Understanding Manx Syndrome in Cats
Related terms: spina bifida, myelodysplasia, spinal cord dysplasia, hydromyelia, spinal dysraphism, syringomyelia, spinal dysplasia
The Manx Cat, instantly recognizable for its lack of a tail, carries a genetic mutation that, unfortunately, extends beyond just this unique physical trait. This mutation often leads to serious health issues known collectively as Manx Syndrome. This syndrome arises from the gene’s impact on the development of the spine and spinal cord, resulting in various forms of spina bifida. These conditions can significantly compromise a cat’s quality of life, leading to partial paralysis, abnormal behaviors, incontinence, and painful infections. It’s crucial to remember that cats evolved with tails for vital functions such as balance and communication. The continued demand for Manx cats unfortunately perpetuates the prevalence of this genetic mutation and the associated health and welfare challenges.
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Key Information at a Glance
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1. Brief Description
“Manx syndrome” is the term used to describe a range of health problems seen in Manx cats. These issues are directly linked to the genetic mutation responsible for their defining characteristic: a shortened or absent tail. This visible vertebral mutation is frequently associated with serious developmental abnormalities in the spinal cord, leading to significant neurological conditions, or diseases of the nervous system.
Spina bifida is the most common developmental issue in Manx cats. This term encompasses several conditions where the neural tube, which forms the spinal cord, fails to close completely. Additionally, the vertebral arches, the bony structures that protect the spinal cord, also fail to develop fully.
The symptoms of spina bifida in Manx cats vary widely depending on the severity of the spinal cord abnormality. These can include an unusual “hopping” gait, a plantigrade stance (walking with more of the hind leg on the ground than normal), urinary and fecal incontinence, and a lack of sensation in the hind legs and the perineal area (the skin around the anus and urethra). In severe cases, the deformities can be so debilitating that they are fatal.
2. Welfare Impact Severity
The welfare impact on Manx cats is highly variable. Some individuals may show no signs of spinal cord issues, while others endure significant problems. These can include impaired hind limb function and loss of bladder and bowel control. Cats with incontinence are prone to being constantly soiled with urine and feces, leading to skin inflammation, irritation, and infections. Hind limb dysfunction restricts their ability to perform a full range of normal feline behaviors.
In the most severe instances, affected kittens may die before birth or require euthanasia at a young age due to the severity of their condition.
3. Duration of Welfare Impact
Symptoms of Manx Syndrome can be apparent at birth or develop in the weeks and months following. Unfortunately, there is typically no effective cure, making this a lifelong condition. While surgical interventions are sometimes possible, they can also introduce their own welfare concerns.
4. Prevalence in Manx Cats
Spina bifida is a common occurrence in Manx cats. “Rumpy” Manx cats, those completely without tails, are particularly susceptible to these issues (Kroll and Constantinescu 1994).
5. Diagnosis
Diagnosing spina bifida involves a combination of veterinary examination techniques, including x-rays, myelography (a contrast x-ray of the spinal cord), and magnetic resonance imaging (MRI) scans.
6. Genetic Basis
The tail-less trait in Manx cats is caused by a mutant gene, denoted as M. This gene disrupts the normal development of the coccygeal (tail) and sacral vertebrae (the sacrum is located at the base of the spine, near the hips). All Manx cats are heterozygous (Mm) for this gene, meaning they possess one copy of the mutant M gene and one copy of the normal m gene. The mutant M gene is dominant over the normal m gene (Long 2006). Cats that are homozygous dominant (MM), inheriting two copies of the mutant gene, are so severely malformed that they typically die in the uterus before birth. This makes the Manx gene a lethal gene (Long 2006).
7. Identifying Carriers and Affected Cats
Affected Manx kittens are usually identifiable before leaving the breeder. It is crucial that all Manx kittens undergo a thorough veterinary examination before purchase.
All Manx cats, by definition, carry the mutant M gene and can potentially produce offspring with Manx Syndrome.
8. Addressing and Eliminating the Problem
Currently, there are no programs in place to reduce the negative impacts of the mutant M gene. The gene is intrinsically linked to the defining characteristic of the Manx cat – its lack of tail. Therefore, breeding Manx cats inevitably perpetuates these welfare concerns.
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1. Clinical and Pathological Effects of Manx Syndrome
The Manx cat breed is renowned for its tailless appearance. However, this striking vertebral mutation is frequently linked to severe developmental abnormalities of the spinal cord, leading to neurological diseases affecting the nervous system.
To fully grasp the clinical problems associated with Manx Syndrome, understanding normal feline anatomy and development is essential. The feline spine, or vertebral column, is composed of numerous bones called vertebrae, divided into five regions. These are the cervical (neck) region with 7 vertebrae, the thoracic (chest) region with 13, the lumbar (lower back) region with 7, and the sacrum (hips) formed by 3 fused vertebrae. Lastly, there are the tail (coccygeal) bones, typically ranging from 18 to 20 in number (Hudson and Hamilton 1993). Vertebrae are numbered according to their spinal region, starting from the head towards the tail. The first cervical vertebra is C1, the second C2, and the first thoracic vertebra is T1, and so forth.
Vertebrae are complex bony structures. The body, the largest part of each vertebra, is positioned ventrally (towards the underside). Dorsal to the vertebral body is the vertebral canal, a bony opening formed during development by the fusion of two vertebral arches originating from each vertebral body. The spinal cord, a delicate neurological pathway connecting the brain and peripheral nerves, passes through and is protected by the vertebral canal. Spinal nerves emerge in pairs between each vertebra, forming peripheral nerves that transmit sensation and control movement to all parts of the body except the head.
Spinal cord regions are named corresponding to the spinal column regions. There are 8 cervical segments (one preceding the first cervical vertebra), 13 thoracic, 7 lumbar, 3 sacral, and approximately 7 caudal (coccygeal) segments, labeled similarly to vertebrae (C1, T1, L1, etc.). Due to differing growth rates between the spine and spinal cord, the spinal cord typically ends around the L7 vertebra level in normal cats. As the spinal cord is shorter than the vertebral column, spinal cord segments don’t perfectly align with their corresponding vertebrae. For instance, the S2 cord segment is located within the L6 vertebra in healthy cats (Hudson and Hamilton 1993).
The taillessness in Manx cats originates from a mutant, autosomal dominant gene M, disrupting the development of coccygeal and sacral vertebrae. All Manx cats are heterozygous (Mm) for this gene. Homozygous MM cats, inheriting two mutant genes, are so severely affected that they die early in uterine development, classifying the Manx gene as lethal (Long 2006). Cats homozygous for the normal gene (mm) possess tails and are not considered Manx cats, even if born to Manx parents.
The mutant M gene exhibits variable expressivity, resulting in varying degrees of taillessness. Deforest and Basrur (1979) categorize Manx cats into four types:
- Rumpy cats: Completely lack coccygeal vertebrae.
- Rumpy-riser cats: Have 1-7 coccygeal vertebrae fused in an upright position.
- Stumpy cats: Possess 2-14 coccygeal vertebrae, often kinked and abnormal in shape. They have limited tail movement.
- Normal cats (“Longie” Cats): Have longer tails despite carrying the M gene (Mm), and are not considered Manx in breed standards.
The first three categories encompass cats with vertebral abnormalities (Deforest and Basrur 1979).
Vertebral development in the fetus is closely linked to spinal cord development. During early embryonic development, the neural tube, precursor to the spinal cord and brain, forms from an invagination (inward folding) of the ectoderm (outer tissue layer). This fold curls into a tube, detaches from the surface tissue, and forms the neural tube and nervous tissue. Subsequently, the mesoderm (middle tissue layer) segments into somites, further dividing into three regions. The sclerotome, closest to the fetal midline, forms 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 underlying nervous system defect causes aberrant vertebral column development in Manx cats. While Manx cats are bred for taillessness, this trait is a consequence of abnormal spinal cord and vertebral arch development caused by the gene. This explains why spinal cord abnormalities are frequently observed and are the source of severe clinical and welfare issues in Manx cats.
Spina bifida is the most common developmental problem in Manx cats. It is a broad term describing conditions where the neural tube, forming the spinal cord, fails to close to varying degrees, and vertebral arches also fail to fully form.
Various types of spina bifida and spinal cord abnormalities can occur (Kroll and Constantinescu 1994), each associated with specific clinical and welfare concerns:
- Meningeal dysplasia: Abnormal formation of the meninges, the protective tissue layers surrounding the spinal cord.
- Spinal cord dysplasia (myelodysplasia) (Hopkins 1992): Malformation of the spinal cord, potentially including:
- Absent or duplicated central canal (a canal running through the spinal cord’s center).
- Hydromyelia: Dilated central canal.
- Syringomyelia: Formation of cavities or spaces 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 typically clinically normal (Kroll and Constantinescu 1994).
- Spina bifida manifesta: Spina bifida with evident nervous system abnormalities.
- Spina bifida cystica: Vertebral arch defect with herniation (ballooning out) of meninges (meningocele) or meninges and spinal cord (meningomyelocele) through the defect. Meningomyeloceles typically cause severe spinal cord problems.
- Spina bifida aperta: Spinal cord open to the skin surface, posing a high infection risk leading to severe illness and deterioration.
Rumpy Manx cats often lack sacral and sometimes lumbar vertebrae and may have missing spinal cord segments (spinal cord dysgenesis) (Kroll and Constantinescu 1994).
Symptoms of spina bifida and spinal cord dysgenesis in Manx cats vary based on the severity of the spinal cord abnormality at birth. Common signs include:
- Plantigrade hind limb stance and gait (Hopkins 1992): Walking on the hock to toe area, like humans, instead of toes, due to partial hind limb paralysis. Normal, rapid movement is difficult, leading to “hopping” (Deforest and Basrur 1979). A rabbit-like hopping gait is common (Kroll and Constantinescu 1994). Cats may appear crouched and less coordinated.
A Manx cat, showcasing the breed’s characteristic lack of tail due to a genetic mutation linked to Manx Syndrome.
- Lack of perineal skin sensation (Deforest and Basrur 1979).
- Urinary incontinence: Inability to control urine release, leading to secondary urinary tract infections.
- Fecal incontinence: Inability to control feces release, potentially causing megacolon (colon distension) and abdominal distension from constipation. Constipation here is due to impaired nerve function for defecation. Fecal and urinary incontinence causes perineal skin soiling.
- Rectal prolapse: Rectum protrusion through the anus (Deforest and Basrur 1979).
- Severely affected individuals may have spinal abnormalities like meningomyelocele, manifesting as a dorsal midline lump covered by a membrane (Kroll and Constantinescu 1994). Open lesions may leak CSF (cerebrospinal fluid), increasing infection risk, leading to rapid decline, lethargy, fever, severe neurological signs, and death (Evans 1985).
Sometimes, more severe signs develop weeks to months after birth due to spinal cord “tethering,” where the spinal cord abnormally attaches to the vertebral canal. As the cat grows, the spinal cord stretches, causing progressive sensory and motor impairment in hind legs and incontinence (Kroll and Constantinescu 1994), particularly in Rumpy cats. These signs stem from sensory and motor nerve abnormalities in hind limbs, bladder, bowel, and perineal region (Kroll and Constantinescu 1994).
- Stumpy Manx cats, with short, deformed tails, are prone to arthritis in tail bone joints, causing pain (Feline Advisory Bureau).
- Exencephally: Incomplete skull development with brain partially outside the skull.
- Kyphoscoliosis: Dorsal and lateral spinal column curvature (Evans 1985).
Surgery may sometimes help treat specific Manx Syndrome forms. Constipation can be managed medically to some extent. However, generally, effective treatments for these problems are limited.
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2. Intensity of Welfare Impact
The welfare impact of Manx Syndrome varies significantly. Some Manx cats appear normal, except for their tail, and show no spinal cord dysfunction. Others suffer major spinal and spinal cord abnormalities, resulting in hind limb dysfunction and urinary/fecal incontinence. These cats may be constantly soiled, causing skin irritation, inflammation, and infection, requiring intensive care. Impaired mobility restricts their ability to express normal feline behaviors. Spina bifida itself is not painful unless spinal cord infection occurs. However, stumpy cats are prone to painful arthritis in their tail stumps.
Severely affected 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). This highlights that the desirable tailless trait is linked to a range of severe health problems.
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3. Duration of Welfare Impact
Abnormalities may be evident at birth, or signs may emerge over weeks to months as the cat develops (Kroll and Constantinescu 1994). These conditions are typically untreatable, and severe cases may lead to illness and death from complications, unless euthanasia is chosen. Life expectancy is significantly reduced in affected individuals. Less severely affected cats may manage in protected environments with dedicated owners. Surgery may occasionally offer limited help.
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4. Number of Animals Affected
Spina bifida is common in Manx cats. Deforest and Basrur (1979) noted that “Manx breeders soon discover that a considerable percentage of kittens suffer from severe congenital abnormalities.” Their study reported 7 out of 44 kittens (16%) were affected, all of whom were rumpies. Rumpy Manx cats are frequently clinically affected (Evans 1985) and have higher juvenile mortality rates (Kroll and Constantinescu 1994). Despite this, they may be preferred by breeders and owners focused on taillessness without considering welfare implications. Breeders often euthanize affected kittens early, so potential buyers primarily see healthier individuals.
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5. Diagnosis of Manx Syndrome
Detecting the various abnormalities caused by the Manx gene mutation can be challenging. An experienced veterinarian may palpate (feel) abnormalities in the caudal or sacral vertebral area. A skin dimple in the lumbosacral region may indicate an underlying meningocele (Kroll and Constantinescu 1994). Veterinarians also assess spinal reflexes to identify spinal cord abnormalities. Radiography (x-rays) reveals bony defects, while myelography or MRI scans are needed to confirm the type and extent of spinal cord abnormalities (Kroll and Constantinescu 1994).
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6. Genetics of the Manx Cat
Taillessness in Manx cats is due to the mutant, autosomal dominant M gene, which disrupts coccygeal and sacral vertebral development. All Manx cats are heterozygous (Mm), possessing one mutant M gene and one normal m gene, inherited from each parent. The M gene is a mutant form of the normal m gene and is dominant (Long 2006). Homozygous MM cats, with two mutant genes, are so severely abnormal they die during fetal development, making the Manx gene lethal (Long 2006).
Variable expression of the mutant M gene in heterozygous (Mm) individuals is influenced by other, currently unidentified, modifying genes (Long 2006). Robinson (1993) suggests that genetic factors only partially explain expression variation. Heritability is estimated around 0.40 ± 0.11 (Robinson, 1993), meaning about 40% of variation is due to modifying genes and the rest to environmental factors.
Because Manx cats must be tailless to some degree to be classified as Manx, they are all heterozygous and do not “breed-true.” Breeding Manx cats results in some kittens (about 25%) being genetically mm, having normal tails and avoiding Manx Syndrome, but these are not considered Manx cats.
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7. Identifying Carriers and Risk of Being Affected
All Manx cats, defined by their taillessness, carry the mutant M gene and can produce affected offspring, making them gene carriers. While stumpy cats might seem less prone to disease, breeding from them does not reduce the risk of producing rumpies (more prone to severe disease). Unknown modifying genes and environmental factors determine the severity of the condition, and these cannot be tested for or identified before breeding.
Breeding Manx (tailless) cats perpetuates Manx Syndrome. Cats evolved with tails for communication and balance. Continuing to purchase or desire Manx cats sustains the serious health and welfare problems caused by this genetic mutation inherent in all Manx cats.
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8. Elimination and Mitigation Strategies
Manx breeders may breed Manx (Mm) cats with “normal” (mm) cats to avoid producing severely affected MM fetuses that die before birth. However, this still results in the possible production of affected Mm individuals.
Currently, there are no programs to mitigate the adverse effects of the mutant M gene. The gene is inextricably linked to the tailless Manx phenotype, so breeding Manx cats inherently maintains the diseases and welfare issues caused by the mutant gene. The Feline Advisory Bureau (FAB) suggests that informed breeding practices have reduced problem occurrences, but supporting evidence is lacking. Breeding of Manx and Cymric (long-haired Manx) cats appears to have declined in the UK recently (http://www.danzantemanx.com). Future identification of genes and environmental factors influencing M gene expression might enable methods to reduce its adverse effects. However, the ethical implications of continuing a breed based on such a harmful gene should be seriously considered.
Tailed cats (not considered Manx) produced from Manx breeding are mm homozygous, do not carry the mutant gene, are free from Manx Syndrome, 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 in compiling this information.
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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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