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Rat-Mouse — Care & Reference Manual

LLM-refined manual (v2 pipeline, kimi, 2026-08-04; docs/MANUAL_V2_DESIGN.md). This manual assembles the verified fact blocks in Pet Data Station that mention rat-mouse, organised along a pet owner's journey. Every quoted fact is reproduced verbatim from its cited first-hand source ([n] superscripts; see References, each tagged with a computed trust grade per docs/topic_grading_guide.md) and is independently checkable. Guide sections (checklists, red-flag box) are orientation prose in which every factual sentence carries its own [n]; derived-summary blocks from non-Open-Access sources keep their Paraphrased derived summary mark. Mis-sectioned, duplicate, off-topic and image-residue fragments were removed by the v2 builder (build-gate enforced).

Contents

1. Species Profile
2. Life-Stage Care
3. Is this pet right for you?
4. Daily & Weekly Care Checklist
5. Nutrition
6. Husbandry
7. Behavior & Training
8. Enrichment & Exercise
9. When to call a vet NOW
10. Health & Disease
11. Toxicology & Hazards
12. Grooming
13. Breeding & Neutering
14. Regulations & Legality
15. Breed-Specific Health
16. Appendix A — Commercial Food & Regulatory Notes
17. Appendix B — Research Evidence

Species Profile

The profile below records this species' taxonomy, natural origin and lifespan as documented in the cited reference.

Fancy mouse (Mus musculus) — species profile (taxonomy, geographic range, habitat, physical description, behavior, wild diet, reproduction, lifespan)

Mus musculus may have originally been distributed from the Mediterranean region to China, but it has now been spread throughout the world by humans and lives as a human commensal. [1]

House mice generally live in close association with humans-- in houses, barns, granaries, etc. [1]

They also occupy cultivated fields, fencerows, and even wooded areas, but they seldom stray far from buildings. [1]

Some individuals spend the summer in fields and move into barns and houses with the onset of cool autumn weather. [1]

Because of their association with humans, house mice have been able inhabit inhospitable areas (such as tundra and desert) which they would not be able to occupy independently. [1]

Their fur ranges in color from light brown to black, and they generally have white or buffy bellys. [1]

They have long tails that have very little fur and have circular rows of scales (annulations). [1]

House mice tend to have longer tails and darker fur when living closely with humans. [1]

They range from 12 to 30 g in weight. [1]

In the wild state, house mice generally dwell in cracks in rocks or walls or make underground burrows consisting of a complex network of tunnels, several chambers for nesting and storage, and three or four exits. [1]

When living with humans, house mice nest behind rafters, in woodpiles, storage areas, or any hidden spot near a source of food. [1]

They construct nests from rags, paper, or other soft substances and line them with finer shredded material. [1]

House mice are generally nocturnal, although some are active during the day in human dwellings. [1]

House mice are quick runners (up to 8 miles per hour), good climbers, jumpers, and also swim well. [1]

In the wild, house mice eat many kinds of plant matter, such as seeds, fleshy roots, leaves and stems. [1]

Insects ( beetle larvae, caterpillars, and cockroaches ) and meat (carrion) may be taken when available. [1]

In human habitation, Mus musculus consumes any human food that is accessible as well as glue, soap, and other household materials. [1]

Many mice store their food or live within a human food storage facility. [1]

The recent discovery of ultrasonic songs produced by male mice, when exposed to female sex pheromones, suggests that this behavior may be involved in mate choice. [1]

Breeding occurs throughout the year, although wild mice may have a reproductive season extending only from April to September. [1]

Where house mice are abundant they can consume huge quantities of grains, making these foods unavailable to other (perhaps native) animals. [1]

House mice are also important prey items for many small predators. [1]

House mice are eaten by a wide variety of small predators throughout the world, including cats, foxes, weasels, ferrets, mongooses, large lizards, snakes, hawks, falcons, and owls. [1]

House mice try to avoid predation by keeping out of the open and by being fast. [1]

They are also capable of reproducing very rapidly, which means that populations can recover quickly from predation. [1]

Commensal populations of Mus musculus are generally stable and densities can be as high as 10 mice per square meter. [1]

In the wild, populations are less stable and densities may be less than 1 mouse per 100 square meters. [1]

Overall, populations are flourishing and are in fact aided by human construction of houses, barns, and other structures. [1]

Fancy rat (Rattus norvegicus) — species profile (taxonomy, geographic range, habitat, physical description, behavior, wild diet, reproduction, lifespan)

Norway rats ( Rattus norvegicus ) are originally native to northern China. [2]

Following a series of introductions, the species had found its way to Eastern Europe by the early eighteenth century. [2]

By the year 1800, they occurred in every European country. [2]

norvegicus was native to forests and brushy areas. [2]

Today, however, Norway rats find preferred habitat to be alongside the rapid expansion of the human population. [2]

Nearly every port city in the world has a substantial population of these rodents. [2]

They occupy a variety of habitats including garbage dumps, sewers, open fields and woodlands, basements, and nearly anywhere else that food and shelter might be found. [2]

Rattus norvegicus is a rather large member of the mouse family. [2]

On average, these rats reach nearly 400 mm nose-to-tail, and weigh 140 to 500 g. [2]

Males are usually larger than females. [2]

In natural populations, these rats are covered with coarse, brownish fur (sometimes splotched with black or white hairs) on their dorsal surface, which usually lightens to a gray or tan color nearing the underside. [2]

Often, these rats take up residence in areas near water. [2]

There is much learning capacity in Norway rats. [2]

They are able to remember their way around complex sewer and burrow networks. [2]

Using their sense of smell and touch, they are able to survive quite easily given that there is a steady supply of any type of food. [2]

In metropolitan areas, they survive mainly on discarded human food, and anything else that can be eaten without negative consequences. [2]

Some Norway rats living near the sea have been observed catching fish with their paws. [2]

Social animals, Norway rats tend to breed in large groups. [2]

Once a female enters her six-hour estrus period, she may mate as many as five-hundred times with competing males. [2]

Norway rats are excellent competitors and will readily drive out competing rat species, such as Rattus rattus. [2]

Their burrows also tend to aerate the soil. [2]

As prey, they help to sustain predator populations. [2]

Rattus norvegicus is preyed on by any number of carnivorous mammals, birds, and reptiles. [2]

Humans also kill very large numbers of Norway rats as pests. [2]

These animals are not a conservation concern. [2]

In fact, humans spend a great deal of effort trying to eradicate them. [2]

Life-Stage Care

Young, adult and senior care for this species, drawn from first-hand care pages and veterinary references.

Rat Mouse — life stage (owner-practical care, Merck Veterinary Manual pet-owner)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Avoid fatty treats, since older rats are prone to obesity. [3]

Food should be available constantly, but remove uneaten food before feeding fresh (at least daily). [3]

Wire climbing shelves should have openings no wider than ½ × ½ inch. [3]

Bottle holders with chew guards are available. [3]

Avoid ammonia buildup from urine by changing litter often enough. [3]

If a house mouse is a pet, the average life span is about 2 years [1]

The maximum lifespan of R. norvegicus is 4 years (in captivity). [2]

Is this pet right for you?

• They are social and need company: domesticated rats are social, active and intelligent and make good pets; mice are very social and prefer group living, and singly housed rats may develop isolated-rat stress syndrome (increased startle, elevated stress hormones). [3] [4]
• Size: Norway rats are large rodents — on average nearly 400 mm nose-to-tail and 140–500 g — and are social animals that breed in large groups; house mice are much smaller, weighing 12–30 g. [2] [1]
• Right cage: the best cages are easy to clean and resist chewing, with solid (not wire-mesh) floors so feet and hind limbs do not get trapped, plus good ventilation and escape-proof latches, and large enough for toys and free movement. [3] [4]
• They breed fast: rats breed prolifically, so keep only same-sex individuals together; male rats reach sexual maturity at about 6–10 weeks and females at 8–12 weeks. [3]
• Daily commitment: they need daily feeding, water-bottle checks, cage cleaning and social time — they are not low-maintenance. [3]

Daily & Weekly Care Checklist

Every day:

• Feed the right chow: feed mice a good-quality commercial mouse food (nuggets) and rats a commercial pellet made specifically for rats — not rabbit/guinea-pig/hamster feed, which lacks the nutrients rats need; supplement with small amounts of fruit/veg as part of the daily allowance, not in addition. [5] [6] [4]
• Constant water: give constant access to clean drinking water in bottles (mice can die without water even for short periods) and clean food/water containers daily. [5] [3]
• Health watch: check each animal for illness signs — appetite or weight loss, hunched posture, eye/nose discharge, hair loss, matted fur, trauma or dullness; watch rats for red staining around the eyes/nostrils (chromodacryorrhoea). [3] [7]
• Exercise + company: give rats time out of the cage to exercise (wheels at least 12–14 in, tubes, ladders, climbing blocks) and social contact; scatter food to encourage natural foraging. [3] [5]
• Ammonia control: avoid ammonia buildup from urine by changing litter often enough, because high-ammonia air worsens respiratory disease. [3]

Every week:

• Weigh + teeth: weigh and check body condition; rats have incisor teeth that grow continuously and need materials to gnaw, and a vet can trim overgrown teeth when needed. [3] [8]
• Clean + climate: clean the cage thoroughly and keep temperatures at 18–26°C; temperatures above 30°C can cause heat exhaustion, especially if the cage is overcrowded. [4] [3]
• Young rats: raise young rats with adequate humidity, since low humidity can cause annular constrictions that may lead to loss of the distal tail. [8]

Nutrition

The short version: base the diet on a good-quality commercial rodent chow (rodent chows should have a minimum of 16% protein and 4–5% fat), with other foods not more than 20% of the total diet and small daily amounts of fruit/veg; rats and mice are omnivores but lab-style diets are high-fat and low-fiber, so supplement fibre and avoid obesity. [9] [4] [6] The sourced details follow.

The quotes below summarise this species' dietary requirements and nutrition-related disease risks, drawn from professional veterinary references.

Ball python feeding — obligate carnivore; whole prey mice/rats; pre-killed frozen-thawed; separate cage

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Ball pythons are obligate carnivores and need to eat whole animals to get the right nutrition; most keepers feed appropriately sized mice or rats. [10]

Only pre-killed prey that has been frozen and thawed should be fed, because live rodents can severely injure or kill a snake. [10]

Ball pythons are nighttime feeders. [10]

Prey should be about the same width as the ball python's body at mid-body; for example, a snake whose midsection is 1½ inches in diameter should be fed prey no wider than 1½ inches. [10]

Juvenile ball pythons are fed about once a week, adults about every 1–2 weeks, and baby ball pythons every other day. [10]

Fresh, clean water should always be available to a ball python and be replaced daily. [10]

Mouse feeding — commercial mouse nuggets; fruit/veg supplement; coprophagic; water bottles

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Feed mice a good-quality commercial mouse food (nuggets), which gives a complete and balanced diet. [5]

Offer small amounts of fresh fruit and vegetables as part of the daily allowance (not in addition). [5]

Mice are coprophagic rodents and eat their faeces to absorb essential nutrients such as vitamin B12 and folic acid. [5]

Give constant access to clean drinking water in bottles with metal sipper tubes, as mice can die without water even for short periods. [5]

Nutrition of rats and mice (Merck): omnivorous diet, obesity risk, coprophagy

Rats and mice are omnivores, eating foods of both plant and animal origin. [4]

Formulated pelleted diets for laboratory rodents are convenient and nutritionally balanced diets for early life and reproduction. However, laboratory rodent diets are relatively high in fat and low in fiber, and when provided ad libitum, they cause obesity. [4]

Owners should supplement their pet’s diet with feeds high in fiber such as vegetables, limited amounts of fruit, and occasional treats. [4]

Coprophagy is a normal behavior in rats and mice. [4]

Rat & mouse safe greens & vegetables — opportunistic omnivore; nugget base, small fresh veg/fruit, rodent toxins

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Mice are opportunistic omnivores; wild mice eat a wide variety of seeds, grains and other plant material plus invertebrates, small vertebrates and carrion. [5]

A good-quality commercial mouse food (recommended as nuggets/pellets) provides a complete and balanced diet. [5]

Mice are coprophagic, re-eating their faeces to absorb essential nutrients such as vitamin B12 and folic acid. [5]

Rat feeding — rat-specific commercial pellets; omnivore supplements; water bottles

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Feed rats a commercial food pellet made specifically for rats, not pellets formulated for rabbits, guinea pigs, hamsters or other herbivores, which lack the nutrients rats need. [6]

Rats are omnivores; supplement the diet with small amounts of fruit, vegetables, cooked egg, grains and seeds as part of the daily food allowance (not in addition, to avoid obesity). [6]

Provide a continuous supply of fresh, clean drinking water in bottles rather than bowls, with several bottles so all rats can drink at the same time. [6]

Rat, mouse, hamster and gerbil nutrition — rodent chow composition and treat limits (VIN Veterinary Partner)

Rats, mice, hamsters and gerbils have similar dietary requirements. [9]

The basic diet for this group should consist of a good quality rodent chow or lab block. [9]

Rodent chows should have a minimum of 16% protein and 4 to 5% fat content. [9]

Good quality rodent chows are considered to be fairly complete diets for this group. [9]

Other foods can be fed in addition to the commercial pellets but should not constitute more than 20% of the total diet. [9]

Fruit and vegetables as described for the rabbits, guinea pigs and chinchillas can be offered at a rate of about 1 teaspoon/day. [9]

A reasonable amount of nuts and or seeds would be a total of 1 teaspoon/day for rats and about ½ teaspoon for the other species. [9]

Pelleted food should be purchased in amounts that will be used within three months to prevent spoilage. [9]

Mostly nocturnal or active at dusk, Norway rats go about digging burrows, foraging for food, and preparing nests during these hours. [2]

They are excellent swimmers, and are often referred to as "water rats." Foraging behaviors can take the rats on long nightly excursions to areas known to be rich in food resources via learned routes. [2]

Norway rats are excellent foragers. [2]

Because of their foraging habits, Norway rats act as seed dispersers. [2]

Husbandry

The home is a chew-resistant cage with solid floors, good ventilation and escape-proof latches; aquariums are not suitable because inadequate air circulation lets ammonia build up and worsens respiratory disease. [4] [8] The sourced details follow.

Housing, environment and daily-care essentials for this species.

Husbandry of pet rats and mice (caging, solid floors, bedding, ammonia control)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Best cages for pet rats and mice are easy to clean and deodorise and resist rodent chewing or digging; solid (not wire-mesh) floors are preferred because feet and hind limbs can get trapped and injured in the gaps. [4]

Good husbandry protects rats' and mice's health: suitable bedding plus frequent cage cleaning helps prevent respiratory disease, which worsens in high-ammonia air. [4]

Husbandry of rats and mice (Merck): caging, substrate, social needs

The best cages for pet mice and rats are made of a material that is easy to clean and deodorize and that is indestructible to rodent chewing or digging in the corners. [4]

Wire-mesh floors should be avoided because rats and mice can trap their feet, and especially hindlimbs, in the openings, resulting in fractures and injuries. [4]

Husbandry of Mice and Rats The best cages for pet mice and rats are made of a material that is easy to clean and deodorize and that is indestructible to rodent chewing or digging in the corners. [4]

Pet owners generally choose bedding on the basis of cost and availability; laboratory veterinarians choose bedding on the basis of cost and water-holding capacity. [4]

This type of bedding irritates pet rodents, and the coloring agents can stain the coat of white rats or mice. [4]

Historically, owners of pet rats or mice preferred paper and softwood chips, such as kiln-dried pine or aspen, over straw because it requires fewer bedding changes. [4]

Wood chip bedding (such as pine and aspen) that has not been heat treated should not be used, because it contains volatile chemicals that can irritate the respiratory tract and activate liver enzymes in rodents ( 1, 2 ). [4]

Owners must combine frequent bedding changes with good husbandry practices, such as regular cage cleaning, low animal density, and low environmental temperature and humidity. [4]

Aquariums are not suitable cages for rats and mice, because air circulation is inadequate and therefore ammonia builds up. [4]

Pearls & Pitfalls Aquariums are not suitable cages for rats and mice, because air circulation is inadequate and therefore ammonia builds up. [4]

Environmental temperature and relative humidity can depend on husbandry and housing design and can differ considerably between the cage and the room the cage is in. [4]

Factors that contribute to variation in temperature and humidity include cage material and construction, number of animals in the cage, frequency of bedding changes, and bedding type. [4]

The main factors that determine the type of bedding material for pet mice and rats are size and manipulability. [4]

Mice and rats avoid bedding consisting of small particles; they prefer bedding consisting of large, fibrous particles. [4]

Mice and rats are optimally maintained at temperatures of 18–26°C (64–79°F). [4]

[Paraphrased derived summary — non-Open-Access source.] A separate feeding cage is recommended so the snake associates the cage with feeding rather than the handler's hand. [10]

[Paraphrased derived summary — non-Open-Access source.] Scatter portions of the daily food allowance around the cage to encourage natural foraging behaviour. [5]

[Paraphrased derived summary — non-Open-Access source.] Use a solid cage floor; wire mesh can damage feet and legs. [3]

[Paraphrased derived summary — non-Open-Access source.] Water-bottle holders let the bottle hang inside the cage. [3]

[Paraphrased derived summary — non-Open-Access source.] Fresh water should always come from a bottle mounted in the cage. [3]

[Paraphrased derived summary — non-Open-Access source.] The cage should be large enough for toys and free movement. [3]

[Paraphrased derived summary — non-Open-Access source.] In general, a cage should have good ventilation, be easy to clean, and be escape proof. [3]

[Paraphrased derived summary — non-Open-Access source.] Rats are social and spend much time grooming themselves and cage-mates. [3]

[Paraphrased derived summary — non-Open-Access source.] Prevent injuries by keeping the cage hazard-free and handling the animal gently. [3]

[Paraphrased derived summary — non-Open-Access source.] The enclosure needs space for exercise plus feeding and nesting areas. [3]

[Paraphrased derived summary — non-Open-Access source.] Powder-coated wire cages with solid metal shelves and a plastic tray base are easy to clean and rats enjoy climbing the levels. [3]

[Paraphrased derived summary — non-Open-Access source.] A cage should be well ventilated, easy to clean and escape-proof. [3]

[Paraphrased derived summary — non-Open-Access source.] Recycled-paper bedding is safe and easy to clean. [3]

[Paraphrased derived summary — non-Open-Access source.] Temperatures above 30°C (86°F) can cause heat exhaustion, especially if the cage is overcrowded. [3]

[Paraphrased derived summary — non-Open-Access source.] Keep the cage quiet and do not disturb the litter for at least 7 days after birth, especially for a first litter. [3]

[Paraphrased derived summary — non-Open-Access source.] Rats breed prolifically, so keep males and females in separate cages. [3]

[Paraphrased derived summary — non-Open-Access source.] The best cages for pet mice and rats are easy to clean and deodorize and indestructible to rodent chewing or corner digging. [8]

[Paraphrased derived summary — non-Open-Access source.] Appropriate bedding and frequent cage cleaning help prevent respiratory diseases worsened by high ammonia levels. [8]

Behavior & Training

Rats and mice are active, social and intelligent; rats enjoy climbing and play, and you should move slowly to avoid startling a rat (one that rears to face an approaching hand is more likely to bite) — keep same-sex groups and provide enrichment. [3] The sourced details follow.

Socialisation, bonding, play and preventing boredom / behaviour problems.

Rat Mouse — behavior (owner-practical care, Merck Veterinary Manual pet-owner)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Rats are very active and enjoy exercise and play. [3]

Discharge around the eyes or nose can signal illness or stress. [3]

Domesticated rats are social, active and intelligent and make good pets. [3]

Move slowly to avoid startling; a rat that rears to face an approaching hand is more likely to bite. [3]

Rats are social and best kept in groups. [3]

Aggression is uncommon among litter-mate rats raised together. [3]

Mice are very active and enjoy exercise and play. [3]

Mice are very social and prefer group living. [3]

Watch mice for excessive scratching. [3]

Mice are social and best kept in groups. [3]

[Paraphrased derived summary — non-Open-Access source.] A pet rat needs a suitable cage, a balanced diet, and opportunity for exercise and socialisation with its owner to stay healthy. [3]

[Paraphrased derived summary — non-Open-Access source.] Aggression is uncommon among litter-mate mice raised together. [3]

Enrichment & Exercise

Toys, foraging, hiding and exercise to prevent boredom.

Rat Mouse — enrichment (owner-practical care, Merck Veterinary Manual pet-owner)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Rats may chew through wood and escape. [3]

Routine exercise is needed for good health. [3]

Wheels, tubes, ladders and climbing blocks provide stimulation. [3]

A rat exercise wheel should be at least 12–14 inches in diameter. [3]

Wheels should have a smooth (not perforated) surface to avoid trapping toes. [3]

When to call a vet NOW

• Mice decline fast: mice can become unwell and deteriorate quickly, often showing only subtle signs of pain until severe — check them regularly and act fast. [11]
• Rat early signs: watch rats for changes in feeding, drinking, social behaviour or activity as an early problem sign; red staining around the eyes/nostrils (chromodacryorrhoea) can signal stress or health problems — consult a vet if concerned. [7]
• Poisoning is urgent: rats cannot vomit, so even a small amount of a harmful substance can be fatal — contact a vet immediately if you think a rat ate something poisonous, and avoid onion, citrus, walnuts, rhubarb, grapes, raisins and chocolate. [7] [6]
• Mice + toxins: keep poisonous materials (grapes, rhubarb, plants, chemicals) away from mice and contact a vet immediately if exposure is suspected; mice should not be fed onion, grapes, rhubarb or chocolate. [11] [5]
• Bite warning (zoonotic): rat-bite fever is a potentially fatal human disease — Streptobacillus moniliformis lives in rats' nasal passages and a bite can transmit it — so seek medical care for any rat bite. [8]
• Common rat tumours: the most common subcutaneous tumour in rats is the mammary fibroadenoma, which can reach 8–10 cm and occur in both sexes — have a vet check any lump. [8]

Health & Disease

The recurring themes: continuously growing incisors (overgrown incisors are the usual dental issue), mammary fibroadenomas in rats, respiratory disease driven by ammonia, and the zoonotic risk of rat-bite fever. [8] [4] The sourced details follow.

Common conditions and their clinical signs, drawn from professional veterinary references. If you notice worrying signs, contact a species-experienced veterinarian promptly.

Dental disease in pet rats and mice (continually erupting incisors; overgrown incisors most common)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Pet rats and mice commonly develop dental problems because their incisors grow continuously; overgrown incisors are the usual issue (unlike guinea pigs and chinchillas, where cheek-tooth malocclusion is more common). [4]

Mammary fibroadenoma in rats (most common subcutaneous tumor; up to 8–10 cm, both sexes)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

The most common subcutaneous tumour in rats is the mammary fibroadenoma; mammary tissue extends widely so tumours can appear anywhere from the neck to the groin, reach 8–10 cm across, and occur in both sexes. [4]

Mouse emergency / urgent signs — rapid decline, keep poisons away, vet immediately

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Mice can become unwell and deteriorate quickly, often showing only subtle signs of pain until severe; check them regularly. [11]

Rat emergency / urgent signs — behaviour changes, chromodacryorrhoea, no vomiting

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Watch for changes in feeding, drinking, social behaviour or activity as an early sign of a problem. [7]

Red staining around the eyes and nostrils (chromodacryorrhoea) can signal stress or health problems; consult a vet if concerned. [7]

Rat-bite fever in pet rats and mice (Streptobacillus moniliformis, potentially fatal zoonosis)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Streptobacillus moniliformis normally lives in rats' nasal passages without making them ill, but if a rat bites a person the bacterium can cause rat-bite fever, a potentially fatal human disease. [4]

Toxicology & Hazards

Substances and environmental hazards to avoid.

Low-humidity tail annular constriction / tail-loss hazard in young rats

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Intense pruritus, often at the neck and ears, leads to self-trauma. [8]

Raising young rats in low humidity can cause annular constrictions that may result in loss of the distal tail. [8]

Mouse toxic / harmful foods — onion, grapes, rhubarb, chocolate (rodent poisons)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Like other rodents, mice should not be fed toxic foods such as onion, grapes, rhubarb and chocolate. [5]

Rat toxic / harmful foods — onion, citrus, walnuts, rhubarb, grapes, raisins, chocolate; limit sugars/dairy

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Avoid harmful foods for rats: onion, citrus fruits, walnuts, rhubarb, grapes, raisins and chocolate. [6]

Avoid sugars and high-fat foods such as dairy; these are acceptable only as occasional training treats in small amounts. [6]

[Paraphrased derived summary — non-Open-Access source.] Safe greens include small amounts of fresh vegetables and fruits fed as part of the daily allowance (not in addition); however grapes/raisins and rhubarb are poisonous to mice and lettuce can cause diarrhoea. [5]

[Paraphrased derived summary — non-Open-Access source.] Wooden gnawing blocks help wear teeth (avoid wood treated with toxic substances). [3]

[Paraphrased derived summary — non-Open-Access source.] Keep poisonous materials (including grapes, rhubarb, plants and chemicals) away from mice; contact a vet immediately if exposure is suspected. [11]

[Paraphrased derived summary — non-Open-Access source.] Rats cannot vomit, so even a small amount of a harmful substance can be fatal; contact a vet immediately if you think a rat has eaten something poisonous. [7]

Grooming

Brushing / bathing, nails, coat / skin and dental care.

Rat Mouse — grooming (owner-practical care, Merck Veterinary Manual pet-owner)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

A food dish should be easy to clean and sturdy enough not to tip. [3]

Commercial rat food provides all needed vitamins and minerals and includes hard pellets that wear down the continuously growing incisors. [3]

Food and water containers should be cleaned thoroughly each day. [3]

Illness signs include appetite or weight loss, hunched posture, eye or nose discharge, hair loss, matted fur, trauma (bites, wounds, limping) or dullness. [3]

Rats have incisor teeth that grow continuously. [3]

They need materials to gnaw to wear their growing teeth down. [3]

A vet can trim overgrown teeth periodically when needed. [3]

Rats are social animals, and grooming is a socially affiliative behavior. If left alone without human contact and environmental enrichment, singly housed rats might develop isolated-rat stress syndrome, which includes signs such as increased startle reflex and elevated basal levels of stress hormones ( 6 ). [4]

Breeding & Neutering

Neutering / spaying, reproduction and preventing unwanted litters.

Rat Mouse — breeding (owner-practical care, Merck Veterinary Manual pet-owner)

All lines in this block are paraphrased derived summaries — non-Open-Access source.

Rats breed prolifically, so keep only same-sex individuals together. [3]

Male rats reach sexual maturity at about 6–10 weeks; females at 8–12 weeks. [3]

Average gestation is 21–23 days; pregnancy may be detected at about 2 weeks via abdominal palpation or weight or mammary changes. [3]

Females can become pregnant again soon after birth; being pregnant while nursing is unhealthy. [3]

Give females at least 2 months' rest between pregnancies and litter-rearing to recover. [3]

Reproductive problems are uncommon in healthy rats. [3]

House mice have a polygynous mating system. [1]

Regulations & Legality

Legality crosswalk lines for this species, where available. Jurisdiction-specific pet law is frequently a gap — see the roadmap.

Rat Mouse — species legality crosswalk (US/CA/FL named lists + EU/JP/CITES framework)

Rats and mice — EU-IAS: Not on the landed EU Union list of IAS of Union concern (species not enumerated) — Art 7 prohibition applies only to listed species. Basis: Negative finding: enumerated scan of landed EU Union list.

Rats and mice — JP-IAS: Not designated in the landed JP specified-invasive alien species list (species not enumerated) — Art 4 prohibition applies only to designated species. Basis: Negative finding: enumerated scan of landed JP designated list.

Breed-Specific Health

Appenzeller Sennenhund — Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (dogs, cats, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. (hereditary; OMIA-verified breed predisposition)

Breed: Appenzeller Sennenhund (Dog) [12]

Disorder: Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (dogs, cats, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. [12]

Mode of inheritance: X-linked incomplete dominant [12]

Summary: De Lucia et al. (2019): Veterinary clinicians should be aware of cutaneous mosaicism and consider X-linked genodermatoses when seeing female cases with segmental cutaneous diseases like the one following the Blaschko’s lines. [12]

Clin feat: Bauer et al. (2017):No abnormalities were found on the affected daughter during general physical examination except a stunted growth. Linear hyperplastic and partially alopecic lesions, covered with thick brown scales and clusters of dilated follicular ostia were the most prominent dermatological features (Figure 1). The lesions were distributed along Blaschko’s lines in a bilateral rather symmetrical fashion and were more evident on the limbs, the head, the neck and the dorsal trunk. The abdominal and inguinal skin appeared normal. Frond like hyperkeratotic lesions at the margin of all the pawpads with occasional horn-like projections were considered the most probable cause of the visible lameness. Cytological examination of the linear hyperplastic lesions, revealed the presence of variable numbers of coccoid bacteria and a large number of Malassezia yeasts which were suspected to substantially contribute to the pruritus and the offensive odor. Results of the blood tests and urinalysis were unremarkable. De Lucia et al. (2019): Alopecic scaly plaques following the Blaschko’s lines on the limbs, the head, the dorsal neck and the trunk, and severe foot pads hyperkeratosis were the most relevant lesions [12]

Pathology: Bauer et al. (2017):The histopathological findings were identical in all biopsies.... Multifocally, the epidermis and the wall of the hair follicular infundibuli were moderately to severely hyperplastic with abrupt transition to normal skin. Within the hyperplastic area the infundibular epithelium was covered by thick layers of densely packed parakeratotickeratin which was distending the infundibuli. The parakeratotic keratin was often protruding above the epidermal surface. The size of the keratohyalin granules within the granular cell layers of the epidermis and the infundibular wall was within the normal range. Within the parakeratotic keratin, multifocally variable numbers of coccoid bacteria were present and occasionally the lumen of infundibuli contained degenerate neutrophils. Sebaceous glands appeared normal. The interfollicular epidermis was covered by moderate to large amounts of laminar to compact mostly orthokeratotic, but also some parakeratotic keratin. Within the keratin layers of the epidermis multifocally degenerate neutrophils, nuclear debris and small numbers of coccoid bacteria were present. Multifocally exocytosis of neutrophils was seen. Within the superficial dermis there was a mild pigmentary incontinence and a moderate perivascular infiltrate composed of neutrophils, mast cells and fewer lymphocytes. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 388248422 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Bauer et al. (2017):"a deletion spanning 14,399 bp including the last three exons of the NSDHL gene . . . . The formal variant designation is chrX:120,749,179_120,763,577del14,399". Leuthard et al. (2019) detected a heterozygous missense variant in NSDHL in a female affected Chihuahua, c.700G>A or p.Gly234Arg. Christen et al. (2020): "A heterozygous frameshift variant,… Evidence (references) - 1998. A hereditary disorder of cornification and multiple congenital defects in five Rottweiler dogs. Vet Dermatol — PubMed:PMID34644958 | DOI:10.1046/j.1365-3164.1998.00079.x — OMIA Phene_Article / Article - 2008. Cornification defect in the golden retriever: clinical, histopathological, ultrastructural and genetic characterisation. Vet Dermatol — PubMed:PMID18477327 | DOI:10.1111/j.1365-3164.2008.00667.x — OMIA Phene_Article / Article - 2017. A large deletion in the NSDHL gene in Labrador Retrievers with a congenital cornification disorder. G3 (Bethesda) — PubMed:PMID28739597 | DOI:10.1534/g3.117.1124 — OMIA Phene_Article / Article - 2019. X-linked cutaneous mosaicism in a dog. Vet Dermatol — PubMed:PMID31012178 | DOI:10.1111/vde.12748 — OMIA Phene_Article / Article - 2019. A missense variant in the NSDHL gene in a Chihuahua with a congenital cornification disorder resembling inflammatory linear verrucous epidermal nevi. Anim Genet — PubMed:PMID31571289 | DOI:10.1111/age.12862 — OMIA Phene_Article / Article - 2020. NSDHL frameshift deletion in a mixed breed dog with progressive epidermal nevi. Genes (Basel) — PubMed:PMID33143176 | DOI:10.3390/genes11111297 — OMIA Phene_Article / Article - 2021. Ichthyosis and hereditary cornification disorders in dogs. Vet Dermatol — PubMed:PMID34796560 | DOI:10.1111/vde.13033 — OMIA Phene_Article / Article - 2022. Genetics of inherited skin disorders in dogs. Vet J — PubMed:PMID34861369 | DOI:10.1016/j.tvjl.2021.105782 — OMIA Phene_Article / Article - 2023. Genome sequencing of 2000 canids by the Dog10K consortium advances the understanding of demography, genome function and architecture. Genome Biol — PubMed:PMID37582787 | DOI:10.1186/s13059-023-03023-7 — OMIA Phene_Article / Article - 2024. Heterozygous deletion of the NSDHL gene in an Appenzeller Mountain Dog with verrucous epidermal keratinocytic nevi. Anim Genet — PubMed:PMID38659285 | DOI:10.1111/age.13436 — OMIA Phene_Article / Article - 2026. Development of cost-effective PCR-RFLP methods for screening Mendelian disorders in Chihuahua dogs. F.U. Vet. J. Health Sci. — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:308050 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:300275 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [12]

Chihuahua — Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (dogs, cats, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. (hereditary; OMIA-verified breed predisposition)

Breed: Chihuahua (Dog) [12]

Domestic Shorthair — Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (cats, dogs, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. (hereditary; OMIA-verified breed predisposition)

Breed: Domestic Shorthair (Cat) [13]

Clin feat: De Lucia et al. (2019): A 2‐year‐old, female, domestic short hair cat with a history of multiple alopecic, verrucous, hyperpigmented and erythematous skin lesions, following Blaschko's lines on the head, the limbs, the trunk and paw pads. The same authors concluded that the clinical signs of this single cat correspond to the feline counterpart of human inflammatory linear verrucous epidermal nevus (ILVEN), which closely resembles a mild form of CHILD syndrome, a disorder caused by mutations in the same gene. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 389725407 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: De Lucia et al. (2019): "a heterozygous missense variant in the NSDHL gene: XM_004000985.5:c.397A>G or XP_004001034.1:p.(Ser133Gly) [omia.variant:1055]. The variant was absent from 93 additional genetically diverse control cats as demonstrated by Sanger sequencing. The variant was predicted to affect the essential serine residue of the catalytic tetrad 109Asn‐133Ser‐160Tyr‐164Lys in the conserv… Evidence (references) - 2019. Genetic variant in the NSDHL gene in a cat with multiple congenital lesions resembling inflammatory linear verrucous epidermal nevi. Vet Dermatol — PubMed:PMID30474267 | DOI:10.1111/vde.12699 — OMIA Phene_Article / Article - 2012. Feline epidermal nevi resembling human inflammatory linear verrucous epidermal nevus. J Vet Med Sci — PubMed:PMID22672841 | DOI:10.1292/jvms.12-0117 — OMIA Phene_Article / Article - 2019. X-linked cutaneous mosaicism in a dog. Vet Dermatol — PubMed:PMID31012178 | DOI:10.1111/vde.12748 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:308050 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:300275 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [13]

Labrador Retriever — Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (dogs, cats, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. (hereditary; OMIA-verified breed predisposition)

Breed: Labrador Retriever (Dog) [12]

Mixed Breed — Many alias names exist for the phenotype. They include congenital cornification disorder; CHILD nevi; CHILD-like nevi; ILVEN. The human phenotype resulting from NSDHL loss-of-function variants is termed congenital hemidysplasia with ichthyosiform erythroderma and limb defects (CHILD syndrome). CHILD syndrome is characterized by epidermal nevi and striking unilateral limb defects. Animals (dogs, cats, mice) with NSDHL variants have similar epidermal nevi, but so far were never reported to also have the limb defects seen in human CHILD syndrome. (hereditary; OMIA-verified breed predisposition)

Breed: Mixed Breed (Dog) [12]

Rat Terrier — Canine degenerative myelopathy, hereditary canine spinal muscular atrophy (hereditary; OMIA-verified breed predisposition)

Breed: Rat Terrier (Dog) [14]

Disorder: Canine degenerative myelopathy, hereditary canine spinal muscular atrophy [14]

Mode of inheritance: Autosomal recessive [14]

Summary: This is an adult onset degeneration of the spinal cord that progresses to paraplegia and tetraparesis. There is no successful treatment. A genetic test is available. A different mutation in the SOD1 gene causes an early onset disease: [OMIA:002322-9615]: Dyskinesia, paroxysmal, SOD1-related in Canis lupus familiaris. [14]

Clin feat: Most dogs are at least 8 years of age at the onset of clinical signs, which include hyporeflexia, upper motor neuron proprioceptive spasticity and ataxia in the pelvic limbs. Widespread limb muscle atrophy can be observed and the disease progresses to paraplegia and eventually flaccid tetraparesis (Awano et al., 2009). Hyperesthesia, cranial nerve signs (e.g. difficulty in swallowing and barking), urinary and fecal incontinence (Coates et al., 2010) can be observed and in final stages of the disease respiratory muscles fail (Nardone et al., 2016). There is no effective treatment. [14]

Pathology: Histopathologic examination of the spinal cord is necessary for definitive diagnosis. Noninflammatory axonal and myelin degeneration is present at all levels of the spinal cord, being most severe in the dorsal lateral funiculus within the middle to caudal thoracic region. Segmental axonal and myelin degeneration, endoneurial fibrosis, hypomyelinated fibers and secondary demyelination are present in peripheral nerves. Axon cylinder vacuolization is characteristic (Coates et al., 2010). [14]

Prevalence: In an extensive project, Zeng et al. (2014) genotyped 33,747 dogs representing 222 breeds for both known mutant alleles, namely c.52T and c.118A. They concluded that the SOD1:c.118A allele is widespread and common among privately owned dogs whereas the SOD1:c.52T allele is rare and appears to be limited to Bernese Mountain Dogs. Full details are available in the paper. Mizukami et al. (2016) reported the frequency of the c.118A allele as 0.008 in 500 Border collies in Japan. Regarding the insertion reported by Turba et al. (2107), these authors reported that The allele containing the insertion was highly prevalent in Hovawart dogs, accounting for the 26.6% of allele frequency. The insertion was also found in other unrelated breeds such as Rough Collies and Standard Poodles. Santos et al. (2020) genotyped 97 German Shepherd dogs for the SOD1:c.118G>A mutation using a PCR/RFLP test. The dogs were located in Brazil and had no clinical signs of degenerative myelopathy at the time of sampling. They “observed genotype frequencies (with 95% confidence interval) of: 0.758 (0.672-0.844), 0.242 (0.156-0.328) and 0.000 (0.000-0.000) for GG, AG and AA genotypes, respectively.” Maki et al. (2022) genotyped 541 German Shepherd Dogs (GSD) registered with the Japanese GSD Registration Society from 2000 to 2019, for the SOD1:c.118G>A likely causal variant (omia.variant:36). They reported 330 G/G dogs (61%), 184 G/A dogs (34%), and 27 A/A dogs (5%), indicating a frequency of the mutant allele of 0.220. For each of the seven A/A dogs over 10 years old (this being an adult-onset disease), the owners reported DM-related clinical signs, indicating a clinical progression rate of 100%. [14]

Control: Due to the high frequency of the causative mutation in Boxers and Pembroke Welsh Corgis, in these breeds it is not practical to exclude carriers from breeding, so it is recommended that carriers be bred to noncarriers. Breeding of affected dogs of any breed should be avoided. [14]

Gen test: Investigating the many discordant findings between the parental and the offspring genotypes found by different laboratories in testing for the c.118G>A variant, Turba et al. (2017) discovered An insertion of 54 nucleotides [in the SOD1 gene] composed of a poly-T stretch and 15 nucleotides containing the duplication of the exon 2-intron 2 junction was... responsible for the partial mismatch of the reverse primer used for a direct sequencing assay. The mismatch hampered the amplification of the corresponding allele and caused an evident drop-out effect. The insertion is in complete linkage disequilibrium with the c.118G allele. Santos et al. (2020) identified “a deletion of one “T” in the position 26540247 described as ENSCAFG00000008859:g.26540247del … located in the intron 1 of the SOD1 gene. … Although the role of the ENSCAFG00000008859:g.26540247del on structure and expression of SOD1 (and consequently its relationship with CDM) was not investigated in this study, its location does not suggest that it can influence the expression of the studied disease.” However, this variant prevented in a small number of dogs adequate genotyping of the SOD1:c.118G>A in the PCR-RFLP test used in this study. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 403559 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - Gene: Entrez Gene ID 389416327 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: The first likely causative variant described is a G to A transition (c.118G>A; p.E40K) in exon 2 of SOD1. All affected dogs tested were homozygous mutant. However, some homozygous mutant dogs had no signs of degenerative myelopathy, which suggests incomplete penetrance or other causative loci (Awano et al., 2009). The mutation is hypothesized to lead to SOD1 aggregation, as cytoplasmic inclusio… Evidence (references) - 1994. Immunohistochemical evidence for immunoglobulin and complement deposition in spinal cord lesions in degenerative myelopathy in German Shepherd dogs. Can J Vet Res — PubMed:PMID8143248 — OMIA Phene_Article / Article - 2002. Degenerative myelopathy in German shepherd dogs. Veterinary Record — OMIA Phene_Article / Article - 2003. Molecular genetic and expression analysis of alpha-tocopherol transfer protein mRNA in German shepherd dogs with degenerative myelopathy. Berl Munch Tierarztl Wochenschr — PubMed:PMID12592926 — OMIA Phene_Article / Article - 2008. Clinical characterization of a familial degenerative myelopathy in Pembroke Welsh Corgi dogs. J Vet Intern Med — PubMed:PMID18196743 — OMIA Phene_Article / Article - 2009. Genome-wide association analysis reveals a SOD1 mutation in canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A — PubMed:PMID19188595 | DOI:10.1073/pnas.0812297106 — OMIA Phene_Article / Article - 2010. Canine degenerative myelopathy. Vet Clin North Am Small Anim Pract — PubMed:PMID20732599 | DOI:10.1016/j.cvsm.2010.05.001 — OMIA Phene_Article / Article - 2009. Degenerative myelopathy in two Boxer dogs. Vet Pathol — PubMed:PMID19276068 | DOI:10.1354/vp.08-VP-0270-M-BC — OMIA Phene_Article / Article - 2012. Genome-wide association studies for multiple diseases of the German Shepherd Dog. Mamm Genome — PubMed:PMID22105877 | DOI:10.1007/s00335-011-9376-9 — OMIA Phene_Article / Article - 2013. Genotyping assays for the canine degenerative myelopathy-associated c.118G>A (p.E40K) mutation of the SOD1 gene using conventional and real-time PCR methods: a high prevalence in the Pembroke Welsh Corgi breed in Japan. J Vet Med Sci — PubMed:PMID23328634 | DOI:10.1292/jvms.12-0451 — OMIA Phene_Article / Article - 2011. Immunohistochemical observation of canine degenerative myelopathy in two Pembroke Welsh Corgi dogs. J Vet Med Sci — PubMed:PMID21628865 | DOI:10.1292/jvms.11-0097 — OMIA Phene_Article / Article - 2012. Degenerative myelopathy associated with a missense mutation in the superoxide dismutase 1 (SOD1) gene progresses to peripheral neuropathy in Pembroke Welsh corgis and boxers. J Neurol Sci — PubMed:PMID22542607 | DOI:10.1016/j.jns.2012.04.003 — OMIA Phene_Article / Article - 2013. Neuronal loss and decreased GLT-1 expression observed in the spinal cord of Pembroke Welsh Corgi dogs with canine degenerative myelopathy. Vet Pathol — PubMed:PMID23839236 | DOI:10.1177/0300985813495899 — OMIA Phene_Article / Article - (59 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:105400 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:147450 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:618598 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [14]

Rat Terrier — Congenital hypothyroidism with goiter (hereditary; OMIA-verified breed predisposition)

Disorder: Congenital hypothyroidism with goiter [15]

Summary: Congenital hypothyroidism (CH) is an endocrine disorder characterized by inadequate T4 levels early in life concurrent with signs of hypothyroidism. Disease can be primary (failure to make T4), which is due to abnormal thyroid development or function. Primary hypothyroidism often presents with goiter but can be due to thyroid dysgenesis. CH can be secondary (failure to make bioactive TSH), which is caused by abnormal pituitary development or function. CH can also be tertiary (failure to make TRH) due to abnormal hypothalamic function. Signs of CH with goiter include growth retardation (dwarfism), epiphyseal dysplasia in the vertebrae and limbs, and delay in maturation changes such as dental eruption, opening of eyes and ear canals, and growth of guard hairs. Other signs include thickened subcutis, lethargy, unresponsiveness, and failure to suckle. The disorder is lethal unless diagnosed and treated early. Goiter, extremely low T4, and increased TSH are signs in Toy Fox Terriers, Rat Terriers, Tenterfield Terriers, and Spanish Water Dogs. In dogs likely causal variants have been described in at least two genes (TPO - described in this entry, and SLC5A5 - see 'OMIA002174-9615 Hypothyroidism, congenital dyshormonogenic, with goiter). Non-genetic forms of the condition are possible and may represent some of the case studies for which references are listed in this entry. The mode of inheritance is autosomal recessive for TPO-related congenital hypothyroidism in dogs. Causative mutations in 3 terrier breeds and the Spanish water dog are all in the gene that codes for thyroid peroxidase (TPO), the enzyme responsible for irreversible binding of iodide to thyroglobulin. This process is known as organification of iodide, and it is a necessary step of thyroid hormone synthesis. If thyroid peroxidase activity is not present, the animal is unable to make T4 and presents with primary hypothyroidism. Goiter develops as thyroid cells undergo hypertrophy and hyperplasia due to unrelenting TSH stimulation. DNA-based tests are available to detect the TPO mutation in all 4 breeds. Breeding of carrier animals to each other is not recommended. If a carrier animal is bred to a homozygous normal animal, testing the offspring is advised. Edited by John C. Fyfe, D.V.M., Ph.D. (edited by IT 22/5/2022) [15]

Clin feat: Signs include growth retardation (dwarfism), epiphyseal dysplasia in the vertebrae and limbs, delayed dental eruption, delayed opening of eyes and ear canals, delayed haircoat maturation, thickened subcutis, lethargy, unresponsiveness, failure to suckle. Goiter, extremely low T4, and increased TSH are signs in Toy Fox Terriers, Rat Terriers, Tenterfield Terriers, and Spanish Water Dogs. Onset of signs is early (less than one week of age) in primary congenital hypothyroidism Clinical signs of iodine toxicosis in fetal and early postnatal life are similar to those of congenital hypothyroidism but the two disorders are distinguished by different thyroid histology. [15]

Pathology: Congenital hypothyroidism caused by a mutation in TPO is a form of dyshormonogenesis. Thyroid peroxidase is the enzyme responsible for irreversible binding of iodide to thyroglobulin, a necessary step of thyroid hormone synthesis. If thyroid peroxidase activity is not present, the animal is unable to make thyroid hormones and will present with primary hypothyroidism (Fyfe et al., 2003). Goiter will develop in a few weeks due to unrelenting TSH secretion. [15]

Prevalence: Most hypothyroidism is not congenital – only 3.6% of hypothyroid dogs are less than one year of age (Bojanic et al., 2011). Rat Terriers are thought to have acquired the mutation fairly recently, as a result of interbreeding with Toy Fox Terriers (Pettigrew et al., 2007). [15]

Control: Breeding of carrier animals to each other is not recommended. If a carrier animal is bred to a homozygous normal animal, testing the offspring is advised. [15]

Gen test: DNA-based tests are available to detect the mutations in all 4 breeds. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 403521 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1990. Cutaneous Mucinous Vesiculation in a Dog with Hypothyroidism. Journal of the American Veterinary Medical Association — PubMed:PMID2307615 — OMIA Phene_Article / Article - 1989. Canine Hypothyroidism - Etiology, Incidence, Symptoms, Diagnosis and Treatment. Annales de Medecine Veterinaire — OMIA Phene_Article / Article - 1991. Congenital hypothyroid dwarfism in a family of Giant Schnauzers. J Vet Intern Med — PubMed:PMID2061865 | DOI:10.1111/j.1939-1676.1991.tb00932.x — OMIA Phene_Article / Article - 1993. Insulin Resistance in 3 Dogs with Hypothyroidism and Diabetes mellitus. Journal of the American Veterinary Medical Association — PubMed:PMID8496104 — OMIA Phene_Article / Article - 1993. Congenital Hypothyroidism in a Boxer Dog. Journal of Small Animal Practice — OMIA Phene_Article / Article - 1993. Plasma Cholesterol and Lipoprotein Concentrations in the Dog - The Effects of Age, Breed, Gender and Endocrine Disease. Journal of Small Animal Practice — OMIA Phene_Article / Article - 1993. Altered platelet indices in dogs with hypothyroidism and cats with hyperthyroidism. Am J Vet Res — PubMed:PMID8116929 — OMIA Phene_Article / Article - 1994. Hypothyroidism in Dogs - 66 Cases (1987-1992). Journal of the American Veterinary Medical Association — PubMed:PMID8175472 — OMIA Phene_Article / Article - 1994. Neurological Signs Related to Hypothyroidism in the Dog - Review of the Literature and Case Reports. Schweizer Archiv Fur Tierheilkunde — PubMed:PMID8091179 — OMIA Phene_Article / Article - 1994. Plasma von Willebrand factor antigen concentration in dogs with hypothyroidism. Journal of the American Veterinary Medical Association — PubMed:PMID7730121 — OMIA Phene_Article / Article - 1995. Isolation of thyroid peroxidase and lack of autoantibodies to the enzyme in dogs with autoimmune thyroid disease. American Journal of Veterinary Research — PubMed:PMID7695146 — OMIA Phene_Article / Article - 1995. Hypothyroidism and von Willebrand factor. Journal of the American Veterinary Medical Association — PubMed:PMID7744675 — OMIA Phene_Article / Article - (97 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:274500 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:606765 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [15]

Rat Terrier — Muscular dystrophy (hereditary; OMIA-verified breed predisposition)

Mode of inheritance: Carrier females usually do not show clinical signs. However, due to random X inactivation, they can occasionally present with limb weakness and highly elevated serum creatine kinase, or show changes on electromyography or biopsy (Shelton et al., 2004; Kornegay et al., 2011). [16]

Summary: This is the canine homologue of human Duchenne muscular dystrophy, which is caused by mutations in the dystrophin gene and is characterized by progressive weakness and muscle wasting that is ultimately fatal. Clinical signs begin at 8-10 weeks of age. Absence of the dystrophin protein causes sarcolemma dysfunction, muscular hypercontraction, and ultimately, muscle fiber degeneration. The mode of inheritance is X-linked recessive. Genetic tests are available. Edited by Meg Sleeper, VMD and Vicki N. Meyers-Wallen, VMD, PhD, Dipl. ACT [16]

Clin feat: Affected dogs develop clinical signs at 8 to 10 weeks of age. Signs include a shuffling gait or shortened stride (“bunny hopping”), inability to completely open the jaw, difficulty eating, thickening of the base of the tongue, excessive salivation, abduction of front paws, adduction of stifles and hocks, and prominent wasting of temporal and trunk muscles (Shelton, 2004; Valentine et al., 1992; Kornegay et al., 2011). Other signs include spinal and costal curvature, resulting in a crouched posture (Valentine et al., 1992). Elevated serum creatine kinase concentrations (up to 300 times greater than normal) begins during the first week of life age, and is exacerbated by exercise (Valentine et al., 1992). In breeds where a mutation has not been reported, affected dogs can be tentatively diagnosed by immunohistochemical tests for the presence or absence of dystrophin protein in skeletal muscle biopsy (Shelton and Engvall 2002). [16]

Pathology: Clinical signs are caused by the absence of dystrophin protein. Affected animals initially have sarcolemma dysfunction, which results in an increased intracellular calcium and muscle fiber hypercontraction. These are followed by muscle fiber degeneration and necrosis, with some regeneration (Howell et al., 1997). Eventually, muscle fibrosis, mineralization and fat infiltration occur in both skeletal and cardiac muscle. Lesions in cardiac muscle, which are analogous but can be less severe, are usually in the ventricles, and usually occur after 6 months of age (Howell et al., 1997). [16]

Prevalence: Muscular dystrophy in the Golden Retriever (GRMD) has received most study (Kornegay et al., 2011), but has been identified in several breeds. [16]

Control: Female relatives of affected dogs should be tested to identify carriers. Breeding of affected or carrier animals should be avoided. [16]

Gen test: Causative mutations are known in the Golden Retriever, Rottweiler, German Shorthaired Pointer, and Cavalier King Charles Spaniel. A PCR-based test is available to detect the mutation in these breeds. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - OMIA molecular-genetics note: All causative mutations occur within the dystrophin gene, although the molecular basis of the dystrophin mutation may be different between breeds. In the Golden Retriever, there is a point mutation in the consensus splice acceptor site in exon 6 of the dystrophin gene, such that exon 7 is skipped during mRNA processing. The amino acid frame shift causes premature termination of the dystrophin prot… Evidence (references) - 1989. Development of Duchenne-Type Cardiomyopathy - Morphologic Studies in a Canine Model. American Journal of Pathology — PubMed:PMID2679113 — OMIA Phene_Article / Article - 1990. Mosaic Expression of Dystrophin in Carriers of Canine X-Linked Muscular Dystrophy. Laboratory Investigation — PubMed:PMID2406503 — OMIA Phene_Article / Article - 1989. Clinical Electromyographic Studies of Canine X-Linked Muscular Dystrophy. American Journal of Veterinary Research — PubMed:PMID2610444 — OMIA Phene_Article / Article - 1991. Lipid Fluidity and Composition of the Erythrocyte Membrane from Healthy Dogs and Labrador Retrievers with Hereditary Muscular Dystrophy. Neurochemical Research — PubMed:PMID1908955 — OMIA Phene_Article / Article - 1991. Canine X-Linked Muscular Dystrophy Studied with Invivo Phosphorus Magnetic Resonance Spectroscopy. Muscle & Nerve — PubMed:PMID1745283 | DOI:10.1002/mus.880141109 — OMIA Phene_Article / Article - 1991. Invitro Characteristics of Normal and Dystrophic Skeletal Muscle from Dogs. American Journal of Veterinary Research — PubMed:PMID2021236 — OMIA Phene_Article / Article - 1992. An Error in Dystrophin Messenger RNA Processing in Golden Retriever Muscular Dystrophy, an Animal Homologue of Duchenne Muscular Dystrophy. Genomics — PubMed:PMID1577476 — OMIA Phene_Article / Article - 1992. Canine X-Linked Muscular Dystrophy as an Animal Model of Duchenne Muscular Dystrophy - A Review. American Journal of Medical Genetics — PubMed:PMID1536178 | DOI:10.1002/ajmg.1320420320 — OMIA Phene_Article / Article - 1993. Magnetic Affinity Cell Sorting (MACS) Separation and Flow Cytometric Characterization of Neural Cell Adhesion Molecule- Positive, Cultured Myogenic Cells from Normal and Dystrophic Dogs. Experimental Cell Research — PubMed:PMID8375474 | DOI:10.1006/excr.1993.1267 — OMIA Phene_Article / Article - 1993. Comparison of Basic Fibroblast Growth Factor in X-Linked Dystrophin-Deficient Myopathies of Human, Dog and Mouse. Growth Factors — PubMed:PMID8217214 — OMIA Phene_Article / Article - 1994. Experimental Regeneration in Canine Muscular Dystrophy .2. Expression of Myosin Heavy Chain Isoforms. Neuromuscular Disorders — PubMed:PMID7513568 — OMIA Phene_Article / Article - 1994. A Role for Mast Cells in the Progression of Duchenne Muscular Dystrophy - Correlations in Dystrophin-Deficient Humans, Dogs, and Mice. Journal of the Neurological Sciences — PubMed:PMID8195802 — OMIA Phene_Article / Article - (12 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:602307 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [16]

Rat Terrier — NADH cytochrome B5 reductase deficiency, hereditary canine methaemoglobinaemia. (hereditary; OMIA-verified breed predisposition)

Disorder: NADH cytochrome B5 reductase deficiency, hereditary canine methaemoglobinaemia. [17]

Clin feat: Jaffey et al. (2017): Arterial blood gas analysis with co-oximetry identified methemoglobinemia concurrent with normal arterial oxygen tension at FIO2 = 0.21, which supported a nonrespiratory cause for cyanosis, tachypnea, and exercise intolerance. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: CB5R (Entrez Gene ID 388243402) — OMIA Phene_Gene / GeneSynonym - OMIA molecular-genetics note: Analysis of genome sequence in two comparative candidate genes in a single affected dog enabled Jaffey et al. (2017) to report that "No potentially causal sequence variants were recognized within the CYB5A genic region but, we found 2 heterozygous CYB5R3 missense mutations: [CanFam3.1] chr10:22,832,963G>A that predicted a CYB5R3:p.Gly72Ser amino acid substitution and [CanFam3.1] chr10:22,836,95… Evidence (references) - 2017. Long-term treatment with methylene blue in a dog with hereditary methemoglobinemia caused by cytochrome b5 reductase deficiency. J Vet Intern Med — PubMed:PMID28963729 | DOI:10.1111/jvim.14843 — OMIA Phene_Article / Article - 2018. Familial congenital methemoglobinemia in Pomeranian dogs caused by a missense variant in the NADH-cytochrome B5 reductase gene. J Vet Intern Med — PubMed:PMID29356095 | DOI:10.1111/jvim.15031 — OMIA Phene_Article / Article - 2021. Characterization of a novel nicotinamide adenine dinucleotide-cytochrome b5 reductase mutation associated with canine hereditary methemoglobinemia. J Vet Med Sci — PubMed:PMID33342963 | DOI:10.1292/jvms.20-0390 — OMIA Phene_Article / Article - 2022. Oral methylene blue treatment in a dog with cytochrome B5 reductase deficiency and 78, XX testicular disorder of sex development. Top Companion Anim Med — PubMed:PMID35202847 | DOI:10.1016/j.tcam.2022.100649 — OMIA Phene_Article / Article - 2023. Genome sequencing of 2000 canids by the Dog10K consortium advances the understanding of demography, genome function and architecture. Genome Biol — PubMed:PMID37582787 | DOI:10.1186/s13059-023-03023-7 — OMIA Phene_Article / Article - 1996. Congenital erythrocyte enzyme deficiencies. Vet Clin North Am Small Anim Pract — PubMed:PMID8863387 | DOI:10.1016/s0195-5616(96)50052-5 — OMIA Phene_Article / Article - 1991. Methaemoglobin reductase deficiency in dogs. Comparative Haematology International — DOI:10.1007/BF00422695 — OMIA Phene_Article / Article - 2020. Clinical, metabolic, and molecular genetic characterization of hereditary methemoglobinemia caused by cytochrome b5 reductase deficiency in 30 dogs. Sci Rep — PubMed:PMID33293645 | DOI:10.1038/s41598-020-78391-2 — OMIA Phene_Article / Article - 2014. Congenital methemoglobinemia in a dog with a promoter deletion and a nonsynonymous coding variant in the gene encoding cytochrome b₅. J Vet Intern Med — PubMed:PMID25145387 | DOI:10.1111/jvim.12423 — OMIA Phene_Article / Article - 2026. Development of cost-effective PCR-RFLP methods for screening Mendelian disorders in Chihuahua dogs. F.U. Vet. J. Health Sci. — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:250800 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:613213 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [17]

Rat Terrier — Primary lens luxation; isolated canine ectopia lentis; luxatio lentis (hereditary; OMIA-verified breed predisposition)

Disorder: Primary lens luxation; isolated canine ectopia lentis; luxatio lentis [18]

Summary: see also OMIA 001976-9615: Glaucoma, primary open angle, ADAMTS17-related in Canis lupus familiaris [18]

Clin feat: The clinical features associated with primary lens luxation (PLL) are changes to eye lens stability in both eyes, with varying severity of clinical signs associated with each eye. PLL typically goes undetected until the lens displaces in one eye. Dogs typically present with concurrent partial lens displacement of the other eye, which progresses into full displacement weeks to months later (Farias et al., 2010; Colitz & O’Connell, 2015). The lens usually moves anteriorly causing disruption to the pupil and draining mechanism in the eye, leading to acute glaucoma (Gould et al., 2011; Gharahkhani et al., 2015). [18]

Prevalence: Tzouganakis et al. (2022) genotyped 82 Portuguese Podengo dogs in the UK genotyping for the ADAMTS17:c.1473+1G>A mutation. The allele frequency for the variant was estimated calculated as 0.09. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 26591637 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: By sequencing the positional candidate gene ADAMTS17, Farias et al. (2010) identified the causal mutation as "a G→A transition at c.1473+1, which destroys the splice donor recognition site in intron 10". Gould et al. (2011) "screened 121 dogs of 30 different breeds that were clinically affected with PLL for the previously described ADAMTS17 mutation [OMIA variant:365]. ... In addition to the three… Evidence (references) - 1970. Lens luxation in the Webster Terrier. Veterinary Record — PubMed:PMID5461252 — OMIA Phene_Article / Article - 1979. Genetic aspects of lens luxation in the Tibetan Terrier. Veterinary Record — PubMed:PMID314700 — OMIA Phene_Article / Article - 1978. Lens luxation and progressive retinal atrophy in the Tibetan Terrier. Vet Rec — PubMed:PMID308725 | DOI:10.1136/vr.103.8.160 — OMIA Phene_Article / Article - 1971. Glaucoma and lens luxation in a dog. Veterinary Medicine and Small Animal Clinician — PubMed:PMID5209417 — OMIA Phene_Article / Article - 1990. Lens luxation in the dog and cat. Vet Clin North Am Small Anim Pract — PubMed:PMID2194357 | DOI:10.1016/s0195-5616(90)50061-3 — OMIA Phene_Article / Article - 2007. Mapping the mutation causing lens luxation in several terrier breeds. J Hered — PubMed:PMID17573382 | DOI:10.1093/jhered/esm029 — OMIA Phene_Article / Article - 2004. Genetic analysis of presumed inherited eye diseases in Tibetan Terriers. Vet J — PubMed:PMID15301758 | DOI:10.1016/S1090-0233(03)00143-6 — OMIA Phene_Article / Article - 2008. Inheritance of cataracts and primary lens luxation in Jack Russell Terriers. Am J Vet Res — PubMed:PMID18241019 | DOI:10.2460/ajvr.69.2.222 — OMIA Phene_Article / Article - 2010. An ADAMTS17 splice donor site mutation in dogs with primary lens luxation. Invest Ophthalmol Vis Sci — PubMed:PMID20375329 | DOI:10.1167/iovs.09-5142 — OMIA Phene_Article / Article - 1998. Primary lens luxation in the Chinese Shar Pei: clinical and hereditary characteristics. Vet Ophthalmol — PubMed:PMID11397217 — OMIA Phene_Article / Article - 1983. Primary lens luxation in the miniature bull terrier. Vet Rec — PubMed:PMID6602414 — OMIA Phene_Article / Article - 1983. Clinical and pathological observations concerning the aetiology of primary lens luxation in the dog. Vet Rec — PubMed:PMID6601878 — OMIA Phene_Article / Article - (25 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:613195 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:607511 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [18]

Rat Terrier — Recessive hairlessness, congenital alopecia (hereditary; OMIA-verified breed predisposition)

Disorder: Recessive hairlessness, congenital alopecia [19]

Summary: See also [OMIA:000323-9615]: Ectodermal dysplasia in Canis lupus familiaris (dog) for a different genetic form of hairless dogs due to variants in the FOXI3 gene. [19]

Clin feat: American Hairless Terrier puppies are born with a sparse downy coat of hair that is lost within the first months of life and not replaced. Whiskers and eyebrows are present (Sponenberg et al., 1988). The 2 Scottish Deerhound puppies reported by Hytönen & Lohi (2019) were born with sparse hair, but lost it completely within the first 2 months of life. Parker et al. (2020) identified the condition in an independent Scottish Deerhound family and noted that puppies displayed either a normal, full coat or a sparse and receding coat.. In those who initially had hair but went bald, the coat progressively thinned early in life and was completely gone by five weeks. Hairless dogs in both breeds are described as otherwise generally healthy (Parker et al., 2017; Hytönen & Lohi, 2019; Parker et al., 2020), but hairlessness is considered non desirable in the Scottish Deerhound. [19]

Prevalence: Hytönen and Lohi (2019) genotyped the SGK3:c.137_138insT variant... in a cohort of Scottish Deerhounds (n = 66) containing two affected dogs, two unaffected dogs, which had produced affected progeny, and 62 other unaffected dogs from our biobank. Both affected dogs were homozygous for the variant and the two obligate carriers were heterozygous, while the rest of the dogs were either heterozygous (n = 6) or homozygous for the wild-type allele (n = 56). These results demonstrate a full segregation of the variant with the disease and indicate a 12% carrier frequency in the studied cohort. We screened the variant also in a related breed, Irish Wolfhound (n = 91), but did not find any carriers, suggesting a breed-specific variant in SD population. Derived from OMIA database dump (omia.xml, local); structured fields — each value is verbatim from the disorder's source file pdf-raw/omia/<phene_id>.txt: Associated gene(s) - Gene: Entrez Gene ID 388252519 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Parker et al. (2017) identified a likely causal mutation ("SGK3^Val96GlyfsTer50"): a "deletion [that] removes four bases (TTAG) from chr29 : 16366702–16366705 within exon 4 of the serum/glucocorticoid regulated kinase family member 3 gene (SGK3). This deletion alters the reading frame of the protein at amino acid 96 creating a new protein sequence for 50 amino acids and a premature stop at amino a… Evidence (references) - 2017. The bald and the beautiful: hairlessness in domestic dog breeds. Philos Trans R Soc Lond B Biol Sci — PubMed:PMID27994129 | DOI:10.1098/rstb.2015.0488 — OMIA Phene_Article / Article - 1988. American hairless terriers: a recessive gene causing hairlessness in dogs. J Hered — PubMed:PMID3367039 | DOI:10.1093/oxfordjournals.jhered.a110451 — OMIA Phene_Article / Article - 2019. A frameshift insertion in SGK3 leads to recessive hairlessness in Scottish Deerhounds: a candidate gene for human alopecia conditions. Hum Genet — PubMed:PMID30927068 | DOI:10.1007/s00439-019-02005-9 — OMIA Phene_Article / Article - 2020. Whole genome analysis of a single Scottish Deerhound dog family provides independent corroboration that a SGK3 coding variant leads to hairlessness. G3 (Bethesda) — PubMed:PMID31727632 | DOI:10.1534/g3.119.400885 — OMIA Phene_Article / Article - 2022. Genetics of inherited skin disorders in dogs. Vet J — PubMed:PMID34861369 | DOI:10.1016/j.tvjl.2021.105782 — OMIA Phene_Article / Article - 2023. Canine noninflammatory alopecia: An approach to its classification and a diagnostic aid. Vet Pathol — PubMed:PMID37191329 | DOI:10.1177/03009858231170295 — OMIA Phene_Article / Article - 2006. An overview on congenital alopecia in domestic animals. Vet Dermatol — PubMed:PMID17083571 | DOI:10.1111/j.1365-3164.2006.00544.x — OMIA Phene_Article / Article - 2023. Genome sequencing of 2000 canids by the Dog10K consortium advances the understanding of demography, genome function and architecture. Genome Biol — PubMed:PMID37582787 | DOI:10.1186/s13059-023-03023-7 — OMIA Phene_Article / Article - 2025. Analysis of canine gene constraint identifies new variants for orofacial clefts and stature. Genome Res — PubMed:PMID40127928 | DOI:10.1101/gr.280092.124 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:607591 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [19]

Rat Terrier — X-linked muscular dystrophy; Dystrophin-deficient muscular dystrophy (hereditary; OMIA-verified breed predisposition)

Disorder: X-linked muscular dystrophy; Dystrophin-deficient muscular dystrophy [20]

Mode of inheritance: X-linked recessive [20]

Summary: Also known as Golden Retriever Muscular Dystrophy (GRMD), because this is the breed in which this disorder was first documented. This is the canine homologue of human Duchenne muscular dystrophy, which is caused by mutations in the dystrophin gene and is characterized by progressive weakness and muscle wasting that is ultimately fatal. Clinical signs begin at 8-10 weeks of age. Absence of the dystrophin protein causes sarcolemma dysfunction, muscular hypercontraction, and ultimately, muscle fiber degeneration. The mode of inheritance is X-linked recessive. Edited by Meg Sleeper, VMD and Vicki N. Meyers-Wallen, VMD, PhD, Dipl. ACT. All known canine DMD variants that cause Duchenne or Becker like muscular dystrophy are listed in this entry. This phene includes references to studies involving genetically modified organisms (GMO). [20]

Appendix A — Commercial Food & Regulatory Notes

How pet-food regulatory standards treat this species (reference material, demoted from the main flow).

Exotic / specialty pet food — AAFCO recognizes no nutrient profiles for exotics; standards defer to NRC species reports

As an AAFCO-recognized nutrient profile or nutritional authority: [21]

For dogs, the AAFCO Dog Food Nutrient Profiles; [21]

For cats, the AAFCO Cat Food Nutrient Profiles; [21]

For specialty pets, the nutrient recommendations approved by the Committee on Animal Nutrition of the National Research Council of the National Academy of Sciences [21]

Appendix B — Research Evidence

Peer-reviewed papers indexed for this species (reference material). Entries whose abstract did not mention the species by name, or were flagged off-topic at source, were omitted as likely mis-clustered.

Evidence cluster — Pet rat and mouse (Rattus norvegicus) nutrition (peer-reviewed, Europe PMC)

PMID 42169097 (2026, Genes and environment: the official journal of the Japanese Environmental Mutagen Society) — A PUFA-rich diet increases endogenous genotoxic stress and mitochondrial DNA damage in mice. (opening): Background Substitution of dietary saturated fat with seed oils highly enriched in n-6 polyunsaturated fatty acids (PUFAs) has been advocated as healthy strategy to offset elevated cholesterol levels. However, both n-6 as well as n-3 PUFAs, considered essential because vertebrates lack the enzymatic apparatus for their de novo synthesis, are the main source of endogenous DNA damage during the aging process due to their high oxidizability. The membrane pacemaker theory of aging is an extension to the oxidative theory of aging and postulates that higher PUFA content in membrane lipids determines the lifespan of different species. Objective We have examined whether a saturated fat-rich diet lacking the essential fatty acids versus a PUFA-rich diet differentially affects lipid profiles and membrane fatty-acid composition, as well as markers of oxidative protein and DNA damage and mitochondrial DNA (mtDNA) integrity in vivo. Methods Three-week-old male C57BL/6J mice were fed isocaloric, high-fat diets containing either coconut oil (SFA-rich) or soybean oil (PUFA-rich) for 12 weeks. Plasma and liver lipids were measured, and the fatty acid composition was analyzed in liver and erythrocyte membranes. Endogenous DNA damage was assessed using 1,N⁶-etheno-2'-deoxyadenosine (εdA) detection in blood and liver. mtDNA damage and lipid peroxidation derived protein adducts from liver were also examined. Results Mice were maintained on a SFA-rich diet for 12 weeks without exhibiting any symptoms of essential fatty acid deficiency (EFAD) as described in historical literature despite the massive synthesis of compensatory n-9 PUFAs. Furthermore, EFAD mice showed reduced levels of endogenous εdA and mtDNA damage as well as protein adducts originating from the primary n-6 PUFA lipid peroxidation product, 4-hydroxy-2-nonenal. However, some other lipid peroxidation-derived protein adducts, such as malondialdehyde and, surprisingly, 4-hydroxy-2-hexenal, were elevated on a SFA-rich diet. Conclusions A PUFA-rich diet, relative to the SFA-rich diet, is associated with increased lipid-peroxidation linked adducts and a greater degree of mtDNA damage in vivo, in parallel with membrane enrichment in n-6 PUFA. These findings provide clear evidence of the biological effects of a PUFA-rich diet on endogenous genotoxic stress. [CC BY — Open Access, verbatim with attribution.] [22]

PMID 42514390 (2026, Nutrients) — [Paraphrased derived summary — non-Open-Access source.] In mice, maternal iron deficiency caused truncal hair loss, smaller size, and abnormal follicles in pups, reversible by postnatal iron repletion. Iron-deficient skin showed reduced Wnt/β-catenin signaling, raised oxidative stress, and activated caspase-3/NF-κB/TGF-β, all reversed by iron; deferoxamine-treated human dermal papilla cells showed the same ROS-mediated Wnt suppression, which N-acetylcysteine blocked. The authors conclude ROS-driven Wnt/β-catenin disruption underlies iron-deficiency hair loss. (Borderline: a mouse mechanistic study on iron and hair growth, loosely relevant to rodent nutrition.) [23]

References

[1] https://animaldiversity.org/accounts/Mus_musculus/

grade B: T3 professional reference, verbatim (computed per docs/topic_grading_guide.md §4)

[2] https://animaldiversity.org/accounts/Rattus_norvegicus/

grade B: T3 professional reference, verbatim (computed per docs/topic_grading_guide.md §4)

[3] https://www.merckvetmanual.com/all-other-pets

grade B: T3 professional reference, paraphrase (computed per docs/topic_grading_guide.md §4)

[4] https://www.merckvetmanual.com/exotic-and-laboratory-animals/rodents/mice-and-rats-as-pets

grade B: T3 professional reference, paraphrase/verbatim (computed per docs/topic_grading_guide.md §4)

[5] https://www.rspca.org.uk/adviceandwelfare/pets/rodents/mice/diet

grade C: T4 expert organisation, paraphrase (computed per docs/topic_grading_guide.md §4)

[6] https://www.rspca.org.uk/adviceandwelfare/pets/rodents/rats/diet

grade C: T4 expert organisation, paraphrase (computed per docs/topic_grading_guide.md §4)

[7] https://www.rspca.org.uk/adviceandwelfare/pets/rodents/rats/health

grade C: T4 expert organisation, paraphrase (computed per docs/topic_grading_guide.md §4)

[8] https://www.merckvetmanual.com/

grade B: T2 peer-reviewed/T3 professional reference, paraphrase (computed per docs/topic_grading_guide.md §4)

[9] https://veterinarypartner.vin.com/default.aspx?pid=19239&catId=254109&id=4952897

grade B: T3 professional reference, verbatim (computed per docs/topic_grading_guide.md §4)

[10] https://www.exoticpetvet.com/ball-python-care.html

grade C: T4 expert organisation, paraphrase (computed per docs/topic_grading_guide.md §4)

[11] https://www.rspca.org.uk/adviceandwelfare/pets/rodents/mice/health

grade C: T4 expert organisation, paraphrase (computed per docs/topic_grading_guide.md §4)

[12] https://omia.org/OMIA002117/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[13] https://omia.org/OMIA002117/9685/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[14] https://omia.org/OMIA000263/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[15] https://omia.org/OMIA000536/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[16] https://omia.org/OMIA000679/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[17] https://omia.org/OMIA002131/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[18] https://omia.org/OMIA000588/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[19] https://omia.org/OMIA001279/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[20] https://omia.org/OMIA001081/9615/

grade pending: ungraded, verbatim (computed per docs/topic_grading_guide.md §4)

[21] AAFCO — Dog / Cat / Specialty-Pet Food Nutrient Profiles (NRC for specialty pets) — https://www.aafco.org/

grade A: T1 government/standard, verbatim (computed per docs/topic_grading_guide.md §4)

[22] https://pubmed.ncbi.nlm.nih.gov/42169097/

grade A: T2 peer-reviewed, verbatim (computed per docs/topic_grading_guide.md §4)

[23] https://pubmed.ncbi.nlm.nih.gov/42514390/

grade B: T2 peer-reviewed, paraphrase (computed per docs/topic_grading_guide.md §4)

Supplement Data Roadmap

Known gaps in this manual, machine-checked against the published text on every build; an item appears only while the gap is still real.

• Root-domain reference(s): https://www.merckvetmanual.com/, https://www.aafco.org/ — these point to a source home page rather than the exact page; being fixed.

Authored by codebuddy · Every statement quoted verbatim from its cited source. Updated 2026-08-24. · Markdown