FELINE MEDICAL CURIOSITIES: MISCELLANEOUS
Note: Contrary to suggestions on some bulletin boards, the images here are not photoshop. With the exception of those labelled as artist's impressions these are photos of medical conditions. Offsite links to images on these pages is not supported - bandwidth costs money!
Cats have "paw dominance" similar to the right-handedness and left-handedness found. Owners will have noticed that some cats tend to prefer one paw over the other for manipulating objects while others use either paw. Studies indicate that 20% of cats are right-pawed; 38.3% of cats are left pawed and the remaining 41.7% are ambidextrous. Preferences are determined by the part of the brain called the sensorimotor cerebral cortex. Paw dominance is fixed and can be modified only slightly by environmental factors, such as convenience for reaching something.
STANDING ON 2 LEGS
Unusually for a predator with long, slender limbs, a cat can stand on its hindlimbs (bipedal posture) for relatively long periods. This posture is most often seen when the cat is begging or searching for food or trying to get a better viewpoint in a situation where there aren't any objects to jump onto for a better vantage point. Some cats have been taught to "waltz" on their hindlimbs and others will do so of their own accord while begging.
FLUORESCENT TURKISH ANGORA CATS (GENETIC MODIFICATION)
In December 2007 it was reported that South Korean scientists had cloned three glow-in-the dark Turkish Angora cats. The scientists manipulated a fluorescent protein (RFP) gene and a side effect is that the cloned genetically modified Turkish Angora cats glow in the dark when exposed to ultraviolet light. The three cats, two live and one stillborn, were born in January and February. The surviving kittens are now adult Turkish Angoras, weighing 3 kg and 3.5 kg (6.5 - 7 lbs). The cloned cats were produced by a team of scientists led by cloning expert Kong Il-keun at Gyeongsang National University.
The ability to produce cloned cats with an altered RFP gene was hailed as significant because it could be used for developing treatments for genetic diseases and for reproducing model (cloned) animals suffering from the same diseases as humans. In the past, protein has been identified by dissecting the tissue and staining it with dye. While the initial cats are much feted, sadly fluorescent cats appear destined to be living tools in research labs.
While fluorescent cats require UV light to make them glow, other animals have been made luminous by introducing a luminosity gene (e.g. from jellyfish) and naturally glow greenish in th dark. There is interest in luminous cats. To be either luminous of fluorescent the visible fur colour needs to be white.
THE DANCING CATS OF JAPAN
Scientists in Japan in the 1950s discovered that fish were tainted with mercury (from pollution) when an epidemic of neurologically poisoned "dancing cats" swept coastal villages. Unfortunately for affected cats, the brain damage cannot be cured.
THE "FLY-CATCHING" CATS OF EAST ANGLIA
Following Britain’s East Coast flooding of the 1950s (affecting the Essex, Suffolk and Norfolk coastal areas), many rescued cats developed abnormal behaviour, particularly the so-called ‘fly-catching syndrome’ where the cat stares upwards or into the distance and snaps at hallucinatory "flies" (it may have involved seizures, but triggered by the stress suffered during the floods). Unfortunately many did not recover and had to be put to sleep. Unlike Japan's "dancing cats" this syndrome had a psychological rather than physical basis. Post traumatic stress disorders are not new in felines. Many cases of apparent shell-shock had been encountered by vets during the Second World War. Some cats were so badly affected that they could not be extricated from the dark corners where they had taken refuge and had to be destroyed on humanitarian grounds. Limb-flicking, most often associated with trying to flick a substance (e.g. water) or item (e.g. piece of adhesive tape) off of the paws. Cats that had eaten LSD showed limb-flicking behaviour even when there is no irritating foreign material on the paws.
Sometimes cats that are otherwise normal cats have episodes of slow-motion movement. These episodes vary in how long they last and may include sleep periods. The cat walks, eats and groom less than half as fast as normal. Urination and defecation have also been seen during slow-motion attacks. The cause has not been identified, but appears to be a temporary anomaly.
TRIPLE THYROID GLANDS
Hyperthyroid is increasingly common in cats, especially older cats, and has been linked to canned food (although survey results are not fully conclusive) or a diet of canned food high in fish products. Cats normally have 2 thyroid glands in their neck, compared to 1 thyroid gland in humans, and hyperthyroid is usually associated with abnormal tissue in one of those glands. One treatment of hyperthyroid is to remove the abnormal thyroid glands. A veterinary practice in Chelmsford, Essex, England, has treated a hyperthyroid cat which had 3 thyroid glands. Two have been removed, still leaving the cat with a functioning thyroid gland (personal discussion, July 2006).
MAD CAT DISEASE (FELINE SCRAPIE, PRION DISEASE)
In 1990, a Siamese cat at Bristol Veterinary School, England, died of FSE during Britain's BSE (Bovine Spongiform Encephalopathy) outbreak. The cat showed symptoms of nervous disease in January 1990. It had poor limb co-ordination, but unlike BSE-affected cattle it was not nervous or aggressive. It was described as appearing "happy, but drunk". There is no treatment for Spongiform Encephalopathy and the cat was euthanized. It was assumed to have eaten cat food containing infected tissue well before the ban on using certain cattle parts. There have been no other confirmed cases of FSE in domestic cats, however in December 2000 a lion at Newquay (Cornwall, UK) zoo fell ill after a fight with another lion. An autopsy revealed its death was due to FSE, possibly from an infected carcase.
Spasticity means "suffering from spasms" and covers several conditions with similar symptoms. It is also known as cerebral palsy and cerebellar hypoplasia (CH). Affected cats may be born to females that contracted Feline Infectious Enteritis (FIE, Feline Panleukopaenia, Feline Distemper) during pregnancy. The virus can cross the blood-brain barrier and cause defects in the cerebellum. Unborn kittens at 1 - 4 weeks gestation are usually killed by the infection and the foetus is reabsorbed by the mother or spontaneously aborted. Kittens at about 4-5 weeks gestation may be stillborn and have major defects; if born live they are unlikely to survive. Kittens infected near the end of the pregnancy may be stillborn or may be born with Cerebellar Hypoplasia (spasticity).
The virus affects the cerebellum area of the brain, an area involved in fine motor control. This causes ataxia (poor co-ordination), gait abnormalities and perception. Affected cats are wobbly and unco-ordinated and have characteristic head tremors which are evident when they try to focus on an object. Barring any accidents caused by their unco-ordination, their life expectancy doesn't seem to be affected and given a safe environment, they live as long as unaffected cats and seem little troubled by their condition.
Turner's Syndrome is a chromosome anomaly where a cat inherits a single X chromosome, but no other sex chromosome. It is usually lethal and the kitten will have several physical abnormalities due to lacking part of the necessary genetic information. In October 2010 I heard of a cream female kitten born to a black silver mother and a cream father (cream is genetically red with the addition of "dilute"). The parents were Maine Coons so their colour genetics were known over several generations. The mother's pedigree showed she could not have inherited a red gene and has never produced red/cream kittens on previous matings to a cream male (i.e. she wasn't a "hidden tortie"). The only way to have a cream female kitten is in the absence of a black gene. This meant the kitten was XO (Turner's syndrome) and had inherited her X gene, with the red gene, from the father. The kitten also had a severely underdeveloped lower jaw, twisted front legs and a kinked shortened tail. She had the neck webbing that is also characteristic of Turner's in humans. She also had a cleft palate and a shortened tongue which prevented her suckling so she was put to sleep soon after birth.
FAINTING SYNDROME (MYOTONIA CONGENITA)
During 2006, two kittens with suspected Myotonia Congenita were reported across the internet. The condition is better known as "fainting goat syndrome". If startled, kittens (tabby Charlie and black-and-white Spike) stumble and fall over into a rigid paralysis lasting about a minute before they return to normal. The kittens appeared generally healthy and were able to walk, but could not run or jump. The kittens came from a pet shop and had been returned there by their purchasers, but Charlies's owner decided to keep his kitten and to take Spike who was due to be put down by the pet shop (note: pet shops are not the best places to obtain kittens from).
According to the Royal Veterinary College, Charlie and Spike are the only known cases of Myotonia Congenita in the UK. There have been only six other feline cases reported worldwide: two from the US and four from New Zealand (being a genetic condition several littermates may be affected). Myotonia Congenita is a genetic condition that is a defining breed trait in so-called "Fainting Goats" hence its common name "fainting goat syndrome". It usually only affects the muscles used for movement, but in extreme cases it can affect the muscles used for breathing, resulting in respiratory failure. Normally, a muscle contracts and then relaxes, but with myotonia congenita, the muscle relaxation is delayed and the muscles remain locked (contracted) so the limbs are rigid.
It was least obvious when the kittens were resting, however Charlie had problems getting to his feet after resting for a while and took a few moments to become steady. Anything stressful or startling, such as a loud noise or even snagging his claws unexpectedly, induced the fainting and locking of the muscles. Vets planned to treat him with drugs to prevent the muscles contracting so much. The drug had not previously been used for cats. Even if the treatment reduced the severity of the symptoms, Charlie would never be able to go outdoors or play like normal cats.
Sadly the condition proved fatal to both cats. Spike died on 27/10/10 due to respiratory failure and Charlie died on 30/10/10. It is hoped that a post mortem and DNA analysis will give clues as to whether this is the same condition as seen in goats. In goats, the condition rarely affects lifespan.
"LIVING ROBOT" DISEASE IN CATS IN SCOTLAND
In 2012, British vets reported on an incurable disease that turned cats from a rural area of Scotland into "living robots". It had been recognised in the area for around 10 years and was compared to "Staggering Disease" reported in cats in Sweden and Austria and I've included information in this section (see foot of page for references).
"Living Robot" disease is a slowly progressing neurologicical disease. Afflicted cats showed personality changes; most became over-affectionate though a few became aggressive. Their movement became stiffer with the head held forward, the chin slightly down and the ears forward. Their legs become rigid, giving them an odd, stiff gait and their tail become stiff and stuck out. The disease got its nickname because the cats walked in a robotic manner. As the disease progressed, they became increasingly disorientated to the point of getting stuck in corners because they didn't know how to turn around or reverse. They also had difficulty grooming. When the illness progressed to a point where cats found it hard to swallow, they had to be euthanized. This was usually within 11 - 12 months of falling ill. A similar condition has been reported in Sweden and Austria where it is known as 'Staggering Disease', however those cats did not exhibit the stiff extended tails seen in the Scottish cats. There is no known treatment or cure. Once symptoms start, they become progressively more disabling until the cats are put down within 11 - 12 months to prevent suffering. Vets have tried a number of treatments including painkillers, vitamins, antibiotics and drugs that are normally given to Multiple Sclerosis sufferers, but none have been effective in slowing the progress of the disease.
The outbreak is centred on a rural area of Scotland between Inverness and Aberdeen (Grampian region) where two vet surgeries have recorded 21 cases. Around 50 cases have been spotted in Scotland in the past ten years. One case was reported in Liverpool in a cat that probably contracted the diease when it lived in the affected region of Scotland. Researchers believe there to be unreported cases elsewhere. It isn't known how long elapses between infection and initial symptoms. Affected cats are usually already elderly. They all had outdoor access and were good hunters, so it is believed they caught the disease through hunting. The disease does not spread from cat to cat suggesting it may be a mutant virus carried by mice or voles in the locality. Tests for numerous viruses (in blood samples, brain/spinal fluid samples and brain tissue) have ruled out many viruses, but not identified a causal agent.
Many neurological conditions have common symptoms because the same areas of the brain/central nervous system are compromised. The "robotic" or "staggering" diseases are not the same as the prion disease Feline Spongiform Encephalopathy (Feline BSE, Chronic Wasting Disease, CWD) which is already documented in cats. Symptoms are also not consistent with Lyme Disease or Domoic Acid Poisoning (suggested in some online comments pages). Owners should not confuse the progressive symptoms of this Staggering Disease with common age-related joint stiffness ("clockwork kitty syndrome") caused by arthritis or with the sudden onset hind-limb weakness caused by saddle thrombus. Fringe theories included radiation from Fukushima or from wireless networking/mobile phone masts!
For comparison, "Staggering Disease" has been observed in Sweden since the early 1970s and was associated with a non-suppurative meningoencephalomyelitis mainly affecting the brain stem and the limbic system. Similar types of feline encephalomyelitis have been reported around the world, including Australia (Borland & McDonald, 1965), the USA (Vandevelde & Braund, 1979) and Austria. It is formally known as Feline Nonsuppurative Meningoencephalitis and has been tentatively linked to Borna Disease Virus (BDV) infection. However, the cats did not originate from areas where Borna Disease was endemic, and did not show typical signs of classic Borna Disease. Only small amounts of Borna Disease antigen were detected in them, which is not consistent with the huge amount of Borna Disease antigen found in infected horses. In a number of studies in the 1990s, the brains of cats showing neurological symptoms were being examined for Feline Spongiform Encephalopathy (FSE) and were also tested for viruses.
Initial reports showed that 44% percentage of Swedish cats suffering from Staggering Disease had BDV antibodies (Lundgren et al., 1993 ; Lundgren & Ludwig, 1993). Immunohistochemistry found viral markers present at very low levels in the brains of only three out of 24 diseased cats (Lundgren et al., 1995a, 1995b). Austrian cats with Staggering Disease lacked detectable levels of BDV markers in the central nervous system (Nowotny & Weissenböck, 1995). Research in Japan (Nakamura et al., 1999) found low levels of BDV antigen or low levels of Borna Virus RNA (the virus's equivalent of DNA), but not both at once, present in the brains of cats exhibiting different neurological symptoms. In Switzerland, only one of 180 brains of cats with neurological disease showed evidence of BDV infection by immunohistochemistry (Bornand et al., 1998). The other 179 cat brains were negative for BDV markers. BDV-specific RNA were found in the cerebral cortex of a cat with paralytic disease (Berg & Berg, 1998) and in the brains of some diseased cats in the United Kingdom (Reeves et al., 1998), but BDV infection was not confirmed by other methods.
Those various results indicate that cats are occasionally infected with Borna Virus, but it is probably not the cause of Staggering Disease. The incidence of antibodies in cats with neurological disease compared to the incidence of antibodies in cats with other types of disease suggests that Borna Virus may play some role in nervous disease in cats. No correlation has been found with established feline viruses such as FeLV, FIV or FIP (FCoV). Borna Disease will already have been ruled out in the Scottish cats.
On March 13th, 2006 it was reported that a cat in gave birth to 5 normal kittens, and one that resembled a mouse. The owner said the nose, mouth, ears and tail of the "kitten" looked like that of a mouse, but the rest of the body was kitten-like. The mother cat nursed and cared for it, just like the kittens. A look at the photos accompanying the story reveal the odd-one-out to be a rodent. It is not unknown for a mother cat to adopt other animals while her maternal instincts are so strong. The rodent, meanwhile, has temporary protection amongst the genuine kittens and has a convenient food source.
See Mosaicism and Gender Anomalies for information on hermaphroditism, Klinefelter syndrome and other gender anomalies in cats.
A "throwback" is an animal whose conformation, and often temperament, resembles the ancestral type rather than resembling its breed. This happens due to recessive (hidden) genes inherited from the parents re-combining or a mutation returning a gene back to its wild type. The complexities of inheritance means that a small percentage of domestic kittens, born to friendly pet cats and raised in a household, do not inherit the necessary genes for them to have domestic temperaments. No matter that they are raised in a loving environment and their siblings and parents are friendly pets, such kittens simply lack the genes that allow a cat to be domesticated. Such cases are rare, but one of the best documented seems to be that of "Thumper" the Manx.
In August 1975, Mrs Rosemary Morley of Brighton, Sussex, England, bought a male Manx from a leading breeder in the Isle of Man. The kitten was flown from the breeder to England at the age of 14 weeks. This is all quite normal. Thumper, described as an "orange" kitten looked nothing like a Manx apart from the absent tail. His body shape was wrong and his face was pointed instead of round. At the age of 14 weeks, Thumper's claws were as large as those of an adult cat. Fearing a mix-up, Mrs Morley contacted the breeder, who assured her that the sire and dam of her odd looking kitten were normal domestic Manx cats born in the Isle of Man. Thumper was an aloof youngster, though this can happen if a breeder does not properly socialise the kittens before homing them. As he matured, he developed huge whiskers, double canines that were chisel-ended and enormously long claws.
Thumper instinctively adopted the lifestyle of a wild cat and shunned the domestic life. He ate everything he killed while out hunting (an activity at which he excelled) and specialised in snakes in lizards. He also developed a banshee-like scream. His mature size was 36 inches (91 cm) long and weighed 12 lbs (5.44 kg). He was not dependent on his owner for anything and did not seek human companionship. Like a wild cat, he spent most of his life hidden in long grass, shrubs or woodland though he did not enjoy hot weather and liked to cool off quickly by lying in the fridge with the door open.
Veterinary surgeons thought that he was either a feral cat or was extremely neurotic. It seemed that he had not inherited the genes for domesticity and he had inherited a bunch of genes that made him look, and act, wild. In June 1978, zoo vet David Taylor identified him as a rare genetic regression to the African wildcat (Felis lybica) - in other words he was a throwback to the wild ancestor of the domestic cat. The scarab beetle marking on Thumper's forehead was said to be the tell-tale sign as this distinguishes F lybica from all other wild cats, however it is widely found in domestic tabby cats and isn't much of an indicator! Sadly, in the summer of 1980, Thumper became seriously ill after eating poison and stopped eating. He risked dehydration because he normally obtained all his fluids from his kills and from assorted vegetation that he also ate. In a rare admission of dependency, he allowed Mrs Morley to dropper feed him while he remained in his "den" - on top of a 4 ft 6 in (1.37 metres) stack of boxes in her attic. Sadly, the poison caused irreparable brain damage, and this rare throwback died on 4 December 1980.
ALLEGED FELINE MATHEMATICIANS
I get regular emails about Cuty Boy the alleged feline mathematician. Cuty Boy is a much publicised cream Persian from Bar Dubai whose alleged passion and talent for arithmetic was discovered when he was a kitten. It is claimed that he can add, divide, multiply, subtract, find square roots and solve algebra problems. Cuty Boy was bought from a Dubai pet shop by Hema Mohan Chandra, from Kerala, who is also his stage handler. Her son, Renjit, noticed Cuty Boy's ability to understand commands. Hema claims the cat can indicate "yes", "no", "left" and "right" and that he replied "yes" when asked if he understood numbers. She then taught him to count up to 20. Cuty Boy gives his answers by nose-bumping her face the correct number of times. Numbers too large for nose-bumping are indicated using a set of answer cards. The cat selects the correct answer by twitching his tail and looking at the card. To convince sceptics of Cuty Boy's abilities, the owners had him tested by maths teacher Sahadevan Panicker from Dubai's Gulf Modern School. Unfortunately, Cuty Boy has to be pushed by his family to perform in public.
But what is really happening? The phenomenon is called involuntary/unconscious cuing. Some cats are adept at reading human body language even if the humans are not aware they are transmitting body language. Studies of "counting horses" (who tapped a hoof the correct number of times in response to an arithmetic puzzle) uncovered the truth. The animals picked up on almost imperceptible twitches from the handler/trainer. The handler was mentally urging the animal to tap again and get the right answer. This mental urging leaked into a facial or body twitch and at each "signal", the horse tapped a hoof. In some cases, the handler was unaware that he was leaking signals to the horse (this may also be true of Cuty Boy's owner). The studies found that when the body language was obscured, or when a the animal worked with an unfamiliar handler, the animal lost its ability to count. When the handler didn't know the answer (or was deliberately given an incorrect answer by the person setting a complex problem), the counting animal also got the answer wrong. Set pieces such as selecting the correct card were learnt in much the same way - picking up on tiny signals, including "left" and "right".
Cuty Boy also understands phrases in 8 languages, including Gujarati, Persian, Malayalam (Hema's mother tongue), English, Arabic and French and can identify objects when asked in those languages. This is not evidence of great linguistic skills or of a psychic cat. While the meanings of some of those words will have been learnt, Cuty Boy will be relying on his owner's involuntary cues regardless of the spoken language.
Counting, linguistic and psychic animals do not perform well in controlled conditions. Owners blame this on the animal being upset and refusing to co-operate, but the truth is that the animal is not being given any cues. Cuty Boy's unwillingness to perform in public is probably linked to difficulty in concentrating on the owner's signals when there are so many distractions for both cat and owner. In a public environment, there is greater tension and this makes the owner's body language unclear. In spite of recent relentless publicity, Cuty Boy is not a mathematical prodigy. He is simply a performing animal with a flair for reading body language and doing a counting trick that was debunked over a century ago. He is the 21st Century version of "Clever Hans".
Note: The most famous counting critter was William von Osten's horse, Clever Hans (Kluge Hans), in Berlin. Hans answered tricky maths questions (including fractions) by tapping out the answer with his hoof. He was first publicly exhibited in 1891 and several scientists became convinced that there was no signalling or trickery. They were impressed that Hans performed almost as well without von Osten as with him. In 1904, psychologist Oskar Pfungst studied Hans and noticed that if the nobody present knew the correct answer, neither did Hans. When the horse wore blinkers to obscure his view or when the questioner was further away, Hans got the answer wrong. He deduced that Hans was getting a signal from the person asking the question. Pfungst noticed that when a person asked a question, they tilted their head slightly without even realising it. This signalled Hans to begin tapping. When Hans got to the right answer, the excited questioner lifted their head, raised an eyebrow or smiled ... and Hans stopped counting! Hans was clever because he could read human body language. Another example was Lady Wonder the "telepathic horse" tested by JB Rhine. In 1927, Lady Wonder was seen to knock over alphabet blocks in response to questions. Two years later, Lady Wonder failed testing and Rhine concluded that the horse had lost its psychic abilities. Like Clever Hans, Lady Wonder had previously been picking up on subtle human body language. Cuty Boy is simply a feline equivalent of Clever Hans.
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BOOKS ABOUT ANOMALIES
If you are interested in medical curiosities, books worth reading are "Mutants: on the Form, Varieties and Errors of the Human Body" by Armand Marie Leroi and "Anomalies and Curiosities of Medicine Vols 1 and 2" by George M. Gould & Walter L. Pyle. The Gould & Pyle books were published in 1896 and are in the public domain. You can download text-only versions of Gould & Pyle from several websites so don't waste money on text-only versions of the book; but if you want the versions with photos, consider the Kessinger editions. The Leroi book explains why and how some deformities and anomalies happen - the mechanism is the same in cats as it is in humans.
Feline Borna Disease/Staggering Disease References<
Berg, A. L. & Berg, M. (1998). A variant form of feline Borna disease. Journal of Comparative Pathology 119, 323-331
Borland, R. & McDonald, N. (1965). Feline encephalomyelitis. British Veterinary Journal 121,479-483.
Bornand, J. V., Fatzer, R., Melzer, K., Jmaa, D. G., Caplazi, P. & Ehrensperger, F. (1998). A case of Borna disease in a cat. European Journal of Veterinary Pathology 4, 33-35.
Kronevi, T., Nordstrom, M., Moreno, W. & Nilsson, P. O. (1974). Feline ataxia due to nonsuppurative meningoencephalomyelitis of unknown aetiology. Nordisk Veterindrmedicin 26, 720-725.
Lundgren, A. L. & Ludwig, H. (1993). Clinically diseased cats with non-suppurative meningoencephalomyelitis have Borna disease virus-specific antibodies. Acta Veterinaria Scandinavica 34, 101-103.
Lundgren, A. L., Czech, G., Bode, L. & Ludwig, H. (1993). Natural Borna disease in domestic animals other than horses and sheep. Journal of Veterinary Medicine Series B 40, 298-303.
Lundgren, A. L., Lindberg, R., Ludwig, H. & Gosztonyi, G. (1995a). Immunoreactivity of the central nervous system in cats with a Borna disease-like meningoencephalomyelitis (staggering disease). Acta Neuropathologica 90, 184-193.
Lundgren, A. L., Zimmermann, W., Bode, L., Czech, G., Gosztonyi, G., Lindberg, R. & Ludwig, H. (1995b). Staggering disease in cats: isolation and characterization of the feline Borna disease virus. Journal of General Virology 76, 2215-2222
Melzer, K. (1999). Untersuchung zur Aetiologie von ZNS-Erkrankungen bei der Katze in der Schweiz mit besonderer Beruecksichtigung der Borna Disease Virus Infektion. Inaugural dissertation (Dr. med. vet.), University of Zürich, Switzerland. [Melzer, K. (1999). [Investigation into the etiology of CNS illnesses of the cat in Switzerland, with special consideration of the Borna Disease virus infection. Inaugural thesis (Dr. med. vet.), University Of Zurich, Switzerland.]
Nakamura, Y., Asahi, S., Nakaya, T., Bahmani, M. K., Saitoh, S., Yasui, K., Mayama, H., Hagiwara, K., Ishihara, C. & Ikuta, K. (1996). Demonstration of Borna disease virus RNA in peripheral blood mononuclear cells derived from domestic cats in Japan. Journal of Clinical Microbiology 34, 188-191.
Nakamura, Y., Watanabe, M., Kamitani, W., Taniyama, H., Nakaya, T., Nishimura, Y., Tsujimoto, H., Machida, S. & Ikuta, K. (1999). High prevalence of Borna disease virus in domestic cats with neurological disorders in Japan. Veterinary Microbiology 70, 153-169.
Nowotny, N. & Weissenböck, H. (1995). Description of feline nonsuppurative meningoencephalomyelitis ('staggering disease') and studies of its etiology. Journal of Clinical Microbiology 33, 1668-1669.
Reeves, N. A., Helps, C. R., Gunn-Moore, D. A., Blundell, C., Finnemore, P. L., Pearson, G. R. & Harbour, D. A. (1998). Natural Borna disease virus infection in cats in the United Kingdom. Veterinary Record 143, 523-526.
Vandervelde, M. & Braund, K. G. (1979). Polioencephalomyelitis in cats. Veterinary Pathology 16, 420~27.
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