Manx Syndrome
Related terms: spina bifida, myelodysplasia, spinal cord dysplasia, hydromyelia, spinal dysraphism, syringomyelia, spinal dysplasia
Outline: The genetic mutation responsible for the Manx cat’s distinctive taillessness unfortunately carries significant health consequences. This mutation frequently disrupts the development of the spine and spinal cord, leading to various forms of spina bifida. These conditions can result in partial paralysis, hinder normal feline behaviors, cause incontinence, and increase susceptibility to painful infections. Tails are not merely cosmetic features for cats; they are vital for communication and balance. The continued demand for Manx Cats perpetuates the serious health and welfare challenges inherent in this breed due to the genetic mutation present in all Manx cats.
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Summary of Information
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1. Brief description
The term “Manx syndrome” encompasses a range of conditions observed in Manx cats, directly linked to their defining characteristic: a shortened or absent tail. Regrettably, this readily apparent vertebral mutation is often associated with severe developmental abnormalities within the spinal cord, leading to significant neurological disorders affecting the nervous system.
Spina bifida is the most prevalent developmental issue in Manx cats. This term broadly describes several conditions where the neural tube, which develops into the spinal cord, fails to close completely, and the vertebral arches, the bony structures of the spine, also do not fully form.
The symptoms of spina bifida in Manx cats vary depending on the severity of the spinal cord abnormality. These can include an unusual “hopping” gait, a plantigrade stance where more of the hind leg touches the ground than normal, urinary and fecal incontinence, and reduced sensation in the hind legs and perineal area (the skin surrounding the anus and urethra). In severe cases, the deformity can be fatal.
2. Intensity of welfare impact
The welfare impact on Manx cats is variable. Some exhibit no signs of spinal cord issues, while others suffer significant problems such as impaired hind limb function and incontinence. Cats with bladder or bowel control issues may frequently soil themselves with urine and/or feces, leading to skin inflammation, irritation, and infections. Hind limb dysfunction restricts their ability to perform a full range of normal behaviors like jumping, running, and climbing.
Severely affected kittens may die in utero or are often euthanized at a young age due to the severity of their condition.
3. Duration of welfare impact
Symptoms can be present at birth or emerge in the weeks and months following. Typically, there is no effective cure, making the condition lifelong. While surgical interventions are sometimes possible, these can also introduce their own welfare concerns.
4. Number of animals affected
Spina bifida is a common occurrence in Manx cats. “Rumpy” Manx cats, those completely without tails, are particularly susceptible (Kroll and Constantinescu 1994).
5. Diagnosis
Diagnosing spina bifida involves a combination of veterinary physical examinations, X-rays, myelography, and Magnetic Resonance Imaging (MRI) scans to assess the spinal cord and vertebral column.
6. Genetics
The taillessness in Manx cats originates from a mutant gene, designated M, which disrupts the normal development of the coccygeal (tail) and sacral vertebrae (located near the hips). All Manx cats are heterozygous (Mm) for this gene, possessing one mutant M gene and one normal m gene. The mutant M gene is dominant over the normal m gene (Long 2006). Homozygous MM cats, inheriting two mutant genes, are so severely deformed that they typically do not survive fetal development. Thus, the Manx gene is considered a lethal gene (Long 2006).
7. How to identify affected or carrier animals?
Affected Manx kittens are usually identifiable before leaving breeders. It is crucial for all new Manx kittens to undergo a thorough veterinary examination prior to purchase.
All Manx cats carry the mutant M gene and can produce offspring with Manx syndrome.
8. Elimination prospects and methods
Currently, there is no established program to mitigate the adverse effects of the mutant M gene. This gene is intrinsically linked to the defining trait of the Manx cat – its taillessness. Therefore, breeding Manx cats inevitably perpetuates these associated welfare issues.
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1. Clinical and Pathological Effects
The Manx cat breed is characterized by its lack of a tail; however, this prominent vertebral mutation is frequently linked to significant developmental abnormalities in the spinal cord, resulting in neurological disease (disorders of the nervous system).
To fully comprehend the clinical problems associated with the Manx anomaly, an understanding of normal feline anatomy and development is necessary. The feline spine, or vertebral column, is composed of numerous bones called vertebrae, divided into 5 regions. These include 7 cervical vertebrae in the neck, 13 thoracic vertebrae in the chest, 7 lumbar vertebrae in the lower back, and 3 fused sacral vertebrae at the hips. Lastly, there are the coccygeal (tail) vertebrae, typically numbering between 18 and 20 but varying (Hudson and Hamilton 1993). Vertebrae are numbered according to their region, starting from the head towards the tail. The first cervical vertebra is C1, the second C2, the first thoracic vertebra is T1, and so on.
Vertebrae are complex bony structures. The vertebral body, the largest part, is positioned ventrally (towards the underside). Dorsal to the vertebral body (towards the cat’s back) is an opening, the vertebral canal, formed during development by the fusion of two vertebral arches extending from each vertebral body. The spinal cord passes through this canal, providing a crucial neurological connection between the brain and peripheral nerves. The vertebral canal offers vital protection for the delicate spinal cord. Pairs of spinal nerves emerge between each vertebra, forming peripheral nerves that transmit sensation and control movement throughout the body (excluding the head).
Spinal cord regions correspond to the vertebral column regions: 8 cervical segments, 13 thoracic segments, 7 lumbar segments, 3 sacral segments, and approximately 7 caudal (coccygeal) segments. These segments are similarly named (C1, T1, L1, etc.). Due to differing growth rates between the spine and spinal cord, the spinal cord in normal cats ends around the level of the L7 vertebra. Consequently, spinal cord segments do not perfectly align with their corresponding vertebrae. For instance, the S2 cord segment is located within the L6 vertebra in normal cats (Hudson and Hamilton 1993).
Diagram illustrating the anatomy of a cat’s spine and spinal cord, highlighting the regions affected by the Manx gene.
Taillessness in Manx cats is caused by a mutant, autosomal dominant gene, M, which disrupts the development of coccygeal and sacral vertebrae. All Manx cats are heterozygous (Mm) for this gene. Homozygous MM cats, with two mutant genes, suffer severe abnormalities and typically die in utero, classifying the Manx gene as lethal (Long 2006). Cats homozygous for the normal gene (mm) are born with tails and, although born to Manx parents, are not classified as Manx cats.
The mutant M gene exhibits variable expressivity, resulting in varying degrees of taillessness. Deforest and Basrur (1979) categorized these into four types:
- Rumpy cats: Completely lack coccygeal vertebrae.
- Rumpy-riser cats: Have a few (1-7) fused coccygeal vertebrae in an upright position.
- Stumpy cats: Possess 2-14 coccygeal vertebrae, often severely kinked and abnormally shaped. These cats have limited tail movement.
- Normal cats (“Longie” Cats): Have longer tails despite carrying the M gene (Mm).
All cats in the first three categories exhibit vertebral abnormalities (Deforest and Basrur 1979).
Vertebral development in the fetus is closely linked to spinal cord development. Early in embryonic development, the neural tube, which forms the spinal cord and brain, originates from an invagination (inward folding) of the ectoderm, the outer tissue layer of the early embryo. This fold curls to form a tube, detaches from the surface tissue, and sinks to become the neural tube and nervous tissue. Following neural tube formation, the mesoderm, the middle tissue layer, segments into somites, which further divide into three regions. The sclerotome, the region closest to the midline of the fetus, develops into vertebrae adjacent to the neural tube (Kroll and Constantinescu 1994).
The Manx anomaly gene disrupts ectodermal tissue, affecting both spinal cord and vertebral arch development (Bailey 1975).
Deforest and Basrur (1979) suggest that this fundamental nervous system defect leads to abnormal vertebral column development in Manx cats. Thus, while Manx cats are bred for taillessness, this trait arises from abnormal spinal cord and vertebral arch development caused by the Manx gene. Consequently, spinal cord abnormalities are frequently present in Manx cats. These spinal cord issues are the root cause of the severe clinical and welfare problems in this breed.
Spina bifida is the most common developmental problem observed in Manx cats. It encompasses various conditions where the neural tube, precursor to the spinal cord, fails to close properly to varying degrees, and vertebral arches also fail to fully form.
Several types of spina bifida and associated spinal cord abnormalities can occur (Kroll and Constantinescu 1994), each with specific clinical and welfare implications:
- Meningeal dysplasia: Abnormal formation of the meninges, the protective tissues surrounding the spinal cord.
- Spinal cord dysplasia (myelodysplasia): Malformation of the spinal cord, potentially including:
- Absent or duplicated central canal (the channel through the spinal cord’s center).
- Hydromyelia: Dilation of the central canal.
- Syringomyelia: Formation of fluid-filled cavities within the spinal cord.
- Abnormal distribution or migration of gray matter (spinal cord tissue type).
- Absence of the ventral median fissure (a normal spinal cord shape feature) (Shell 2003a).
- Sacrocaudal dysgenesis: Absence of sacral and caudal spinal cord segments (Shell 2003b).
- Spina bifida occulta: Localized defect with incomplete vertebral arch formation. Overlying skin is normal, and the cat is clinically normal (Kroll and Constantinescu 1994).
- Spina bifida manifesta: Form with evident nervous system abnormalities.
- Spina bifida cystica: Vertebral arch defect with herniation (protrusion) of the meninges (meningocele) or meninges and spinal cord parts (meningomyelocele) through the defect. Meningomyeloceles often cause severe spinal cord problems.
- Spina bifida aperta: Spinal cord open to the skin surface, posing a high risk of spinal cord infection, severe illness, and deterioration.
Rumpy Manx cats frequently lack sacral and sometimes lumbar vertebrae and often have missing portions of the spinal cord (spinal cord dysgenesis) (Kroll and Constantinescu 1994).
Symptoms of spina bifida and spinal cord dysgenesis in Manx cats vary depending on the severity of the spinal cord abnormality at birth and can include:
- Plantigrade hind limb stance and gait: Walking on the entire area from hock to toe, like a human, instead of on toes, due to hind limb paralysis. Normal rapid movement is difficult, leading to “hopping” (Deforest and Basrur 1979). A rabbit-like gait is common (Kroll and Constantinescu 1994). Cats may appear crouched and have reduced coordination.
- Lack of perineal skin sensation (Deforest and Basrur 1979).
- Urinary incontinence: Inability to control urination, leading to secondary urinary tract infections.
- Fecal incontinence: Inability to control defecation, potentially with megacolon (colon distension) and abdominal distension due to constipation. Constipation is caused by impaired nerve function for expelling feces. Fecal and urinary incontinence leads to perineal skin soiling.
- Rectal prolapse: Protrusion of the rectum through the anus (Deforest and Basrur 1979).
- Severe cases: Spinal abnormalities like meningomyelocele, presenting as a dorsal midline lump covered by membrane (Kroll and Constantinescu 1994). Open meningomyeloceles may leak cerebrospinal fluid (CSF), increasing infection risk and causing rapid decline, lethargy, fever, severe neurological signs, and death (Evans 1985).
More severe clinical signs can develop weeks to months after birth due to “tethering” of the spinal cord, where the spinal cord abnormally attaches to the vertebral canal. As the cat grows, spinal cord stretching and damage cause progressive sensory and motor impairment in hind legs and incontinence (Kroll and Constantinescu 1994). These late-onset signs affect hind limb nerves, bladder, bowel, and perineal region, and are most common in Rumpy cats.
- Stumpy Manx cats: Prone to arthritis in deformed tail bone joints, causing significant pain (Feline Advisory Bureau).
- Exencephally and kyphoscoliosis: Rarely, Manx cats may exhibit exencephally (incomplete skull development with brain protrusion) and kyphoscoliosis (spinal column curvature) (Evans 1985).
Surgical intervention can sometimes benefit certain forms of Manx syndrome. Constipation can be medically managed to some extent. However, effective treatments are generally lacking for most Manx syndrome-related problems.
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2. Intensity of Welfare Impact
While some Manx cats appear normal except for their short tails and show no spinal cord dysfunction, others suffer severe spinal and spinal cord abnormalities, resulting in hind limb dysfunction and urinary and fecal incontinence. These affected cats may constantly soil themselves, leading to skin irritation, inflammation, and infection requiring extensive care. Mobility impairment hinders their ability to express natural behaviors. Spina bifida itself does not cause pain unless spinal cord infection occurs. However, stumpy Manx cats are susceptible to painful arthritis in their tail stumps.
Severely affected Manx cats cannot live normal lives and are often euthanized early. Spina bifida aperta can lead to spinal cord infections, causing rapid, severe illness, pain, and death.
“It must be remembered that the unique appearance of the Manx actually constitutes the relatively normal end of a spectrum of genetically controlled characteristics that include serious and potentially lethal abnormalities” (Kitchen et al 1972 as cited by Kroll and Constantinescu 1994).
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3. Duration of Welfare Impact
Abnormalities may be apparent at birth; otherwise, symptoms appear over weeks to months as the kitten develops (Kroll and Constantinescu 1994). These problems are often untreatable, and severely affected animals are likely to die from complications or require euthanasia. Life expectancy is significantly reduced in affected individuals. Less severely affected cats may manage in protected home environments with dedicated owner care. Surgical treatment is occasionally helpful.
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4. Number of Animals Affected
Spina bifida is common in Manx cats. Deforest and Basrur (1979) state, “the Manx breeder soon discovers that a considerable percentage of kittens suffer from severe congenital abnormalities.” Their study found 16% of kittens were affected (7 out of 44), all of whom were rumpies. Rumpy cats are frequently clinically affected (Evans 1985) and have higher juvenile mortality (Kroll and Constantinescu 1994). Despite health issues, rumpies may be favored by breeders and owners prioritizing taillessness over welfare. Breeders often euthanize affected kittens early, presenting only healthier individuals to potential owners.
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5. Diagnosis
Detecting Manx syndrome abnormalities can be challenging. Expert veterinary examination may reveal vertebral abnormalities in the caudal or sacral region. A lumbosacral skin dimple may indicate an underlying meningocele (Kroll and Constantinescu 1994). Abnormal spinal reflexes can also suggest spinal cord issues. Radiographs (X-rays) show bony defects, and myelography or MRI scans confirm the type and extent of spinal cord abnormalities (Kroll and Constantinescu 1994).
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6. Genetics
Taillessness in Manx cats is due to the dominant mutant gene M, causing abnormal coccygeal and sacral vertebra development. All Manx cats are heterozygous (Mm), carrying one mutant M and one normal m gene, inherited from each parent. M is dominant over m (Long 2006). Homozygous MM cats with two mutant genes are severely abnormal and die in utero, making the Manx gene lethal (Long 2006).
Variable expression of the M gene in heterozygous (Mm) individuals is influenced by other genes (modifying genes) (Long 2006), currently unidentified. Robinson (1993) suggests only part of the variation is genetic, with heritability estimated around 0.40 ± 0.11 (Robinson, 1993), suggesting about 40% is due to modifying genes and the rest to environmental factors.
Manx cats must be tailless to some degree to be classified as Manx, meaning they are all heterozygous and do not “breed-true.” Breeding Manx cats produces some kittens (around 25%) that are genetically mm, possessing normal tails and avoiding Manx syndrome, but these are not considered Manx cats.
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7. How to know if an animal is a carrier or likely to be affected?
All Manx cats (tailless cats) carry the mutant M gene and can produce affected offspring, thus being carriers. Breeding stumpy cats, thought to be less prone to disease, does not reduce the risk of producing rumpy kittens (more prone to severe Manx syndrome). Unknown modifying genes and environmental factors determine the severity, and these are currently untestable before breeding.
Breeding Manx (tailless) cats perpetuates Manx syndrome. Cats evolved with tails for communication and balance. As long as Manx cats are bred and purchased, the serious health and welfare issues caused by the mutant gene will continue.
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8. Methods and prospects for elimination of the problem
Manx breeders may breed Manx (Mm) cats with “normal” (mm) cats to avoid producing severely affected MM fetuses. However, this still results in potentially affected Mm offspring.
Currently, there is no program to reduce the adverse effects of the M gene. The gene is linked to taillessness, the defining Manx cat trait, so breeding Manx cats maintains these welfare problems. The Feline Advisory Bureau (FAB) suggests informed breeding may reduce problems, but evidence is lacking. Manx and Cymric (long-haired Manx) breeding seems to have decreased in the UK recently (http://www.danzantemanx.com). Future identification of modifying genes and environmental factors might help reduce the Manx gene’s adverse effects. However, the ethics of breeding a breed defined by a harmful gene should be seriously considered.
Tailed kittens (not Manx), genetically mm, from Manx breeding are free from the condition and can be safely bred.
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9. Acknowledgements
UFAW expresses gratitude to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their contributions to this section.
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10. References
Bailey C (1975) An embryologic approach to the clinical significance of congenital vertebral and spinal abnormalities. Journal of the American Animal Hospital Association 11: 426-434
Danzante manx (2010) Homepage. (On-line). Available at http://www.danzantemanx.com. Accessed 7.12.2010
Deforest M and Basrur P (1979) Malformations and the Manx Syndrome in Cats. Canadian Veterinary Journal 20 304-314
Evans RJ (1985) The Nervous System. In: Feline Medicine and Therapeutics. Editors E. Chandler, C, Gaskell, & A Hilbery Blackwell scientific publications: London, pp 38
Feline Advisory Bureau (FAB) Available at http://www.fabcats.org/breeders/inherited_disorders/manx.php. Accessed 7.12.2010
Hopkins A (1992) Feline Neurology Part 2: Diseases of the spinal cord, peripheral nerves and neuromuscular system. In Practice, 14 111-117
Hudson L and Hamilton W (1993) Atlas of Feline Anatomy for Veterinarians. W.B Saunders Company: Philadelphia, USA. pp 30.
Kitchen H, Murray R and Cockrell B (1972) Animal model for human disease; spina bifida, sacral dysgenesis and myelocele. American Journal of Pathology 66 203-206
Kroll R and Constantinescu G (1994) Congenital Abnormalities of the Spinal Cord and Vertebrae. In: Consultations in Feline Medicine 2. Editor J. August. W.B Saunders Company: Philadelphia, USA. pp 413
Long S (2006) Veterinary genetics and reproductive physiology. A textbook for veterinary nurses and technicians. Butterworth Heinemann: London. pp 18
Robinson R (1993) Expressivity of the Manx Gene in Cats. Journal of Heredity. 84 170-172
Shell L (2003a) Myelodysplasia (Spinal Dysraphism) (on-line) Available at http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1023. Accessed 30.11.10
Shell L (2003b) Sacrocaudal Dysgenesis. (On-line) Available at http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1024. Accessed 30.11.10
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