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Rabbit — 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 rabbit, 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. Species-Specific Health
17. Appendix A — Commercial Food & Regulatory Notes
18. Appendix B — Research Evidence

Species Profile

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

Domestic rabbit (Oryctolagus cuniculus) — species profile (taxonomy, geographic range, habitat, physical description, behavior, wild diet, reproduction, lifespan)

Oryctolagus cuniculus, also called a European, an Old World, or a domestic rabbit, is the only species in its genus. [1]

cuniculus may be found worldwide. [1]

cuniculus weigh between 1.5 and 2.5 kg, and are from 38 to 50 cm long. [1]

Domestic individuals may be larger. [1]

The coat is generally grayish, with black and brown (and sometimes red) sprinkled throughout. [1]

Gardeners know them to eat lettuce, cabbage, root vegetables, and grains. [1]

cuniculus is one of several rabbit species that are known to reingest feces (coprophagy) to obtain extra nourishment from their food. [1]

The species has a very large caecum, in which bacterial fermentation of otherwise indigestible material occurs. [1]

Domestic rabbits can live to be up to nine years old. [1]

Rabbit summary facts — life expectancy 8-12 years, adult weight 1-8 kg, gestation 30-33 days, litter 4-12 kits, weaning 5-6 weeks (Welsh Government code)

Males are called bucks and females are called does. Baby rabbits are called kits. [2]

Prey species have many predators e.g. owls, buzzards, foxes, dogs and cats. [2]

Life expectancy: 8 to 12 years (can be longer). [2]

Adult body weight: 1 to 8 Kg (this varies with breed and sex). [2]

Most litters will be born between 30 to 33 days. Litter size: 4 to 12 (average = 7) kits in a litter. The size of the litter depends on the breed of the rabbit. Generally smaller dwarf breeds will have litters of 2-4, medium breeds will have litters of 4-6, and larger breeds will have litters of 6-10. [2]

[Paraphrased derived summary — non-Open-Access source.] Rabbits are classified as lagomorphs, not rodents. [3]

Life-Stage Care

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

Rabbit — life-stage care (young/juvenile, adult, senior/older, growth & aging)

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

Kits are usually weaned between 4 and 8 weeks of age. [4]

Rabbits are generally considered senior from about 5 to 8 years of age. [4]

Rabbits suit older children who can handle them gently, with adults prepared to take over care. [4]

No child should be the sole owner of any animal — adult supervision is always recommended. [4]

A rabbit's lifespan depends largely on how healthy and well cared for it is. [4]

Because rabbits live a long time, they are a major commitment needing quality care, routine veterinary visits and constant attention. [4]

Weaning age 5-6 weeks. [2]

[Paraphrased derived summary — non-Open-Access source.] In a safe, stimulating environment with a nutritious diet and plenty of company, a rabbit typically lives 8 to 12 years, though some live longer. [4]

Owning and caring for a rabbit is great fun and very rewarding, but it is also a big responsibility and a long-term caring and financial commitment as they normally live for 7-12 years. [5]

Is this pet right for you?

• A 7–12 year commitment: rabbits normally live 7–12 years, so this is a long-term caring and financial commitment, with routine veterinary visits. [5] [4]
• They need company: rabbits are social animals and should ideally live with a neutered rabbit companion — a neutered male/female pair works best. Companionship is nearly as important to them as a good diet, yet about 42% of UK pet rabbits were kept alone in 2024. [5] [4]
• They need space: the enclosure must let a rabbit take at least three hops from end to end (about 150–180 cm for an average adult) and stand fully upright on its back legs without its ears touching the top. [5]
• They need your time daily: a rabbit should have the opportunity to interact with its owner for several hours a day. [5]
• Children: rabbits suit older children who can handle them gently; no child should be the sole owner of any animal — an adult must stay responsible. [4]
• They are not rodents: rabbits are lagomorphs, with continuously growing teeth and a fibre-driven digestive system — that biology shapes almost everything in this manual. [6] [5]

Daily & Weekly Care Checklist

Every day:

• Hay and/or grass available at all times — at least a bundle a day as big as the rabbit itself; fibre keeps the gut moving and wears down the teeth. [7] [5]
• Fresh water at all times, in a bowl and/or a metal-tipped bottle. [5]
• A large handful of safe leafy greens (ideally 5–6 types) and a small measure of pellets — fruit and root vegetables (carrots included) only as occasional treats. [7]
• Watch your rabbit at least once a day: behaving normally, eating and drinking its usual amount. [5]
• Check underneath and around the bottom for droppings — at least twice daily in warm weather because of fly-strike risk. [5]
• Clean the living area daily; litter/toilet areas daily. [5]
• Daily access to the exercise run, plus interaction with you. [5]

Every week:

• Clean the whole enclosure thoroughly at least once a week. [5]
• Weigh your rabbit and check body condition — you should easily be able to feel its ribs. [5]
• Groom short-coated rabbits weekly; long-haired rabbits need grooming at least once a day. [5]

Nutrition

The short version: unlimited hay and grass (about 85% of the diet), a daily handful of leafy greens (about 10%), a small measure of pellets (about 5%), water always. [7] Avoid muesli-style mixes and never change the diet suddenly — both are linked to dental and digestive disease. [7] The sourced details follow.

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

Nutrition of rabbits (Merck): hay, cecotrophs, calcium, fiber

Rabbits are small herbivores with specialized feeding needs and digestive systems. They are selective eaters and choose nutrient-rich leaves and new plant shoots over mature plant material that is higher in fiber. [8]

Cecotroph ingestion is highest when rabbits are fed a diet high in nondigestible fiber. This reingested material provides microbial protein, vitamins (including all the B vitamins needed), and small quantities of volatile fatty acids, which are essential in rabbit nutrition. [8]

Reducing the calcium level to 0.4%–0.5% of the diet for nonlactating rabbits helps reduce these problems. This can be accomplished by feeding pelleted diets with a timothy hay base. [8]

A rabbit should always have an unlimited supply of hay, because they frequently need to nibble on it to keep peristalsis active. [8]

Rabbit diet — DAERA welfare code: hay-based diet, safe greens, foods to avoid, water, weight

Rabbits are herbivores, they need a diet that is high in fibre to wear down their continuously growing teeth, keep their intestines functioning properly and help prevent them from becoming bored. [5]

A rabbit’s daily diet should consist mainly of large quantities of hay or dried or fresh grass that will provide the necessary fibre for the rabbit. [5]

Rabbits should have access to hay or dried or fresh grass throughout the day and night. [5]

Green plants and a small amount of high quality specialist rabbit food such as extruded nuggets or high quality pellets should make up the remainder of your rabbit’s diet. [5]

Lawn mower clippings should not be fed as they can contain metal slivers and oil which can be harmful. [5]

Root vegetables can be given occasionally but, as carrots are especially high in sugar, you should use the carrot tops and only a little of the carrot itself. [5]

All fruit should be regarded as a treat item and fed in limited quantities as fruit is high in sugar and can lead to gastro-intestinal disturbance as well as causing dental problems. [5]

High-fat or high-carbohydrate foodstuffs should be avoided completely including commercial ‘rabbit treats’, bread, milk, breakfast cereal, nuts, seeds and chocolate. [5]

Do not make any sudden changes to your rabbit’s diet as this could upset its digestive system and make it very ill. [5]

Examples of suitable green plants include broccoli, cabbage, parsley, watercress, celery leaves and kale. [5]

Safe wild plants include chickweed, bramble, raspberry, blackberry and strawberry leaves and dandelion. [5]

Your rabbit must always have access to fresh water in either a bowl and/or a metal-tipped bottle. [5]

Ideally you should easily be able to feel its ribs. Adjust how much you feed your rabbit to make sure that it does not become over or underweight. [5]

Rabbits should be weighed regularly to assess any increases or decreases in weight as rabbits that are over or under weight may suffer. [5]

Rabbit diet — feeding ratio, safe greens and foods to avoid

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

A rabbit's diet should be about 85% hay and fresh grass, 10% leafy green vegetables and herbs, and 5% pellets. [7]

Pet rabbits should always have good-quality hay and/or grass available to eat as much as they want — at least one bundle every day, as big as the rabbit itself. [7]

Rabbits need a large handful of safe, washed leafy green vegetables, herbs and weeds daily, ideally five to six different types; introduce new greens gradually in small amounts to avoid stomach upsets. [7]

Safe leafy greens include spinach, celery, cabbage, kale, broccoli, rosemary, parsley, mint and dandelion leaves. [7]

Fruit and root vegetables (e.g. carrots) should only be given in small amounts as an occasional treat. [7]

Muesli-style foods are not recommended for rabbits: they can cause serious dental disease and digestive problems and can lead to obesity. [7]

Sudden changes in diet can upset a rabbit's digestive system, so any change to a healthier diet should be made gradually over several weeks. [7]

Fresh, clean drinking water must be available to rabbits at all times. [7]

Rabbit nutrition — calcium metabolism and the risk of diet-related hypercalciuria

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

Rabbits handle calcium differently from many mammals, so their normal blood calcium can reach about 16 mg/dL. [6]

Rabbit nutrition — small herbivores with specialized digestive systems; fiber drives GI motility and dental wear

fiber is important for stimulating GI motility, preventing behavioral problems (eg, fur chewing) [8]

Oryctolagus cuniculus is a generalized herbivore, eating a diverse diet of grasses, leaves, buds, tree bark, and roots. [1]

Specialist have continuously growing teeth, produce soft droppings (caecotrophs) which they normally eat and hard waste droppings. [2]

A constant supply of fresh water needs to be provided at all times. [5]

[Paraphrased derived summary — non-Open-Access source.] Indigestible fibre supports gut motility, prevents behaviours like fur-chewing, wears down teeth, and stimulates appetite and caecotroph intake; pet rabbits are generally fed up to 20% crude fibre including about 12.5% indigestible fibre. [6]

foraging for food and having suitable objects to play with are excellent ways of ensuring a rabbit is kept properly occupied [5]

[Paraphrased derived summary — non-Open-Access source.] Rabbits have an unusual digestive system that produces special droppings called caecotrophs. [4]

[Paraphrased derived summary — non-Open-Access source.] Rabbit calcium metabolism yields higher normal blood calcium (up to 16 mg/dL) and a wider range than in other animals, which can prompt a false diagnosis of hypercalcemia. [3]

Husbandry

The home is a resting area permanently attached to an exercise run, with at least one hiding place per rabbit available 24 hours a day. [5] Space dimensions, cleaning rhythm and hazard-proofing follow.

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

Rabbit environment & housing — DAERA welfare code: space, hiding places, cleaning, hazards

The resting area should ideally be permanently attached to an exercise area to which the rabbit has free access at all times. [5]

be high enough for it to stand up fully stretched on its back legs without its ears touching the top [5]

As a guide, your rabbit should be able to take three hops from one end to another as an absolute minimum. For a fully grown average breed of rabbit this can equate to around 150/180cms in length and 60cms in height. [5]

Your rabbit should have daily access to an exercise area (the run). [5]

The run should be as large as possible to allow your rabbit to stretch upwards to full height and to run, as opposed to just hop. [5]

Rabbits should have 24 hour access to appropriate hiding places where they can run if they feel afraid, stressed, unwell, or simply want to be on their own for a while. [5]

There should always be at least the same number of hiding places in any enclosure as there are animals. [5]

Your rabbit’s living area should be cleaned daily. [5]

The entire living area should be cleaned thoroughly at least once a week [5]

Bedding should be provided to give your rabbit extra insulation, somewhere to hide and something to nibble on. It should be clean and dry and should also be safe for your rabbit to eat. Examples include hay and straw. [5]

Use of wood shavings as bedding material should be avoided. [5]

Wood shavings containing pine or clay based cat litters should not be used as they can be hazardous to rabbits. [5]

If let loose indoors particular attention should be given to restricting access to areas where there are electrical cables which rabbits may chew through. [5]

Rabbits should not be left unattended in a car or other vehicle in warm weather. This can be life threatening [5]

Household cleaning materials including liquids, medicines or other products intended for people or other animals should also be kept out of reach. You should contact your vet promptly if you think your rabbit has come into contact with anything that could harm it. [5]

Rabbits can be kept outdoors all year round but ideally their resting area should be brought into a shed or unused garage with natural light and ventilation for the winter months or otherwise protected from bad weather [5]

Rabbit environment — heat sensitivity; water-bowl intake higher than bottle

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

Rabbits are heat-sensitive; hot, humid conditions or poor ventilation (in hutches or during transport) can kill many rabbits, especially pregnant does. They need free access to cool water, and when controllable the optimum is 50–70°F (15.5–21°C), 40–60% relative humidity, and 10–20 air changes/hour. [6]

Rabbits drink significantly more from a bowl than from a cage bottle; research shows bowl water intake is markedly higher. [6]

Rabbit housing & daily care — two-compartment hutch, 'hop three times' size guide, daily run access, transport, daily attendance (Welsh Government code)

Your rabbit’s living area should have at least two compartments: a darkened sheltered area for sleeping and another for eating/relaxing. It should be a comfortable, dry, clean, well-ventilated and draught-free area where your rabbit will feel safe and be protected from predators and extremes of weather and temperature. [2]

The living area should be big enough for it to lie down and stretch out comfortably in all directions, high enough for your rabbit to stand up on its back legs without its ears touching the top, and it should be long enough for your rabbit to move around, feed and drink. As a guide, it should be able to hop three times from one end to another as a minimum. [2]

Your rabbit should have daily access to a safe and secure run where it can run and jump. The run should be as large as possible so that your rabbit can stretch upwards to its full height and run, not just hop. This area should provide protection from predators and extremes of weather and temperature as well as areas where your rabbit can hide if it wants to. [2]

Make sure your rabbit is transported safely. On long journeys, you should regularly offer food, water and a litter tray within the safe confnes of the stationary vehicle. Rabbits should not be left unattended in a vehicle in warm weather. This can be life threatening. [2]

You must arrange for your rabbit to be cared for by a suitable person if you are away from home. A responsible person must attend to your rabbit every single day. [2]

Rabbit housing — durable wire caging; hay/straw bedding; aquariums unsuitable

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

Rabbits chew, so cages must be durable and easy to sanitise; all-wire cages using at least 12-gauge wire (16-gauge recommended for the floor to bear the rabbit's weight) are preferred, and aquariums are unsuitable because of poor air circulation. [6]

Pens need a non-slip floor and can be bedded with straw or shredded paper under straw or hay for absorbency; shavings or sawdust are poorer choices because the dust irritates the airways. [6]

Rabbits are active and need room to hop, run, jump, dig and stretch out fully; for a medium-sized rabbit the minimum living area (shelter plus exercise space) should be no smaller than 3 m × 2 m and 1 m high. [6]

If litter trays are provided, line them with newspaper, hay or straw, shredded paper, and/or paper-based non-clumping litter; clumping litters should be avoided. [6]

When cleaning the enclosure, return a small amount of used bedding so the area keeps a familiar smell. [6]

[Paraphrased derived summary — non-Open-Access source.] A secure shed, hut or playhouse with an attached run makes a suitable home. [4]

[Paraphrased derived summary — non-Open-Access source.] The whole enclosure should be cleaned about once a week. [4]

[Paraphrased derived summary — non-Open-Access source.] If using litter trays, fill them with newspaper, hay, straw, shredded paper or a paper-based non-clumping, non-expanding cat litter. [4]

[Paraphrased derived summary — non-Open-Access source.] Feed hoppers are best made of sheet metal with holes or a screen in the bottom to remove fines (small broken feed particles). [3]

[Paraphrased derived summary — non-Open-Access source.] Poor sanitation leads to disease and death, so cleaning and sanitizing must be constant. [3]

Behavior & Training

Rabbits are social, territorial and trainable with reward-based methods. [4] When lifting, place one hand under the chest and the other under the bottom, holding the rabbit close; never shout at or punish a rabbit. [5] Companionship rules and body-language signals follow.

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

Rabbit behaviour & company — DAERA welfare code: companionship, handling, stress, enrichment

Rabbits are social animals and should ideally be kept with an appropriate companion such as another neutered rabbit, preferably a male/female neutered pair. [5]

An appropriate companion is a neutered rabbit of a similar size and opposite sex. Rabbits of the same sex are more likely to fight. [5]

Rabbits may accept a guinea pig as a companion, but this is not advised. The powerful hind legs of even a small rabbit could cause serious internal injury to a guinea pig that could be fatal. [5]

A rabbit, whether kept alone or with other rabbits, should have the opportunity to interact with its owner for several hours a day. [5]

To lift a rabbit place one hand under the rabbit’s chest and the other hand under its bottom. Hold the rabbit close so that it feels secure and it is prevented from falling. [5]

Never shout at or punish your rabbit. It is unlikely to understand and can become more nervous or scared. [5]

A rabbit with nothing to do will quickly become unhealthy, unhappy and possibly aggressive. [5]

the way each rabbit behaves is largely influenced by experiences during the first few weeks of life. [5]

A prospective owner should be satisfied that the rabbit they are thinking of getting is old enough to live without help from its mother, which is when it is over 8 weeks of age. [5]

Never leave your rabbit alone with a cat or dog, even if they are familiar with each other. [5]

If you see any of these signs of stress you should contact your vet promptly. [5]

rabbits kept in cramped conditions will fight [5]

Rabbit natural history & behaviour — prey-species origins, continuously growing teeth, social groups, scent marking, fear response (Welsh Government code)

All of our rabbits are descended from the wild European rabbit, whose Latin name Oryctolagus cuniculus means ‘Hare-like digger of underground passages’. This name describes the rabbit’s basic behaviour of living underground in a burrow, emerging on the surface in the evening and returning below ground soon after daybreak. Rabbits spend much of their time in dark or low light conditions. They do not like bright lights. [2]

Rabbits eat grasses and herbs. They have adapted in the dry landscape of southern Spain, an area of hot summers and little rainfall, with poor quality herbage. Their teeth and digestive system are designed for this poor quality, high fbre food. They slice the grass stems with their specially shaped, sharp, front teeth and grind them with their back teeth. Their teeth grow continuously throughout their lives. Rabbits spend about 70% of the time they are awake eating. [2]

Rabbits are social creatures, living in stable groups of between 2 and 10 individuals. Groups of two are usually a male and female, but females normally outnumber males in larger groups. The close bonds that form between individuals within a group and the companionship they enjoy helps the rabbits feel safe and secure and gives them and their offspring the best chance of survival. [2]

Rabbits show very subtle changes in behaviour to indicate when they are in pain or are frightened. Often these are misunderstood or not even noticed by owners. [2]

Rabbits rub their chin over objects and other rabbits, but this can also include their owners and visitors. Rabbits of both sexes do this, though males more so, and can have quite damp and sticky chins caused by the secretions from the scent gland located there. Chin marking denotes territory and also acts as a means of identifying members of the rabbit’s own group. It acts to both reassure the rabbit that it is amongst friends and on home territory and to deter intruders. [2]

They also create latrines, and it is this natural behaviour that makes rabbits so easy to housetrain. [2]

Rabbits are animals that are very easily frightened. They can also remember what has frightened them. [2]

A common situation where this may occur, is a rabbit that is scared of being picked up. It will attempt to escape by running round its living area; it may then turn around and bite because it cannot get away. [2]

Rabbit — behavior & socialization (companionship, play, bonding, preventing boredom/behavior problems)

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

Rabbits are territorial and form complex social hierarchies, with some individuals becoming dominant over others. [4]

Rabbits are intelligent and, like dogs, can learn to respond to cues through positive reward-based training. [4]

Boxing — a rabbit rearing on its hind legs, ears up, swatting with its front paws and sometimes growling — signals aggression or distress. [4]

Rabbits are highly social, yet in 2024 about 42% of pet rabbits in the UK were kept alone. [4]

A properly bonded pair of rabbits usually become companions quickly; without a partner they can develop abnormal behaviours. [4]

Companionship is nearly as important to rabbits as a good diet. [4]

Pet rabbits can also form companion bonds with the people who care for them. [4]

A rabbit that must live alone (only on veterinary advice) still needs daily interaction with people. [4]

European rabbits are gregarious, territorial animals. [1]

[Paraphrased derived summary — non-Open-Access source.] Rabbits are social and need companionship; they should be kept with at least one other friendly, compatible rabbit. [6]

[Paraphrased derived summary — non-Open-Access source.] A rabbit's behaviour varies with age, personality and past experience, but frightened or painful rabbits commonly develop habits such as aggression or hiding. [4]

[Paraphrased derived summary — non-Open-Access source.] A gentle nip from a rabbit is usually not aggression — it may be an attempt to groom a person or to get their attention. [4]

[Paraphrased derived summary — non-Open-Access source.] Stress or fear in rabbits can show as bar-chewing, over-grooming, changes in feeding or toileting, or repeatedly circling the enclosure. [4]

[Paraphrased derived summary — non-Open-Access source.] Holding a rabbit on its back (tonic immobility) is often mistaken for relaxation but is actually a fear response. [4]

Enrichment & Exercise

Toys, foraging, hiding and exercise to prevent boredom.

Rabbit — environmental enrichment & exercise (toys, foraging, hiding, exercise, preventing boredom)

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

Hay is essential for rabbit dental health because constant side-to-side chewing of it wears down their continuously growing teeth and prevents problems. [4]

Rabbits can be taught simple tricks such as retrieving a toy; a relaxed rabbit may make a soft purring sound by gently chattering its teeth, although teeth grinding can instead indicate pain. [4]

A rabbit's front teeth grow continuously at about 3 mm per week, so constant chewing of hay is needed to wear them down. [4]

Like people, rabbits need stimulation and activities to enrich their daily lives. [4]

When to call a vet NOW

Rabbits are prey animals: they often do not look ill until they are very unwell, and they can become worse very quickly — act promptly. [5]

• Not eating or drinking, or any sudden change in eating habits — contact a vet immediately; this can signal serious illness, and a stopped gut (GI stasis) is an emergency. [7] [9]
• Maggots on the rabbit, or a dirty/sticky bottom in warm weather — fly strike can kill within hours; call a vet immediately. [5]
• Diarrhoea or abnormal droppings — vet promptly; if minor changes do not return to normal within 24 hours, see a vet. [7] [5]
• Stops eating hay or grass — have a vet check for underlying problems such as dental disease. [7]
• Eating less during any diet change — take the rabbit to a vet immediately. [7]
• Suspected contact with a poisonous plant or a household chemical — contact your vet promptly. [5]

Prevention beats emergencies: vaccinate against myxomatosis and VHD (both usually fatal), keep teeth on a hay-based diet, and neuter — unspayed females over three years old face a uterine-tumour incidence that may reach about 80%. [5] [4]

Health & Disease

The recurring themes below: teeth that grow about 3 mm a week and depend on hay, a gut that depends on fibre (stasis is the classic emergency), and fly strike in warm weather. [4] [9] [5]

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

Rabbit dental disease — continuously growing (elodont) teeth predispose to malocclusion and abscesses

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

Dental disease in rabbits may appear as drooling (slobbers), teeth grinding, or loss of appetite (anorexia). [9]

Sometimes the cheek teeth overgrow and cause serious tongue or cheek (buccal) sores. [9]

Dental abscesses can form as a result of foreign material lodged in the mouth. [9]

Rabbit emergency signs — when to contact a vet

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

If a rabbit's eating or drinking habits change, contact a vet immediately, as this can signal serious illness. [7]

Monitor droppings at least twice daily; if they are soft or runny (diarrhoea) or otherwise abnormal, book a vet appointment as soon as possible, and if minor changes do not return to normal within 24 hours, see a vet. [7]

If a rabbit stops eating hay or grass, have a vet check for underlying health problems, as dental disease can make chewing uncomfortable. [7]

During any diet change, if the rabbit is not eating enough, take it to a vet immediately. [7]

Sticky droppings around the bottom can signal flystrike risk and need a vet check. [7]

Rabbit gastrointestinal (GI) stasis — a species-specific, fiber-dependent emergency

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

Once GI stasis stops the stomach from emptying, gas builds up and causes further abdominal distension and pain (a colic-like picture). [9]

Preventing GI stasis is the best approach: feed a high-fibre diet, avoid stress and obesity, provide environmental enrichment, and groom daily to remove loose hair. [9]

A high-fibre diet forms a fibre mesh that stops gut contents becoming too compact, helping ingested hair pass through more easily. [9]

Rabbit health & welfare — DAERA welfare code: daily/weekly checks, fly strike, vaccination, grooming, neutering

there are vaccines that are designed to protect rabbits from diseases such as Myxomatosis and Viral Haemorrhagic Disease (VHD). Both of these diseases are usually fatal and your rabbit should be vaccinated. [5]

Prevent your rabbit having contact with wild rabbits or areas where wild rabbits have been. [5]

Rabbits are prey animals and, to avoid attracting attention from predators, they often do not look ill until they are very unwell. They can become worse very quickly, so you need to act promptly. [5]

You should consult a vet if your rabbit shows any signs of illness or a change in behaviour. [5]

During warm weather, rabbits should be checked at least twice daily underneath and around the bottom for droppings. Having a dirty bottom can increase the risk of a condition known as fly strike which can kill a rabbit in a matter of hours. [5]

You should contact your vet immediately if you find maggots on your rabbit. [5]

watch your rabbit at least once a day to ensure it is behaving normally as well as eating and drinking its usual amount. [5]

A rabbit with diarrhoea should be seen by a vet promptly. [5]

it is a good idea to check your rabbit’s weight at least once a week. Loss of weight may indicate a dental or other health problem. [5]

Only a veterinarian can check a rabbit’s back teeth and these should be done at least once a year. [5]

Only a vet should correct misaligned or overgrown teeth. [5]

Dental problems can cause a poor appetite, runny eyes, a wet chin or drooling. If your rabbit is showing any of these symptoms you should take it to see your vet promptly. [5]

Rabbit pododermatitis / sore hocks (ulcerative; overweight on hard surfaces predisposed)

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

Pododermatitis ("sore hocks") affects the footpads; overweight rabbits kept on hard surfaces are especially prone to it. [9]

The problem involves the sole (plantar) surface of the hind-foot metatarsals and, less often, the palm (volar) side of the front-foot metacarpophalangeal area — not the hock joint itself. [9]

Rabbit vaccines: RHDV2 and myxomatosis, with country-availability differences (Merck Veterinary Manual; PetMD)

RHDV2 (rabbit hemorrhagic disease virus, a calicivirus) is a fatal disease of rabbits and was first detected in the United States in 2018; as of 2022 it had been documented in 23 states. [10]

In the USA there are no FDA-approved vaccines for RHDV2, but the USDA granted emergency use of the RHDV2 vaccine for pet rabbits in 2021, and the European vaccines can be used. [10]

Vaccines protective against RHDV1 and RHDV2 are available in several countries, and pet rabbits are typically vaccinated at 10 weeks of age with annual boosters recommended. [10]

Myxomatosis is a fatal disease of domestic rabbits caused by myxoma virus; an attenuated myxomatosis vaccine exists but is not available in the USA, where myxomatosis is largely restricted to coastal California and Oregon. [10]

In the United States a myxomatosis vaccine is unavailable and has not been approved by the USDA, whereas the myxomatosis vaccine is available in Europe and the UK. [10]

Toxicology & Hazards

Substances and environmental hazards to avoid.

Antibiotic (enteric dysbiosis / enterotoxemia) toxicity in rabbits — oral antibiotic contraindications

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

Very few products are licensed for rabbits, leading to extra-label use of therapies approved for other species. [3]

Use particular caution with antibiotics that suppress normal gut microflora and cause enteric dysbiosis and/or enterotoxemia. [3]

This 'antibiotic toxicity' means oral clindamycin, lincomycin, erythromycin, ampicillin, amoxicillin/clavulanic acid, and cephalosporins are contraindicated in rabbits. [3]

The flea treatment fipronil is contraindicated in rabbits because of severe toxic reactions in some individuals. [3]

Rabbit non-drug poisons — garden, household and feeding hazards

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

Some garden and household plants are poisonous to rabbits — examples include bluebells, foxgloves, holly and tulips.

Lawnmower clippings should not be fed to rabbits, as they can make them ill.

If in doubt about whether a plant is safe, leave it out; a vet can advise on rabbit-safe and rabbit-toxic plants.

If a rabbit eats any item on the poisonous list, contact a veterinarian immediately; the 24-hour ASPCA Animal Poison Control line (888-426-4435) can be used if the regular vet is closed.

Foods listed as poisonous and needing immediate veterinary contact include chocolate, oleander, poinsettia, bulb flowers, nightshade leaves and stems (including tomato), onions, garlic, spicy peppers, and anything containing essential oils.

Foods that should never be fed to rabbits include corn, nuts, cereal, tomato, iceberg lettuce, seeds, raisins, bread, beans, potato, and animal products such as yogurt drops.

Other items toxic to rabbits include avocado, nightshade leaves, pits from fruit, oleander and bulb plants.

You should not feed any plant to your rabbit unless you are sure of its identity and safety. Many plants can be poisonous to your rabbit. [5]

Grooming

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

Rabbit — grooming & hygiene (brushing/bathing, nails/claws, coat/skin, dental)

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

Rabbits are generally quiet, clean and gentle, can be litter-trained, and can learn simple behaviours. [4]

Toilet areas must be cleaned daily. [4]

Regular grooming is needed to keep your rabbit comfortable and prevent it swallowing lots of fur as this can cause a blockage of the bowel. [5]

Rabbits with a short coat should be groomed weekly but longhaired rabbits should be groomed at least once a day to avoid matts and tangles. [5]

Breeding & Neutering

Neutering / spaying, reproduction and preventing unwanted litters.

Rabbit — breeding & neutering (neutering/spaying, reproduction, preventing unwanted litters)

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

Litters range from one to ten kits, and a doe can mate again within hours of giving birth. [4]

A neutered male and neutered female pair works well, since neutering lowers the risk of fighting in both sexes. [4]

Even neutered rabbits may mount one another to display dominance rather than for mating. [4]

Litters are one to ten kits and does can re-mate within hours; female offspring can themselves become pregnant at only a few months old. [4]

Left unneutered, a single pair could produce around 82 rabbits in a year, so sexing and neutering are essential to prevent unwanted litters. [4]

Unneutered female rabbits are at high risk of uterine tumours; in does over three years old the incidence may reach about 80%, and these tumours are usually fatal. [4]

[Paraphrased derived summary — non-Open-Access source.] A female rabbit (doe) can become pregnant as early as four months of age and has a gestation of about four weeks. [4]

Rabbits that are not neutered tend to show problematic behaviour and may suffer health problems. [5]

Females are usually neutered when they reach sexual maturity, at the age of 4 months, and males at the age of 3 months. [5]

A female rabbit can produce between 4 to 12 babies per litter, and will become pregnant again soon after she has given birth. [5]

[Paraphrased derived summary — non-Open-Access source.] Palpating the doe's abdomen for grape-sized uterine embryos is a much better way to detect pregnancy. [3]

Regulations & Legality

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

⚠️ Incomplete — jurisdiction-specific pet-law data is still being collected. The lines below are unverified statute excerpts, not actionable legal guidance; treat them as honest gaps and consult the relevant authority.

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

( 3 ) any species of European rabbit of the genus Oryctolagus;

Breed-Specific Health

Alaska (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Alaska (Rabbit) [11]

Mode of inheritance: Autosomal [11]

Prevalence: Letko et al. (2020) genotyped 49 rabbits with different coat colours.... Out of 19 black and tan rabbits analysed, 17 carried the deletion in a homozygous state. The remaining two black and tan rabbits were heterozygous for the deletion but also heterozygous for the single base insertion, causing recessive black and thus presumably compound heterozygous a^t/a. As the a allele is recessive to a^t, rabbits with an a^t/a genotype are phenotypically black and tan. None of the 30 rabbits that were not black and tan carried the deletion in a homozygous state. 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 4215581 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2010. Characterization of the rabbit agouti signaling protein (ASIP) gene: transcripts and phylogenetic analyses and identification of the causative mutation of the nonagouti black coat colour. Genomics — PubMed:PMID20004240 | DOI:10.1016/j.ygeno.2009.11.003 — OMIA Phene_Article / Article - 1953. [Studies on the coat markings of wild rabbits; a contribution to the mechanism of the agouti factor.]. Z Indukt Abstamm Vererbungsl — PubMed:PMID13091004 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2019. Multiple conserved elements structuring inverted repeats in the mammalian coat color-related gene Asip. Zoolog Sci — PubMed:PMID31116535 | DOI:10.2108/zs180081 — OMIA Phene_Article / Article - 2020. A deletion spanning the promoter and first exon of the hair cycle-specific ASIP transcript isoform in black and tan rabbits. Anim Genet — PubMed:PMID31729778 | DOI:10.1111/age.12881 — OMIA Phene_Article / Article - 2023. A genome-wide association study of coat color in Chinese Rex rabbits. Front Vet Sci — PubMed:PMID37655262 | DOI:10.3389/fvets.2023.1184764 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:611742 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600201 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [11]

Angora (Rabbit) — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: Angora (Rabbit) [12]

Summary: See Robinson (1958, pp. 248-251) 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 4324720 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1924. Genetics of the Japanese rabbit. Journal of Genetics — OMIA Phene_Article / Article - 2006. Mutations in the melanocortin 1 receptor (MC1R) gene are associated with coat colours in the domestic rabbit (Oryctolagus cuniculus). Anim Genet — PubMed:PMID16978179 | DOI:10.1111/j.1365-2052.2006.01494.x — OMIA Phene_Article / Article - 2010. A composite six bp in-frame deletion in the melanocortin 1 receptor (MC1R) gene is associated with the Japanese brindling coat colour in rabbits (Oryctolagus cuniculus). BMC Genet — PubMed:PMID20594318 | DOI:10.1186/1471-2156-11-59 — OMIA Phene_Article / Article - 1924. On the "Japanese" rabbit. Journal of Genetics — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2007. Non-invasive and simple methods for sampling DNA for PCR analysis of melanocortin 1 receptor (MC1R) gene mutations: a technical note. World Rabbit Science — OMIA Phene_Article / Article - 2019. A novel pale-yellow coat color of rabbits generated via MC1R mutation with CRISPR/Cas9 System. Front Genet — PubMed:PMID31620174 | DOI:10.3389/fgene.2019.00875 — OMIA Phene_Article / Article - 2021. Rabbits - their domestication and molecular genetics of hair coat development and quality. Anim Genet — PubMed:PMID33216407 | DOI:10.1111/age.13024 — OMIA Phene_Article / Article - 2021. Analysis of MC1R, MITF, TYR, TYRP1, and MLPH genes polymorphism in four rabbit breeds with different coat colors. Animals (Basel) — PubMed:PMID33466315 | DOI:10.3390/ani11010081 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:266300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:155555 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [12]

Angora (Rabbit) — Hair, long (hereditary; OMIA-verified breed predisposition)

Mode of inheritance: Autosomal recessive [13]

Summary: See Robinson (1958, pp. 292-297). 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 389093243 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Fatima et al. (2023) "discovered that the homozygous missense mutation T19234C within Fgf5 might contribute to the long-hair trait of Angora rabbits by reducing its receptor binding capacity." Evidence (references) - 1924. Linkage of Dutch, English, and Angora in Rabbits. Proc Natl Acad Sci U S A — PubMed:PMID16576789 | DOI:10.1073/pnas.10.3.107 — OMIA Phene_Article / Article - 1905. Mendelism. Macmillan and Bowes, Cambridge — OMIA Phene_Article / Article - 2006. A first-generation microsatellite-based integrated genetic and cytogenetic map for the European rabbit (Oryctolagus cuniculus) and localization of angora and albino. Anim Genet — PubMed:PMID16879342 | DOI:10.1111/j.1365-2052.2006.01462.x — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2000. [Some misunderstandings about the angora rabbit]. Tijdschr Diergeneeskd — PubMed:PMID11060929 — OMIA Phene_Article / Article - 2001. Scanning electron microscopic study of different hair types in various breeds of rabbits. Folia Morphol (Warsz) — PubMed:PMID11234696 — OMIA Phene_Article / Article - 2007. Characteristics of Angora rabbit fiber using optical fiber diameter analyzer. J Anim Sci — PubMed:PMID17644779 | DOI:10.2527/jas.2007-0109 — OMIA Phene_Article / Article - 2009. Genetic description of a divergent selection experiment in Angora rabbits with overlapping generations. J Anim Breed Genet — PubMed:PMID19646147 | DOI:10.1111/j.1439-0388.2008.00769.x — OMIA Phene_Article / Article - 2010. Genetics of fibre production and fleece characteristics in small ruminants, Angora rabbit and South American camelids. Animal — PubMed:PMID22444694 | DOI:10.1017/S1751731110000029 — OMIA Phene_Article / Article - 1903. The heredity of 'Angora' coat in mammals. Science — PubMed:PMID17844480 | DOI:10.1126/science.18.467.760.b — OMIA Phene_Article / Article - 2018. MicroRNAs Profiling Identifies miR-125a and Its Target Gene Wnt2 in Skins of Different Haired Rabbits. Front Genet — PubMed:PMID30619457 | DOI:10.3389/fgene.2018.00628 — OMIA Phene_Article / Article - 2019. Analyses of histological and transcriptome differences in the skin of short-hair and long-hair rabbits. BMC Genomics — PubMed:PMID30770723 | DOI:10.1186/s12864-019-5503-x — OMIA Phene_Article / Article - (8 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:190330 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:165190 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [13]

Blauer Wiener (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Blauer Wiener (Rabbit) [11]

California (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: California (Rabbit) [11]

Champagne-Silberkaninchen, Germany (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Champagne-Silberkaninchen, Germany (Rabbit) [11]

Checkered Giant — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Checkered Giant [11]

Checkered Small — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Checkered Small [11]

Chinchilla (Rabbit) — Tremor, X-linked (hereditary; OMIA-verified breed predisposition)

Breed: Chinchilla (Rabbit) [14]

Mode of inheritance: X-linked [14]

Summary: This is an X-linked disorder that affects myelination of the central nervous system. 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: PLP (Entrez Gene ID 4118891) — OMIA Phene_Gene / GeneSynonym - OMIA molecular-genetics note: Building on the results of Tosic et al. (1993) that this disorder is primarily due to faulty expression of the proteolipid protein (PLP) gene, Tosic et al. (1994) sequenced PLP cDNA from normal and affected rabbits and showed that the disorder is due to a point mutation in exon 2 of the PLP gene, corresponding to the end of the first potential transmembrane domain of the protein. The mutation remo… Evidence (references) - 1993. Paralytic Tremor (pt) Rabbit - A Sex-Linked Mutation Affecting Proteolipid Protein-Gene Expression. Brain Research — PubMed:PMID8275312 — OMIA Phene_Article / Article - 1994. Paralytic tremor (pt): A new allele of the proteolipid protein gene in rabbits. Journal of Neurochemistry — PubMed:PMID7525875 — OMIA Phene_Article / Article - 2005. Rabbit paralytic tremor phenotype--a plp1 gene mutation as a model of human Pelizaeus-Merzbacher disease. Acta Neurobiol Exp (Wars) — PubMed:PMID15960310 — OMIA Phene_Article / Article - 1995. Oligodendrocyte development in PLP "pt" mutant rabbits: glycolipid antigens and PLP gene expression. Metab Brain Dis — PubMed:PMID8847995 — OMIA Phene_Article / Article - 1995. Expression of myelin-specific proteins during development of normal and hypomyelinated Paralytic tremor mutant rabbits. II. Studies on the purified myelin. Mol Chem Neuropathol — PubMed:PMID8588825 | DOI:10.1007/BF02814942 — OMIA Phene_Article / Article - 1995. Expression of myelin-specific proteins during development of normal and hypomyelinated Paralytic tremor mutant rabbits. I. Studies on the brain homogenates. Mol Chem Neuropathol — PubMed:PMID8588824 | DOI:10.1007/BF02814941 — OMIA Phene_Article / Article - 1988. Myelin composition and activities of CNPase and Na+,K+-ATPase in hypomyelinated "pt" mutant rabbit. J Neurochem — PubMed:PMID2826682 — OMIA Phene_Article / Article - 1996. pt point mutation in plp gene results in hyperexpression of MOG in hypomyelinated rabbit. Acta Neurobiol Exp (Wars) — PubMed:PMID8787215 — OMIA Phene_Article / Article - 1997. Intracellular transport of the DM-20 bearing shaking pup (shp) mutation and its possible phenotypic consequences. J Neurosci Res — PubMed:PMID9418971 | DOI:10.1002/(SICI)1097-4547(19971201)50:53.0.CO;2-# — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 1976. Elektronenmikroskopische Untersuchung der intrazerebralen Verkalkungen bei dem erblichen paralytischen Tremor der pt-Kaninchen [Electron microscopic studies of intracerebral calcifications in hereditary paralytic tremor in pt rabbits]. Neuropatol Pol — PubMed:PMID967309 — OMIA Phene_Article / Article - 1986. Brain lipids of a myelin-deficient rabbit mutant during development. Neurochem Pathol — PubMed:PMID3561890 | DOI:10.1007/BF02834354 — OMIA Phene_Article / Article - (13 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:312080 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:300401 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [14]

Coloured dwarf — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Coloured dwarf [11]

Dutch (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Dutch (Rabbit) [11]

Dwarf, long-haired — Dwarfism, generic (hereditary; OMIA-verified breed predisposition)

Breed: Dwarf, long-haired [15]

Mode of inheritance: Autosomal incomplete dominant [15]

Summary: Robinson (1958, pp. 343-346) provides an extensive summary of this form of proportionate dwarfism. The effect of the mutant dw allele on a wide range of traits was reported by Crary and Sawin (1949), Sawin and Dietz (1950), Sawin and Curran (1952), and in three 1955 papers by Latimer and Sawin. The results of Carneiro et al. (2017) imply that small size in dwarf rabbits results from a large effect, loss-of-function (LOF) mutation in HMGA2 combined with polygenic selection. Bovo et al. (2025) provide evidence for a polygenic architecture underlying small size in rabbits, influenced by a few major loci. [15]

Clin feat: As reported by Green et al. (1934): The [homozygous] dwarfs of this stock are born alive and occasionally they are capable of nursing, but so far, none of them has lived longer than a few days. They are delicately formed and to outward appearance are fully developed except for the bones of the calvarium, which, as a rule, are incompletely calcified. Carneiro et al. (2016) summarise the phenotype information reported by Robinson (1958): The dwarf allele is recessive lethal. Homozygotes (dw/dw) are smaller than litter mates and exhibit a characteristic swollen head, tiny ears, and are usually called peanuts.. Peanuts are viable up to the time of birth but typically die within a few days of birth. Heterozygotes (Dw/dw) reach ∼2/3 of the size of wild-type litter mates (Dw/Dw) and in adulthood are typically under 1 kg in body weight, have compact and rounded bodies, a disproportionately larger head when compared to the rest of the body, small ears, and a short snout due to altered craniofacial development.. Several resources suggest that the altered craniofacial development may predispose dwarf rabbits to an increased risk to develop dental disease (e.g. Harcourt-Brown, 1997; Wegner, 1997; van Caelenberg et al., 2008; Koroleva and Titova, 2022). [15]

Pathology: The pathology in individuals homozygous for the dwarf mutation leads to death. [15]

Control: Breeding of two animals that are both heterozgyous for the dwarf mutation should be avoided. For the breeding of dwarf rabbits, each breeding pair should include an animal heterozygous for the dwarf mutation (dwarf rabbit) and an animal that does not have the dwarf mutation. This will avoid the birth of non viable homozygous dwarfs and result in the birth of 50% viable (heterozygous) dwarfs and 50% normal sized rabbits. 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 394535807 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Carneiro et al. (2017) showed "that the dwarf allele constitutes a ~12.1 kb deletion overlapping the promoter region and first three exons of the HMGA2 gene leading to inactivation of this gene." Very interestingly, mutation in this same gene is associated with body-size variation in dogs (OMIA:001968-9615) and horses ( Evidence (references) - 1940. A dwarf mutation in the rabbit: the constitutional influence on homozygous and heterozygous individuals. J Exp Med — PubMed:PMID19871001 — OMIA Phene_Article / Article - 1990. Hereditary C8-alpha-gamma deficiency associated with dwarfism in the rabbit. Journal of Heredity — OMIA Phene_Article / Article - 1997. Zur Problematik der Zwergkanninchen-Zucht [Problematic aspects of breeding dwarf rabbits]. Dtsch Tierarztl Wochenschr — PubMed:PMID9289403 — OMIA Phene_Article / Article - 1981. In vitro culture of rabbit growth plate chondrocytes. 2. Chondrodystrophic mutants. Growth — PubMed:PMID6458543 — OMIA Phene_Article / Article - 1934. A lethal dwarf mutation in the rabbit with stigmata of endocrine abnormality. Science — PubMed:PMID17840734 | DOI:10.1126/science.79.2056.487 — OMIA Phene_Article / Article - 1955. Morphogenetic studies of the rabbit. XIII. The influence of the dwarf gene upon organ size and variability in race X. Anat Rec — PubMed:PMID13292775 — OMIA Phene_Article / Article - 1957. Morphogenetic studies of the rabbit. XV. Measurements of the digestive tube and of its parts in normal and dwarf rabbits of race X. Anat Rec — PubMed:PMID13509179 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1941. Genetic linkage in the rabbit. Proc Natl Acad Sci U S A — PubMed:PMID16588495 | DOI:10.1073/pnas.27.11.519 — OMIA Phene_Article / Article - 1949. Morphogenetic studies in the rabbit. VI. Genetic factors influencing the ossification pattern of the limbs. Genetics — PubMed:PMID17247330 | DOI:10.1093/genetics/34.5.508 — OMIA Phene_Article / Article - 1950. Morphogenetic studies of the rabbit. IX. Masking of prenatal growth gradients in adults. Moderne Biologie (eds Griineberg, H. and Ulrich, W.) — OMIA Phene_Article / Article - 1952. Genetic and physiological background of reproduction in the rabbit. 1. The problem and its biological significance. Journal of Experimental Zoology — OMIA Phene_Article / Article - (12 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:600768 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600509 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [15]

English Lop — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: English Lop [12]

English Spot (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: English Spot (Rabbit) [11]

Fairly Pearly — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Fairly Pearly [11]

Fauve de Borgogne (Rabbit) — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: Fauve de Borgogne (Rabbit) [12]

Flemish Giant (Rabbit) — Yellow fat (hereditary; OMIA-verified breed predisposition)

Breed: Flemish Giant (Rabbit) [16]

Summary: See Robinson (1958, p. 313). 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 389110988 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Strychalski et al. (2015): "novel AAT-deletion mutation at codon 248 of the BCO2 gene, which has been found in homozygous yellow-fat rabbits. The deletion mutation, located at the beginning of exon 6, results in the absence of asparagine in protein" Evidence (references) - 1933. The linkage relations of yellow fat in rabbits. Proc Natl Acad Sci U S A — PubMed:PMID16577589 | DOI:10.1073/pnas.19.11.947 — OMIA Phene_Article / Article - 1965. "Yellow fat" in the wild rabbit. Nature — PubMed:PMID4161266 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2015. A novel AAT-deletion mutation in the coding sequence of the BCO2 gene in yellow-fat rabbits. J Appl Genet — PubMed:PMID26002694 | DOI:10.1007/s13353-015-0290-9 — OMIA Phene_Article / Article - 1930. The inheritance of yellow-fat in rabbits. Verh 1 Internat Kaninchenzuchter Kongresses, Leipzig — OMIA Phene_Article / Article - 1946. Fat colour and fur colour in different varieties of rabbit. J Genet — PubMed:PMID20995079 | DOI:10.1007/BF02986253 — OMIA Phene_Article / Article - 1969. Aetiology of "yellow fat" disease (pansteatitis) in the wild rabbit. J Comp Pathol — PubMed:PMID5348109 | DOI:10.1016/0021-9975(69)90046-2 — OMIA Phene_Article / Article - 1928. Yellow fat in rabbits, a linked character?. Verh. V. Intern. Kongr. Vererbungswissenschaft — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:611740 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [16]

Giant Grey — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Giant Grey [11]

Havanna (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Havanna (Rabbit) [11]

Havanna (Rabbit) — Coat colour, brown, TYRP1-related (hereditary; OMIA-verified breed predisposition)

Summary: See Robinson (1958, p. 238) 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: TRP-1 (Entrez Gene ID 389108532) — OMIA Phene_Gene / GeneSynonym - OMIA molecular-genetics note: Utzer et al. (2014): "A mutation in exon 2 (g.41360196G>A) leads to a premature stop codon at position 190 of the deduced amino acid sequence (p.Trp190ter). Therefore, translation predicts a truncated TYRP1 protein lacking almost completely the tyrosinase domain." Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2014. A premature stop codon in the TYRP1 gene is associated with brown coat colour in the European rabbit (Oryctolagus cuniculus). Anim Genet — PubMed:PMID24814776 | DOI:10.1111/age.12171 — OMIA Phene_Article / Article - 1924. On the Occurrence in Rabbits of Linkage in Inheritance between Albinism and Brown Pigmentation. Proc Natl Acad Sci U S A — PubMed:PMID16576859 | DOI:10.1073/pnas.10.12.486 — OMIA Phene_Article / Article - 2021. Rabbits - their domestication and molecular genetics of hair coat development and quality. Anim Genet — PubMed:PMID33216407 | DOI:10.1111/age.13024 — OMIA Phene_Article / Article - 2021. Analysis of MC1R, MITF, TYR, TYRP1, and MLPH genes polymorphism in four rabbit breeds with different coat colors. Animals (Basel) — PubMed:PMID33466315 | DOI:10.3390/ani11010081 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:612271 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:203290 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:115501 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [17]

Holland Lop (Rabbit) — Dwarfism, generic (hereditary; OMIA-verified breed predisposition)

Breed: Holland Lop (Rabbit) [15]

Japanese (Rabbit) — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: Japanese (Rabbit) [12]

Lionhead Dwarf — Neuronal ceroid lipofuscinosis, 7 (hereditary; OMIA-verified breed predisposition)

Breed: Lionhead Dwarf [18]

Mode of inheritance: Probably autosomal recessive [18]

Clin feat: Böttcher-Künneke et al. (2020) reported a 2 year old female lionhead dwarf rabbit which was presented due to behavioural changes, acute anxiety, hyperaesthesia, disorientation, ataxia, loss of vision, phantom scratching, epileptic seizures and a severe nasal dermatitis; all of which progressed within the following twelve months.. Due to the progressive deterioration of its clinical signs and poor quality of life, the rabbit was euthanised. [18]

Pathology: Böttcher-Künneke et al. (2020) report pathological findings in the affected lionhead dwarf rabbit: At necropsy, a symmetrical internal hydrocephalus of the lateral ventricles was present. Histologically, neurons of the cerebrum, hippocampus, cerebellum, brain stem and spinal cord were enlarged due to the accumulation of an eosinophilic, partially granular intracytoplasmic material, which led to the diagnosis of a neuronal storage disease. Christen et al. (2024) report additional pathological findings: Cytoplasmic pigment present in neurons was weakly positive with Sudan black B and autofluorescent. Immunohistology revealed astrogliosis, microgliosis and axonal degeneration. 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 398298897 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Christen et al. (2024) "the genome of the affected [lionhead dwarf] rabbit was sequenced and examined for private variants in NCL candidate genes. The analysis revealed a homozygous ~10.7 kb genomic duplication on chromosome 15 comprising parts of the MFSD8 gene, NC_013683.1:g.103,727,963_103,738,667dup. The duplication harbors two internal protein coding exons and is predicted to in… Evidence (references) - 2024. Intragenic MFSD8 duplication and histopathological findings in a rabbit with neuronal ceroid lipofuscinosis. Anim Genet — PubMed:PMID38712841 | DOI:10.1111/age.13441 — OMIA Phene_Article / Article - 2020. Neuronale Speicherkrankheit bei einem ausgewachsenen weiblichen Kaninchen. Kleintierpraxis — DOI:doi.org/10.2377/0023-2076-65-656 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:610951 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:611124 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [18]

Lop dwarf — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Lop dwarf [11]

Lop — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Lop [11]

Marburger Feh (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Marburger Feh (Rabbit) [11]

Mini Silver — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Mini Silver [11]

Netherland dwarf (Rabbit) — Dwarfism, generic (hereditary; OMIA-verified breed predisposition)

Breed: Netherland dwarf (Rabbit) [15]

New Zealand Red (Rabbit) — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: New Zealand Red (Rabbit) [12]

New Zealand White (Rabbit) — Amelogenesis imperfecta, FAM83H-related (hereditary; OMIA-verified breed predisposition)

Breed: New Zealand White (Rabbit) [19]

Summary: Zhang et al. (2022): Fam83h mutations cause human amelogenesis imperfecta (AI), an inherited disorder characterized by severe hardness defects in dental enamel.. a large deletion of the Fam83h gene (900 bp) was generated via a dual sgRNA-directed CRISPR/Cas9 system in rabbits. This study involves genetically modified organisms (GMO). [19]

Clin feat: Zhang et al. (2022): Abnormal tooth mineralization and loose dentine were found in homozygous Fam83h knockout (Fam83h-/-) rabbits compared with WT rabbits. In addition, reduced hair follicle counts in dorsal skin, hair cycling dysfunction and hair shaft differentiation deficiency were observed in Fam83h-/- rabbits. Moreover, X-rays and staining of bone sections showed abnormal bending of the ulna and radius and an ulnar articular surface with insufficient trabecular bone in Fam83h-/- rabbits. 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 394534710 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2022. CRISPR/Cas9-mediated deletion of Fam83h induces defective tooth mineralization and hair development in rabbits. J Cell Mol Med — PubMed:PMID36300761 | DOI:10.1111/jcmm.17597 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:611927 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:130900 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [19]

New Zealand White (Rabbit) — Cerebral palsy, RHOB-related (hereditary; OMIA-verified breed predisposition)

Summary: Wu et al. (2024) created a rabbit model using the SpG-BE4max system to mimic a de novo RhoB p.S73F mutation associated with cerebral palsy in humans. This study involves genetically modified organisms (GMO).brbr 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 398298915 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2024. The RhoB p.S73F mutation leads to cerebral palsy through dysregulation of lipid homeostasis. EMBO Mol Med — PubMed:PMID39080495 | DOI:10.1038/s44321-024-00113-2 — OMIA Phene_Article / Article [20]

New Zealand White (Rabbit) — Coat/skin colour, oculocutaneous albinism type I (OCA1), TYR-related (hereditary; OMIA-verified breed predisposition)

Summary: See Robinson (1958, pp. 338-340) 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 4118478 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1987. Linkage of albino and hemoglobin beta-chain loci in the rabbit. Journal of Heredity — PubMed:PMID3584936 — OMIA Phene_Article / Article - 1993. Drug-Induced Retinal Toxicity in Albino Rabbits - The Effects of Imipenem and Aztreonam. Investigative Ophthalmology & Visual Science — PubMed:PMID8225881 — OMIA Phene_Article / Article - 1994. Blue-Light-Induced Dysfunction of the Blood-Retinal Barrier at the Pigment Epithelium in Albino Versus Pigmented Rabbits. Experimental Eye Research — PubMed:PMID8157099 | DOI:10.1006/exer.1994.1192 — OMIA Phene_Article / Article - 1995. Comparative ocular pharmacokinetics of brimonidine after a single dose application to the eyes of albino and pigmented rabbits. Drug Metabolism and Disposition — PubMed:PMID7587958 — OMIA Phene_Article / Article - 2000. Tyrosinase gene variants in different rabbit strains. Mamm Genome — PubMed:PMID10920244 | DOI:10.1007/s003350010120 — OMIA Phene_Article / Article - 1996. Expression of the murine wild-type tyrosinase gene in transgenic rabbits. Transgenic Res — PubMed:PMID8840523 | DOI:10.1007/BF01980205 — OMIA Phene_Article / Article - 1996. YAC transgenesis in farm animals: rescue of albinism in rabbits. Mol Reprod Dev — PubMed:PMID8722692 | DOI:10.1002/(SICI)1098-2795(199605)44:13.0.CO;2-S — OMIA Phene_Article / Article - 1964. Catechol-O-methyl transferase and monamine oxidase activity in the ocular tissue of albino rabbits. Invest Ophthalmol — PubMed:PMID14238873 — OMIA Phene_Article / Article - 1905. Mendelism. Macmillan and Bowes, Cambridge — OMIA Phene_Article / Article - 2006. A first-generation microsatellite-based integrated genetic and cytogenetic map for the European rabbit (Oryctolagus cuniculus) and localization of angora and albino. Anim Genet — PubMed:PMID16879342 | DOI:10.1111/j.1365-2052.2006.01462.x — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1973. Recombination between buphthalmos and albino loci in the rabbit. J Hered — PubMed:PMID4782848 | DOI:10.1093/oxfordjournals.jhered.a108442 — OMIA Phene_Article / Article - (9 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:203100 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:606952 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:606933 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [21]

Rex (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Rex (Rabbit) [11]

Rheinische Schecken (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Rheinische Schecken (Rabbit) [11]

Russian (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Russian (Rabbit) [11]

Sauteur d'Alfort — disrupted saltatorial locomotion, sauteur phenotype, acrobat (hereditary; OMIA-verified breed predisposition)

Breed: Sauteur d'Alfort [22]

Disorder: disrupted saltatorial locomotion, sauteur phenotype, acrobat [22]

Summary: Carneiro et al. (2021): Saltatorial locomotion is a type of hopping gait that in mammals can be found in rabbits, hares, kangaroos, and some species of rodents.. Here, we take advantage of one strain of domesticated rabbits, the sauteur d’Alfort, that exhibits an abnormal locomotion behavior defined by the loss of the typical jumping that characterizes wild-type rabbits. Strikingly, individuals from this strain frequently adopt a bipedal gait using their front legs.. Additional anatomical problems have also been described in sauteur rabbits, they are born blind because of retinal dysplasia and start developing cataracts after their first year of life [Theret, 1961; Boucher et al., 1996]. [22]

Pathology: Carneiro et al., 2021: immunohistochemistry (IHC) was performed on the spinal cord of newborn rabbits from our experimental cross.. In rabbits homozygous for the wild-type allele, RORB is localized in the nucleus of a population of dorsal horn neurons.. In the spinal cord from rabbits heterozygous for the sauteur allele (+/s^am), the number of neurons expressing RORB was approximately 25% lower than in the wild-type animals.. In contrast, in rabbits homozygous for the sauteur allele (s^am/ s^am), the expression of RORB was undetectable by IHC. 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 389111649 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Using the whole-genome sequencing data generated for the bulked segregant analysis, Carneiro et al. (2021) searched the 5.4 Mb candidate region for potential causal variants and identified a splice site mutation in RORB as likely causal variant. "This variant corresponds to a change from GT to AT in the 5’ donor site of intron 9 (chr1: 61,103,503bp)" (Carneiro et al., 2021). RORB cDNA analysis ide… Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1961. Aspects génétiques de quelques anomalies oculaires chez les animaux domestiques. [Genetic aspect of some ocular anomalies in domestic animals]. Bull Mem Soc Fr Ophtalmol — PubMed:PMID13980887 — OMIA Phene_Article / Article - 2021. A loss-of-function mutation in RORB disrupts saltatorial locomotion in rabbits. PLoS Genet — PubMed:PMID33764968 | DOI:10.1371/journal.pgen.1009429 — OMIA Phene_Article / Article - 1935. Une mutation nouvelle chez le lapin. Bull Acad Vet Fr — OMIA Phene_Article / Article - 1943. Troubles de la locomotion et troubles de la vision chez le lapin, liaison héréditaire. Bull Acad Vet Fr — OMIA Phene_Article / Article - 1996. The “Alfort jumper” rabbit: historic, description and characterization. Proc 6th World Rabbit Congr. — OMIA Phene_Article / Article - 1991. Le lapin Sauteur d’Alfort. Rev Avic — OMIA Phene_Article / Article - 2002. Les allures du lapin normal peuvent-elles expliquer la marche acrobatique du «lapin sauteur d’Alfort»?. Mammalia — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:601972 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [22]

Saxon Gold — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: Saxon Gold [12]

Silver (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Silver (Rabbit) [11]

Thüringer (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Thüringer (Rabbit) [11]

Weisse Wiener (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: Weisse Wiener (Rabbit) [11]

White Giant (Rabbit) — Coat colour, extension (hereditary; OMIA-verified breed predisposition)

Breed: White Giant (Rabbit) [12]

White Hotot (Rabbit) — Coat colour, agouti (hereditary; OMIA-verified breed predisposition)

Breed: White Hotot (Rabbit) [11]

Zika, Hungary (Rabbit) — Coat/skin colour, oculocutaneous albinism type I (OCA1), TYR-related (hereditary; OMIA-verified breed predisposition)

Breed: Zika, Hungary (Rabbit) [21]

Species-Specific Health

Rabbit (Oryctolagus cuniculus) — Achondroplasia-1 (hereditary; OMIA-verified species predisposition)

Species: Rabbit (Oryctolagus cuniculus) [23]

Disorder: Achondroplasia-1 [23]

Clin feat: As first reported by Brown and Pearce (1945), this form of achondroplasia "is present at birth and is characterized by size reduction, by a disproportion of bodily parts, most marked in the extremities, and by an invariably lethal effect. The animals are still-born or die very shortly after birth. In physical appearance and in the character of the skeletal changes as shown by x-ray photographs, achondroplasia in the rabbit has a remarkable resemblance to the disease in man and in cattle and dogs." 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 entry symbol: Initially ac; later (Robinson, 1958) ac-1 (no structured Phene_Gene link) Evidence (references) - 1972. Studies of oxidative energy deficiency. I. Achondroplasia in the rabbit. Arch Biochem Biophys — PubMed:PMID4337533 | DOI:10.1016/0003-9861(72)90020-3 — OMIA Phene_Article / Article - 1945. Hereditary achondroplasia in the rabbit: III. Genetic aspects; general considerations. J Exp Med — PubMed:PMID19871500 | DOI:10.1084/jem.82.4.281 — OMIA Phene_Article / Article - 1945. Hereditary achondroplasia in the rabbit: II. Pathologic aspects. J Exp Med — PubMed:PMID19871499 | DOI:10.1084/jem.82.4.261 — OMIA Phene_Article / Article - 1945. Hereditary achondroplasia in the rabbit: I. Physical appearance and general features. J Exp Med — PubMed:PMID19871498 | DOI:10.1084/jem.82.4.241 — OMIA Phene_Article / Article - 1963. Morphogenetic studies of the rabbbit. XXXII. Qualitative skeletal variations induced by the ac gene (achondroplasia). Am J Anat — PubMed:PMID14042510 | DOI:10.1002/aja.1001130103 — OMIA Phene_Article / Article - 1971. Organ-culture studies of achondroplastic rabbit cartilage: evidence for a metabolic defect in glucose utilization. J Embryol Exp Morphol — PubMed:PMID5556980 — OMIA Phene_Article / Article - 1981. In vitro culture of rabbit growth plate chondrocytes. 2. Chondrodystrophic mutants. Growth — PubMed:PMID6458543 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1969. Microscopic studies of achondroplastic rabbit cartilage. Teratology — PubMed:PMID5797691 | DOI:10.1002/tera.1420020103 — OMIA Phene_Article / Article [23]

Rabbit (Oryctolagus cuniculus) — Achondroplasia-2 (hereditary; OMIA-verified species predisposition)

Disorder: Achondroplasia-2 [24]

Mode of inheritance: Sawin and Crary (1959) reported many body measurements that suggested a relatively small effect of the mutant gene in heterozygotes. [24]

Clin feat: Sawin and Crary (1959): "The homozygous dachs manifests certain of the typical characteristics of chondrodystrophy but there are certain unique differences. Diminished size and shortening of the limbs appear to be consistent but variable in their expression. Hyperplasia of cartilage in the region of the metaphysis and any profound enlargement of the head seem to be absent except as they may be secondary manifestations or are mildly expressed by individual bone measurements. The depression at the nasion appears to have migrated posteriorly and is accompanied by depression and shift of the orbit and optic foramen. Associated with these are highly localized disproportionate differences which are unlike those noted in any other inherited chondrodystrophy thus far described." As summarised by Robinson (1958, p. 341), "The present case differs from... [Achondroplasia-1; OMIA 001996-9986] in several respects. The animals are fully viable and appear quite normal at birth but when adult have the characteristic short legs. Externally the achondroplasia can be recognised by a small cartilaginous papilla arising at the base of the ear. This is present at hirth but is not fully detectable until the ear flap opens at approximately the sixth day and the papilla separates from the remainder of the ear. X-ray plates reveal abnormalities of the leg bones which at a later age may result in crippled legs and a peculiar undulating gait. Dislocations of the hip or knee may appear and become more pronounced as maternity is reached, interfering with normal and successful mating. However, it has been possible to produce young from one [homozygous] female by a normal male. Ear carriage is modified so that it tends to project downward and outward instead of upward and backward. SAWIN (1955) notes that the heterozygote... possesses a remnant of the papilla in the same relative position at the ear base." 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 entry symbol: ac-2 (no structured Phene_Gene link) Evidence (references) - 1962. Morphology of the external ear of the dachs (chondrodystrophy) rabbit. American Zoologist — OMIA Phene_Article / Article - 1958. Morphogenetic studies of the rabbit. XXI. The nature of disproportionate dwarfism induced by the Da gene revealed by the early fetal ossification pattern. American Journal of Anatomy — PubMed:PMID13626838 | DOI:10.1002/aja.1001030104 — OMIA Phene_Article / Article - 1952. A second achondroplasia in the rabbit. Journal of Heredity — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1965. Morphogenetic studies of the rabbit. XXXV. Pleiotropic effects of the Dachs gene and the gradient growth pattern. J Morphol — PubMed:PMID14336226 | DOI:10.1002/jmor.1051170106 — OMIA Phene_Article / Article - 1959. Morphogenetic Studies of the Rabbit. XXIII. the Effects of the Dachs Gene Da (Chondrodystrophy) upon Linear and Lateral Growth of the Skeleton as Influenced in Time. Genetics — PubMed:PMID17247845 | DOI:10.1093/genetics/44.4.609 — OMIA Phene_Article / Article - 1959. Morphogenetic studies of the rabbit. XXV. The spheno-occipital synchondrosis of the dachs (chondrodystrophy) rabbit. Am J Anat — PubMed:PMID14442107 | DOI:10.1002/aja.1001050206 — OMIA Phene_Article / Article - 1962. Morphogenetic studies of the rabbit. XXIX. Accessory ossification centers at the occipitovertebral articulation of the dachs (chondrodystrophy) rabbit. Am J Anat — PubMed:PMID13986942 | DOI:10.1002/aja.1001110302 — OMIA Phene_Article / Article - 1963. Morphogenetic studies of the rabbit. XXXIII. Cartilages and muscles of the external ear as affected by the dachs gene (Da). Am J Anat — PubMed:PMID14072363 | DOI:10.1002/aja.1001130303 — OMIA Phene_Article / Article - 1964. Development of the external ear in the dachs rabbit. Anat Rec — PubMed:PMID14248315 | DOI:10.1002/ar.1091500413 — OMIA Phene_Article / Article - 1955. Recent genetics of the domestic rabbit. Adv Genet — PubMed:PMID13258375 | DOI:10.1016/s0065-2660(08)60096-6 — OMIA Phene_Article / Article [24]

Rabbit (Oryctolagus cuniculus) — Adrenoleukodystrophy, ABCD1-related (hereditary; OMIA-verified species predisposition)

Disorder: Adrenoleukodystrophy, ABCD1-related [25]

Summary: Zhou et al. (2024) created a rabit model for X-linked adrenoleukodystrophy using CRISPR/Cas9 technology to knock out ABCD1 and evaluated rAAV9-based gene therapy in these knockout rabbits. This phene includes references to studies involving gene edited or genetically modified organisms (GMO). 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 398299010 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2025. Development of a rabbit model for adrenoleukodystrophy: A pilot study on gene therapy using rAAV9. Mol Ther Nucleic Acids — PubMed:PMID40027885 | DOI:10.1016/j.omtn.2025.102469 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:300371 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:300100 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [25]

Rabbit (Oryctolagus cuniculus) — Agenesis, renal (hereditary; OMIA-verified species predisposition)

Disorder: Agenesis, renal [26]

Summary: See Robinson (1958, p. 355). 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 entry symbol: ra (no structured Phene_Gene link) Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1943. [Renal agenesis, a new mutation in the rabbit]. Rev. Med. vet. (Lisboa) — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:617805 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:601076 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:277000 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [26]

Rabbit (Oryctolagus cuniculus) — Also known as buphthalmia (hereditary; OMIA-verified species predisposition)

Disorder: Also known as buphthalmia [27]

Summary: See Robinson (1958, p. 325) 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 entry symbol: bu (no structured Phene_Gene link) Evidence (references) - 1995. Development of ocular hypertension in congenitally buphthalmic rabbits. Laboratory Animal Science — PubMed:PMID7474889 — OMIA Phene_Article / Article - 1987. Optic nerve head axonal transport in rabbits with hereditary glaucoma. Exp Eye Res — PubMed:PMID2439361 | DOI:10.1016/s0014-4835(87)80162-8 — OMIA Phene_Article / Article - 1997. Ultrastructural studies of primary congenital glaucoma in rabbits. J Pediatr Ophthalmol Strabismus — PubMed:PMID9430063 | DOI:10.3928/0191-3913-19971101-08 — OMIA Phene_Article / Article - 1951. Buphthalmos in the rabbit. Br J Ophthalmol — PubMed:PMID14830731 | DOI:10.1136/bjo.35.4.232 — OMIA Phene_Article / Article - 1952. The neurovascular mechanism controlling ocular tension in congenital glaucoma of rabbits. Am J Ophthalmol — PubMed:PMID14923742 | DOI:10.1016/0002-9394(52)90947-1 — OMIA Phene_Article / Article - 1962. Recessive buphthalmos in the rabbit. Genetics — PubMed:PMID13904370 | DOI:10.1093/genetics/47.5.519 — OMIA Phene_Article / Article - 1965. BUPHTHALMIA IN THE RABBIT: A TEST FOR EARLY DIAGNOSIS. Proc Soc Exp Biol Med — PubMed:PMID14297855 | DOI:10.3181/00379727-119-30144 — OMIA Phene_Article / Article - 1967. A comparison of the findings from the corneal epithelium of the normal and the buphthalmic rabbit eye. Trans Am Ophthalmol Soc — PubMed:PMID4169897 — OMIA Phene_Article / Article - 1967. The rate of aqueous humor formation in buphthalmic rabbit eyes. Invest Ophthalmol — PubMed:PMID6016389 — OMIA Phene_Article / Article - 1967. Buphthalmia in the rabbit: effect of age and repeated testing on the cornified cell count diagnostic technique. Proc Soc Exp Biol Med — PubMed:PMID6066166 | DOI:10.3181/00379727-126-32405 — OMIA Phene_Article / Article - 1968. Gonioscopic study of hereditary buphthalmia in rabbits. Arch Ophthalmol — PubMed:PMID5652269 | DOI:10.1001/archopht.1968.03850040777022 — OMIA Phene_Article / Article - 1969. Buphthalmia in the rabbit. Pleiotropic effects of the (bu) gene and a possible explanation of mode of gene action. J Hered — PubMed:PMID5365620 | DOI:10.1093/oxfordjournals.jhered.a107973 — OMIA Phene_Article / Article - (22 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:137700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:137750 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:137760 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:137763 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:231300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:231300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600510 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600975 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [27]

Rabbit (Oryctolagus cuniculus) — Ataxia, generic (hereditary; OMIA-verified species predisposition)

Disorder: Ataxia, generic [28]

Summary: See Robinson (1958, p. 330-331) 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 entry symbol: ax (no structured Phene_Gene link) Evidence (references) - 1942. "Ataxia," a Hereditary Nervous Disorder of the Rabbit. Proc Natl Acad Sci U S A — PubMed:PMID16588528 | DOI:10.1073/pnas.28.4.123 — OMIA Phene_Article / Article - 1962. Hereditary ataxia of rabbits. Histopathological alterations. Arch Neurol — PubMed:PMID14480890 | DOI:10.1001/archneur.1962.00450200037004 — OMIA Phene_Article / Article - 1964. Hereditary ataxia in the rabbit: amino acid analyses of blood and brain. J Nerv Ment Dis — PubMed:PMID14206450 | DOI:10.1097/00005053-196408000-00004 — OMIA Phene_Article / Article - 1965. Ultrastructural lesions in rabbit hereditary ataxia. Arch Neurol — PubMed:PMID5832261 | DOI:10.1001/archneur.1965.00470030018002 — OMIA Phene_Article / Article - 1966. [Familial ataxia of the rabbit, different from the hereditary disease of Sawin-Anders. Preliminary communication]. Acta Neuropathol — PubMed:PMID6006977 | DOI:10.1007/BF00687854 — OMIA Phene_Article / Article - 1966. Carbohydrate metabolites in rabbit hereditary ataxia. Arch Neurol — PubMed:PMID5912009 | DOI:10.1001/archneur.1966.00470150061010 — OMIA Phene_Article / Article - 1967. Glycogen and glycolytic intermediates in rabbit hereditary ataxia. J Neuropathol Exp Neurol — PubMed:PMID6022138 — OMIA Phene_Article / Article - 1967. Inositide metabolism in rabbit hereditary ataxia. Arch Neurol — PubMed:PMID4293372 | DOI:10.1001/archneur.1967.00470300103017 — OMIA Phene_Article / Article - 1968. Hereditary ataxia of animals. Arch Neurol — PubMed:PMID5676918 | DOI:10.1001/archneur.1968.00480010052003 — OMIA Phene_Article / Article - 1970. Glucose 14C metabolism in rabbit hereditary ataxia. Arch Neurol — PubMed:PMID5435666 | DOI:10.1001/archneur.1970.00480230063007 — OMIA Phene_Article / Article - 1974. Familial ataxia of the rabbit Sawin-Anders type. Ultrastructural analysis of degeneration of the cochlear nuclei. Acta Neuropathol — PubMed:PMID4446957 | DOI:10.1007/BF00685318 — OMIA Phene_Article / Article [28]

Rabbit (Oryctolagus cuniculus) — Brachydactyly (hereditary; OMIA-verified species predisposition)

Disorder: Brachydactyly [29]

Summary: See Robinson (1958, pp. 341-342) 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 entry symbol: (no structured Phene_Gene link) Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1935. Hereditary brachydactylia and associated abnormalities in the rabbit. Science — PubMed:PMID17799086 | DOI:10.1126/science.81.2104.405-a — OMIA Phene_Article / Article - 1939. Hereditary brachydactylia and allied abnormalities in the rabbit. J Exp Med — PubMed:PMID19870848 | DOI:10.1084/jem.69.2.301 — OMIA Phene_Article / Article - 1977. Simultaneous prevention of blood abnormalities and hereditary congenital amputations in a brachydactylous rabbit stock. Teratology — PubMed:PMID301294 | DOI:10.1002/tera.1420150204 — OMIA Phene_Article / Article - 1984. Prevention of thrombocytic defects in the br/ rabbit with folic acid and vitamin B12: analogy with the T.A.R. syndrome in humans. Int J Vitam Nutr Res — PubMed:PMID6500844 — OMIA Phene_Article / Article - 1989. Animal models with inherited hematopoietic abnormalities as tools to study thrombopoiesis. Blood Cells — PubMed:PMID2649183 — OMIA Phene_Article / Article [29]

Rabbit (Oryctolagus cuniculus) — C3 deficiency (hereditary; OMIA-verified species predisposition)

Disorder: C3 deficiency [30]

Summary: C3 deficiency was discovered in a line of rabbits undergoing selection for high and low total complement haemolytic activity (Komatsu, 1985). Preliminary molecular studies by Komatsu (1992) showed that the mutant allele produces only very low levels of C3 mRNA, suggesting a mutation in a control region of the gene. Sequencing is now underway to determine the exact molecular defect. [30]

Clin feat: 10% of normal C3 serum levels; low survival rate; reduced serum bactericidal activity; suppressed delayed-type hypersensitivity [30]

Gen test: Using a 1.6 kb fragment of rabbit C2 cDNA as a probe in Southern analysis, the three genotypes at this locus can be detected with either BglII, StuI, or SacI (Komatsu, 1992). 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 entry symbol: C3D (no structured Phene_Gene link) Evidence (references) - 1988. Hereditary C3 hypocomplementemia in the rabbit. Immunology — PubMed:PMID3410489 — OMIA Phene_Article / Article - 1992. Molecular Biology for Genetic Deficiencies of Complement Components in Rabbits - C8alpha-gamma Deficiency and C3- Hypocomplementemia. JARQ - Japan Agricultural Research Quarterly — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:613779 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:120700 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [30]

Rabbit (Oryctolagus cuniculus) — C8 deficiency (hereditary; OMIA-verified species predisposition)

Disorder: C8 deficiency [31]

Summary: C8 deficiency was discovered in a line of rabbits undergoing selection for high and low total complement haemolytic activity (Komatsu, 1985). Both the alpha and gamma genes are transcribed, producing normal quantities of mRNA. However, the mature mRNA from the alpha gene of C8-deficient rabbits includes a 93-bp intron, suggesting that the disorder is due to a mutation at an exon/intron junction (Komatsu, 1992). Sequencing of mutant and normal genes is underway, to determining the exact mutation. [31]

Clin feat: dwarfism (non-pituitary); small litter size; small thymus; low survival rate; severely reduced bactericidal activity; enhanced delayed-type hypersensitivity 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 43731941 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1991. Genetic Deficiency of Complement Component-C8 in the Rabbit - Evidence of a Translational Defect in Expression of the alpha-gamma Subunit. Biochemical Genetics — PubMed:PMID1772398 — OMIA Phene_Article / Article - 1990. Hereditary C8-alpha-gamma deficiency associated with dwarfism in the rabbit. Journal of Heredity — OMIA Phene_Article / Article - 1992. Molecular Biology for Genetic Deficiencies of Complement Components in Rabbits - C8alpha-gamma Deficiency and C3- Hypocomplementemia. JARQ - Japan Agricultural Research Quarterly — OMIA Phene_Article / Article - 1985. Genetic deficiency of the alpha-gamma subunit of the eighth complement component in rabbits. Journal of Immunology — PubMed:PMID3973389 — OMIA Phene_Article / Article - 1985. A method for developing hereditary deficiency of complement component in the rabbit. Experimental Animals — PubMed:PMID4018150 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:120950 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:613790 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [31]

Rabbit (Oryctolagus cuniculus) — Cataract, GJA8-related (hereditary; OMIA-verified species predisposition)

Disorder: Cataract, GJA8-related [32]

Summary: Yuan et al. (2016) generated GJA8-deficient rabbits using CRISPR/Cas9 gene editing to develop a rabbit model for congenital cataracts. Rabbits with impaired GJA8 function presented with microphthalmia, small lens size and cataracts. (GMO) 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 389124555 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2016. CRISPR/Cas9-mediated GJA8 knockout in rabbits recapitulates human congenital cataracts. Sci Rep — PubMed:PMID26912477 | DOI:10.1038/srep22024 — OMIA Phene_Article / Article - 2023. Congenital cataracts affect the retinal visual cycle and mitochondrial function: A multi-omics study of GJA8 knockout rabbits. J Proteomics — PubMed:PMID37467890 | DOI:10.1016/j.jprot.2023.104972 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:116200 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600897 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [32]

Rabbit (Oryctolagus cuniculus) — Cataract, generic (hereditary; OMIA-verified species predisposition)

Disorder: Cataract, generic [33]

Summary: See Robinson (1958, p. 326) 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 entry symbol: ca (no structured Phene_Gene link) Evidence (references) - 2002. Spontaneous cataracts in laboratory rabbits. Vet Ophthalmol — PubMed:PMID12236868 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1964. [Histological findings in hereditary cataract in animals]. Ber Zusammenkunft Dtsch Ophthalmol Ges — PubMed:PMID14260526 — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 2015. High incidence of spontaneous cataracts in aging laboratory rabbits of an inbred strain. Vet Ophthalmol — PubMed:PMID25123814 | DOI:10.1111/vop.12203 — OMIA Phene_Article / Article [33]

Rabbit (Oryctolagus cuniculus) — Cleft lip, GADD45G-related (hereditary; OMIA-verified species predisposition)

Disorder: Cleft lip, GADD45G-related [34]

Summary: Lu et al. (2019) "reported the generation of a novel GADD45G mutated rabbit model by CRISPR/Cas9 and CRISPR-based BE4-Gam systems. The homozygous (GADD45G-/-) while not heterozygous (GADD45G+/-) pups died after birth due to severe craniofacial defects of unilateral or bilateral cleft lip (CL)." [34]

Clin feat: Lu et al. (2019): "all GADD45G−/− rabbits died within three days of birth and exhibited unilateral (10%) or bilateral (90%) cleft lip (CL) at the postnatal 3 days." 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 389120055 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2019. Mutations of GADD45G in rabbits cause cleft lip by the disorder of proliferation, apoptosis and epithelial-mesenchymal transition (EMT). Biochim Biophys Acta Mol Basis Dis — PubMed:PMID31150757 | DOI:10.1016/j.bbadis.2019.05.015 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:604949 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [34]

Rabbit (Oryctolagus cuniculus) — Coat colour, English spotting (hereditary; OMIA-verified species predisposition)

Disorder: Coat colour, English spotting [35]

Mode of inheritance: As summarised by Fontanesi et al. (2014), who provided additional segregation data that supported single-locus inheritance, "Rabbits homozygous for the recessive non-mutated allele (en/en) are self-colored (not spotted). Heterozygous En/en rabbits are normally spotted and possess far larger patches of colored fur compared to the homozygous En/En animals that have a reduced spotted pattern". [35]

Summary: Also known as Dominant White Spotting. For a through summary of early literature, see Robinson (1958, p. 263-265). [35]

Clin feat: As summarised by Fontanesi et al. (2014) "En/En rabbits are subvital compared to vital heterozygous En/en rabbits because dominant homozygous animals are affected by an underlying megacolon" (Robinson, 1958; Bodeker et al., 1995; Wieberneit and Wegner, 1995) 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 entry symbol: En (no structured Phene_Gene link) - OMIA molecular-genetics note: Because this coat-colour locus is associated with megacolon (see Clinical features), Fontanesi et al. (2010) investigated EDNRB as a comparative functional candidate gene, because mutations in this gene give rise to megacolon in horse (OMIA 000629-9796) and human (OMIM 600155). However, they were able to rule out EDNRB as the causative gene for this trait in rabbits. Evidence (references) - 1992. [The problem of breeding for spots in rabbits. 2. Further results on the variation of characteristics in fattening and breeding animals]. Dtsch Tierarztl Wochenschr — PubMed:PMID1576947 — OMIA Phene_Article / Article - 1993. [The problems of breeding spotted rabbits. 3. Variability of the pigmentation grade, ganglionic intestinal wall supply, relationship to pathogenesis--animal breeding and animal welfare aspects]. Dtsch Tierarztl Wochenschr — PubMed:PMID8339710 — OMIA Phene_Article / Article - 1994. [The problems of spotted breeds of rabbits. 4. Morpho- and histometric findings in the CNS and thyroid glands and the hormone content in blood at slaughter of hybrid rabbits, and estimation of the heterosis effect]. Dtsch Tierarztl Wochenschr — PubMed:PMID7895623 — OMIA Phene_Article / Article - 1995. Pathophysiological and functional aspects of the megacolon-syndrome of homozygous spotted rabbits. Zentralbl Veterinarmed A — PubMed:PMID8822192 | DOI:10.1111/j.1439-0442.1995.tb00410.x — OMIA Phene_Article / Article - 1954. White spotting in mice and rabbits. Genetica — PubMed:PMID14366219 — OMIA Phene_Article / Article - 2010. Endothelin receptor B (EDNRB) is not the causative gene of the English spotting locus in the domestic rabbit (Oryctolagus cuniculus). Anim Genet — PubMed:PMID20497153 | DOI:10.1111/j.1365-2052.2010.02084.x — OMIA Phene_Article / Article - 1924. Linkage of Dutch, English, and Angora in Rabbits. Proc Natl Acad Sci U S A — PubMed:PMID16576789 | DOI:10.1073/pnas.10.3.107 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2014. The KIT gene is associated with the english spotting coat color locus and congenital megacolon in Checkered Giant rabbits (Oryctolagus cuniculus). PLoS One — PubMed:PMID24736498 | DOI:10.1371/journal.pone.0093750 — OMIA Phene_Article / Article - 1995. Albino rabbits can suffer from Megacolon-Syndrome when they are homozygous for the “English-spot” gene (En En). World Rabbit Science — OMIA Phene_Article / Article - 1991. [The problems of spotted breeds of rabbits. 1. Fattening and body condition at slaughter, organ parameters]. Dtsch Tierarztl Wochenschr — PubMed:PMID1954863 — OMIA Phene_Article / Article - 2021. Rabbits - their domestication and molecular genetics of hair coat development and quality. Anim Genet — PubMed:PMID33216407 | DOI:10.1111/age.13024 — OMIA Phene_Article / Article - (2 additional references in OMIA) [35]

Rabbit (Oryctolagus cuniculus) — Congenital adrenal hyperplasia (hereditary; OMIA-verified species predisposition)

Disorder: Congenital adrenal hyperplasia [36]

Clin feat: Death within 3 days of birth; complete feminization of external genitalia of males; grossly enlarged adrenals (195 mg cf 3 mg); hypertrophied zona fasciculta cells with multiple vacuolization 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: CYPXIA1 (Entrez Gene ID 175428176) — OMIA Phene_Gene / GeneSynonym - OMIA molecular-genetics note: Molecular evidence provided by Yang et al. (1993) implicates a large deletion in the gene for cholesterol side-chain cleavage enzyme (P450SCC, renamed CYP11A1). Sequencing of the normal and mutant forms should provide definitive evidence of the nature of the mutation. Evidence (references) - 1993. Inherited congenital adrenal hyperplasia in the rabbit is caused by a deletion in the gene encoding cytochrome-P450 cholesterol side-chain cleavage enzyme. Endocrinology — PubMed:PMID7682938 | DOI:10.1210/endo.132.5.7682938 — OMIA Phene_Article / Article - 1994. Evidence of a steroidogenic enzyme gene dose effect on adrenal gene expression in hereditary rabbit congenital adrenal hyperplasia. Pediatric Research — PubMed:PMID7877888 — OMIA Phene_Article / Article - 1978. Genetics and pathology of hereditary adrenal hyperplasia in the rabbit. Journal of Heredity — PubMed:PMID731013 — OMIA Phene_Article / Article - 1992. Inherited congenital adrenal hyperplasia in the rabbit: absent cholesterol side-chain cleavage cytochrome P450 gene expression. Endocrinology — PubMed:PMID1611996 — OMIA Phene_Article / Article - 2023. Models of congenital adrenal hyperplasia for gene therapies testing. Int J Mol Sci — PubMed:PMID36982440 | DOI:10.3390/ijms24065365 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:118485 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:613743 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [36]

Rabbit (Oryctolagus cuniculus) — Cyclopia (hereditary; OMIA-verified species predisposition)

Disorder: Cyclopia [37]

Summary: See Robinson (1958, p. 348) 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: Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article [37]

Rabbit (Oryctolagus cuniculus) — Cystic fibrosis (hereditary; OMIA-verified species predisposition)

Disorder: Cystic fibrosis [38]

Summary: Yang et al. (2020) "report the production of CFTR-ΔF508 rabbits by CRISPR/Cas9-mediated gene editing." This study involves genetically modified organisms (GMO). 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 398298869 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2024. Sotagliflozin attenuates liver associated disorders in cystic fibrosis rabbits. JCI Insight — PubMed:PMID38358827 | DOI:10.1172/jci.insight.165826 — OMIA Phene_Article / Article - 2021. Phenotypes of CF rabbits generated by CRISPR/Cas9-mediated disruption of the CFTR gene. JCI Insight — PubMed:PMID33232302 | DOI:10.1172/jci.insight.139813 — OMIA Phene_Article / Article - 2020. Production of CFTR-ΔF508 rabbits. Front Genet — PubMed:PMID33552140 | DOI:10.3389/fgene.2020.627666 — OMIA Phene_Article / Article - 2023. Cystic fibrosis rabbits develop spontaneous hepatobiliary lesions and CF-associated liver disease (CFLD)-like phenotypes. PNAS Nexus — PubMed:PMID36712930 | DOI:10.1093/pnasnexus/pgac306 — OMIA Phene_Article / Article - 2021. Intestinal dysbiosis in young cystic fibrosis rabbits. J Pers Med — PubMed:PMID33669429 | DOI:10.3390/jpm11020132 — OMIA Phene_Article / Article - 2024. Endocrine pathology in young rabbits with cystic fibrosis. eGastroenterology — PubMed:PMID39605883 | DOI:10.1136/egastro-2024-100102 — OMIA Phene_Article / Article - 2026. Male reproductive phenotype in cystic fibrosis: comparison of existing animal models. Lab Anim (NY) — PubMed:PMID42380629 | DOI:10.1038/s41684-026-01763-0 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:219700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:602421 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [38]

Rabbit (Oryctolagus cuniculus) — Delta 9-tetrahydrocannabinol seizure (hereditary; OMIA-verified species predisposition)

Disorder: Delta 9-tetrahydrocannabinol seizure [39]

Summary: Fish et al. (1981): "Delta 9-Tetrahydrocannabinol (THC), the major psychoactive ingredient of marijuana, causes nonfatal convulsions in rabbits of a closed colony of New Zealand White rabbits (Uaz: NZW). The convulsive phenotype appears to be associated with homozygous expression of a single autosomal recessive gene with full penetrance." 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 entry symbol: thc (no structured Phene_Gene link) Evidence (references) - 1981. Inheritance of delta 9-tetrahydrocannabinol seizure susceptibility in rabbits. J Hered — PubMed:PMID6268703 — OMIA Phene_Article / Article - 1983. The ontogeny of delta-9-tetrahydrocannabinol responsiveness in the rabbit. Dev Psychobiol — PubMed:PMID6299864 | DOI:10.1002/dev.420160207 — OMIA Phene_Article / Article - 1983. Convulsant-anticonvulsant properties of delta-9-tetrahydrocannabinol in rabbits. Behav Genet — PubMed:PMID6305325 | DOI:10.1007/BF01065669 — OMIA Phene_Article / Article [39]

Rabbit (Oryctolagus cuniculus) — Diabetes mellitus (hereditary; OMIA-verified species predisposition)

Disorder: Diabetes mellitus [40]

Summary: Song et al. (2019) developed a "rabbit with a non-frameshift mutation of GCK gene (GCK-NFS) by cytoplasm microinjection of Cas9 mRNA and gRNA. These GCK-NFS rabbits showed typical features of MODY-2 including hyperglycemia and glucose intolerance with similar survival rate and weight compared to wild-type (WT) rabbits." This is a genetically-modified organism (GMO). 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 389108310 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1998. Diabetes mellitus in rabbits, guinea pigs and chinchillas [German]. Kleintierpraxis — OMIA Phene_Article / Article - 2019. Genetic deletion of a short fragment of glucokinase in rabbit by CRISPR/Cas9 leading to hyperglycemia and other typical features seen in MODY-2. Cell Mol Life Sci — PubMed:PMID31720743 | DOI:10.1007/s00018-019-03354-4 — OMIA Phene_Article / Article - 2023. Contribution of animal models to diabetes research: Its history, significance, and translation to humans. J Diabetes Investig — PubMed:PMID37401013 | DOI:10.1111/jdi.14034 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:125850 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:125851 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:125852 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:125853 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:176730 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:222100 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:222300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:520000 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [40]

Rabbit (Oryctolagus cuniculus) — Difference of sexual development, DMRT1-related (hereditary; OMIA-verified species predisposition)

Disorder: Difference of sexual development, DMRT1-related [41]

Summary: Dujardin et al. (2023) "abolished DMRT1 expression by CRISPR/Cas9 in. the rabbit. First, we observed that gonads from XY DMRT1−/− rabbit fetuses differentiated like ovaries, highlighting that DMRT1 is involved in testis determination.. Second, we highlighted another function of DMRT1 in the germline since XX and XY DMRT1−/− ovaries did not undergo meiosis and folliculogenesis. XX DMRT1−/− adult females were sterile, showing that DMRT1 is also crucial for female fertility." This study involves genetically modified organisms (GMO). 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 389106167 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2023. DMRT1 is a testis-determining gene in rabbits and is also essential for female fertility. Elife — PubMed:PMID37847154 | DOI:10.7554/eLife.89284 — OMIA Phene_Article / Article - 2024. [Dmrt1 is a major gene for testicular determination and for male and female fertility in rabbits]. Med Sci (Paris) — PubMed:PMID38520096 | DOI:10.1051/medsci/2024004 — OMIA Phene_Article / Article - 2025. DMRT1 haploinsufficiency leads to secondary infertility in XY male rabbits. Biol Reprod — PubMed:PMID40169148 | DOI:10.1093/biolre/ioaf064 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:602424 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [41]

Rabbit (Oryctolagus cuniculus) — Dwarfism, Dahlem (hereditary; OMIA-verified species predisposition)

Disorder: Dwarfism, Dahlem [42]

Clin feat: As summarised by Robinson (1958): "These dwarfs are a little more viable, many surviving to the age of 3 weeks, although some die soon after birth. The gene, da, is not fully recessive and homozygous dwarfs, dada, are approximately half the normal weight and their subsequent growth is very tardy. The head is abnormally short and the lower incisors may lie in front of the upper instead of behind; consequently the teeth may be excessively long. The forehead appears swollen and the eyeballs 'protrude (exophthalmus). The heterozygote is smaller than the homozygous normal somewhat similarly to the other dwarf types." 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 entry symbol: da (no structured Phene_Gene link) Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1937. Erbpathologie des Kaninchen. Erbarzt (Leipzig) — OMIA Phene_Article / Article - 1941. Zwergwuch beim Kaninchen und seine Vererbung. Z. Menschl. Vererbgs. Konstl — OMIA Phene_Article / Article [42]

Rabbit (Oryctolagus cuniculus) — Dwarfism, generic (hereditary; OMIA-verified species predisposition)

Disorder: Dwarfism, generic [15]

Mode of inheritance: As reported by Carneiro et al. (2017), "The dwarf phenotype characterizes the smallest of rabbit breeds and is governed largely by the effects of a single dwarfing allele with an incompletely dominant effect on growth. Dwarf rabbits typically weigh under 1 kg and have altered craniofacial morphology. The dwarf allele is recessive lethal and dwarf homozygotes die within a few days of birth. The dwarf phenotype is expressed in heterozygous individuals and rabbits from dwarf breeds homozygous for the wild-type allele are normal, although smaller when compared to other breeds." The mode of inheritance has been changed from 'autosomal recessive lethal' to 'autosomal incompletely dominant' in May 2022 to reflect that animals with a single copy of the HMGA2 mutation present with a milder form of dwarfism.Bovo et al. (2025) report that additional genes contribute to dwarfism in rabbits and their study supports a polygenic mode of inheritance. [15]

Clin feat: As reported by Green et al. (1934): "The [homozygous] dwarfs of this stock are born alive and occasionally they are capable of nursing, but so far, none of them has lived longer than a few days. They are delicately formed and to outward appearance are fully developed except for the bones of the calvarium, which, as a rule, are incompletely calcified." Carneiro et al. (2016) summarise the phenotype information reported by Robinson (1958): " The dwarf allele is recessive lethal. Homozygotes ( dw/dw ) are smaller than litter mates and exhibit a characteristic swollen head, tiny ears, and are usually called peanuts.. Peanuts are viable up to the time of birth but typically die within a few days of birth. Heterozygotes ( Dw/dw ) reach ∼2/3 of the size of wild-type litter mates ( Dw / Dw ) and in adulthood are typically under 1 kg in body weight, have compact and rounded bodies, a disproportionately larger head when compared to the rest of the body, small ears, and a short snout due to altered craniofacial development.." Several resources suggest that the altered craniofacial development may predispose dwarf rabbits to an increased risk to develop dental disease (e.g. Harcourt-Brown, 1997; Wegner, 1997; van Caelenberg et al., 2008; Koroleva and Titova, 2022). [15]

Rabbit (Oryctolagus cuniculus) — Ectodermal dysplasia-9 (hereditary; OMIA-verified species predisposition)

Disorder: Ectodermal dysplasia-9 [43]

Summary: This entry describes a genetically-modified organism (GMO) 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 389118648 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Deng et al. (2019) created a rabbit model of human ectodermal dysplasia-9 by ablating the rabbit Hoxc13 gene. Evidence (references) - 2019. The disrupted balance between hair follicles and sebaceous glands in Hoxc13-ablated rabbits. FASEB J — PubMed:PMID30125135 | DOI:10.1096/fj.201800928RR — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:614931 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:142976 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [43]

Rabbit (Oryctolagus cuniculus) — Epilepsy (hereditary; OMIA-verified species predisposition)

Disorder: Epilepsy [44]

Summary: See Robinson (1958, pp. 331-333). 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 entry symbol: ep (no structured Phene_Gene link) Evidence (references) - 1979. Genetic animal models of epilepsy. Introduction. Fed Proc — PubMed:PMID478016 — OMIA Phene_Article / Article - 1957. Familial epileptiform disease in a breed of rabbits. Wiener Tierärztliche Monatsschrift — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1955. Recent genetics of the domestic rabbit. Adv Genet — PubMed:PMID13258375 | DOI:10.1016/s0065-2660(08)60096-6 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:104130 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:117100 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:121200 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:121201 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:125370 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:132090 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:132100 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:132300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:159600 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:182610 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:203600 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:208700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:220300 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:226750 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:226800 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:226810 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:226850 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:254770 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:254780 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:254800 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:266270 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:267740 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:270805 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:301900 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:310370 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:545000 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600131 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600143 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600512 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600513 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600669 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:601068 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:245570 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [44]

Rabbit (Oryctolagus cuniculus) — Furless (hereditary; OMIA-verified species predisposition)

Disorder: Furless [45]

Summary: See Robinson (1958, p. 337-339) 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 entry symbol: f; na (no structured Phene_Gene link) Evidence (references) - 2006. Inheritance of the naked gene and associations with postweaning performance and thermotolerance characters in fryer rabbits from an F2 generation. World Rabbit Science — OMIA Phene_Article / Article - 1996. Phenotypical description of hairless rabbits appeared in three different herds. Proceedings of the 6th World Rabbit Congress,Toulouse, France . — OMIA Phene_Article / Article - 1928. Naked – a recessive mutation in the rabbit. Journal of Heredity — OMIA Phene_Article / Article - 2004. Effects of the naked gene on postweaning performance and thermotolerance characters in fryer rabbits. World Rabbit Science — OMIA Phene_Article / Article [45]

Rabbit (Oryctolagus cuniculus) — Furless (hereditary; OMIA-verified species predisposition)

Summary: See Robinson (1958, pp. 337-338). 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 entry symbol: f (no structured Phene_Gene link) Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1933. The furless rabbit. Journal of Heredity — OMIA Phene_Article / Article - 1933. An anatomical study of the furless condition in rabbits. Journal of Morphology — OMIA Phene_Article / Article - 2006. Fiber production and properties in genetically furred and furless rabbits. J Anim Sci — PubMed:PMID16908662 | DOI:10.2527/jas.2006-106 — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article [46]

Rabbit (Oryctolagus cuniculus) — H ydrocephalia (hereditary; OMIA-verified species predisposition)

Disorder: H ydrocephalia [47]

Summary: See Robinson (1958, pp. 333-334). 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: Evidence (references) - 1966. Hydrocephalus and cleft palate in an inbred rabbit colony. Journal of Heredity — PubMed:PMID6007532 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1966. Hydrocephalus and cleft palate in an inbred rabbit colony. Journal of Heredity — PubMed:PMID6007532 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:109400 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:112240 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:123155 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:209970 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236600 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236635 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236640 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236660 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236670 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236690 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:273730 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:276950 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:307000 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:307010 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:314390 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:123155 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600257 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600559 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600991 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:615181 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:109400 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:112240 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:123155 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:209970 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236600 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236635 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236640 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236660 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236670 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236690 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:273730 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:276950 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:307000 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:307010 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:314390 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:123155 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600257 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600559 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600991 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:615181 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [47]

Rabbit (Oryctolagus cuniculus) — Hydrops foetalis (hereditary; OMIA-verified species predisposition)

Disorder: Hydrops foetalis [48]

Summary: See Robinson (1958, pp. 352-353). 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: Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:215140 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236750 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:215140 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:236750 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [48]

Rabbit (Oryctolagus cuniculus) — Hypercholesterolaemia, PCSK9-related (hereditary; OMIA-verified species predisposition)

Disorder: Hypercholesterolaemia, PCSK9-related [49]

Summary: Genetically-modified organism; GMO 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 389105140 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2021. Construction of point mutation rabbits using CRISPR/Cas9. Zhejiang Da Xue Xue Bao Yi Xue Ban — PubMed:PMID34137224 | DOI:10.3724/zdxbyxb-2021-0133 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:603776 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:607786 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [49]

Rabbit (Oryctolagus cuniculus) — Hyperlipidaemia/atherosclerosis, APOE-related (hereditary; OMIA-verified species predisposition)

Disorder: Hyperlipidaemia/atherosclerosis, APOE-related [50]

Summary: This is a genetically-modified organism (GMO) 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 388912575 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2016. ApoE knockout rabbits: A novel model for the study of human hyperlipidemia. Atherosclerosis — PubMed:PMID26724529 | DOI:10.1016/j.atherosclerosis.2015.12.002 — OMIA Phene_Article / Article - 2020. Animal models of human atherosclerosis: current progress. Braz J Med Biol Res — PubMed:PMID32428130 | DOI:10.1590/1414-431x20209557 — OMIA Phene_Article / Article - 2020. Apolipoprotein E knockout rabbit model of intracranial atherosclerotic disease. Animal Model Exp Med — PubMed:PMID32613180 | DOI:10.1002/ame2.12125 — OMIA Phene_Article / Article - 2021. Research methods for animal models of atherosclerosis (Review). Mol Med Rep — PubMed:PMID34713295 | DOI:10.3892/mmr.2021.12511 — OMIA Phene_Article / Article - 2024. Enhanced atherosclerosis in apolipoprotein E knockout rabbits: role of apoB48-rich remnant lipoproteins. Front Cardiovasc Med — PubMed:PMID39087075 | DOI:10.3389/fcvm.2024.1424064 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:107741 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:617347 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [50]

Rabbit (Oryctolagus cuniculus) — Hypophosphatemic rickets, autosomal recessive, 1 (hereditary; OMIA-verified species predisposition)

Disorder: Hypophosphatemic rickets, autosomal recessive, 1 [51]

Summary: Liu et al. (2019) "deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR" [autosomal recessive form of hypophosphatemic rickets]. This model is, therefore, a genetically-modified organism (GMO). 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 389111537 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2019. DMP1 ablation in the rabbit results in mineralization defects and abnormalities in Haversian canal/osteon microarchitecture. J Bone Miner Res — PubMed:PMID30827034 | DOI:10.1002/jbmr.3683 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:241520 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600980 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [51]

Rabbit (Oryctolagus cuniculus) — Hypoxanthine guanine phosphoribosyltransferase deficiency (hereditary; OMIA-verified species predisposition)

Disorder: Hypoxanthine guanine phosphoribosyltransferase deficiency [52]

Summary: This phene includes references to studies involving gene edited or genetically modified organisms (GMO). 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 398298898 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene - OMIA molecular-genetics note: Yin et al. (2024) created a rabbit model for Lesch-Nyhan syndrome using CRISPR/Cas9 HPRT knock out. Evidence (references) - 2024. Establishment and characterization of Lesch-Nyhan syndrome rabbit model. Yi Chuan — PubMed:PMID38763775 | DOI:10.16288/j.yczz.24-012 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:300322 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:308000 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [52]

Rabbit (Oryctolagus cuniculus) — Leg weakness (hereditary; OMIA-verified species predisposition)

Disorder: Leg weakness [53]

Mode of inheritance: Joosten et al. (1981): "Pedigree analysis and genetic mating tests showed that, in contrast to published reports, the disease is not determined by a single recessive gene with complete expressivity. The underlying genetic system is composed of one recessive gene with reduced expressivity or of more genes with the probable involvement of environmental factors." [53]

Clin feat: Joosten et al. (1981): "Femurs of abnormal limbs displayed endotorsion of the shaft and anteversion of the neck as the main features. Endotorsion of the femur was associated with exotorsion of the tibia. Dislocation of the hip was not observed. There was no abnormnal laxity of the joint capsule or the ligamentaum teres." [53]

Pathology: Joosten et al. (1981): "A study on muscle fiber diameter showed that fibers of splayleg animals were in general smaller, particularly in the semitendinosus. Atypical mitochondria of muscles were observed in all rabbits, but more frequently in splayleg animals." 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: Evidence (references) - 1981. Splayleg: a spontaneous limb defect in rabbits. Genetics, gross anatomy, and microscopy. Teratology — PubMed:PMID7302875 | DOI:10.1002/tera.1420240110 — OMIA Phene_Article / Article - 1981. Splayleg: a spontaneous limb defect in rabbits. Genetics, gross anatomy, and microscopy. Teratology — PubMed:PMID7302875 | DOI:10.1002/tera.1420240110 — OMIA Phene_Article / Article [53]

Rabbit (Oryctolagus cuniculus) — Lethality, RYR2-related (hereditary; OMIA-verified species predisposition)

Disorder: Lethality, RYR2-related [54]

Summary: Zheng et al. (2022) "used a constitutive knock-out of RyR2 in rabbits (RyR2-KO) to assess the extent to which a stable decrease in RyR2 expression modulates Ca2+ handling in the heart. We found that homozygous knock-out of RyR2 in rabbits is embryonic lethal. Remarkably, heterozygotes (KO+/-) show ~50% loss of RyR2 protein without developing an overt phenotype at the intact animal and whole heart levels." This study involves genetically modified organisms (GMO). 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: RYR-2 (Entrez Gene ID 388912770) — OMIA Phene_Gene / GeneSynonym Evidence (references) - 2022. Preserved cardiac performance and adrenergic response in a rabbit model with decreased ryanodine receptor 2 expression. J Mol Cell Cardiol — PubMed:PMID35413295 | DOI:10.1016/j.yjmcc.2022.04.004 — OMIA Phene_Article / Article [54]

Rabbit (Oryctolagus cuniculus) — Luxate femur (hereditary; OMIA-verified species predisposition)

Disorder: Luxate femur [55]

Summary: See Robinson (1958, pp. 347-348). 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: Evidence (references) - 1959. "Inherited dysplasia" of the hip joint in dogs and rabbits. Lab Invest — PubMed:PMID13852893 — OMIA Phene_Article / Article - 2001. Hip dysplasia in rabbits: association with nest box flooring. Comp Med — PubMed:PMID11926308 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1957. Splayleg in rabbits; an inherited disease analogous to joint dysplasia in children and dogs. Lab Invest — PubMed:PMID13406999 — OMIA Phene_Article / Article - 1959. "Inherited dysplasia" of the hip joint in dogs and rabbits. Lab Invest — PubMed:PMID13852893 — OMIA Phene_Article / Article - 2001. Hip dysplasia in rabbits: association with nest box flooring. Comp Med — PubMed:PMID11926308 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1957. Splayleg in rabbits; an inherited disease analogous to joint dysplasia in children and dogs. Lab Invest — PubMed:PMID13406999 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:142669 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:142700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:244510 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:265050 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:615612 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:142669 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:142700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:244510 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:265050 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:615612 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [55]

Rabbit (Oryctolagus cuniculus) — Marfan syndrome (hereditary; OMIA-verified species predisposition)

Disorder: Marfan syndrome [56]

Summary: Chen et al. (2018) "describe the generation of a rabbit MPL [Marfanoid-progeroid-lipodystrophy] model with C-terminal truncation of fibrillin-1 using a CRISPR/Cas9 system. FBN1 heterozygous (FBN1 Het) rabbits faithfully recapitulated the phenotypes of MFS [Marfan syndrome], including muscle wasting and impaired connective tissue, ocular syndrome and aortic dilation. Moreover, skin symptoms, lipodystrophy, growth retardation and dysglycemia were also seen in these FBN1 Het rabbits.. " This phene includes references to studies involving gene edited or genetically modified organisms (GMO). 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 398298828 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2024. Genetic models of fibrillinopathies. Genetics — PubMed:PMID37972149 | DOI:10.1093/genetics/iyad189 — OMIA Phene_Article / Article - 2018. Truncated C-terminus of fibrillin-1 induces Marfanoid-progeroid-lipodystrophy (MPL) syndrome in rabbit. Dis Model Mech — PubMed:PMID29666143 | DOI:10.1242/dmm.031542 — OMIA Phene_Article / Article - 2024. Marfan syndrome: insights from animal models. Front Genet — PubMed:PMID39834548 | DOI:10.3389/fgene.2024.1463318 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:154700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:134797 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:604308 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [56]

Rabbit (Oryctolagus cuniculus) — Microcephaly, YIPF5-related (hereditary; OMIA-verified species predisposition)

Disorder: Microcephaly, YIPF5-related [57]

Summary: Liu et al. (2023) "constructed a rabbit PMCPH [primary microcephaly] model harboring YIPF5 (p.W218R) mutation using SpRY-ABEmax mediated base substitution, which precisely recapitulated the typical symptoms of human PMCPH." This study involves genetically modified organisms (GMO). 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 389123594 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2023. YIPF5 (p.W218R) mutation induced primary microcephaly in rabbits. Neurobiol Dis — PubMed:PMID37142085 | DOI:10.1016/j.nbd.2023.106135 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:611483 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:619278 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [57]

Rabbit (Oryctolagus cuniculus) — Muscle contracture (hereditary; OMIA-verified species predisposition)

Disorder: Muscle contracture [58]

Summary: See Robinson (1958, p. 334) 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: Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1955. Recent genetics of the domestic rabbit. Adv Genet — PubMed:PMID13258375 | DOI:10.1016/s0065-2660(08)60096-6 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1955. Recent genetics of the domestic rabbit. Adv Genet — PubMed:PMID13258375 | DOI:10.1016/s0065-2660(08)60096-6 — OMIA Phene_Article / Article [58]

Rabbit (Oryctolagus cuniculus) — Muscular dystrophy, ANO5-related (hereditary; OMIA-verified species predisposition)

Disorder: Muscular dystrophy, ANO5-related [59]

Summary: Sui et al. (2018) "engineered mutant ANO5 rabbits via co-injection of Cas9 mRNA and sgRNA into the zygotes. CRISPR-mediated small indels in the exon 12 and/or 13 in the mutant rabbits lead to the development of typical signs of muscular dystrophy with increased serum creatine kinase (CK), muscle necrosis, regeneration, fatty replacement and fibrosis." These animals are genetically-modifeed organisms (GMO). 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 389106752 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2018. Development of muscular dystrophy in a CRISPR-engineered mutant rabbit model with frame-disrupting ANO5 mutations. Cell Death Dis — PubMed:PMID29789544 | DOI:10.1038/s41419-018-0674-y — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:613319 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:611307 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:608662 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [59]

Rabbit (Oryctolagus cuniculus) — Osteopetrosis (hereditary; OMIA-verified species predisposition)

Disorder: Osteopetrosis [60]

Summary: See Robinson (1958, pp. 348-349). 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 entry symbol: os (no structured Phene_Gene link) Evidence (references) - 1991. Congenitally osteosclerotic (os/os) rabbits are not cured by bone marrow transplantation from normal littermates. Am J Anat — PubMed:PMID1759690 | DOI:10.1002/aja.1001920307 — OMIA Phene_Article / Article - 1948. Hereditary osteopetrosis of the rabbit. Fed Proc — PubMed:PMID18932635 — OMIA Phene_Article / Article - 1948. Hereditary osteopetrosis of the rabbit; general features and course of disease; genetic aspects. J Exp Med — PubMed:PMID18103397 | DOI:10.1084/jem.88.6.579 — OMIA Phene_Article / Article - 1948. Hereditary osteopetrosis of the rabbit; X-ray, hematologic, and chemical observations. J Exp Med — PubMed:PMID18103398 — OMIA Phene_Article / Article - 1950. Hereditary osteopetrosis of the rabbit. III. Pathologic observations; skeletal abnormalities. J Exp Med — PubMed:PMID14784539 — OMIA Phene_Article / Article - 1950. Hereditary osteopetrosis of the rabbit. IV. Pathologic observations; general features. J Exp Med — PubMed:PMID14784540 — OMIA Phene_Article / Article - 1986. The osteopetrotic rabbit: general and skeletal features of a new outbred stock. Bone — PubMed:PMID3790375 — OMIA Phene_Article / Article - 1987. The osteopetrotic rabbit: skeletal cytology and ultrastructure. Am J Anat — PubMed:PMID3578090 | DOI:10.1002/aja.1001780310 — OMIA Phene_Article / Article - 1989. Treatment of congenital osteopetrosis in the rabbit with high-dose 1,25-dihydroxyvitamin D. J Bone Miner Res — PubMed:PMID2718779 | DOI:10.1002/jbmr.5650040109 — OMIA Phene_Article / Article - 1990. Relationship of abnormalities in dental and skeletal development in the osteopetrotic (os) rabbit. J Oral Pathol Med — PubMed:PMID2313606 — OMIA Phene_Article / Article - 1990. Defective osteoclast differentiation and function in the osteopetrotic (os) rabbit. Am J Anat — PubMed:PMID2393000 | DOI:10.1002/aja.1001880412 — OMIA Phene_Article / Article - 1990. Effects of 1,25 dihydroxyvitamin D on osteoclast number and cytochemistry in normal and osteopetrotic (os) rabbits. Am J Anat — PubMed:PMID2148052 | DOI:10.1002/aja.1001890309 — OMIA Phene_Article / Article - (1 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:259700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:259710 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:259720 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:259730 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:600329 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [60]

Rabbit (Oryctolagus cuniculus) — Paresis, posterior (hereditary; OMIA-verified species predisposition)

Disorder: Paresis, posterior [61]

Summary: See Robinson (1958, p. 335). 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: Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article [61]

Rabbit (Oryctolagus cuniculus) — Pelger-Huet anomaly (hereditary; OMIA-verified species predisposition)

Disorder: Pelger-Huet anomaly [62]

Mode of inheritance: Undritz (1939) and Nachsteim (1950) presented evidence of single-locus inheritance, with heterozygotes showing the disorder and homozygotes showing an extreme form of the disorder, including chondrodysplasia, that results in neonatal death in almost all cases. [62]

Summary: See Robinson (1958, pp. 354-355). 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 entry symbol: Pg (no structured Phene_Gene link) Evidence (references) - 1977. [Studies on the frequency of the Pelger anomaly in the domestic rabbit population]. Zentralbl Veterinarmed A — PubMed:PMID407754 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1950. The Pelger-anomaly in man and rabbit; a mendelian character of the nuclei of the leucocytes. J Hered — PubMed:PMID15436969 | DOI:10.1093/oxfordjournals.jhered.a106108 — OMIA Phene_Article / Article - 1952. Beitrage zur Morphologic und Gtnetik der Pelger-Anomalie bei Mensch und Kaninchen [Morphology and genetics of the Pelger anomaly in man and the rabbit]. Zeitschrift fur menschliche Vererbungs- und Konstitutionslehre — OMIA Phene_Article / Article - 1939. Das Pelger-Huetsche Blutbild beim Tier und seine Bedeutung fiir die Entwicklungsgeschichte des Blutes. Schweizerische medizinische Wochenschrift — OMIA Phene_Article / Article - 1943. Das ausschliessliche Vorkommen reifer rundkerniger Leukozyten bei der reingezüchteten Pelger−Huëtschen Anomalie des Kaninchens und die Bedeutung der Pelger−Leukozyten in der vergleichenden Hämatologie. Folia Haemat. — OMIA Phene_Article / Article - 1949. Die Pelger-Anomalie der Leukocyten und die pathologische Anatomie des neugeborenen homozygoten Pelger-Kaninchens. Zeitschrift fur menschliche Vererbungs- und Konstitutionslehre — OMIA Phene_Article / Article - 2003. Congenital abnormalities reported in Pelger-Huët homozygosity as compared to Greenberg/HEM dysplasia: highly variable expression of allelic phenotypes. J Med Genet — PubMed:PMID14684694 | DOI:10.1136/jmg.40.12.937 — OMIA Phene_Article / Article - 1964. [On the activity of neutrophilic alkaline phosphatase with Pelger-Huet anomaly in rabbits]. Patol Pol — PubMed:PMID14241274 — OMIA Phene_Article / Article - 1953. [Effect of colchicine on the white blood picture of Pelger and non-Pelger rabbits]. Acta Haematol — PubMed:PMID13091700 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:169400 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [62]

Rabbit (Oryctolagus cuniculus) — Pelt-loss (hereditary; OMIA-verified species predisposition)

Disorder: Pelt-loss [63]

Summary: See Robinson (1958, p. 338). 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 entry symbol: pl (no structured Phene_Gene link) Evidence (references) - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article [63]

Rabbit (Oryctolagus cuniculus) — Precocious puberty, MKRN3-related (hereditary; OMIA-verified species predisposition)

Disorder: Precocious puberty, MKRN3-related [64]

Summary: Chen et al. (2025) developped a MKRN3-modified rabbit using CRISPR gene editing technology (GMO) as a model for central precocious puberty (CPP) in children. 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 398298979 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2025. A novel model of central precocious puberty disease: Paternal MKRN3 gene-modified rabbit. Animal Model Exp Med — PubMed:PMID39854156 | DOI:10.1002/ame2.12544 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:615346 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:603856 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [64]

Rabbit (Oryctolagus cuniculus) — Premature aging syndrome (hereditary; OMIA-verified species predisposition)

Disorder: Premature aging syndrome [65]

Summary: The affected rabbits produced by Sui et al. (2019) are the result of "precise LMNA targeting in rabbits via co-injection of Cas9/sgRNA mRNA into zygotes", i.e. it is a knock-out model of human premature aging inherited disorders. 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 389109936 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 1960. Hereditary premature sensescence of the rabbit. I. Chronic form; general features. J Exp Med — PubMed:PMID13733754 | DOI:10.1084/jem.111.4.485 — OMIA Phene_Article / Article - 1960. Hereditary premature senescence of the rabbit. II. Acute form; general features. J Exp Med — PubMed:PMID13733753 | DOI:10.1084/jem.111.4.505 — OMIA Phene_Article / Article - 2019. LMNA-mutated rabbits: A model of premature aging syndrome with muscular dystrophy and dilated cardiomyopathy. Aging Dis — PubMed:PMID30705772 | DOI:10.14336/AD.2018.0209 — OMIA Phene_Article / Article - 2018. Highly efficient RNA-guided base editing in rabbit. Nat Commun — PubMed:PMID30006570 | DOI:10.1038/s41467-018-05232-2 — OMIA Phene_Article / Article - 2020. Efficient base editing with high precision in rabbits using YFE-BE4max. Cell Death Dis — PubMed:PMID31959743 | DOI:10.1038/s41419-020-2244-3 — OMIA Phene_Article / Article - 2022. Highly efficient A-to-G base editing by ABE8.17 in rabbits. Mol Ther Nucleic Acids — PubMed:PMID35282412 | DOI:10.1016/j.omtn.2022.01.019 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:150330 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:176670 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [65]

Rabbit (Oryctolagus cuniculus) — Rex coat, plaice type (hereditary; OMIA-verified species predisposition)

Disorder: Rex coat, plaice type [66]

Summary: Without citing references, Pan et al. (2015) explained that "In recent years, some rex rabbits have shown wrinkles in abdomen and extremities during production; this phenotype is known as plaice. The skin size of wrinkle rabbits was found to be 15% larger than that of un-wrinkle animals, with the same quality fur." 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: From a gene transcription study, Pan et al. (2015) reported that "A total of 308 differentially expressed genes were obtained by transcriptome analysis of plaice and un-plaice phenotype animals; 209 additional differentially expressed genes were not found in any database. These genes included 49 that were only expressed in plaice skin rabbits." Evidence (references) - 2015. Solexa-Sequencing Based Transcriptome Study of Plaice Skin Phenotype in Rex Rabbits (Oryctolagus cuniculus). PLoS One — PubMed:PMID25955442 | DOI:10.1371/journal.pone.0124583 — OMIA Phene_Article / Article [66]

Rabbit (Oryctolagus cuniculus) — Short QT syndrome, KCNH2-related (hereditary; OMIA-verified species predisposition)

Disorder: Short QT syndrome, KCNH2-related [67]

Rabbit (Oryctolagus cuniculus) — Syringomyelia (hereditary; OMIA-verified species predisposition)

Disorder: Syringomyelia [68]

Summary: See Robinson (1958, p. 335-336). 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: Evidence (references) - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:186700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:186700 (type: trait) — OMIA Group_OMIM (via OMIA_ID) [68]

Rabbit (Oryctolagus cuniculus) — Tremor, X-linked (hereditary; OMIA-verified species predisposition)

Disorder: Tremor, X-linked [14]

Rabbit (Oryctolagus cuniculus) — Usher syndrome, USH2A-related (hereditary; OMIA-verified species predisposition)

Disorder: Usher syndrome, USH2A-related [69]

Rabbit (Oryctolagus cuniculus) — Watanabe heritable hyperlipidemia (hereditary; OMIA-verified species predisposition)

Disorder: Watanabe heritable hyperlipidemia [70]

Summary: In addition to naturally-occurring variants for this trait, variants have been created artificially: Genetically-modifed organism; GMO. 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: Evidence (references) - 1993. Is the Watanabe Heritable Hyperlipidemic Rabbit a Suitable Experimental Model for Percutaneous Transluminal Coronary Angioplasty in Humans? - A Light Microscopic, Immunohistochemical and Ultrastructural Study. Journal of the American College of Cardiology — PubMed:PMID8473661 — OMIA Phene_Article / Article - 1993. Absence of Glomerulosclerosis in Watanabe Heritable Hyperlipidemic Rabbits. Nephron — PubMed:PMID8502322 — OMIA Phene_Article / Article - 1993. Natural History of Atherosclerosis and Hyperlipidemia in Heterozygous WHHL (WHHL-Hh) Rabbits .1. The Effects of Aging and Gender on Plasma Lipids and Lipoproteins. Journal of Laboratory and Clinical Medicine — PubMed:PMID8426086 — OMIA Phene_Article / Article - 1993. Natural History of Atherosclerosis and Hyperlipidemia in Heterozygous WHHL (WHHL-Hh) Rabbits .2. Morphologic Evaluation of Spontaneously Occurring Aortic and Coronary Lesions. Journal of Laboratory and Clinical Medicine — PubMed:PMID8426070 — OMIA Phene_Article / Article - 1993. Invivo Kinetics of Lipoprotein(a) in Homozygous Watanabe Heritable Hyperlipidaemic Rabbits. European Journal of Clinical Investigation — PubMed:PMID8243527 — OMIA Phene_Article / Article - 1993. The Effects of High Levels of Vitamin-E on the Progression of Atherosclerosis in the Watanabe Heritable Hyperlipidemic Rabbit. Journal of Nutritional Biochemistry — OMIA Phene_Article / Article - 1993. Increased Platelet GPIIb/IIIa Receptor Sensitivity in Watanabe Heritable Hyperlipidemic Rabbits. Biochemical Archives — OMIA Phene_Article / Article - 1993. Hyperreactivity of Aortic Smooth Muscle to Serotonin Is Related to the Presence of Atheroma in Watanabe Heritable Hyperlipidaemic Rabbits. Cardiovascular Research — PubMed:PMID8313424 — OMIA Phene_Article / Article - 1994. Whole Blood and Plasma Concentrations of 4-Hydroxy-2-Nonenal in Watanabe Heritable Hyperlipidemic Versus New Zealand White Rabbits. Biochemical and Biophysical Research Communications — PubMed:PMID8135808 | DOI:10.1006/bbrc.1994.1280 — OMIA Phene_Article / Article - 1994. In Vivo Correction of Low Density Lipoprotein Receptor Deficiency in the Watanabe Heritable Hyperlipidemic Rabbit with Recombinant Adenoviruses. Journal of Biological Chemistry — PubMed:PMID8175805 — OMIA Phene_Article / Article - 1994. Increased mRNA for CD63 antigen in atherosclerotic lesions of Watanabe heritable hyperlipidemic rabbits. Cell Structure and Function — PubMed:PMID7820873 — OMIA Phene_Article / Article - 1994. Expression of mRNA for matrix gamma-carboxyglutamic acid protein during progression of atherosclerosis in aortae of Watanabe heritable hyperlipidemic rabbits. Journal of Biochemistry — PubMed:PMID7883748 — OMIA Phene_Article / Article - (60 additional references in OMIA) - 1993. Is the Watanabe Heritable Hyperlipidemic Rabbit a Suitable Experimental Model for Percutaneous Transluminal Coronary Angioplasty in Humans? - A Light Microscopic, Immunohistochemical and Ultrastructural Study. Journal of the American College of Cardiology — PubMed:PMID8473661 — OMIA Phene_Article / Article - 1993. Absence of Glomerulosclerosis in Watanabe Heritable Hyperlipidemic Rabbits. Nephron — PubMed:PMID8502322 — OMIA Phene_Article / Article - 1993. Natural History of Atherosclerosis and Hyperlipidemia in Heterozygous WHHL (WHHL-Hh) Rabbits .1. The Effects of Aging and Gender on Plasma Lipids and Lipoproteins. Journal of Laboratory and Clinical Medicine — PubMed:PMID8426086 — OMIA Phene_Article / Article - 1993. Natural History of Atherosclerosis and Hyperlipidemia in Heterozygous WHHL (WHHL-Hh) Rabbits .2. Morphologic Evaluation of Spontaneously Occurring Aortic and Coronary Lesions. Journal of Laboratory and Clinical Medicine — PubMed:PMID8426070 — OMIA Phene_Article / Article - 1993. Invivo Kinetics of Lipoprotein(a) in Homozygous Watanabe Heritable Hyperlipidaemic Rabbits. European Journal of Clinical Investigation — PubMed:PMID8243527 — OMIA Phene_Article / Article - 1993. The Effects of High Levels of Vitamin-E on the Progression of Atherosclerosis in the Watanabe Heritable Hyperlipidemic Rabbit. Journal of Nutritional Biochemistry — OMIA Phene_Article / Article - 1993. Increased Platelet GPIIb/IIIa Receptor Sensitivity in Watanabe Heritable Hyperlipidemic Rabbits. Biochemical Archives — OMIA Phene_Article / Article - 1993. Hyperreactivity of Aortic Smooth Muscle to Serotonin Is Related to the Presence of Atheroma in Watanabe Heritable Hyperlipidaemic Rabbits. Cardiovascular Research — PubMed:PMID8313424 — OMIA Phene_Article / Article - 1994. Whole Blood and Plasma Concentrations of 4-Hydroxy-2-Nonenal in Watanabe Heritable Hyperlipidemic Versus New Zealand White Rabbits. Biochemical and Biophysical Research Communications — PubMed:PMID8135808 | DOI:10.1006/bbrc.1994.1280 — OMIA Phene_Article / Article - 1994. In Vivo Correction of Low Density Lipoprotein Receptor Deficiency in the Watanabe Heritable Hyperlipidemic Rabbit with Recombinant Adenoviruses. Journal of Biological Chemistry — PubMed:PMID8175805 — OMIA Phene_Article / Article - 1994. Increased mRNA for CD63 antigen in atherosclerotic lesions of Watanabe heritable hyperlipidemic rabbits. Cell Structure and Function — PubMed:PMID7820873 — OMIA Phene_Article / Article - 1994. Expression of mRNA for matrix gamma-carboxyglutamic acid protein during progression of atherosclerosis in aortae of Watanabe heritable hyperlipidemic rabbits. Journal of Biochemistry — PubMed:PMID7883748 — OMIA Phene_Article / Article - (60 additional references in OMIA) Comparative medicine (human OMIM) - OMIM:143890 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:606945 (type: gene) — OMIA Group_OMIM (via OMIA_ID) - OMIM:143890 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:606945 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [70]

Rabbit (Oryctolagus cuniculus) — XY sex reversal, SRY-related (hereditary; OMIA-verified species predisposition)

Disorder: XY sex reversal, SRY-related [71]

Summary: Song et al. (2017) "mutated Sp1-binding sites in the 5′ flanking region of the rabbit SRY gene using the CRISPR/Cas9 system. As expected, the [resultant] SRY-Sp1 knockout rabbits had female external and internal genitalia and exhibited normal female copulatory behaviors, but they were infertile, and the adults displayed reduced follicles." Thus, these animals are genetically-modified organisms (GMO) 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 389099481 (no symbol in OMIA GeneSynonym) — OMIA Phene_Gene Evidence (references) - 2017. Mutation of the Sp1 binding site in the 5' flanking region of SRY causes sex reversal in rabbits. Oncotarget — PubMed:PMID28445127 | DOI:10.18632/oncotarget.16979 — OMIA Phene_Article / Article Comparative medicine (human OMIM) - OMIM:400044 (type: trait) — OMIA Group_OMIM (via OMIA_ID) - OMIM:480000 (type: gene) — OMIA Group_OMIM (via OMIA_ID) [71]

Rabbit (Oryctolagus cuniculus) — maxillary brachygnathism, congenital malocclusion, mandibular prognathism, crossbite (hereditary; OMIA-verified species predisposition)

Disorder: maxillary brachygnathism, congenital malocclusion, mandibular prognathism, crossbite [72]

Mode of inheritance: Nachtheim (1937) suggested a recessive mode of inheritance. Huang et al. (1981) proposed a "simple autosomal recessive inheritance with incomplete penetrance for this condition". Korn et al. (2016) estimated heritability to be 25%. [72]

Summary: Disproportions in jaw length between upper and lower jaw result in teeth that are not positioned correctly and to dental malocclusion. Brachygnathia superior is observed in rabbits, most frequently in dwarf breeds. [72]

Clin feat: In rabbits, teeth grow throughout their life. Rabbits with brachygnathia superior can have severely overgrown teeth due to abnormal wear. This can result in difficulties to feed and groom and associated severe health problems (Harcourt-Brown 1997, 2009). Affected animals require regular veterinary treatment. 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: Evidence (references) - 1974. Inheritance of brachygnathia superior in rabbits. Zeitschrift fur Tierzuchtung und Zuchtungsbiologie — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2016. Genetic and environmental factors influencing tooth and jaw malformations in rabbits. Vet Rec — PubMed:PMID26908159 | DOI:10.1136/vr.103293 — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 2016. Breeding for good dental and oral health in rabbits. [Comment on Genetic and environmental factors influencing tooth and jaw malformations in rabbits; Vet Rec. 2016 Apr 2;178(14):341]. Vet Rec — PubMed:PMID27034298 | DOI:10.1136/vr.i1808 — OMIA Phene_Article / Article - 1981. Mandibular prognathism in the rabbit: discrimination between single-locus and multifactorial models of inheritance. J Hered — PubMed:PMID7288146 | DOI:10.1093/oxfordjournals.jhered.a109507 — OMIA Phene_Article / Article - 1971. Mandibular prognathism in the rabbit. Genetic studies. J Hered — PubMed:PMID5094712 | DOI:10.1093/oxfordjournals.jhered.a108111 — OMIA Phene_Article / Article - 1967. J Hered — DOI:10.1093/oxfordjournals.jhered.a107602 — OMIA Phene_Article / Article - 1997. Diagnosis, treatment and prognosis of dental disease in pet rabbits. In Practice — DOI:10.1136/inpract.19.8.407 — OMIA Phene_Article / Article - 2009. Dental disease in pet rabbits. In Practice — DOI:10.1136/inpract.31.8.370 — OMIA Phene_Article / Article - 2021. Exceptional changes in skeletal anatomy under domestication: The case of brachycephaly. Integr Org Biol — PubMed:PMID34409262 | DOI:10.1093/iob/obab023 — OMIA Phene_Article / Article - 2025. Rethinking brachycephaly: Anatomical implications and health considerations in lagomorphs. Anat Rec (Hoboken) — PubMed:PMID41431133 | DOI:10.1002/ar.70123 — OMIA Phene_Article / Article - 1974. Inheritance of brachygnathia superior in rabbits. Zeitschrift fur Tierzuchtung und Zuchtungsbiologie — OMIA Phene_Article / Article - 1958. Genetic studies of the rabbit. Bibliographia Genetica — OMIA Phene_Article / Article - 2016. Genetic and environmental factors influencing tooth and jaw malformations in rabbits. Vet Rec — PubMed:PMID26908159 | DOI:10.1136/vr.103293 — OMIA Phene_Article / Article - 1937. Erbpathologische Untersuchungen am Kaninchen [Investigation of inherited defects in rabbits]. Z. indo Abst. u. Vererbgs — DOI:10.1007/BF01847500 — OMIA Phene_Article / Article - 2016. Breeding for good dental and oral health in rabbits. [Comment on Genetic and environmental factors influencing tooth and jaw malformations in rabbits; Vet Rec. 2016 Apr 2;178(14):341]. Vet Rec — PubMed:PMID27034298 | DOI:10.1136/vr.i1808 — OMIA Phene_Article / Article - 1981. Mandibular prognathism in the rabbit: discrimination between single-locus and multifactorial models of inheritance. J Hered — PubMed:PMID7288146 | DOI:10.1093/oxfordjournals.jhered.a109507 — OMIA Phene_Article / Article - 1971. Mandibular prognathism in the rabbit. Genetic studies. J Hered — PubMed:PMID5094712 | DOI:10.1093/oxfordjournals.jhered.a108111 — OMIA Phene_Article / Article - 1967. J Hered — DOI:10.1093/oxfordjournals.jhered.a107602 — OMIA Phene_Article / Article - 1997. Diagnosis, treatment and prognosis of dental disease in pet rabbits. In Practice — DOI:10.1136/inpract.19.8.407 — OMIA Phene_Article / Article - 2009. Dental disease in pet rabbits. In Practice — DOI:10.1136/inpract.31.8.370 — OMIA Phene_Article / Article - 2021. Exceptional changes in skeletal anatomy under domestication: The case of brachycephaly. Integr Org Biol — PubMed:PMID34409262 | DOI:10.1093/iob/obab023 — OMIA Phene_Article / Article - 2025. Rethinking brachycephaly: Anatomical implications and health considerations in lagomorphs. Anat Rec (Hoboken) — PubMed:PMID41431133 | DOI:10.1002/ar.70123 — OMIA Phene_Article / Article [72]

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: [73]

For dogs, the AAFCO Dog Food Nutrient Profiles; [73]

For cats, the AAFCO Cat Food Nutrient Profiles; [73]

For specialty pets, the nutrient recommendations approved by the Committee on Animal Nutrition of the National Research Council of the National Academy of Sciences [73]

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 — Rabbit (Oryctolagus cuniculus) clinical cases (peer-reviewed, Europe PMC)

PMID 42464972 (2026, Veterinary ophthalmology) — [Paraphrased derived summary — non-Open-Access source.] A 2-year-old male giant rabbit with chronic recurrent corneal erosions due to eyelid/third-eyelid conformational abnormality was treated by wedge excision of the upper eyelid and shortening of the third-eyelid cartilage; erosions resolved completely with no recurrence over 1 year. (Source excerpt truncated at abstract opening.) [74]

PMID 42063453 (2026, Case reports in veterinary medicine) — Cutaneous Melanoma in a Rabbit With Multiple Metastatic Lesions: A Case Report. (opening): Background Neoplasia is increasingly common in senior pet rabbits, with cutaneous melanoma being a rare but aggressive type. Its characteristics in rabbits are not fully understood. Case description A 5-year-old rabbit initially presented with a cutaneous mass at the ear base. Despite surgical excision, it recurred rapidly with multiple facial/chest masses and pulmonary metastases, leading to euthanasia. Pathological evaluation confirmed malignant melanoma, revealing features such as high mitotic activity and lymphovascular invasion; immunohistochemistry provided the definitive diagnosis. Conclusion and clinical relevance This case highlights the highly aggressive and metastatic nature of cutaneous melanoma in rabbits, often resulting in a poor prognosis. Clinicians should be aware of melanoma's aggressive potential in rabbits. Surgical intervention alone may prove inadequate, and current treatment options in rabbits are limited. In this case, surgical intervention was not effective, likely because micrometastasis was already present. Treatment options remain limited, and euthanasia is often required in metastatic cases. [CC BY — Open Access, verbatim with attribution.] [75]

Evidence cluster — Rabbit (Oryctolagus cuniculus) husbandry, health & nutrition (peer-reviewed, Europe PMC)

PMID 42353440 (2026, Animals: an open access journal from MDPI) — [Paraphrased derived summary — non-Open-Access source.] A survey of 529 pet-rabbit owners in Croatia found 85.6% reported high rabbit-care knowledge, but higher perceived knowledge was only weakly-to-moderately associated with better husbandry (enrichment, housing type, cleaning frequency) and showed little association with social housing, free movement, or feeding — revealing a substantial knowledge–practice gap. (Source excerpt truncated at abstract opening.) [76]

PMID 42471482 (2026, Scientific reports) — [Paraphrased derived summary — non-Open-Access source.] An animal-economics study of 8 group-housed New Zealand White rabbit does assessed motivation to push weighted doors to access compartments (none, hiding box, sand, straw); does allocated most time to straw (17.5%) then hiding box (8.6%), with visit probability declining as workload increased — suggesting individual seclusion is a price-dependent, non-essential resource under these conditions. (Source excerpt truncated.) [77]

References

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

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

[2] https://www.gov.wales/sites/default/files/publications/2021-02/rabbit-welfare-code-of-practice.pdf

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

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

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

[4] https://www.rspca.org.uk/adviceandwelfare/pets/rabbits

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

[5] https://www.daera-ni.gov.uk/sites/default/files/publications/daera/20.21.048%20Code%20of%20Practice%20Rabbits.PDF

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

[6] https://www.merckvetmanual.com/exotic-and-laboratory-animals/rabbits

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

[7] https://www.rspca.org.uk/adviceandwelfare/pets/rabbits/diet

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

[8] https://www.merckvetmanual.com/exotic-and-laboratory-animals/rabbits/nutrition-of-rabbits

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

[9] https://www.merckvetmanual.com/exotic-and-laboratory-animals/rabbits/noninfectious-diseases-of-rabbits

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

[10] https://www.merckvetmanual.com/exotic-and-laboratory-animals/rabbits/viral-diseases-of-rabbits

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

[11] https://omia.org/OMIA000201/9986/

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

[12] https://omia.org/OMIA001199/9986/

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

[13] https://omia.org/OMIA000439/9986/

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

[14] https://omia.org/OMIA000770/9986/

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

[15] https://omia.org/OMIA000299/9986/

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

[16] https://omia.org/OMIA001079/9986/

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

[17] https://omia.org/OMIA001249/9986/

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

[18] https://omia.org/OMIA001962/9986/

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

[19] https://omia.org/OMIA002600/9986/

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

[20] https://omia.org/OMIA002865/9986/

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

[21] https://omia.org/OMIA000202/9986/

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

[22] https://omia.org/OMIA002317/9986/

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

[23] https://omia.org/OMIA001996/9986/

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

[24] https://omia.org/OMIA001997/9986/

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

[25] https://omia.org/OMIA002955/9986/

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

[26] https://omia.org/OMIA002007/9986/

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

[27] https://omia.org/OMIA000411/9986/

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

[28] https://omia.org/OMIA000077/9986/

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

[29] https://omia.org/OMIA000146/9986/

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

[30] https://omia.org/OMIA000155/9986/

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

[31] https://omia.org/OMIA000156/9986/

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

[32] https://omia.org/OMIA002735/9986/

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

[33] https://omia.org/OMIA000168/9986/

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

[34] https://omia.org/OMIA002394/9986/

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

[35] https://omia.org/OMIA001597/9986/

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

[36] https://omia.org/OMIA000017/9986/

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

[37] https://omia.org/OMIA000249/9986/

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

[38] https://omia.org/OMIA001794/9986/

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

[39] https://omia.org/OMIA000267/9986/

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

[40] https://omia.org/OMIA000279/9986/

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

[41] https://omia.org/OMIA001709/9986/

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

[42] https://omia.org/OMIA001998/9986/

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

[43] https://omia.org/OMIA002157/9986/

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

[44] https://omia.org/OMIA000344/9986/

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

[45] https://omia.org/OMIA000700/9986/

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

[46] https://omia.org/OMIA002002/9986/

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

[47] https://omia.org/OMIA000487/9986/

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

[48] https://omia.org/OMIA000493/9986/

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

[49] https://omia.org/OMIA002329/9986/

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

[50] https://omia.org/OMIA002063/9986/

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

[51] https://omia.org/OMIA001542/9986/

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

[52] https://omia.org/OMIA002855/9986/

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

[53] https://omia.org/OMIA000585/9986/

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

[54] https://omia.org/OMIA002577/9986/

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

[55] https://omia.org/OMIA000473/9986/

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

[56] https://omia.org/OMIA000628/9986/

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

[57] https://omia.org/OMIA002688/9986/

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

[58] https://omia.org/OMIA000674/9986/

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

[59] https://omia.org/OMIA002242/9986/

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

[60] https://omia.org/OMIA000755/9986/

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

[61] https://omia.org/OMIA000011/9986/

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

[62] https://omia.org/OMIA000783/9986/

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

[63] https://omia.org/OMIA002003/9986/

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

[64] https://omia.org/OMIA002920/9986/

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

[65] https://omia.org/OMIA001213/9986/

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

[66] https://omia.org/OMIA001994/9986/

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

[67] https://omia.org/OMIA002441/9986/

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

[68] https://omia.org/OMIA000965/9986/

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

[69] https://omia.org/OMIA002624/9986/

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

[70] https://omia.org/OMIA000499/9986/

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

[71] https://omia.org/OMIA001230/9986/

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

[72] https://omia.org/OMIA000149/9986/

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

[73] 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)

[74] https://pubmed.ncbi.nlm.nih.gov/42464972/

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

[75] https://pubmed.ncbi.nlm.nih.gov/42063453/

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

[76] https://pubmed.ncbi.nlm.nih.gov/42353440/

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

[77] https://pubmed.ncbi.nlm.nih.gov/42471482/

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.

• Regulations & Legality depth: only 1 verified legality line(s) so far — coverage is still being collected; consult your local authority before relying on this section.
• 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