturer, MA, USA

BASICS 3111 Summary In petspecific care there is a focus on prevention and - фото 185BASICS

3.11.1 Summary

In pet‐specific care, there is a focus on prevention and early detection. To accomplish early detection, both genotypic and phenotypic tests are needed. Genotypic tests examine an individual's DNA for mutations (variants) or markers that may be correlated with traits and disease risk. Phenotypic tests measure observable features (e.g., blood test results, heart rhythm, body weight, etc.) and diagnostic judgments are made on that basis, and comparisons with so‐called “normal” reference intervals (ranges).

Genotypic tests on their own have value, but they cannot always predict actual risk of diseases. In addition, genotypic tests are available primarily for conditions transmitted as simple Mendelian traits (e.g., von Willebrand disease, progressive rod‐cone dysplasia, mdr1 , etc.), mostly controlled by one set of genes. On the other hand, the most common hereditary conditions encountered in veterinary practice (e.g., atopic dermatitis, hip dysplasia, seizure disorders, etc.) have a more complex pattern of inheritance, often influenced by environmental factors and multiple genes, and confirmed principally through phenotypic testing. Because of this, both genotypic and phenotypic testing are needed as part of most early detection schemes.

3.11.2 Terms Defined

Genotypic Testing:Testing that determines actual genetic mutations (variants) or markers of traits or conditions.

Phene:A trait or characteristic that is genetically determined.

Phenotypic testing:Testing that determines observable features of traits or conditions and compares them to normal or typical values.

MAIN CONCEPTS Genotypic tests those that rely on the detection of actual - фото 186MAIN CONCEPTS

Genotypic tests, those that rely on the detection of actual genetic mutations (variants) or markers ( Table 3.11.1), have a lot of benefits. They can be detected at an early age, even as early as one day of age. They don't change over time, so if a genetic mutation is present (or not present) when tested, repeat testing is not needed – the results should not change over time. In fact, if the parents have been tested for a specific variant, the status of the offspring can be inferred from such testing. So, if two Labrador retrievers are both “clear” for progressive rod‐cone degeneration (prcd) and they are bred together, theoretically it should not be possible for the pups to develop that specific form of progressive retinal atrophy (PRA) if the testing has been done by a reliable genetic testing facility ( http://bit.ly/2YWXBscor https://dogwellnet.com/ctp). Of course, mistakes do happen. In this instance, the most likely cause for pups testing “affected” for prcd when the parents tested “clear” would be that the breeders made a mistake in identifying which animals were the actual parents. Theoretically, it would also be possible that the pups developed a spontaneous mutation, but this is very rare.

Table 3.11.1 Some of the genotypic tests currently available

2,8‐Dihydroxyadenine Urolithiasis Type IA
Achromatopsia
Acral Mutilation Syndrome
Acute Respiratory Distress Syndrome
Aggression (markers)
Alanine Aminotransferase (ALT) Activity
Alexander Disease
Amelogenesis Imperfecta
Arrhythmogenic Right Ventricular Cardiomyopathy
Autoimmune lymphoproliferative Syndrome
Bardet–Biedl Syndrome
Bernard Soulier Syndrome
Brain Hypomyelination
Burmese Head Defect
Canine Leukocyte Adhesion Deficiency Types I & III
Canine Multifocal Retinopathy (CMR 1, 2 & 3)
Canine Multiple System Degeneration
Cardiomyopathy, Dilated (DCM1 and DCM2)
Cardiomyopathy, Hypertrophic
Catalase Deficiency
Centronuclear Myopathy
Cerebellar Ataxia
Cerebellar Cortical Degeneration
Cerebellar Hypoplasia
Cerobellar Abiotrophy
Chondrodysplasia
Chondrodystrophy and intervertebral Disc Disease
Ciliary Dyskinesia
Cleft Lip with Syndactyly
Cleft Lip/Palate
Cobalamin Malabsorption
Collie Eye Anomaly/Choroidal Hypoplasia
Color Dilution Alopecia
Complement 3 (C3) deficiency
Cone Degeneration
Cone‐Rod Dystrophy (1, 2, 3, 4, SWD)
Congenital Hypothyroidism with Goiter
Congenital Keratoconjunctivities Sicca and Ichthyosiform Dermatosis
Congenital Macrothrombocytopenia
Congenital Myasthenic Syndrome
Congenital Stationary Night Blindness
Copper Toxicosis
Craniomandibular Osteopathy
Curly Coat Dry Eye Syndrome
Cyclic Hematopoiesis
Cyclic Neutropenia
Cystic renal Dysplasia and Hepatic Fibrosis
Cystinuria (Types I‐A, II‐A, II‐B)
Dandy–Walker Malformation
Day Blindess
Deafness and Vestibular Syndrome
Degenerative Myelopathy
Dental Hypomineralization
Dermatomyositis
Dystrophic Epidermolysis Bullosa
Early Adult Onset Deafness
Early Onset Progressive Polyneuropathy
Ectodermal Dysplasia
Elliptocytosis
Encephalopathy
Epidermolysis Bullosa Simplex
Epidermolytic Hyperkeratosis
Epilepsy (variants)
Episodic Falling Syndrome
Exercise‐Induced Collapse
Exercise‐Induced Metabolic Myopathy
Factor IX Deficiency (Hemophilia B)
Factor VII Deficiency
Factor VIII Deficiency (Hemophilia A)
Factor XI Deficiency
Factor XII Deficiency
Familial Congenital Methemoglobinemia
Familial Juvenile Epilepsy
Familial Nephropathy
Fanconi Syndrome
Fucosidosis
Gall Bladder Mucocele Formation
Gangliosidosis (GM1 & GM2)
Generalized Myoclonic Epilepsy
Glanzmann's Thrombasthenia
Glaucoma
Globoid Cell Leukodystrophy/Krabbe’s Disease
Glomerulopathy KIRREL2
Glycogen Storage Disease IA, II, III, IIIA
Goniodysgenesis and Glaucoma
Hereditary Ataxia
Hereditary Cataracts
Hereditary Deafness (PTPRQ)
Hereditary Footpad Hyperkeratosis
Hereditary Nasal Parakeratosis
Hereditary Nephropathy
Hereditary Nephropathy (Alport Syndrome)
Hip Dysplasia (markers)
Histiocytic Sarcoma (marker)
Hyperekplexia (Startle Disease)
Hyperoxaluria
Hyperuricosuria
Hypoadrenocorticism
Hypocatalasia
Hypokalemic Polymyopathy
Hypomyelination and Tremors
Ichthyosis
Inflammatory Myopathy
Inherited Myopathy
Iron‐Deficiency Anemia
Juvenile Encephalopathy
Juvenile Epilepsy
Juvenile Laryngeal Paralysis and Polyneuropathy
Juvenile Myoclonic Epilepsy
Juvenile Onset Polyneuropathy
L2‐ Hydroxyglutaric Aciduria
Lagotto Storage Disease
Laryngeal Paralysis
Lethal Acrodermatitis MKLN1
Leukoencephalomyelopathy
Ligneous Membranitis
Lipoprotein Lipase Deficiency
Long QT Syndrome
Lundehund Syndrome
Lupoid Dermatosis
Macrothrombocytopenia
Macular Corneal Dystrophy
Malignant Hyperthermia
Mannosidosis
May–Hegglin Anomaly
Microphthalmia, Anophthalmia, and Coloboma
Mucolipidosis II
Mucopolysaccharidosis (I, IIIa, VI, VII, VIII)
Mullerian Duct Syndrome
Multidrug Resistance 1
Multiple System Degeneration
Muscular Dystrophy
Musladin–Lueke Syndrome
Mycobacterium Avium Susceptibility
Myeloperoxidase deficiency
Myostatin Deficiency
Myotonia Congenita
Myotonia Hereditaria
Myotubular Myopathy
Narcolepsy
Necrotizing Meningoencephalitis
Nemaline Myopathy
Neonatal Ataxia
Neonatal Cerebellar Cortical Degeneration
Neonatal Encephalopathy
Neonatal Encephalopathy with Seizures
Neonatal Neuroaxonal Dystrophy
Neuroaxonal Dystrophy
Neurodegenerative Vacuolar Storage Disease
Neuronal Ceroid Lipofuscinosis 1, 2, 4a, 5, 6, 7, 8, 10, A, MFSD8
Niemann‐Pick C
Oculoskeletal Dysplasia
Osteochondrodysplasia
Osteochondromatosis
Osteogenesis Imperfecta
P2Y12 Receptor Platelet Disorder
Palmoplantar Keratoderma
Pancreatitis (marker)
Pannus (marker)
Paroxysmal Dyskinesia
Periodic Fever Syndrome
Persistent Mullerian Duct Syndrome
Phosphofructokinase Deficiency
Pituitary Dwarfism
Platelet Dysfunction
Platelet Procoagulant Deficiency – Scott Syndrome
Polycystic Kidney Disease
Polyneuropathy
Pompe Disease
Porphyria
Postoperative Hemorrhage
Prekallikrein Deficiency
Primary Ciliary Dyskinesia
Primary Lens Luxation
Primary Open Angle Glaucoma
Progress Retinal Atrophy ‐ crd4/cord1
Progressive Neuronal Abiotrophy
Progressive Retinal Atrophy ‐ AD/RHO
Progressive Retinal Atrophy ‐ CNGA
Progressive Retinal Atrophy ‐ CNGB1
Progressive Retinal Atrophy ‐ crd (1, 2, 3, 4)
Progressive Retinal Atrophy ‐ erd
Progressive Retinal Atrophy ‐ Golden Retriever (1 & 2)
Progressive Retinal Atrophy ‐ IG‐PRA1
Progressive Retinal Atrophy ‐ Late Onset
Progressive Retinal Atrophy ‐ rcd (1, 1a, 2, 3, 4)
Progressive Retinal Atrophy ‐ RdAc
Progressive Retinal Atrophy ‐ Rdy
Progressive Retinal Atrophy ‐ SAG
Progressive Retinal Atrophy ‐ Type 1, 3, 4
Progressive Retinal Atrophy ‐ Type A, B
Progressive Retinal Atrophy ‐ Type III
Progressive Retinal Atrophy ‐ X‐linked
Progressive Rod Cone Degeneration (prcd)
Protein‐Losing Nephropathy
Pyruvate Dehydrogenase Phosphatase Deficiency
Pyruvate Kinase Deficiency
Raine Syndrome Dental Hypomineralization
Renal Cystadenocarcinoma and Nodular Dermatofibrosis
Renal Dysplasia
Retinal Degeneration
Rickets
Rod‐Cone Dysplasia 1, 1a, 3
Sanfilippo Syndrome Type A / Mucopolysaccharidosis IIIA (Dachshund Type)
Scott Syndrome
Sensory Ataxic Neuropathy
Sensory Neuropathy
Severe Combined Immunodeficiency (Autosomal)
Severe Combined Immunodeficiency (X‐linked)
Shaking Puppy
Shar‐Pei Inflammatory Disease
Short Tail (Brachyury)
Skeletal Dysplasia
Spinal Dysraphism
Spinal Muscular Atrophy
Spinocerebellar Ataxia
Spondylocostal Dysostosis
Spongiform Leukoencephalomyelopathy
Spongy Degeneration with Cerebellar Ataxia (1 & 2)
Stargardt Disease
Startle Disease
Subacute Necrotizing Encephalopathy
Thrombopathia
Trapped Neutrophil Syndrome
van den Ende‐Gupta Syndrome
von Willebrand Disease Types I, II, and III
Xanthuria Type 1a, 2a, 2b
X‐Linked Ectodermal Dysplasia
X‐Linked Generalized Tremor Syndrome
X‐Linked Hereditary Nephropathy
X‐Linked Myotubular Myopathy

The other big problem with relying on genotypic testing alone is that, at the present time at least, genetic testing is only available for a relatively small number of phenes (conditions, traits, etc.), representing perhaps 20–30% of heritable conditions. Some of the most common conditions with a heritable component, such as allergies or hip dysplasia, have more complex inheritance, often influenced by environmental factors. Such tests that get developed will likely not be entirely predictive, but may indicate whether risk is higher, lower or moderate for an individual, compared to the relevant population base.

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