Camelids get their own BVDV strain, causing ill-thrift, respiratory failure and abortion. Whole-blood PCR screens crias to confirm they are not persistent carriers.

Camelid red blood cells are small, flat and oval rather than round, so the slide must be read by a technician familiar with camelids to tell true anemia from dehydration.

Alpaca panels centre on fleece-density mutations; llama panels, bred as pack and guardian animals, centre on structural soundness and ancestral lineage markers instead.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A cerebrospinal fluid tap looking for raised eosinophils, the sign that deer-borne meningeal worm has reached the spinal cord and is causing hind-limb paralysis.

A high-density centrifugation method needed to catch Eimeria macusaniensis (E. mac), a giant coccidial parasite that can kill a camelid and that ordinary flotation misses.

Guards against severe skin disease from zinc deficiency and rickets from too little ultraviolet light. Dense-fleeced alpacas need this watched far more closely than coarser-fibred llamas.

Handling stress can trigger fatal capture myopathy. After any restraint, creatine kinase and AST are checked for the spikes that mean muscle is breaking down.

Macropods ferment in the foregut, so their normal fecal flora differs completely from a rodent's and standard rodent wet-mount criteria do not apply.

The number-one health threat in captive macropods. Oral exams, deep tissue culture and jaw X-rays catch aggressive bone infection before it deforms the skull.

Macropod glucose, protein and red-cell counts have to be read against macropod reference intervals, not a rodent or placental-mammal baseline.

Macropods are uniquely prone to white muscle disease from these deficiencies, so levels are checked to confirm muscle tissue is not degrading.

Marsupials have no natural immunity to Toxoplasma gondii, shed by cats. Where a placental mammal often tolerates it, a macropod collapses neurologically, so routine titers matter in captivity.

Detects an environmental fungus that grows in damp bedding or feed and invades the air sacs and respiratory tract.

Counted by hand, because bird red blood cells carry a nucleus and mammalian analysers cannot read them. A high white count often flags hidden infection or respiratory stress.

Checks for avian bornavirus, which attacks the nerves of the digestive tract so the bird cannot digest food and loses weight severely.

Screens for a bacterium that causes respiratory disease in birds and can pass to people as a severe flu-like illness.

Most birds have no external reproductive organs, so a drop of blood or a freshly pulled feather follicle establishes sex.

Companion birds chew cages, toys and household items. This blood test measures the lead or zinc behind sudden neurological signs or weakness.

A respiratory swab used for poultry and exotic birds alike, monitoring for lethal flu strains that trigger government-mandated quarantine.

Tracks organ function using uric acid rather than BUN or creatinine for the kidneys, and bile acids for the liver.

Determines whether a cat carries blood type A, B, or the rare AB type, information breeders need because mismatched matings between a type B queen and a type A or AB tom can cause fatal newborn blood incompatibility.

Visualises soft-tissue organ changes that an X-ray cannot show.

A recessive gene controlling whether hair pigment bands into the ticked agouti pattern or lies flat as solid color, the switch behind tabby versus solid coats.

A rare recessive TYR gene mutation causing a white coat with blue eyes and a near total lack of pigment, distinct from the other white coat genes.

A recessive MC1R variant in Norwegian Forest Cats that gradually replaces black pigment with a golden, amber tone as kittens mature into adults.

A mail-in or at-home kit screening urine parameters or mapping genetic health mutations without a clinic visit.

Brainstem auditory evoked response testing, confirming hearing in each ear.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Detects systemic hypertension, which often travels with feline hyperthyroidism or chronic kidney disease.

Two TYRP1 mutations that lighten black pigment to chocolate or the lighter cinnamon shade, each reducing eumelanin production in the coat.

A recessive skull and facial malformation, congenital frontonasal dysplasia, that produces stillbirths or kittens too deformed to survive.

A recessive disorder causing episodes of low blood potassium and skeletal muscle weakness, most visible in the neck, in Burmese and related breeds.

A recessive coloration seen in Burmese lines from Australia and New Zealand that develops with age, adding progressive reddish pigment across the head and back.

A combination of a domestic non-agouti variant and a wild Asian Leopard Cat agouti variant that darkens and extends the face mask and dorsal stripe in Bengals.

Temperature-sensitive pigment variants that restrict color to the cooler extremities, producing the recessive Siamese pattern or the more pigmented Burmese pattern, which is incompletely dominant to it.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A recessive LPAR6 gene deletion that produces the short, soft, curly coat fixed in the Cornish Rex breed and also found in German Rex cats.

X-rays for bone fractures and chest structures.

A recessive variant that clumps pigment granules unevenly in the hair shaft, softening black to gray and red to cream across all coat colors.

Two separate dominant variants at the same gene, one producing an all- white coat often linked to some hearing loss, the other producing patches of white spotting.

A recessive enzyme deficiency causing intermittent hemolytic anemia, with variable age of onset and signs ranging from lethargy and weight loss to jaundice.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Screens hereditary risks including hypertrophic cardiomyopathy (HCM) and polycystic kidney disease (PKD).

Checks for antibodies to the slow-acting virus that weakens cell-mediated immunity over years.

Detects active viral protein in the blood, identifying a highly contagious retrovirus that suppresses the immune system.

A recessive KIT gene variant responsible for the Birman breed's characteristic white gloved feet, distinguishing true gloving from ordinary white spotting.

A fatal recessive glycogen branching enzyme defect causing abnormal glycogen buildup in muscle, liver, and nerve cells, usually lethal by about 5 months of age.

A fatal recessive lysosomal storage disorder that impairs a neuron's ability to clear metabolic waste, causing tremors and loss of coordination starting at 6 to 8 weeks of age.

A breed-specific MYBPC3 variant that raises the risk of thickened heart muscle and sudden death, with two copies carrying markedly higher risk than one.

A breed-specific MYBPC3 variant, R820W, associated with heart muscle thickening; two copies bring high risk of severe early disease while one copy is usually silent.

A fatal recessive storage disease from a GLB1 mutation causing tremors, ataxia, and blindness beginning around 3 months of age and ending near 9 to 10 months.

A fatal recessive HEXB mutation causing rapidly progressing tremors and ataxia starting as early as 4 weeks of age, with death typically before 8 months.

Four variants in one gene that produce a long coat, three fairly breed specific and one found across all long-haired breeds and crossbreds.

A recessive lysosomal storage disorder with mild and severe forms causing facial changes, stunted growth, joint and mobility problems, and heart valve thickening.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

A dominant PKD1 variant causing multiple kidney cysts from an early age that often progresses to renal failure later in life, common in Persian-derived breeds.

Tests for progressive retinal atrophy, an inherited cause of blindness.

A recessive CEP290 mutation causing slow, late-onset blindness first detectable around seven months of age and usually complete by 3 to 5 years.

A rare dominant CRX mutation causing early photoreceptor degeneration and blindness by about seven weeks of age, with one or two copies causing disease.

A recessive form of blindness destroying light-sensing retinal cells beginning around 7 weeks of age, with vision severely compromised by roughly 2 years.

A recessive AIPL1 variant, comparable to Leber congenital amaurosis in humans, causing retinal thinning starting around 5 weeks and severe loss by 16 weeks of age.

A dominant TRPV4 variant that folds ear cartilage; one copy gives the breed's folded ears while two copies bring a higher risk of painful cartilage and bone problems.

An early kidney biomarker that flags declining function months or years before creatinine rises. Used for the high rate of chronic kidney disease in cats and of renal amyloidosis in ageing captive lorises.

A dominant variant producing curly hair, one copy gives a loosely wavy coat and two copies give a tighter curl along with a slimmer body and longer ears.

Two mutations at the KRT71 gene, one recessive to normal coat causing the Sphynx's near hairlessness, the other causing the Devon Rex's curly coat, itself recessive to the hairless variant.

A recessive COLQ mutation causing generalized muscle weakness worsened by exertion or excitement, often producing a characteristic dog- begging stance from about 3 weeks of age.

A recessive chromosome deletion causing motor neuron loss and hindlimb muscle wasting starting around 3 to 4 months of age; the condition is not painful or fatal.

Measures thyroid hormone to diagnose canine hypothyroidism or feline hyperthyroidism, a very common metabolic disease in ageing cats.

Analyzes urine concentration, pH and protein loss to catch early diabetes, bladder crystals or kidney stress.

Beta-casein comes in two main forms, A1 and A2, differing by one amino acid; breeders select toward A2/A2 herds because milk carrying only A2 is of interest to some health-conscious buyers.

The main whey protein gene in cattle, carrying A and B variants that shift the balance of whey against casein and fat, information breeders use to suit cows for drinking milk or cheese production.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Screens blood for bovine leukemia virus to control the spread of infectious lymphosarcoma through a herd.

Monitors bulk milk or individual blood for Brucella abortus, maintaining disease-free status and preventing transmission to people.

Counts white blood cells in milk to judge herd udder health and screen for subclinical mastitis.

A recessive lethal defect of Dexter cattle caused by either of two mutations that produce severely disproportionate dwarf fetuses with short spines and oversized heads, aborted around seven months.

A recessive lethal defect of Miniature Zebu cattle caused by an ACAN gene mutation that produces disproportionate dwarf fetuses with short limbs and a large head, aborted around seven months.

An antigen-capture ELISA or PCR on a small ear tissue sample, identifying calves persistently infected with bovine viral diarrhea virus.

A panel bundling three separate milk protein tests, beta-casein, kappa-casein and beta-lactoglobulin, reporting variants linked to milk yield, protein content and cheese-making quality.

A recessive metabolic defect of Holstein cattle, caused by an APOB gene mutation, that blocks normal fat and cholesterol transport, leaving affected calves with chronic diarrhea and poor growth.

A coat colour dilution trait caused by PMEL17 gene variants that lighten black or red pigment in a dose-dependent way, one copy giving a duller shade and two copies a much paler, near-white coat.

A recessive SLC45A2 variant that dilutes black Dexters to chocolate or red Dexters to cream, letting breeders predict or select for diluted coat colour in calves before they are born.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A dominant variant in the COPA gene that overrides the usual black-or- red coat gene to give Holsteins a red and white coat instead of black and white, helping breeders predict calf colour.

A recessive myostatin (MSTN) gene deletion causing muscle hypertrophy, known as double muscling, that raises muscle mass and lean meat yield in Belgian Blue and several other beef breeds.

A recessive TYRP1 gene variant that dilutes black pigment to a dun, dark brown to gold, shade in Dexter cattle, showing as dun or red depending on the animal's separate MC1R genotype.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

Detects XX/XY chimerism in a female born twin to a male, which leaves her sterile with an underdeveloped reproductive tract. Reported as positive or negative, in cattle and goats alike.

Checks blood or milk for antibodies to Mycobacterium avium subspecies paratuberculosis, the cause of chronic wasting disease.

A milk protein gene with A and B variants; the B allele is linked to higher casein content and better cheese yield, letting dairy breeders select cattle suited to cheese-making.

The Extension locus that controls black versus red coat pigment in cattle, with dominant black, wild-type and recessive red alleles combining to predict calf colour; Holsteins need a separate test.

A Holstein-specific Extension-locus test in which the Black/Red (Telstar) variant makes a calf born red turn black by 3 to 6 months, alongside the breed's usual dominant black and red alleles.

Non-esterified fatty acids and beta-hydroxybutyrate in blood or milk, diagnosing subclinical ketosis and negative energy balance in transition dairy cows.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

A recessive lethal defect of Romagnola cattle causing abnormal organ development, a fluid-filled abdomen, craniofacial deformities and liver fibrosis, with affected calves typically stillborn.

Polledness is dominant in cattle, so one copy of a polled variant, from either the Holstein-Friesian/Jersey or the Celtic-origin lineage, prevents horn growth; animals with neither copy grow horns.

Confirms pregnancy from a blood sample as early as 28 days after breeding, a highly accurate alternative to manual palpation.

A recessive neurodegenerative disease of Charolais cattle that damages myelin in the brain and spinal cord, causing an unsteady gait and stiff hind limbs that worsen until the animal cannot stand.

A recessive muscle disorder of Chianina and Romagnola cattle causing exercise-induced cramping and stiffness, sometimes making the animal hop or fall, that eases once it stops moving.

A recessive lethal defect of Dexter cattle that leaves the lungs underdeveloped and causes severe fluid buildup under the skin, so affected pregnancies end in abortion or a stillborn calf.

Calcium, magnesium and phosphorus, to prevent and manage milk fever (periparturient hypocalcemia) and grass tetany.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Cavy micronutrient requirements are high; calcium is tracked to prevent metabolic bone disease.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A small scope inside the mouth, checking for sharp enamel spurs, molar overgrowth and ulcers on the tongue and cheeks.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Hindgut fermenters with a large cecum have their own normal gut flora, so the wet mount is read against cavy criteria and checked for pinworms and Giardia.

Open-rooted teeth grow for life. X-rays are the only way to see root elongation, back-tooth impaction and the painful jaw abscesses that stop an animal eating.

Cavies cannot make their own vitamin C. Blood levels are tracked to prevent scurvy, which brings painful joints, bleeding gums and immune collapse.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Degus have an unusual insulin molecule and go diabetic on ordinary rodent food, going blind from cataracts as they do. Long-range markers are used because the stress of being held spikes a single glucose reading on its own.

A small scope inside the mouth, checking for sharp enamel spurs, molar overgrowth and ulcers on the tongue and cheeks.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Hindgut fermenters with a large cecum have their own normal gut flora, so the wet mount is read against cavy criteria and checked for pinworms and Giardia.

Screens for a rodent-borne virus that is mild or silent in the animal but causes meningitis and neurological disease in people.

Clear tape pressed to the skin around the anus picks up pinworm eggs that a flotation misses, since the female lays outside the gut rather than in it.

Open-rooted teeth grow for life. X-rays are the only way to see root elongation, back-tooth impaction and the painful jaw abscesses that stop an animal eating.

Visualises soft-tissue organ changes that an X-ray cannot show.

Controls how black and red pigment are distributed across the coat, from solid black to sable to solid yellow or tan points. Inherited as an allelic series with partial codominance between the A locus variants.

A fatal neurological disorder of Alaskan Huskies causing seizures, an abnormal high-stepping gait, trouble eating, and vision problems in young dogs, usually appearing before adulthood.

A nerve and muscle disorder of Alaskan Malamutes causing exercise intolerance, a changed bark, noisy breathing, and worsening hind leg gait problems starting between 3 and 19 months of age.

A mail-in or at-home kit screening urine parameters or mapping genetic health mutations without a clinic visit.

Brainstem auditory evoked response testing, confirming hearing in each ear.

Variants in a dopamine transporter gene linked to owner-reported adverse behaviors in Belgian Malinois, such as seizure-like episodes, glazing over, and unpredictable biting, worst with two copies of the A22 allele.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Dilutes black pigment to brown or liver without affecting red or yellow pigment, so two copies turn a black-based coat brown and give red or yellow dogs brown noses and paw pads.

A board-certified ophthalmologist's exam screening for inherited eye disease.

A panel of genome-wide and DLA-region markers that measures how genetically diverse an individual dog is relative to its breed, helping breeders plan matings that avoid excessive inbreeding.

An immune and blood clotting disorder of German Shepherd Dogs causing recurrent skin and bone infections, gum disease, and lameness, usually fatal early despite some dogs surviving for years.

An immune and blood clotting disorder of Irish Setters causing recurrent infections, poor weight gain in puppies, and gum disease, with most affected dogs dying early despite occasional longer survival.

An eye disorder causing round blister-like areas of retinal detachment that appear around 11 to 16 weeks of age, progress slowly for about a year, and then stabilize without causing blindness.

An eye disorder of Coton de Tulear dogs causing round blister-like retinal detachments beginning around 15 weeks of age that progress slowly for about a year and then stop without causing blindness.

An eye disorder of Lapphund breeds causing round blister-like retinal detachments between 9 and 24 months of age that usually progress slowly and typically do not lead to blindness.

A fatal heart disorder of Nova Scotia Duck Tolling Retrievers, caused by an LMNA gene deletion, that produces dilated cardiomyopathy and sudden death in young adult dogs carrying two copies.

A muscle disorder of Labrador Retriever puppies causing loss of muscle tone, exercise intolerance, and an awkward gait, typically appearing between 2 and 5 months of age with two copies of the PTPLA mutation.

A progressive balance and coordination disorder of Spinone Italiano puppies caused by a repeat expansion in the ITPR1 gene, starting around 4 months of age and often severe enough to require euthanasia before one year.

A neurological disorder of Nova Scotia Duck Tolling Retrievers caused by an SLC25A12 gene mutation, producing stumbling, an abnormal high- stepping gait, weakness, and episodic collapse as early as 10 weeks of age.

Screens for two separate extra-copy insertions of the FGF4 gene that shorten the legs, one of which (CDDY) also raises the risk of premature disc degeneration and Hansen type I disc disease in dogs carrying it.

An FGF4 retrogene insertion in Nova Scotia Duck Tolling Retrievers that shortens the legs and raises the risk of premature intervertebral disc degeneration and painful disc herniation.

A birth defect in Nova Scotia Duck Tolling Retriever puppies causing cleft palate, cleft lip, or both, sometimes along with fused toes, in puppies that inherit two copies of the CLPS variant.

The most common inherited cause of cleft palate in Nova Scotia Duck Tolling Retriever puppies, a hole in the roof of the mouth that raises the risk of aspiration pneumonia from nursing difficulty.

Screens five recessive FGF5 gene variants that produce a long hair coat, with dogs carrying two copies of any long hair variant expected to grow longer hair than their short coated relatives.

A brown coat color in French Bulldogs, slightly darker than the classic brown, caused by a different gene than the usual chocolate variant and requiring two copies to appear.

An inherited eye disorder in herding breeds with Collie ancestry, causing underdeveloped blood vessels behind the retina and, in more severe cases, a small eye, retinal detachment, or vision loss.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A retinal disorder causing day blindness and light sensitivity from either of two CNGB3 gene variants, appearing around 8 to 12 weeks of age while night vision stays normal.

An early onset retinal disease causing progressive blindness in American Staffordshire Terriers and American Pit Bull Terriers, with two breed-specific variants each needing two copies to cause disease.

A nerve insulation disorder of Golden Retrievers causing early muscle weakness, exercise intolerance, and swallowing difficulty from infancy, arising from any of three separate gene variants with different inheritance patterns.

A skin disorder of Golden Retrievers causing scaling that can darken into thick gray or black patches, arising from either of two gene variants and appearing as early as 3 to 6 weeks of age.

A skin disorder in Labrador Retrievers, genetically distinct from the Golden Retriever forms, causing mild to severe scaling that can darken into gray or black patches over most of the body.

A neuromuscular disorder of Golden Retrievers caused by a COLQ gene variant that disrupts nerve to muscle signaling, producing progressive weakness in dogs with two copies of the mutation.

A neuromuscular disorder of Labrador Retrievers causing puppies to collapse after a few minutes of vigorous exercise and recover with rest, usually appearing between 6 and 12 weeks of age.

Covers two copper metabolism disorders: an X-linked ATP7A variant causing fatal Menkes-type copper deficiency, and an ATP7B variant causing copper buildup and liver damage in several breeds.

Measures cortisol to check for Cushing's disease (hyperadrenocorticism).

Two KRT71 gene variants that produce wavy hair with one copy and a fully curly coat with two copies, found across many curly and wavy coated breeds such as Poodles and Portuguese Water Dogs.

A blood disorder of Collies, also called Gray Collie Syndrome, causing recurring drops in infection-fighting white cells roughly every two weeks, leading to fevers, infections, and often death before age two.

A kidney disorder in Labrador Retrievers that prevents reabsorption of the amino acid cystine, allowing crystals and stones to form in the urinary tract and potentially causing a painful blockage.

An inner ear disorder of Doberman Pinschers from either of two gene variants, causing deafness in one or both ears along with possible balance and coordination problems in dogs with two copies.

Tests the SOD1 mutation behind degenerative myelopathy, a progressive spinal cord disease.

X-rays for bone fractures and chest structures.

Two gene variants linked to dilated cardiomyopathy in Doberman Pinschers, a heart muscle disease that thins the heart wall and can lead to congestive failure, affecting roughly half the breed in its lifetime.

Lightens black to a gray-blue shade and brown to a pale silvery shade, caused by any of three recessive gene variants that must be present in two copies to change coat color.

A beta-defensin gene variant that produces a solid black or brindle patterned coat by overriding the red and yellow pigment pattern otherwise controlled by the Agouti gene.

A commercial DNA panel mapping breed makeup alongside a wide set of genetic health mutations.

A neuromuscular disorder causing weakness, loss of coordination, and collapse after 5 to 20 minutes of intense exercise in otherwise healthy dogs, usually resolving within about 25 minutes of rest.

A mild to moderate inherited blood clotting disorder that leaves affected dogs mostly healthy but prone to excess bleeding, found across several hound, spaniel, and terrier breeds.

A tooth enamel disorder in Italian Greyhounds causing pitting, discoloration, and small, gapped teeth, estimated to affect about 14 percent of the breed with roughly 30 percent carrying one copy.

A tooth enamel disorder in Samoyeds, caused by a breed-specific gene variant, that thins or removes the outer enamel layer, causing sensitivity, staining, premature wear, and gum disease.

A kidney disorder of Basenjis, usually appearing between 4 and 8 years of age, that causes glucose to leak into the urine despite normal blood sugar and can progress to kidney failure if untreated.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

An RSPO2 gene variant that produces the long mustache and eyebrow hair called furnishings in wire coated breeds, with dogs lacking the variant showing a softer, incorrect coat texture instead.

A fatal, progressive storage disorder in Shiba Inus caused by a beta- galactosidase gene deletion, producing vision loss, tremors, and balance problems by 6 months of age and death by about 18 months.

A fatal nerve storage disorder in Toy Poodles caused by a HEXB gene deletion, producing tremor, stumbling, and progressive neurological decline starting around 9 to 12 months of age.

An SGK3 gene deletion behind the American Hairless Terrier's coat: puppies are born with thin hair that is lost within the first months of life when two copies of the hairless variant are present.

A PSMB7 gene variant that, combined with Merle, produces the Great Dane's dark patches on a white background. Two copies are believed fatal before birth, so every harlequin dog carries only one.

Detects proteins shed by adult heartworms from a quick blood draw, before they block the heart and lungs.

A blood clotting disorder in Boxers caused by a Factor VIII gene mutation, producing easy bruising, prolonged bleeding after injury, and occasional nosebleeds, with males needing only one copy to be affected.

A blood clotting disorder in German Shepherd Dogs from either of two Factor VIII gene mutations, causing bruising, prolonged bleeding, and nosebleeds, with affected males showing signs and carrier females usually unaffected.

A cataract disorder in Australian Shepherds appearing after age 2, where one copy of the mutation usually causes a mild, non-progressive cataract and two copies cause a faster form that can lead to blindness.

A recessive skin defect that thickens and cracks the nose's surface cells, giving dogs a dry, crusty nose from a young age; carriers show no signs but pass the mutation to half their pups.

An inherited defect in urate transport raises uric acid levels in urine, increasing the risk of bladder and kidney stones; dogs with two copies are affected and pass the variant to every offspring.

A recessive nerve-coating defect causing whole-body tremors in Weimaraner puppies from about two weeks old, usually easing by three to four months, though a mild hind-leg tremor can persist.

A recessive gut defect that blocks vitamin B12 absorption, causing lethargy, poor weight gain and anemia in Beagles and Border Collies from six to twelve weeks old, with lasting nerve damage if untreated.

A recessive BIN1 gene mutation causing rapidly progressive muscle wasting and exercise intolerance in Great Danes from about six months old; only around a fifth of affected dogs reach a good-quality adulthood.

A coat variant that fades red or yellow pigment toward cream or white while leaving black or brown pigment unchanged; dogs with two copies show the diluted, lighter phaeomelanin coat.

An early-onset, incompletely penetrant recessive form of Addison's disease in young Tollers, usually appearing around five months old with lethargy, vomiting and poor appetite, sometimes with autoimmune eye inflammation.

A recessive cataract disorder affecting both eyes, starting before one year old and progressing to blindness by two to three years, seen in Boston Terriers, Staffordshire Bull Terriers and French Bulldogs.

A recessive NAPEPLD gene disorder causing progressive loss of balance and paw dragging or knuckling in Rottweilers and Great Danes, usually starting before one year old without causing pain.

A recessive SLC45A2 gene variant producing a white or off-white coat, pink skin and blue eyes in Lhasa Apsos and related breeds, with some added sensitivity of the skin and eyes to bright light.

Six pigment-switch variants at one gene control black eumelanin versus red or yellow phaeomelanin, producing a melanistic mask, a grizzle pattern, or recessive red, yellow or pale coats by allele combination.

An incompletely dominant PMEL gene insertion produces patchy areas of diluted and solid pigment; the inserted repeat can vary in length between a dog's own cells, changing how much dilution shows.

A recessive lysosomal storage disease in Brazilian Terriers causing skeletal abnormalities, developmental delay and excessively lax, disabling joints; two copies of the variant are needed to be affected.

A recessive lysosomal storage disease in German Shepherds causing skeletal deformity, developmental delay and excessively lax joints that make standing and walking difficult; carriers show no signs.

An ABCB1 gene deletion lets certain drugs, including ivermectin and loperamide, cross into the brain and cause neurotoxicity such as tremors, poor coordination and seizures; herding breeds are most affected.

A recessive connective-tissue disorder in Beagles affecting bone, heart, skin and muscle, producing small size, tight thickened skin, stiff joints, a broadened skull and a stilted tip-toe gait.

A recessive sleep disorder in Dobermans causing bouts of irresistible sleepiness and cataplexy, a sudden full-body muscle collapse while the dog stays conscious, often triggered by excitement.

A rare recessive HCRTR2 gene sleep disorder in Labradors causing daytime sleepiness and sudden muscle-weakness episodes triggered by play or food, usually stable in severity after the first year.

A dominant T-box gene mutation that shortens the tail; a second copy is lethal in the womb, so breeding two bobtail dogs together is expected to cut litter size by about a quarter from lost embryos.

A recessive SPTBN2 gene disorder causing loss of coordination, a wide stance and tremors in Beagle puppies noticed around three weeks old as they start to walk, from cerebellum degeneration.

A recessive ATF2 gene brain disease in Standard Poodles and Poodle- derived crosses causing weakness, mobility problems and seizures; affected pups do not survive past about seven weeks old.

A recessive VPS11 gene degenerative nerve disease in Rottweilers causing incoordination, high-stepping gait, tremors and involuntary eye movements, first seen in young adult dogs.

A rare recessive CLN5 gene brain disease in Golden Retrievers starting between one and two years old with anxiety, compulsive circling, tremors, seizures and vision loss, usually fatal by age three.

A recessive SLC45A2 deletion tracing to a single 1976 female produces a cream coat with blue eyes and little pigment around the eyes, mouth and nose, along with heightened sensitivity to bright light.

An echocardiogram read to OFA standards, clearing a dog of congenital heart disease.

An OFA-graded elbow radiograph screening for elbow dysplasia.

An OFA-graded hip radiograph screening for hip dysplasia.

Screens the kneecaps for luxating patella.

An OFA-registered autoimmune thyroiditis screen.

A recessive skeletal disorder in Miniature Poodles causing stunted growth, splayed hind limbs, enlarged joints, a flattened rib cage and bent, shortened bones, noticeable from about three weeks old.

A recessive SERPINH1 gene disorder in Dachshunds that leaves bones and teeth fragile and easily fractured from a defect in collagen processing; two copies of the variant are needed to be affected.

A dominant KIT gene variant, traced to one female born in 2000, produces symmetrical white forelock, muzzle, chest and collar markings; a second copy is lethal before birth, though one copy causes no health issues.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

Measures hip joint laxity as a distraction index, a numeric alternative to OFA hip grading.

An MITF gene variant produces white body spotting, less symmetric than Irish or mantle patterns; inheritance runs incompletely dominant in some breeds and fully recessive in others, with two copies giving more white.

A recessive, fatal nerve disorder in Rottweilers and Black Russian Terriers causing throat paralysis, eye problems, limb weakness and motor deficits from about three months old, ending in death by one year.

Tests for progressive retinal atrophy, an inherited cause of blindness.

A recessive ADAMTS17 mutation lets the eye's lens detach from its normal position, causing painful inflammation and glaucoma that can rapidly lead to blindness if untreated, typically starting between three and eight years old.

A recessive ADAMTS10 mutation in Beagles raises pressure inside the eye over time, leading to nerve damage, vision loss and blindness if untreated; about one percent of Beagles carry the variant.

A recessive ADAMTS17 gene inversion causing rising eye pressure from three to four years old, later lens displacement, an enlarged eye and vision loss from nerve and retinal degeneration.

An early-onset recessive rod-cone dysplasia from a PDE6B gene mutation in Irish and Irish Red and White Setters, typically causing complete blindness before two years old with signs from six weeks.

An adult-onset recessive retinal degeneration in Basenjis from an S-antigen gene variant, starting with night-vision loss that can progress to complete blindness, though daylight vision often lasts for years.

Two distinct recessive retinal-degeneration mutations found in Golden Retrievers, with PRA1 signs appearing around age six and PRA2 around age four; two copies of either variant leads to progressive blindness.

A late-onset recessive rod-cone dysplasia in Sloughis, also called rcd1a, causing visual impairment that starts around two to three years old and progresses toward blindness.

A recessive C2orf71 frameshift mutation causing late-onset photoreceptor degeneration and eventual blindness across several breeds, including setters, Dachshunds and Golden Retrievers.

A recessive CNGA1 gene retinal degeneration specific to Shetland Sheepdogs, typically diagnosed in adulthood with low-light vision loss; it is not the only known cause of PRA in the breed.

A widespread recessive late-onset retinal disease affecting many breeds, first destroying low-light night vision in the rods and later daytime color vision in the cones, usually noticeable by four years old.

A recessive enzyme defect causing severe hemolytic anemia from premature red blood cell death, with lethargy and poor exercise tolerance from four months to two years old and liver failure often by age five.

A Labrador-specific recessive PKLR gene mutation causing severe hemolytic anemia, with lethargy and poor stamina from four months to two years old and typically fatal liver failure by around age five.

A Basenji-specific recessive PKLR gene deletion causing severe hemolytic anemia, with lethargy and poor stamina between four months and two years old and often fatal liver failure by around age five.

A dominant FLCN gene mutation causing late-onset firm skin nodules by around six years old plus paired kidney tumors in German Shepherds; a single copy causes disease and passes to half of offspring.

An early-onset recessive retinal degeneration in Collies causing night blindness by six weeks old and complete blindness by six to eight months, with visible eye changes around three to four months.

A recessive metabolic brain disorder, succinic semialdehyde dehydrogenase deficiency, in Salukis causing seizures, an exaggerated gait and abnormal vocalizing within the first ten weeks of life.

A maternally inherited mitochondrial DNA disorder in Golden Retrievers causing progressive loss of muscle control, abnormal posture and reduced spinal reflexes without muscle wasting; only females pass on the risk.

Variants in two genes, MC5R and RSPO2, combine to predict how much a dog sheds relative to its breed's typical rate, ranging from minimal to average shedding depending on the combination inherited.

A recessive COL11A2 gene mutation causing mild disproportionate dwarfism with short, thickened, slightly curved legs in Labradors, more common in working lines; not every dog with two copies shows obvious signs.

Swabs analysed under the microscope to identify the yeast or bacterial overgrowth behind chronic ear and skin infections.

A recessive NKX2-8 gene defect present at birth causing a malformed spinal canal, weak rear-leg coordination and a bunny-hopping gait in Weimaraners; the condition is not painful and does not worsen with age.

A recessive ABCA4 gene mutation in Labradors causing progressive loss of the retina's light-sensing cells, reducing vision in both daylight and dim light while some sight is usually kept lifelong.

An immune-mediated skin and muscle disease in Collies and Shetland Sheepdogs whose risk is set by genotypes at three loci, ranging from hair loss and scaly skin to, in severe cases, muscle wasting and trouble eating.

Two linked mutations raise the risk of sudden, painful pressure buildup in the eye that can cause blindness if untreated; Italian Greyhounds with two copies are about sixty times more likely to develop it.

Variants across five gene loci together explain about ninety percent of progressive retinal atrophy risk in Italian Greyhounds, with some combinations raising risk up to thirty times above baseline.

Genetic markers near the dog leukocyte antigen region raise the risk of necrotizing meningoencephalitis, a usually fatal brain inflammation in Pugs; two copies make a dog roughly thirteen times more likely to develop it.

Screens for the tick-transmitted bacterial infections - Lyme disease, Ehrlichia and Anaplasma.

Measures thyroid hormone to diagnose canine hypothyroidism or feline hyperthyroidism, a very common metabolic disease in ageing cats.

A recessive VPS13B gene mutation in Border Collies that lowers white blood cell counts, weakening the immune system and causing chronic infections, smaller size and developmental delay from six weeks old.

Assesses how well the kidneys concentrate urine and screens for urinary tract infections, crystals and early diabetes.

The most common inherited bleeding disorder in dogs, from low levels of clotting protein von Willebrand factor, causing spontaneous or prolonged bleeding; a single copy can cause it, though not every carrier shows symptoms.

A rare, more severe recessive form of von Willebrand bleeding disorder in German Shorthaired and Wirehaired Pointers, from abnormal clotting- protein structure; two copies are needed to cause bleeding problems.

The most severe form of von Willebrand bleeding disorder, from a near- total lack of clotting protein; each affected breed carries its own distinct mutation, and two copies are needed to cause bleeding.

Tests for von Willebrand disease, an inherited clotting disorder.

A commercial breed and genetic health DNA panel.

An X-linked EDA gene defect in German Shepherds causing missing hair on the forehead and tail, abnormal teeth, frequent eye and lung infections and reduced sweat and other exocrine glands; males need only one copy.

An X-linked MTM1 gene mutation in Labradors causing early muscle weakness, wasting, a hoarse bark and collapse episodes from about seven weeks old; affected puppies typically need euthanasia by three to six months.

A distinct X-linked MTM1 mutation in Rottweilers causing progressive muscle wasting, weakness and poor coordination from about seven weeks old, usually fatal by six months; it differs from the Labrador form.

A CACNA1F gene deletion causing X-linked retinal degeneration in racing Greyhounds, with vision impairment usually diagnosed in early adulthood; males need only one copy, while the risk from one copy in females is still under study.

Detects antibodies to equine infectious anemia. Legally required for interstate travel, boarding, sales and competition - for donkeys exactly as for horses.

Donkeys hide pain, so routine panels are run far earlier than for a horse. A donkey with a serious condition may only stand quietly and eat a little less.

Donkey thyroid levels differ from a horse's. Read against equine ranges a healthy donkey looks severely hypothyroid, so donkey-specific reference scales are required.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

Resting insulin or an oral sugar test, diagnosing equine metabolic syndrome (EMS), which puts a horse at high risk of laminitis.

Nerve blocks, flexion tests and digital radiographs used together to isolate the exact source of joint or soft tissue pain.

Donkeys are the natural host for lungworm and carry heavy loads without coughing, but pass it to horses, which get very sick. The Baermann technique catches the larvae; flotation does not.

A stressed or off-feed donkey mobilises fat into the bloodstream, which brings on liver and kidney failure. Run at the first sign of even a minor illness.

Visualises soft-tissue organ changes that an X-ray cannot show.

A blood screen (CIEP, ELISA or qPCR) for a highly contagious parvovirus causing slow immune-mediated wasting, organ failure and hind-limb weakness. Incurable, so breeding stock is screened rather than treated.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

X-rays for bone fractures and chest structures.

Measured after a strict 4-to-6 hour fast to catch insulinoma, a pancreatic tumour that overproduces insulin and causes dangerously low blood sugar.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Diagnoses ferret adrenal disease, which is driven by overproduced sex hormones rather than cortisol - the panel looks for high estradiol, progesterone and androstenedione.

Assesses how well the kidneys concentrate urine and screens for urinary tract infections, crystals and early diabetes.

Measures active oxygen saturation in the water column with a digital probe.

A skin, fin or gill mucus scrape read live under the microscope for external parasites and bacteria.

Tracks biological filtration. Raised nitrite causes brown blood disease, where hemoglobin can no longer carry oxygen.

Monitors acid-base balance and the water's buffering capacity, which is what prevents a sudden fatal pH crash.

Measures the toxic waste excreted through the gills. High levels cause acute neurological damage and respiratory failure.

Measures active oxygen saturation in the water column with a digital probe.

A skin, fin or gill mucus scrape read live under the microscope for external parasites and bacteria.

Tracks biological filtration. Raised nitrite causes brown blood disease, where hemoglobin can no longer carry oxygen.

Monitors acid-base balance and the water's buffering capacity, which is what prevents a sudden fatal pH crash.

Measures the toxic waste excreted through the gills. High levels cause acute neurological damage and respiratory failure.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Genets take feline reference intervals and feline viruses with them. This identifies the parvovirus that destroys the immune system and the gut lining.

A serum neutralising titer in IU/mL, reported against the 0.5 IU/mL export threshold. For wolves and wolf-hybrids it is the only proof of immunity, because no rabies vaccine is federally approved for them and a vaccination certificate is legally invalid after a bite; for mink, genets and kinkajous it is the standard export requirement.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A needle aspirate or tissue biopsy read by a pathologist, separating benign growths from aggressive cancer. Rats and mice have a very high rate of mammary tumours; more than half of older hedgehogs develop a tumour of some kind, most often in the mouth or uterus.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A fresh smear under the microscope for Giardia, Spironucleus and the bacterial overgrowth behind 'wet tail' (proliferative ileitis) in hamsters.

PCR and culture on placental tissue after a miscarriage, identifying contagious pathogens that also infect people - Chlamydia pecorum and Campylobacter.

A milk protein gene variant that determines how much alpha-s1 casein a doe produces, grouped into high, intermediate or low output, with higher levels linked to better cheese yield.

Beta-hydroxybutyrate in blood or urine. Ewes are tested in late pregnancy for twin-lamb disease, dairy goats in early lactation when heavy milk production makes ketosis likely.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

The critical goat-specific blood test. Where sheep get OPP, goats get CAE - a retrovirus causing hard udder, chronic arthritis and brain inflammation in kids.

Blood antibody test for the internal and external abscesses caused by Corynebacterium pseudotuberculosis, which ruin wool and meat quality.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A recessive neuromuscular disorder caused by a CLCN1 gene mutation that slows muscle relaxation after contraction, causing sudden stiffness and brief falling, most common in Myotonic goats.

Goats need far more copper than sheep, who are poisoned by it. Serum or liver biopsy checks for the deficiency behind a faded coat, fishtail and immune failure.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

Detects XX/XY chimerism in a female born twin to a male, which leaves her sterile with an underdeveloped reproductive tract. Reported as positive or negative, in cattle and goats alike.

A recessive metabolic disorder found mainly in Nubian goats and their crosses that blocks breakdown of cell waste products, causing delayed growth, poor motor skills and early death in affected kids.

Reports PRNP prion protein gene variants, such as S146 and K222, that shift a goat's relative risk of classical scrapie, a fatal brain disease, rather than guaranteeing immunity or infection.

The blood ELISA used for cattle and sheep is unreliable in goats, so Johne's disease is confirmed by fecal PCR instead.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

Camelids get their own BVDV strain, causing ill-thrift, respiratory failure and abortion. Whole-blood PCR screens crias to confirm they are not persistent carriers.

Camelid red blood cells are small, flat and oval rather than round, so the slide must be read by a technician familiar with camelids to tell true anemia from dehydration.

Alpaca panels centre on fleece-density mutations; llama panels, bred as pack and guardian animals, centre on structural soundness and ancestral lineage markers instead.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A cerebrospinal fluid tap looking for raised eosinophils, the sign that deer-borne meningeal worm has reached the spinal cord and is causing hind-limb paralysis.

A high-density centrifugation method needed to catch Eimeria macusaniensis (E. mac), a giant coccidial parasite that can kill a camelid and that ordinary flotation misses.

Guards against severe skin disease from zinc deficiency and rickets from too little ultraviolet light. Dense-fleeced alpacas need this watched far more closely than coarser-fibred llamas.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Cavy micronutrient requirements are high; calcium is tracked to prevent metabolic bone disease.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A small scope inside the mouth, checking for sharp enamel spurs, molar overgrowth and ulcers on the tongue and cheeks.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Hindgut fermenters with a large cecum have their own normal gut flora, so the wet mount is read against cavy criteria and checked for pinworms and Giardia.

Open-rooted teeth grow for life. X-rays are the only way to see root elongation, back-tooth impaction and the painful jaw abscesses that stop an animal eating.

Cavies cannot make their own vitamin C. Blood levels are tracked to prevent scurvy, which brings painful joints, bleeding gums and immune collapse.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A needle aspirate or tissue biopsy read by a pathologist, separating benign growths from aggressive cancer. Rats and mice have a very high rate of mammary tumours; more than half of older hedgehogs develop a tumour of some kind, most often in the mouth or uterus.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A fresh smear under the microscope for Giardia, Spironucleus and the bacterial overgrowth behind 'wet tail' (proliferative ileitis) in hamsters.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Ultrasound of the beating heart, measuring how well it empties. Larger old-world monkeys have a high genetic incidence of heart-muscle scarring; hedgehogs are prone to dilated cardiomyopathy, where the muscle stretches and weakens before any outward sign appears.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A needle aspirate or tissue biopsy read by a pathologist, separating benign growths from aggressive cancer. Rats and mice have a very high rate of mammary tumours; more than half of older hedgehogs develop a tumour of some kind, most often in the mouth or uterus.

Identifies the fungi behind flaky, crusting skin. Worth knowing about because the same infection passes to people as ringworm.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Spinal radiographs, or CT/MRI where available, looking for the disc disease, arthritis and tumours that cause wobbliness. In a live hedgehog this is how Wobbly Hedgehog Syndrome is approached: by ruling everything else out, because nothing tests for WHS itself.

Cultures serial fecal or cloacal samples - at least three, because shedding comes and goes - for gut bacteria the animal carries silently but that cause severe illness in people, especially young children.

Crusts, a skin scrape or plucked quills read under the microscope for the mites behind heavy crusting, constant scratching and quill loss.

The only test that confirms Wobbly Hedgehog Syndrome, and it can only be done after death, on brain and spinal cord tissue. There is NO blood, DNA or antemortem test for WHS - a living hedgehog cannot be cleared of it. Because the disease is inherited, a confirmed result is what tells a breeding programme the line carries it.

A gene controlling whether black pigment is confined to the mane, tail and legs, giving a bay coat, or spread over the whole body for black, one of the two base color genes in horses.

An X-linked androgen receptor defect that makes genetic males (XY) develop as sterile, outwardly female horses, while carrier mares look and reproduce normally but can pass the variant on.

A bundled panel of the white spotting genes the American Paint Horse Association accepts for registration, letting a breeder confirm in one submission which patterns a horse carries.

A modifier gene that, only in horses also carrying the leopard complex mutation, greatly increases how much white spotting covers the body, with no visible effect on its own.

A recessive SEL1L gene variant in Thoroughbreds that impairs platelet function, raising the risk of prolonged or excessive bleeding after an injury, surgery or foaling.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

An X-linked mutation causing striped, texturally distinct hair in heterozygous mares, while males carrying it and homozygous mares instead just have sparse, thin manes and tails.

A dominant KIT region variant causing an all white coat with pink skin, found only in the Camarillo White Horse. Two copies have never been observed and are thought to be lethal before birth.

Arabian lines. Affected foals appear normal at birth, then lose balance and coordination as the cerebellum degenerates. Not fatal in itself, but affected horses are unsafe to ride.

A dominant coat dilution that lightens both red and black pigment and gives pinkish lavender skin and amber eyes, producing gold, tan or dark tan shades depending on the horse's base color.

Detects antibodies to equine infectious anemia. Legally required for interstate travel, boarding, sales and competition - for donkeys exactly as for horses.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A recessive CLCN1 muscle chloride channel variant in New Forest Ponies that delays muscle relaxation, so affected foals are born normal but develop stiffness and trouble rising within a few months.

A recessive variant causing an inability to see in low light from birth, found in Tennessee Walking Horses, Standardbreds and Missouri Fox Trotters, separate from the leopard complex gene's night blindness.

A recessive variant in Connemara Ponies causing a hoof wall that easily cracks and breaks despite a normal looking coronary band, while carriers stay unaffected but can pass the variant on.

An incompletely dominant dilution gene that lightens coat color, turning chestnut horses palomino or cremello, bay horses buckskin or perlino, and black horses smoky black or smoky cream.

A recessive Friesian eyelid condition in which lashes grow from an abnormal spot and can rub the cornea, causing squinting, tearing and ulcers, though some carriers show no signs at all.

A family of KIT gene mutations that cause white spotting ranging from large white markings to an all-white coat, and some combinations of these variants do not survive to birth.

A coat color dilution gene that lightens the body while leaving the head, legs, mane and tail dark, often paired with a dorsal stripe and other primitive markings seen in wild-type equids.

Measures adrenocorticotropic hormone to diagnose pituitary pars intermedia dysfunction (PPID), better known as equine Cushing's disease.

A recessive nerve and calcium regulation disorder in Thoroughbred foals that causes muscle tremors and seizures from low blood calcium and is usually fatal without early treatment.

A laboratory's bundled panel, reported as one document. Record the individual conditions below as well - a buyer looks for 'SCID: Clear', not for a PDF.

A recessive neurological disorder of Quarter Horse foals causing progressive incoordination in the hind legs starting at one to four weeks old, leading to an inability to stand within days.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A recessive immune deficiency of Fell and Dales ponies that leaves foals unable to fight infection once maternal antibodies fade, causing fatal anemia and illness by two to three months old.

Warmblood lines. Affected foals are born with skin and joints too fragile to survive. Carriers are unaffected and common.

A recessive skeletal disorder in Friesians that shortens the limbs and ribs while the head and back stay normal sized, leaving affected foals with hyperextended fetlocks in every limb.

A recessive brain disorder in Friesians causing fluid to build up inside the skull, usually resulting in stillbirth or a foal that must be euthanized soon after a difficult birth.

A recessive platelet disorder identified in several breeds that impairs blood clotting and can cause prolonged or excessive bleeding after an injury or surgery.

Quarter Horse and Paint lines. Affected foals are aborted or die within weeks; carriers are healthy, so only testing finds it.

A dominant coat gene causing progressive whitening with age, where extra copies of the variant mean faster graying and a much higher lifetime risk of melanoma than a single copy.

A dominant coat gene that causes a horse to progressively turn white with age regardless of its base color, reported simply as present or absent without counting how many copies it carries.

Cutting-bred Quarter Horses. Skin along the back separates under the saddle and does not heal, usually ending a riding career.

A laboratory procedure that screens biopsied embryos for sex, coat color genes or a known familial disease mutation before implantation, letting breeders avoid transferring an affected embryo.

Quarter Horse lines descending from Impressive. Causes episodes of muscle tremor and collapse. Dominant, so a single copy shows - record N/H and H/H distinctly where the lab reports them.

Resting insulin or an oral sugar test, diagnosing equine metabolic syndrome (EMS), which puts a horse at high risk of laminitis.

A recessive LAMC2 mutation in Belgian draft horses that prevents the skin from anchoring properly, causing severe blistering, mouth lesions and hoof sloughing in newborn foals that do not survive.

A recessive LAMC2 mutation distinct from the Belgian variant, found in Saddlebreds and related breeds, causing the same fatal blistering of skin and hooves when two copies are inherited.

Nerve blocks, flexion tests and digital radiographs used together to isolate the exact source of joint or soft tissue pain.

Arabian lines. Affected foals are born with a diluted coat and seizures they cannot recover from.

An incompletely dominant Appaloosa spotting gene where one copy gives a variable white pattern and two copies give a lighter pattern plus reliable night blindness and higher uveitis risk.

Frame overo Paint and pinto lines. Two carriers can produce an all-white foal with an unformed colon, which always dies. The carrier pattern is not reliably visible, so testing is the only way to plan around it.

Quarter Horse lines. A potentially fatal reaction to anaesthesia or stress. Worth knowing before any surgery, not only before breeding.

An eye disorder linked to the Silver dilution gene, where one copy brings a milder form with ocular cysts and abnormal cornea or iris development and two copies bring a more severe form.

A recessive dilution found mainly in Shetland Ponies that gives a distinctive sepia toned coat with a flaxen mane and tail, visible only on a chestnut based coat and carried quietly by heterozygotes.

A Quarter Horse muscle disease, formerly called IMM, causing either immune mediated muscle wasting or non exercise related tying up, with two copies of the variant linked to more severe disease.

A recessive Akhal-Teke disorder causing foals to be born with little or no hair coat, abnormal teeth, digestive problems and persistent diarrhea, a condition that is not compatible with life.

A recessive Arabian disorder in which the skull and upper neck vertebrae develop abnormally, compressing the spinal cord and causing incoordination, limb weakness and unusual neck carriage.

A recessive DDB2 gene variant that raises the risk of ocular squamous cell carcinoma, the most common eye tumor in horses, notably in Haflingers and Belgians carrying two copies.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

A recessive dilution gene at the same locus as Cream that lightens coat, mane, tail and skin when two copies are present, or when one Pearl allele pairs with one Cream allele, giving a champagne-like look.

Stock, draft and warmblood breeds. Sugar stored abnormally in muscle, causing tying-up. Manageable by diet and exercise, which is why knowing before purchase matters.

The extension gene decides whether a horse produces black pigment for a black or bay base coat or lacks it for a chestnut coat, and this variant can be carried quietly by any breed.

A dominant white patterning gene mixing white and colored hairs through the body while the head, lower legs, mane and tail stay solid colored, with one or two copies both giving the classic roan look.

An incompletely dominant white spotting gene giving white leg markings, a facial blaze and body roaning with one copy, and an at least 90 percent white coat when two copies are present.

Arabian and part-Arabian lines. An affected foal is born with no functioning immune system and dies of infection within months; two carriers bred together give a one-in-four chance of it.

A dominant PMEL17 gene variant that dilutes black pigment in the mane, tail and coat to silvery gray or chocolate tones while leaving red pigment largely unaffected.

A recessive bone development disorder in Miniature Horses and Shetland Ponies causing short legs, clubfoot and worsening knee and hock deformity, usually requiring euthanasia by six months old.

A bundle of eight MITF and PAX3 gene variants, each producing its own splashed white spotting pattern with blue eyes, where some variants carry a deafness risk and some homozygous states are lethal.

A DMRT3 gene variant that enables lateral gaits such as ambling, tolting and pacing and inhibits shifting to a gallop, with two copies giving the strongest effect on gait and leg coordination.

A recessive dilution of iris color to yellow, amber or bright orange, described so far only in Puerto Rican Paso Fino horses and caused by either of two distinct gene variants.

A dominant white spotting pattern from a KIT gene chromosome inversion, giving rounded white patches that cross the topline while the head usually stays colored, found across many horse breeds.

A high-density flotation for raccoon roundworm. Ordinary flotation solution is not dense enough to float the eggs, which cause permanent brain damage if a person swallows them.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Detects an airborne virus that is very nearly always fatal in these species, causing respiratory failure, thickened skin and seizures.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A serum neutralising titer in IU/mL, reported against the 0.5 IU/mL export threshold. For wolves and wolf-hybrids it is the only proof of immunity, because no rabies vaccine is federally approved for them and a vaccination certificate is legally invalid after a bite; for mink, genets and kinkajous it is the standard export requirement.

Identifies the wasting-disease virus that causes fatal liver and gut inflammation in juvenile bearded dragons, and leaves survivors immunosuppressed.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Counted by hand on a stained film, because reptile red cells, white cells and thrombocytes are all nucleated. An automated mammalian analyser counts those nuclei as white cells and reports a wildly false result.

Tests regurgitated stomach contents, a stomach wash or fresh feces for the parasite behind incurable gastric thickening in snakes and chronic wasting in geckos.

Reptiles pass nitrogen as uric acid rather than urea, so BUN does not track kidney failure the way it does in a mammal. This reads uric acid, phosphorus and the calcium-to-phosphorus ratio, which shifts long before uric acid rises.

Cultures serial fecal or cloacal samples - at least three, because shedding comes and goes - for gut bacteria the animal carries silently but that cause severe illness in people, especially young children.

A skin swab or lesion biopsy for the fungi that eat through scales, skin and eventually facial bone.

Camelids get their own BVDV strain, causing ill-thrift, respiratory failure and abortion. Whole-blood PCR screens crias to confirm they are not persistent carriers.

Camelid red blood cells are small, flat and oval rather than round, so the slide must be read by a technician familiar with camelids to tell true anemia from dehydration.

Alpaca panels centre on fleece-density mutations; llama panels, bred as pack and guardian animals, centre on structural soundness and ancestral lineage markers instead.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A cerebrospinal fluid tap looking for raised eosinophils, the sign that deer-borne meningeal worm has reached the spinal cord and is causing hind-limb paralysis.

A high-density centrifugation method needed to catch Eimeria macusaniensis (E. mac), a giant coccidial parasite that can kill a camelid and that ordinary flotation misses.

Guards against severe skin disease from zinc deficiency and rickets from too little ultraviolet light. Dense-fleeced alpacas need this watched far more closely than coarser-fibred llamas.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Primate guts mirror ours. Fecal culture and PCR screen for Shigella, Salmonella, Campylobacter and Yersinia, which spread readily between primates and their keepers.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Blood PCR and ELISA for simian retrovirus, simian immunodeficiency virus and simian T-cell leukemia virus, which cause lifelong immune suppression.

An early kidney biomarker that flags declining function months or years before creatinine rises. Used for the high rate of chronic kidney disease in cats and of renal amyloidosis in ageing captive lorises.

Tuberculin is injected into the skin of the upper eyelid and read at 24, 48 and 72 hours. Swelling means exposure to human or bovine tuberculosis and immediate isolation. The most important test any captive primate gets.

Measures protein leaking into urine, which alongside SDMA is how renal amyloidosis and chronic kidney disease are caught in ageing captive lorises.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Cavy micronutrient requirements are high; calcium is tracked to prevent metabolic bone disease.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A small scope inside the mouth, checking for sharp enamel spurs, molar overgrowth and ulcers on the tongue and cheeks.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Hindgut fermenters with a large cecum have their own normal gut flora, so the wet mount is read against cavy criteria and checked for pinworms and Giardia.

Open-rooted teeth grow for life. X-rays are the only way to see root elongation, back-tooth impaction and the painful jaw abscesses that stop an animal eating.

Cavies cannot make their own vitamin C. Blood levels are tracked to prevent scurvy, which brings painful joints, bleeding gums and immune collapse.

A blood screen (CIEP, ELISA or qPCR) for a highly contagious parvovirus causing slow immune-mediated wasting, organ failure and hind-limb weakness. Incurable, so breeding stock is screened rather than treated.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Detects an airborne virus that is very nearly always fatal in these species, causing respiratory failure, thickened skin and seizures.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A serum neutralising titer in IU/mL, reported against the 0.5 IU/mL export threshold. For wolves and wolf-hybrids it is the only proof of immunity, because no rabies vaccine is federally approved for them and a vaccination certificate is legally invalid after a bite; for mink, genets and kinkajous it is the standard export requirement.

Regulatory surveillance on farmed mink, which can catch COVID-19 from people, pass it back, and mutate it in between.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Ultrasound of the beating heart, measuring how well it empties. Larger old-world monkeys have a high genetic incidence of heart-muscle scarring; hedgehogs are prone to dilated cardiomyopathy, where the muscle stretches and weakens before any outward sign appears.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Primate guts mirror ours. Fecal culture and PCR screen for Shigella, Salmonella, Campylobacter and Yersinia, which spread readily between primates and their keepers.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Essential for macaques. The virus is mild in a macaque but near-uniformly fatal to a person infected through a scratch or saliva, so antibody titers are tracked regularly.

Blood PCR and ELISA for simian retrovirus, simian immunodeficiency virus and simian T-cell leukemia virus, which cause lifelong immune suppression.

Tuberculin is injected into the skin of the upper eyelid and read at 24, 48 and 72 hours. Swelling means exposure to human or bovine tuberculosis and immediate isolation. The most important test any captive primate gets.

Assesses how well the kidneys concentrate urine and screens for urinary tract infections, crystals and early diabetes.

High-priority regulatory surveillance, run to catch a foreign animal disease outbreak early.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Screens for the destructive gut pathogens - porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis (TGE) and Salmonella.

Tests feed rations for fungal toxins such as aflatoxin and zearalenone, which cause severe reproductive failure and immune suppression.

Cotton ropes hung in the pen collect herd saliva, screening a whole group at once for PRRS and influenza A.

Analyses the fluids collected during routine piglet processing to track disease passed down from the sows.

Confirms negative status for a regulatory disease, which is what permits international pork trade and domestic movement.

Evaluates breeding-herd immunity and screens for production-limiting pathogens such as Mycoplasma hyopneumoniae.

Lungs and livers are inspected at the processing plant to grade how severe herd-wide enzootic pneumonia or parasite scarring has become.

A gene controlling whether black pigment is confined to the mane, tail and legs, giving a bay coat, or spread over the whole body for black, one of the two base color genes in horses.

An X-linked androgen receptor defect that makes genetic males (XY) develop as sterile, outwardly female horses, while carrier mares look and reproduce normally but can pass the variant on.

A bundled panel of the white spotting genes the American Paint Horse Association accepts for registration, letting a breeder confirm in one submission which patterns a horse carries.

A modifier gene that, only in horses also carrying the leopard complex mutation, greatly increases how much white spotting covers the body, with no visible effect on its own.

A recessive SEL1L gene variant in Thoroughbreds that impairs platelet function, raising the risk of prolonged or excessive bleeding after an injury, surgery or foaling.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

An X-linked mutation causing striped, texturally distinct hair in heterozygous mares, while males carrying it and homozygous mares instead just have sparse, thin manes and tails.

A dominant KIT region variant causing an all white coat with pink skin, found only in the Camarillo White Horse. Two copies have never been observed and are thought to be lethal before birth.

Arabian lines. Affected foals appear normal at birth, then lose balance and coordination as the cerebellum degenerates. Not fatal in itself, but affected horses are unsafe to ride.

A dominant coat dilution that lightens both red and black pigment and gives pinkish lavender skin and amber eyes, producing gold, tan or dark tan shades depending on the horse's base color.

Detects antibodies to equine infectious anemia. Legally required for interstate travel, boarding, sales and competition - for donkeys exactly as for horses.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A recessive CLCN1 muscle chloride channel variant in New Forest Ponies that delays muscle relaxation, so affected foals are born normal but develop stiffness and trouble rising within a few months.

A recessive variant causing an inability to see in low light from birth, found in Tennessee Walking Horses, Standardbreds and Missouri Fox Trotters, separate from the leopard complex gene's night blindness.

A recessive variant in Connemara Ponies causing a hoof wall that easily cracks and breaks despite a normal looking coronary band, while carriers stay unaffected but can pass the variant on.

An incompletely dominant dilution gene that lightens coat color, turning chestnut horses palomino or cremello, bay horses buckskin or perlino, and black horses smoky black or smoky cream.

A recessive Friesian eyelid condition in which lashes grow from an abnormal spot and can rub the cornea, causing squinting, tearing and ulcers, though some carriers show no signs at all.

A family of KIT gene mutations that cause white spotting ranging from large white markings to an all-white coat, and some combinations of these variants do not survive to birth.

A coat color dilution gene that lightens the body while leaving the head, legs, mane and tail dark, often paired with a dorsal stripe and other primitive markings seen in wild-type equids.

Measures adrenocorticotropic hormone to diagnose pituitary pars intermedia dysfunction (PPID), better known as equine Cushing's disease.

A recessive nerve and calcium regulation disorder in Thoroughbred foals that causes muscle tremors and seizures from low blood calcium and is usually fatal without early treatment.

A laboratory's bundled panel, reported as one document. Record the individual conditions below as well - a buyer looks for 'SCID: Clear', not for a PDF.

A recessive neurological disorder of Quarter Horse foals causing progressive incoordination in the hind legs starting at one to four weeks old, leading to an inability to stand within days.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A recessive immune deficiency of Fell and Dales ponies that leaves foals unable to fight infection once maternal antibodies fade, causing fatal anemia and illness by two to three months old.

Warmblood lines. Affected foals are born with skin and joints too fragile to survive. Carriers are unaffected and common.

A recessive skeletal disorder in Friesians that shortens the limbs and ribs while the head and back stay normal sized, leaving affected foals with hyperextended fetlocks in every limb.

A recessive brain disorder in Friesians causing fluid to build up inside the skull, usually resulting in stillbirth or a foal that must be euthanized soon after a difficult birth.

A recessive platelet disorder identified in several breeds that impairs blood clotting and can cause prolonged or excessive bleeding after an injury or surgery.

Quarter Horse and Paint lines. Affected foals are aborted or die within weeks; carriers are healthy, so only testing finds it.

A dominant coat gene causing progressive whitening with age, where extra copies of the variant mean faster graying and a much higher lifetime risk of melanoma than a single copy.

A dominant coat gene that causes a horse to progressively turn white with age regardless of its base color, reported simply as present or absent without counting how many copies it carries.

Cutting-bred Quarter Horses. Skin along the back separates under the saddle and does not heal, usually ending a riding career.

A laboratory procedure that screens biopsied embryos for sex, coat color genes or a known familial disease mutation before implantation, letting breeders avoid transferring an affected embryo.

Quarter Horse lines descending from Impressive. Causes episodes of muscle tremor and collapse. Dominant, so a single copy shows - record N/H and H/H distinctly where the lab reports them.

Resting insulin or an oral sugar test, diagnosing equine metabolic syndrome (EMS), which puts a horse at high risk of laminitis.

A recessive LAMC2 mutation in Belgian draft horses that prevents the skin from anchoring properly, causing severe blistering, mouth lesions and hoof sloughing in newborn foals that do not survive.

A recessive LAMC2 mutation distinct from the Belgian variant, found in Saddlebreds and related breeds, causing the same fatal blistering of skin and hooves when two copies are inherited.

Nerve blocks, flexion tests and digital radiographs used together to isolate the exact source of joint or soft tissue pain.

Arabian lines. Affected foals are born with a diluted coat and seizures they cannot recover from.

An incompletely dominant Appaloosa spotting gene where one copy gives a variable white pattern and two copies give a lighter pattern plus reliable night blindness and higher uveitis risk.

Frame overo Paint and pinto lines. Two carriers can produce an all-white foal with an unformed colon, which always dies. The carrier pattern is not reliably visible, so testing is the only way to plan around it.

Quarter Horse lines. A potentially fatal reaction to anaesthesia or stress. Worth knowing before any surgery, not only before breeding.

An eye disorder linked to the Silver dilution gene, where one copy brings a milder form with ocular cysts and abnormal cornea or iris development and two copies bring a more severe form.

A recessive dilution found mainly in Shetland Ponies that gives a distinctive sepia toned coat with a flaxen mane and tail, visible only on a chestnut based coat and carried quietly by heterozygotes.

A Quarter Horse muscle disease, formerly called IMM, causing either immune mediated muscle wasting or non exercise related tying up, with two copies of the variant linked to more severe disease.

A recessive Akhal-Teke disorder causing foals to be born with little or no hair coat, abnormal teeth, digestive problems and persistent diarrhea, a condition that is not compatible with life.

A recessive Arabian disorder in which the skull and upper neck vertebrae develop abnormally, compressing the spinal cord and causing incoordination, limb weakness and unusual neck carriage.

A recessive DDB2 gene variant that raises the risk of ocular squamous cell carcinoma, the most common eye tumor in horses, notably in Haflingers and Belgians carrying two copies.

A DNA marker profile compared against the presumed sire and dam to confirm or exclude parentage. It says nothing about breed, colour or disease status.

A recessive dilution gene at the same locus as Cream that lightens coat, mane, tail and skin when two copies are present, or when one Pearl allele pairs with one Cream allele, giving a champagne-like look.

Stock, draft and warmblood breeds. Sugar stored abnormally in muscle, causing tying-up. Manageable by diet and exercise, which is why knowing before purchase matters.

The extension gene decides whether a horse produces black pigment for a black or bay base coat or lacks it for a chestnut coat, and this variant can be carried quietly by any breed.

A dominant white patterning gene mixing white and colored hairs through the body while the head, lower legs, mane and tail stay solid colored, with one or two copies both giving the classic roan look.

An incompletely dominant white spotting gene giving white leg markings, a facial blaze and body roaning with one copy, and an at least 90 percent white coat when two copies are present.

Arabian and part-Arabian lines. An affected foal is born with no functioning immune system and dies of infection within months; two carriers bred together give a one-in-four chance of it.

A dominant PMEL17 gene variant that dilutes black pigment in the mane, tail and coat to silvery gray or chocolate tones while leaving red pigment largely unaffected.

A recessive bone development disorder in Miniature Horses and Shetland Ponies causing short legs, clubfoot and worsening knee and hock deformity, usually requiring euthanasia by six months old.

A bundle of eight MITF and PAX3 gene variants, each producing its own splashed white spotting pattern with blue eyes, where some variants carry a deafness risk and some homozygous states are lethal.

A DMRT3 gene variant that enables lateral gaits such as ambling, tolting and pacing and inhibits shifting to a gallop, with two copies giving the strongest effect on gait and leg coordination.

A recessive dilution of iris color to yellow, amber or bright orange, described so far only in Puerto Rican Paso Fino horses and caused by either of two distinct gene variants.

A dominant white spotting pattern from a KIT gene chromosome inversion, giving rounded white patches that cross the topline while the head usually stays colored, found across many horse breeds.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Blood antibody test for the microsporidian parasite behind neurological head tilt, cataracts and chronic kidney failure.

A small scope inside the mouth, checking for sharp enamel spurs, molar overgrowth and ulcers on the tongue and cheeks.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

The primary tool for evaluating gut stasis, measuring gas build-up in the cecum and seeing tooth roots elongating inside the skull.

Deep nasal or abscess swabs tracing the bacterium behind 'snuffles' - severe upper respiratory and deep tissue infections.

Liver and kidney enzymes plus glucose. A sharp glucose spike is a primary indicator of severe pain or an acute gut blockage.

Diagnoses a highly contagious, fatal calicivirus that causes sudden death and internal bleeding.

Open-rooted teeth grow for life. X-rays are the only way to see root elongation, back-tooth impaction and the painful jaw abscesses that stop an animal eating.

Assesses how well the kidneys concentrate urine and screens for urinary tract infections, crystals and early diabetes.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

A needle aspirate or tissue biopsy read by a pathologist, separating benign growths from aggressive cancer. Rats and mice have a very high rate of mammary tumours; more than half of older hedgehogs develop a tumour of some kind, most often in the mouth or uterus.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A fresh smear under the microscope for Giardia, Spironucleus and the bacterial overgrowth behind 'wet tail' (proliferative ileitis) in hamsters.

PCR and culture on placental tissue after a miscarriage, identifying contagious pathogens that also infect people - Chlamydia pecorum and Campylobacter.

Beta-hydroxybutyrate in blood or urine. Ewes are tested in late pregnancy for twin-lamb disease, dairy goats in early lactation when heavy milk production makes ketosis likely.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Blood antibody test for the internal and external abscesses caused by Corynebacterium pseudotuberculosis, which ruin wool and meat quality.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

Checks blood or milk for antibodies to Mycobacterium avium subspecies paratuberculosis, the cause of chronic wasting disease.

Screens for a slow, incurable lentivirus that causes wasting, hard udder and respiratory failure through a flock.

DNA testing of codon 171 to establish whether a sheep is resistant, intermediate or susceptible to scrapie, a fatal transmissible spongiform encephalopathy.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Checks boas and pythons for a contagious, untreatable virus behind the neurological disease keepers know as star-gazing. Confirmed on a blood smear by the inclusion bodies it is named for.

Counted by hand on a stained film, because reptile red cells, white cells and thrombocytes are all nucleated. An automated mammalian analyser counts those nuclei as white cells and reports a wildly false result.

Tests regurgitated stomach contents, a stomach wash or fresh feces for the parasite behind incurable gastric thickening in snakes and chronic wasting in geckos.

Reptiles pass nitrogen as uric acid rather than urea, so BUN does not track kidney failure the way it does in a mammal. This reads uric acid, phosphorus and the calcium-to-phosphorus ratio, which shifts long before uric acid rises.

Cultures serial fecal or cloacal samples - at least three, because shedding comes and goes - for gut bacteria the animal carries silently but that cause severe illness in people, especially young children.

An oral and cloacal swab for the highly infectious respiratory virus behind proliferative pneumonia and the chronic mucous discharge that goes with it.

A skin swab or lesion biopsy for the fungi that eat through scales, skin and eventually facial bone.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

A fecal gram stain and toxin test for the bacterial overgrowth behind sudden, life-threatening diarrhea.

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

A fecal antigen test for the gut protozoa behind persistent diarrhea, both of which can pass between pets and people.

Whole-body radiographs read alongside calcium, ionised calcium and phosphorus, diagnosing the calcium deficiency behind hind-leg weakness and paralysis.

A nasal flush or choanal swab for the bacteria behind chronic, flock-wide runny nose and eye swelling in tortoises and turtles.

Examines a stool sample under a microscope for intestinal parasites such as roundworms, hookworms, tapeworms, Giardia and Coccidia.

Counted by hand on a stained film, because reptile red cells, white cells and thrombocytes are all nucleated. An automated mammalian analyser counts those nuclei as white cells and reports a wildly false result.

Reptiles pass nitrogen as uric acid rather than urea, so BUN does not track kidney failure the way it does in a mammal. This reads uric acid, phosphorus and the calcium-to-phosphorus ratio, which shifts long before uric acid rises.

Cultures serial fecal or cloacal samples - at least three, because shedding comes and goes - for gut bacteria the animal carries silently but that cause severe illness in people, especially young children.

Screens for the herpesviruses behind mouth rot and severe oral ulceration. Carriers stay infectious for life, so new arrivals are tested before they meet the collection.

Camelids get their own BVDV strain, causing ill-thrift, respiratory failure and abortion. Whole-blood PCR screens crias to confirm they are not persistent carriers.

Camelid red blood cells are small, flat and oval rather than round, so the slide must be read by a technician familiar with camelids to tell true anemia from dehydration.

Alpaca panels centre on fleece-density mutations; llama panels, bred as pack and guardian animals, centre on structural soundness and ancestral lineage markers instead.

Compares the colour of the inner eyelid against a chart to gauge anemia from the barber's pole worm (Haemonchus contortus). Used alongside a fecal egg count, not instead of one.

Counts parasite eggs per gram of manure to identify high and low shedders before deworming, and to track pasture contamination and dewormer resistance.

A cerebrospinal fluid tap looking for raised eosinophils, the sign that deer-borne meningeal worm has reached the spinal cord and is causing hind-limb paralysis.

A high-density centrifugation method needed to catch Eimeria macusaniensis (E. mac), a giant coccidial parasite that can kill a camelid and that ordinary flotation misses.

Guards against severe skin disease from zinc deficiency and rickets from too little ultraviolet light. Dense-fleeced alpacas need this watched far more closely than coarser-fibred llamas.

Handling stress can trigger fatal capture myopathy. After any restraint, creatine kinase and AST are checked for the spikes that mean muscle is breaking down.

Macropods ferment in the foregut, so their normal fecal flora differs completely from a rodent's and standard rodent wet-mount criteria do not apply.

The number-one health threat in captive macropods. Oral exams, deep tissue culture and jaw X-rays catch aggressive bone infection before it deforms the skull.

Macropod glucose, protein and red-cell counts have to be read against macropod reference intervals, not a rodent or placental-mammal baseline.

Macropods are uniquely prone to white muscle disease from these deficiencies, so levels are checked to confirm muscle tissue is not degrading.

Marsupials have no natural immunity to Toxoplasma gondii, shed by cats. Where a placental mammal often tolerates it, a macropod collapses neurologically, so routine titers matter in captivity.

Visualises soft-tissue organ changes that an X-ray cannot show.

Evaluates organ function, tracking the liver (ALT), kidneys (BUN, creatinine) and pancreas (glucose).

Measures red blood cells, white blood cells and platelets to detect anemia, inflammation or an immune response.

X-rays for bone fractures and chest structures.

Wolves host wild parasites domestic dogs rarely see, including the hydatid tapeworm Echinococcus granulosus, which can infect people. Simple flotation is not enough.

Wolves carry lower, chronic worm burdens whose antigen is masked by immune complexes, so the sample is heat-treated to break those bonds first. A standard in-clinic snap test misses them.

A serum neutralising titer in IU/mL, reported against the 0.5 IU/mL export threshold. For wolves and wolf-hybrids it is the only proof of immunity, because no rabies vaccine is federally approved for them and a vaccination certificate is legally invalid after a bite; for mink, genets and kinkajous it is the standard export requirement.

Swabs analysed under the microscope to identify the yeast or bacterial overgrowth behind chronic ear and skin infections.

Restraint sends a wolf's glucose and cortisol sharply up. A handling baseline is what stops a stressed wolf being read as diabetic or Cushingoid against domestic dog guidelines.

Screens for the tick-transmitted bacterial infections - Lyme disease, Ehrlichia and Anaplasma.

Measures thyroid hormone to diagnose canine hypothyroidism or feline hyperthyroidism, a very common metabolic disease in ageing cats.

Assesses how well the kidneys concentrate urine and screens for urinary tract infections, crystals and early diabetes.