Following Valerie’s experience with Bezique (Dec 99) , we have an update on his condition (and she had another fellow - Khendjer bitten, almost the identical pattern, found later, slower to recover, but also OK!!!) and an excellent slightly technical article on the topic.
has fully recovered from his snakebite but it took him four weeks to do
so. He was still wobbly on his legs when he came home but gradually
He was very hungry and started to put weight back on in the third week
and the shine returned to his coat in the fourth. The fact that Bezique
is a show cat helped while he was in hospital as he was used to a cage,
to being handled and people coming and going and so remained still and
quiet - he must have thought it was a very long show!
The day Bezique was bitten I had the misting system on in the cattery (which I thought was snake proof! !) and I'm sure the water brought the snake in. Don 't forget snakes can get through the smallest spaces - particularly young ones and they can flatten themselves to do so.
My vet has given me a paper by Dr. Peter Little on snakebite in animals and the following are the salient points applicable to cats.
Cats appear to be more resistant to the effects of snakebite than other species. They are approximately three times less sensitive to Tiger and Brown Snake venom than dogs, and are also less likely to receive the full force of the strike due to their greater agility Weakness and flaccid paralysis are often the first presenting signs in cats following snakebite. Often the time of bite is not known. Owners sometimes report that the cat has been missing for a few days, and that they found it in a collapsed state. Other signs of envenomation in cats include dilated pupils, poor response of pupils to light, vomiting, difficulty breathing and disorientation. The most common sign in domestic animals following a serious snakebite is weakness followed by paralysis. Paralysis is usually ascending, affecting the hindlimbs first and then progressing to complete paralysis, with death due to respiratory failure.
clinical signs is usually sudden with collapse or vomiting within
of being bitten. Recovery may occur within 30 minutes to be followed by
a progressive onset of clinical signs. Any or all of the following may
be observed: trembling, vomiting, salivation, defecation, ataxia.
pupils, slow or absent pupillary light reflexes, respiratory distress;
shallow or abdominal respiration, hindquarter weakness, pallor,
non-clotting blood. extended coagulation time, proteinuria, haematuria,
haematemesis, continued bleeding from fang marks or other wounds, and
paralysis progressing to coma or respiratory failure.
Myotoxins cause damage to muscle cells. Most of the dangerous Australian snakes have a component in their venom that can cause damage to skeletal muscles to some extent, with the Brown Snakes being an exception. Myotoxins bind to the muscle fibres, causing progressive destruction of muscle cells with release of breakdown products such as myoglobin (the red-brown muscle pigment) and creatinine kinase (CK) into the circulation. This process can take hours to become apparent, by which time irreversible damage may be done. The result is progressive muscle weakness and pain on movement The myoglobin is passed into the urine resulting in a dark red-brown colouration. The myoglobin can also cause irreversible kidney damage resulting in renal failure in some cases.
Neurotoxins are particularly important in Australian snake venom. Neurotoxins act at the skeletal neuromuscular junction (NMJ), causing progressive paralysis of voluntary muscles (such as limb muscles) and respiratory muscles, by preventing the messages from the brain getting to the muscle fibres. Death occurs due to respiratory paralysis and thus lack of oxygen. The first effects of these neurotoxins are not seen less than one hour after the bite, and usually the earliest signs take 2-4 hours or more to develop. Complete paralysis may take from 3 hours to more than 18 hours to develop. However, breathing difficulty due to paralysis of the tongue and pharynx may develop much earlier than full respiratory paralysis. Animals with severe breathing difficulties or complete paralysis require intubation and artificial ventilation until the effects of the venom are reversed.
ProcoaguIants are chemicals in snake venom that covert prothrombin to thrombin, resulting in consumption of fibrinogen. This is part of the blood clotting system. The result of this is that important blood clotting factors can be consumed (possibly within 30 minutes of the bite). which can result in internal or external bleeding. This problem is particularly severe with Brown Snakes and may last for many days if antivenom treatment is delayed, or not enough antivenom is administered initially. In some cases a brain haemorrhage may occur, which can result in a sudden deterioration in the patient's condition.
Treatment of snakebite in domestic animals can vary widely depending on the species of snake and the severity of envenomation. Clinical scenarios can range from a flaccid. weak cat requiring supportive treatment for several days, to a severely envenomed patient in respiratory arrest with a severe coagulopathy requiring large doses of antivenom. intensive care and artificial ventilation for many days. It is also important to remember that the patient' s condition can change very rapidly - an animal showing no clinical signs can be on the brink of death only 30 minutes later There appears to be a good correlation between the time from snake bite to treatment. and the recovery time - that is, the earlier the administration of the correct antivenom the more rapid the recovery . Also, lower doses of antivenom are generally required if antivenom is administered prior to the onset of paralysis.
Prior to Antivenom Administration
Animals should be premedicated with antihistamine and adrenaline prior to antivenom to help prevent an anaphylactic reaction.
Intravenous fluids are important in all cases of snakebite to treat or prevent dehydration and to maintain urine output to help protect the kidneys from the effects of the venom or myoglobin from muscle cell breakdown. It is important to ensure that the fluids are kept running all the time, so they should be checked frequently.
Excellent nursing care is essential when treating snakebite cases in domestic animals. Paralysed animals should be kept warm and their temperature monitored frequently to prevent the onset of hypothermia. Hypothermia is a common complication in severe snakebite cases and makes the prognosis much worse.
Paralysed animals should be kept in sternal recumbency or turned frequently from side to side. Gentle physiotherapy and massage of muscles can be valuable for paralysed patients, however care must be taken in animals with painful muscles due to the myotoxins present in some snake venoms. Intravenous catheters and nasal oxygen tubes must be checked frequently to ensure that they are not checked or displaced. Animals that are paralysed or weak may not be able to eat voluntarily, so may require feeding via a nasogastric tube Breathing, heart rate, pulse pressure, mucous membranes, pupils, urine output and hydration status should all be monitored frequently. Patients that are stressed or excited should be kept in a quiet environment and sedated if necessary.
From 'On the Spot' 50 June 2000
In response to the Snake Section above, as included in Issue 49, Lesley Roberts wrote:
in the newletter article on snake bites. I've had baby Dugites in
the back garden every February/March for the past three years. I
live opposite a river reserve and for ten years never saw a snake. The
snake catchers say the snakes are now coming into suburbia because of
in the general area. I've currently got four cats and two dogs in
the house full-time - fortunately I work near home so I drive home and
spend lunchtime with the menagerie ... and I'm getting fit walking the
dogs twice a day!
Last year my white/grey domestic neuter, Splodge, found a wiggling baby Dugite and started playing with it. As I dashed for the broom he made the tactical error of killing the snake the same way he would kill a mouse - by biting and crushing its head. Half an hour later he started intermittently panting in distress so I rushed him to a vet. He was given antivenom, put in an oxygen cage, and was on a saline drip overnight to flush the poison from his kidneys. He came home the next day but had to stay in a dark and quiet room for two weeks. Because I took Splodge to the vet quickly he made a 100% recovery and didn't even lose weight. Splodge is now referred to as "Splodge the Snakebuster".
The snake episode cost me $600 but it could easily have cost hundreds of dollars more if I hadn't have been able to identify the type of poisoning and type of snake. Also, the vet told me some cats are extremely allergic to antivenom. Needless to say I'm paranoid about snakes now. I keep the garden as clear of undergrowth as possible, wear boots in the garden, and use the garden hose (on as high pressure as possible) to squirt around plantpots and the stack of spare pavers. The hose is fairly efficient at flushing baby snakes along the path and driveway and over the road into the reserve. I've got an extra-long hose and run behind the snake like a fireman. The cold water slows themdown a bit too.
the garden with wire mesh hooked/clipped to the top of the "asbestos"
so the cats can't get out, but unfortunately the baby snakes still
through thin cracks in the "asbestos" - probably heading for water
I've watered the garden. The snake catchers say dugites lay up to
30 eggs at a time in undisturbed ground and then hang around the nest
special vibrating noises which help the eggs mature and hatch.
rather dubious words of the last snake catcher I spoke to were:
absolutely no way a snake will hang around in a dog's backgarden - too
much ground vibration!"
Bye for now,
P.S. Satu Gamelan sends his regards.
nothing about Dugites, I asked Lesley to tell me more about them ....
I've had a quick search around the Internet for a general description of the Western Australian Dugite (Pseudonaja affinis), 14th most venomous snake in the world, but there isn't much.
Lesley did find this site, however:
Brian Bush's web site: http://members.iinet.net.au/~bush/index.html
Manager of Snakes Harmful and Harmless.
Snakes H & H is a Western Australian based company since April, 1987.
And here is an extract on Dugites
The Dugite is an especially mobile snake that will forage widely into backyards and buildings in search of mice. The potential for snakebite is far greater in the backyard. A feeling of security and a reduced awareness of snakes in this environment increases the chance of treading on one that maybe there.
In southern Western Australia large numbers of hatchling dugites occur mid-February through to mid-April. These are 15-35 cm in length and can be brown, green or yellowish in colour, but always hatch with at least part of the head black. Although best treated with caution, the bite from a juvenile is unlikely to cause more than local symptoms in a healthy adult. Potentially dangerous to children and pets.
In the Perth area two common snakes bite dogs and cats. One is the Dugite or Spotted Brown Snake (Pseudonaja affinis), a very mobile, nomadic snake that has small fangs and small yields of very toxic venom. Often the symptoms are slow in onset and include a progressive paralysis beginning at the back legs and extending forward. It is not uncommon to observe a dog or cat after a bite from a Dugite having problems supporting the hind part of the body. Eventually paralysis becomes total with a lolling of the tongue, non-responsive pupils and laboured breathing. Brown Snake antivenom is used for bites from this species and the Gwardar or Western Brown Snake (P. nuchalis).
Cats are natural hunters and often find snakes. A problem to owners of snake-catching cats is their habit of returning to the house with a live snake. Little will discourage cats from hunting snakes.
Enclosures or backyards where dogs are kept in outer suburban and rural areas should be free of long grass and rubbish. This applies for the area surrounding those enclosures also. The addition of a low (to 1 metre) continuous corrugated iron or cement sheet wall around the perimeter of the enclosure will generally exclude snakes. Dry dog food should be stored in such a way as to lessen its availability and attractiveness to mice.
a dog in bushland during spring, summer and autumn, it is advisable to
restrain it on a leash. If the dog is exercised, choose an open area
you can have visual contact with it always.
From On the Spot, 52 Dec 2000
Spider Envenomation in Dogs and Cats
This is the first part of a CSL Publication - Technical Update No 013, kindly supplied by Valerie. Hamilton.
Virtually all spiders are equipped with both venom glands and fangs, so are capable of causing bites that produce some degree of local injury and occasionally systemic effects. However, to date, only the male Funnel Web Spider, and the female Red Back Spider, which is found in all states of Australia (and New Zealand, where it is known as Kapito) appear capable of causing significant systemic effects.
Red Back Spider
In humans, this spider is the commonest single cause of potentially serious envenomation in Australia1 . The Red back Spider is a member of the Black Widow spider group found world wide, and properly known as Lactrodectus mactans hasselti. Some 250 case reports of red Back spider antivenom use in humans have been received annually by CSL over the last 10 years, a consistency not seen with other antivenoms2. Although fewer Red Back spiders now bite buttocks, or genitalia in outdoor toilets (21.9% in 1961, 9.7% in 1978, 2.3% in 1989), more bites to the head and neck from spiders making homes in ear muffs and safety helmets have kept the numbers constant.3
The Red Back spider is dark brown to jet black in colour with a longitudinal red or orange stripe running down the centre of the back (abdomen) and curving under the distal end. The body is globular in shape and usually about 1 cm in diameter. only the female spider is potentially dangerous. The male spider is considerably smaller and is relatively harmless, because, although it is venomous, it’s small fangs cannot injure humans. the Red Back is not aggressive and if disturbed will usually fall to the ground, curl up and feign death. 1
The spider may be found under logs or bark on the ground, in empty containers, wood sheds and other sheltered places protected from light, where it spins a coarse irregular web. They seem to prefer locations in which the outer portion of the web has some exposure to sunlight, and the inner portion of the web is tucked away in a cool dark crevice.4
The female is able to store the sperm of the male and use it over a period of up to two years to lay several batches of eggs ( the male is sometimes eaten after mating). A female may lay eggs every 25-30 days and may lay up to 5000 eggs. The eggs hatch three weeks after being laid and maturity is reached, on average, in about 3-4 months. Females live for 2-3 years; males live up to 6-7 months 1,5
Although insects are the usual prey of Red back spiders, they are capable of killing and digesting larger animals, such as lizards and frogs. When prey becomes entangled in the web, the spider climbs down and bites it, then retreats for a moment to allow the venom to take effect. She then approaches the victim, swathes it in silk, and lifts it up into her retreat.4
Red Back spider venom has a unique and selective action at the nerve endings where it causes a depletion of either acetylcholine or catecholamines. The mechanism of pain production either at the bite site or in regions far removed from the actual bitten area is not understood. 6
There is considerable species variation in susceptibility to envenomation. Guinea pigs and horses are highly susceptible, cats are moderately susceptible, whilst the dog is relatively resistant to the effects of venom - it is seldom lethal unless a considerable number of bites have been inflicted, as would only occur under experimental conditions.7
The clinical signs in animals are essentially similar to that seen in humans, ie. variable disturbances of the autonomic nervous system and muscular paresis (paralysis).. There is initial pain reaction at the bite site, with animals probably chewing at the bite site, followed by restlessness with abnormal posture (pain), tachycardia (abnormally rapid heart beat), hypertension (high blood pressure), hyperaesthesia (oversensitivity particularly of the skin), hyperaemia of the skin (reddening of the skin, due increased blood flow) and weight loss.
In dogs there may be vomiting, diarrhoea, generalised tremors or chronic contractions of skeletal muscles, rigidity of the abdominal wall, irregular breathing due to muscular contractions of thorax and abdomen, malaise, paresis and prostration.7
In cats there may be hyperexcitability, salivation7 as well as ataxia (uncoordinated walking, inability to walk) and various nervous signs.6
In humans the diagnostic indication of Red Back spider bite is localised sweating at the site of the bite4. Without specific treatment (in humans) it may be months before the resolution of sequelae such as muscle weakness and spasm.6
No special first aid (such as pressure bandage) is recommended because of the relatively slow action of the venom and because the restriction of the circulation may increase the severity of the local pain. Serious illness apparently does not develop for at least three hours4.. Application of ice packs (not local freezing) may give some relief.1
If 24 hours have elapsed since a known bite, and only mild local effects have occurred, then antivenom should be withheld. Use of antivenom during the early acute stages of envenomation will effectively and quickly abolish all results. Results may be less dramatic if used after the paralysis stage or during the convalescent stage.
Red Back spider antivenom is prepared from the sera of horses which have been hyperimmunised against the venom. An initial dose of 500 units (one vial) should be used for any species. This is the amount that will neutralise the ‘average’ spider venom dose.
In contrast to snake antivenom, this antivenom is preferably given by the intramuscular route instead of intravenously. This route has been proven to be clinically satisfactory over many years because of the small volume involved and the relatively slow onset of serious effects of the venom.
In cases of severe envenomation, however, the intravenous route should be used because absorption of intramuscular antivenom is slow6. A further ampoule of antivenom may be indicated in severe cases where the initial response to the antivenom is incomplete, or a relapse occurs . Improvement and disappearance of clinical signs should be expected within a few hours, particularly when the antivenom is given within 24 hours after the bite. general supportive measures and symptomatic treatment may also be required.7
Premedication with subcutaneous (1:1000) adrenaline and intravenous antihistamine may be of help in animals who have previously received horse serum. The routine use of premedication is controversial. A syringe already loaded with 1:1000 adrenaline must be available during antivenom therapy in case of anaphylactic shock, though it is extremely rare, especially when the antivenom is given intramuscularly3,8..
Red Back spider bite is one of the few cases where antivenom may be effective days (even months) after the bite. If the symptoms fit Red Back spider bite, it is quite acceptable to try a dose of antivenom a week or more after the original bit occurred. Multiple doses may be required.8,9
to do if there is an
immediate untoward reaction to the antivenom?
If there is a serious anaphylactic reaction after giving the antivenom, give adrenaline by subcutaneous injection (0.01mL/kg initially of 1:1000 solution), give 100% O2 and IV fluids. Repeat adrenaline and try IM injection if no response to subcutaneous injection.8
From On the Spot 53: March 2001
Spider Envenomation in Cats and Dogs continued
The Funnel Web Spider
The venom of the male spider is five times more toxic, experimentally, to animals, than that of the female. This fact is just one of a number of most ‘unspider-like’ features of this spider. Another unusual feature is that man and monkeys appear to have special susceptibility to the venom (Sutherland 1990 1) Dogs and cats can receive very large doses of the venom with no apparent effect, apart from mild, transient cardiovascular signs (transient moderate hypertension, tachycardia, atrial fibrillation and flutter and ventricular irritability 2 . There are no reports of domestic animals dying after bites of this spider.
encompasses a broad spectrum of responses to spider bite, from very
local skin damage through to major skin damage and systemic illness. It
is a phenomenon seen in many parts of the world, but particularly in
where it is caused by recluse spiders (Loxosceles reclusa, L. laeta, L. gaucho and others, ‘Loxoscelism’). In Australia local skin damage of animals following presumed spider bite is rare, with few cases reported to CSL. Several spiders have been suggested as causes of these
ulcers (eg White tailed spider) but until recently, none was proven. Recently in South Australia there have been cases where the spider was caught at the time of biting and in these cases it was a relative of the recluse spider (fiddleback spider Loxosceles rufescens). This spider is not native to Australia but has been accidentally introduced and is establishing itself in metropolitan areas. However, it cannot be said that all cases of ‘necrotic arachnidism’ in Australia are due to this spider. Indeed, it is likely that in many cases the cause of the ulcer is secondary infection.
A typical case of necrotic arachnidism will present with an ulcer or a full thickness skin defect which is both painful and slow to heal - it may take weeks and even months to fully heal. Treatment includes careful cleaning, antibiotics (after culture), and DELAYED surgical debridement. 3
K (1990) Antivenom use in Australia. Medical Journal of Australia
2 Tibbals J, Sutherland SK, Duncan AW (1987) Effects of male Sydney funnel web spider venom in a cat and a dog. Australian Veterinary Journal 64:63-64
3 White, J. (1995) CSL Antivenom Handbook. CSL Limited, Melbourne
'On the Spot' 55, September 2001
Cat Scratch Fever
Reprinted from Warrnambool Veterinary Clinic ‘Vet Chat’, Small Animal Edition, Winter 2000
What is cat scratch fever?
Cat Scratch fever is a disease of humans caused by a bacterium-like organism called Bartonella henselae. This disease is often associated with the person being scratched by a cat.
People suffering from this disease have fevers, chills and lethargy accompanied by enlarged lymph nodes(glands) and skin or eye lesions. Most symptoms last for a few days only but the enlarged lymph nodes may persist for weeks or months. In a minority of people a more serious disease may develop.
common is this
It is not possible to give accurate estimates of the prevalence of Cat Scratch Disease in this country, but it is probably a fairly common disease. it is likely that many infections do not give rise to symptoms or are of a trivial nature such as mild ‘cold’.
may cause cat
Although many cases of Cat Scratch Disease follow a cat scratch, this is not always so. There have been a few cases in people with no apparent contact with cats.
Recent evidence suggests that a possible route of infection is by a flea bite. Infected cats carry the micro-organism in their blood where it can be present in extremely high numbers. When a flea feeds on an infected cat, it ingests large numbers of Bartonella, some of which may be inoculated into a human if the flea bites them.
The bacterium is found mainly in younger cats and kittens and many of these do not show any sign of disease. The infected cats remain infectious for weeks to months, after which time the organism disappears from the blood.
It is not clear whether cats can be reinfected but there are no reported cases of any human beings being infected more than once.
there a vaccine or
for Cat Scratch Disease?
There is no vaccine available against Cat Scratch Disease either for cats or for humans. Bartonella henselae is sensitive to a number of antibiotics including erythromyxin, trimethoprim/sulpha, enrofloxacin and doxycycline (eg Vibravet), but NOT to penicillin, ampicillin or Clavulox. The disease is self-limiting, and mild cases will resolve without recourse to antibiotics.
Spot 56 December 2001
Another article from the Warrnambool Veterinary Clinic ‘Vet Chat’, Winter 2000 Issue.
EYE ULCERS OR CORNEAL ULCERS
What is a corneal
The cornea is the transparent, shiny membrane which makes up the front of the eyeball. Think of it as a clear window. A corneal ulcer is when the surface of the cornea is damaged, if the damage is the full depth of the cornea the fluid inside the eye will leak causing blindness and a misshapen eye.
What causes ulcers?
There are several causes for corneal ulcers in pets. The most common is trauma. An ulcer may result from the pet rubbing its eye on the carpet, from grass seeds in the eye, or due to laceration, such as a cat scratch. Another cause is chemical burn of the cornea. This may happen when irritating shampoo gets in the eye.
Less common causes of corneal ulcers include bacterial infections, viral infections, and other diseases. These may originate in the eye or develop secondary to disease elsewhere in the body. A common example of this is ‘Dry Eye’, a condition in which the animal does not produce enough tears. Without tears to protect the eyeball the cornea dries out and is easily damaged.
ANY PAINFUL RED EYE SHOULD BE EXAMINED URGENTLY BY YOUR VET
How is a corneal ulcer
Corneal ulcers are not always visible with the naked eye but vets have a special stain they put in the pet’s eye. With this stain if there is an ulcer present it will stain up bright green.
How is a corneal ulcer
The first step in examining the eye is always to check for any foreign bodies, in particular grass seeds. These are often hidden under the third eyelid and cannot be seen. If grass seeds are not found and removed, the ulcer will not heal.
Very mild ulcers may heal with medical treatment. We use a special mixture of drops that prevent infection and relieve pain, as well as having enzymes to protect the eye surface and promote healing. If we use medical treatment we will need to keep a close eye on the ulcer, as sometimes they will deepen rapidly, and a change of treatment will be needed.
In non responsive, or more severe ulcers, measures must be taken to protect the eye and to promote healing. Since pets do not wear eye patches well, surgical techniques are often used to close the eyelids and cover the ulcer.
Ulcers which do not heal well often have an accumulation of dead cells at the ulcer edge. These dead cells prevent normal cells from the corneal surface from sliding over the ulcer edge and filling in the defect to heal it. If this appears to be part of the healing problem, the dead cells are removed from the edges of the ulcer before the eye is surgically closed.
Severe ulcers can cause muscle spasm inside the eye. This muscle spasm effects the pupil and can cause serious long term problems, even loss of the eye. This is known as ‘Uveitis’ and when it occurs, we will vary the treatment further.
be a scar?
The normal cornea has no blood vessels going through it, however, new blood vessels are created in an attempt by the body to heal the ulcer. This is a good response, because it hastens healing, but after the ulcer is healed these vessels remain in the cornea. They are not painful, and do not obstruct vision.
The vessels and some of the white scar tissue that persists after the ulcer heals, can be reduced with the use of ophthalmic drops or ointment containing corticosteroid. It is important that steroids are not used in the eye too soon, because they will stop the healing process. Usually after the ulcer has healed, there will be a small white scar, this will be bigger with more severe ulcers.
OF EYE PROBLEMS IS ESSENTIAL,
OR BLINDNESS MAY ENSUE
From my personal experience tiny doses of systemic cortisone are often a more easily controlled way to reduce blood vessels and scar tissue after healing. And patience -its slow. Truda
From On the Spot 57 March 2002
UPDATE ON FELINE LEUKAEMIA/LEUCOGEN VACCINATION
I have recently received a circular from Virbac concerning various products, including Leucogen, which they produce. I though it might be of interest to include some of their comments - but then I thought that it might also be a good idea to remind everyone about Feline Leukaemia itself. Hence I am reprinting here the Appendix 15 from part 2 of Breeding Cats..... A practical guide.
In 1987 I had the saddest experience of my whole breeding career. My new breed, Spotted Mist (now Australian Mist) had just been recognised as worthy of Championship status, after 10 years of experimental breeding. All should have been rosy - but it was not, I was having many health problems in my cats. Not all the same problem, but pointing to some underlying common cause.
Leukaemia was at the back of my mind.
Testing had recently become much more available in Australia, and I had had a few cats tested in 1985 & 86, with no positive results. But still I was sure that my instinct was right. I had a huge cattery (well over 100 cats), bred four different breeds, and was becoming increasingly concerned that I had a Leukaemia problem - all the signs pointed that way.
Then, right at the end of February 1987, a new, much more sensitive test became available, and I found that my hunch was correct. I carried out a mass testing, 14 cats (including my favourite queen and her week old litter, and my first full register stud) were buried that first test day, 40 more were positive. Twenty or so cats were desexed and given away as pets. The cats were rearranged, taking into account their leukaemia status. Three weeks later we retested all contact cats, and positives. There were very few new positives, and most of the previous positives were now negative. I went into quarantine for more than six months - no-one knew how to interpret the quarantine regulations, but I was far too poor to show anyway with all the testing and desexing. I then instituted ‘leukaemia free’ management practises, and was ready to take up the new Leucogen Vaccine when it became available in 1989.
I am relieved that no one would now be faced with doing what I had to do, not only do we now know a great deal more about leukaemia itself, but the availability of a vaccine completely changes the need to euthanase any positive cats, other than those actually exhibiting clinical signs.
This article presents basic information about the virus, but concentrates mainly on the creation and management of a Leukaemia free cattery, using a combination of testing and vaccination.
Feline Leukaemia is caused by a retrovirus, a group now remarkably notorious, since HIV, the causative agent for AIDS belongs to this same group.
FeLV was one of the first retroviruses to be discovered in the early 1960s, isolates taken and stored from those first samples were examined again in the mid 80’s, when the vaccine was being developed. They were found to be identical with contemporary isolates of the virus - this is, unlike HIV, FeLV is a very stable virus, hence an excellent subject for the production of a preventative vaccine.
Retroviruses unlike many other viruses, do not exist primarily in the usual ‘template’ form of DNA (like our genes), but as the messenger form, RNA. Retroviruses produce reverse transcriptase (which gives them their name). This enzyme enables the newly introduced viral particles to immediately commandeer the cell’s protein factory to manufacture DNA, which is integrated into the genome of the infected cell. All descendants of the cat’s infected cells will contain the ‘hidden’ FeLV DNA template.
This ultimate in parasitism poses the problem that cats may become long term carriers of FeLV, while being both asymptomatic, and giving negative test results. These carrier cats are NOT infectious (shedding) while testing negative, but MAY start to shed again under certain circumstances.
Of most concern to breeders are carriers that shed during the stress of pregnancy. Not only are unvaccinated contact cats then at risk, but the unborn kittens can also be infected. Other environmental stresses, aging, kidney deterioration, illnesses or accidents can trigger shedding. Any factor which reduces or overloads the body’s immune vigilance can allow FeLV to reactivate into an infectious state, a factor which should be born in mind in managing a cattery undergoing the transition to Leukaemia free.
To infect other cells, the incorporated FeLV DNA produces viral RNA which is assembled into new viral particles as buds off the membrane of the host cell. This membrane has been stimulated to form protective coat proteins (gp 70 glycoproteins) which protect the FeLv RNA as it makes its way to infect another cell. This coat protein gp70 (not the infective core) is the portion on which the Leucogen vaccine is based, it is this protein which stimulates the cat’s own immune system to fight off the invader.
The vaccine cannot give the cat Leukaemia, yet it is made from the part of the virus most able to stimulate an immune response.
Core proteins are produced in excess, and are released into the body fluids when the buds break off from the host cell. It is on the detection of the presence of these proteins, specifically protein p27 that laboratory tests are based.
The detection of p27 in a cat’s body fluid indicates that an active infection is present.
AND THE CAT
The most common route of transmission is through the mouth and nose. All body fluids of an infected cat contain viral particles, which can be transmitted by licking, biting and sneezing (and through mother’s milk). The virus is fairly fragile, so that quarters vacated by an infected cat can be readily cleaned and sterilised using household bleach.
Infection by the FeLV virus has three possible consequences:
of the virus
This happens in 40% of cases
Immune response is massive and complete
Cats are immune to any further infection
This is also how the Leucogen vaccine works
Never infectious, test negative
In 30% of infected cats, the virus continues to multiply, leading to clinical
disease from 3 months to 3 years after initial infection
Always infectious, test positive
30% of cats become carriers
May be infectious but test negative
Of the carriers, 50% remain so for life, 40% progressively eliminate the virus, 10% become viraemic, shedding under stress.
Unfortunately, after infection by the natural virus, those cats which test negative cannot be assigned with any certainty to either category 1 or 3 - all exposed cats must remain suspect. In contrast exposure to the coat protein gp70 only, in the Leucogen vaccine means a sure outcome - immune and unable to shed, for life.
Symptoms of Feline Leukaemia
Immunosupression would be the most common sign of FeLV infection - though this can be caused by other conditions (including FIV, “Cat AIDS”). Even the most minor infection becomes a major challenge - bacterial infections, cat flu, ringworm, all career out of control. Other major cat diseases, such as Feline Infectious Peritonitis are much more likely to be fatal, indeed, old literature often associates the two conditions.
Anaemia which may start out as regenerative, but may progress to non-regenerative, death is generally the outcome.
Panleucopaenia, where the white blood cell count drops rapidly, with symptoms similar to that caused by Feline Parvovirus (Infectious Enteritis). Often associated with anaemias. Outcome is death in two to three months.
Renal insufficiency, where the filtration system of the kidneys becomes blocked by deposits of immune complex proteins. This is common in young cats. After my outbreak in 1987, many young cats which were positive but had become negative died very young - of renal failure. Cats which I had castrated were particularly prone to die not long after the operation - presumably because their very limited kidney function had been reduced to zero by the added stress of the anaesthetic.
Reproductive failure, particularly late abortion of the foetuses is very common, 75% of all late abortions in cats are linked to infection with FeLV. Reabsorption, endometriosis and sterility can also be linked to FeLV. It was a growing incidence of such events amongst my own cats which fuelled my suspicions about the possibility that FeLV was present. When a program of eradication is taking place within a cattery in which there have been positive tests in the past, the re-emergence of such signs amongst negative cats which have been, or have been in contact with, positive cats in the past should prompt a retest. The aborting/ resorbing queen is likely to be a carrier who has become positive under the stress of pregnancy.
FeLV is an oncorna virus - that is, it is a retrovirus which is capable of being responsible for the appearance of tumours. Feline Sarcoma Virus (FeSV) is another such oncornavirus, but a defective one, incapable of multiplying by itself, but found in the genome of many cats. It is activated by the presence of FeLV, and sarcomatous tumours due to it can appear quite rapidly.
Tumours due FeLV itself, may on the other hand take several years to appear, as chance combinations of the viral genome with the cat genome need to arise, where an ONC gene from the cat is caught up near an FeLV activating gene. Certainly a surprising number of my cats died of various cancers in the years after my outbreak of FeLV - on looking back through my records, these cats had at some time either tested positive themselves, or been in contact with positive cats.
A LEUKAEMIA FREE CATTERY
If you have a suspicion that you have a leukaemia problem in your cattery, it is worth carrying out some tests.
The modern tests are done in a few minutes by the veterinarian using a very small quantity of blood. The test is based on detecting p27 in the blood, and a positive result indicates that viral replication is occurring at the time of testing . The test is usually combined with one for FIV, a good investment in clearing up two immunosuppressive diseases.
The cats to test in the first instance are those which show any symptoms which make you suspicious - specially queens which suffer late abortion, or cats that seem to ‘go down with everything’.
On finding a positive cat, test all its contacts - both those that share its housing, and those with which it has had recent contact, or that are not separated by nose and paw proof walls. The positive cat should be separated from all other cats and retested 3-4 weeks later.
the cat may be positive again, in which case you should consider
it and finding it a pet home.
If the second test is negative, remember that you do not know whether it has become immune, or is a carrier. Unless you really need to breed from it, it is wisest to desex it, but you may keep it, provided that you never allow unvaccinated kittens near it. If you have more than one cat in this category, they may make a happy little colony.
If you need to breed from this cat, it is quite possible. For a queen, try to make this her last litter, so choose the sire carefully, and be prepared for more expense during the pregnancy, as well as considerable effort in early weaning the kittens, and for a possibly distressing outcome. Retest the queen at the end of the sixth week of pregnancy, if she has become positive again she was a carrier, and it is likely that the pregnancy may not last to term. The kittens are also likely to be positive, and if they are not, they will become so if you allow her to suckle them.
It is worth trying to foster the kittens at birth (or hand rear them), but the foster mother herself must have been vaccinated with Leucogen at least a month beforehand, or you run the risk of infecting her also. Test the kittens when they are 3-4 weeks old, if you are lucky they might be negative. Of course these fosterlings must have their foster mother to themselves - if she had any kittens of her own they need to have been moved on to another vaccinated mother.
If the mother is still negative six weeks into the pregnancy, test her again about one week after the birth. You may have played safe and fostered some or all of the kittens at birth anyway, but if not, and she is still negative, plan to wean the kittens from her completely by six weeks of age. Retest the kittens at seven to eight weeks, and if negative, vaccinate immediately with Leucogen (a half shot each is sufficient), give a second vaccination a month later.
The female you keep from this litter forms the basis of your new leukaemia free stock - and she may even live with cats which have been positive in the past - until you are ready to breed from her. Strict isolation from all other cats from 2 weeks before birth, until 10 days after the kittens have had their first Leucogen vaccination is essential to create more leukaemia free stock.
A stud cat that has tested positive, or indeed that is still positive, is still possible to breed from. All queens visiting him must themselves be vaccinated at least a month before mating - they then only catch his genes, not his leukaemia.
If you do not wish to take the test and remove pathway, but would eventually like to arrive at the stage where Leukaemia is not a potential problem amongst your cats, you can simply start vaccinating healthy kittens at 6, 10 & 14 weeks of age. As your population ages, and new stock grows up, all the young cats will be immune, so that the odd older cat which may shed will not have any influence on the health of the young ones.
If you take this path, it is particularly important that you keep a strict eye on hygiene standards, being careful never to allow any utensils used for older cats near the unvaccinated kittens, without disinfecting them in between. Each litter of kittens MUST be reared separately, and isolation maintained until 10 days after the first vaccination.
If you are satisfied that you have worked your way through all the cats, testing, separating, finding new homes, you have been vaccinating all kittens for a couple of years and are now breeding from females vaccinated as kittens, it is possible to relax your vaccination regime - two shots, at 8 and 12 weeks are now satisfactory. Once all cats not vaccinated as kittens are out of your population, a single vaccination of kittens which you intend to keep, at 16 weeks is adequate, kittens sold as pets are vaccinated on request for the purchaser at 12 weeks, kittens sold for breeding are also vaccinated before they are transferred.
For Leucogen the manufacturers (Virbac) recommended that the vaccination be given at 8,12 & 16 weeks, then annually. At the time that the vaccine came on the market this was the ‘safe’ advice - certainly no cats had lived out their lives on this regime, so the manufacturers were playing it safe.
I never subscribed to this regime, having studied the literature, and considered the nature of the vaccine, I could not see why a vaccine made of the natural antibody inducing gp70 should not confer lifelong immunity, just as contact with the disease does to the 40% of cats which reject the virus. The degree of cover provided by the vaccine is extremely high when two doses are administered to kittens under 12 weeks of age. Over 14 weeks of age, the cover is just as high with a single vaccination. Therefore I arrived at the regimes suggested above - without annual boosters - with one exception - I revaccinate breeding queens that have had a single dose at 16 weeks when they have their 15 month Feline-3 vaccination.
Well, yes, it is simple to start on the road to eliminating leukaemia forever.
In addition to the measures outlined above which you have taken in your own cattery, never buy a kitten which has not been vaccinated under a compatible management scheme, or tested negative, then vaccinated.
Vaccinate all your stud cats - if they are truly negative and unexposed, it prevents them from catching leukaemia through contact with a positive queen. If they are already immune, or even carriers, it does no harm. I vaccinated all my studs, and still do so for any unvaccinated adult cat which comes into my colony - just one full shot.
If all your own breeding stock is vaccinated, you may in complete confidence accept any queen, take your own to any stud, without even mentioning the word Leukaemia - safe in the knowledge that your cats can neither give it to another cat, nor catch it from one.
I am rather distressed at the poor response by breeders to this truly ground breaking vaccine - the first ever retrovirus vaccine produced by genetic engineering. It is so straight forward to use and so safe; the diminution in the severity of all other contagious diseases in a fully vaccinated cattery is so obvious, rewarding and money saving that I am still at a loss to explain their reluctance.
Efficacy of FeLv vaccines (not just Leucogen) is generally accepted to be between 80 & 90% (the study results range from 70-100%). Protective titres have been demonstrated with Leucogen 3 years after vaccination in a group of cats housed with infected cats, hence under continual challenge, however duration of immunity for more than one year has not been clearly demonstrated in specific pathogen free (laboratory) trials. An additional benefit of recombitant FeLV vaccine has been shown in the increased survival rate of cats infected with FIV (Feline Aids).
With reference to control of FeLV in the cat population, among low risk, free roaming cats (where the prevalence is < 1%) an effective immunisation rate of 4%pa is predicted to be adequate to control the disease completely. Under higher risk (10% prevalence), an effective immunisation rate of 23-72% pa is required for control.
(Extracted from FELV VACCINATION IN AUSTRALIA, by Rebecca Higgins BVM&S, Veterinary Services Manager, Virbac Australia Pty Ltd accompyaning letter dated 11 March 2002)
To tease this out, I think it means that we should keep up our cattery vaccinations, specially as I have suggested where there is a past history of positive tests, specially if these cats are still present, to protect our own cats. To contribute to the overall improvement of the resistance of the free roaming population, it is also worthwhile to encourage kitten buyers, who are intending to allow their cat outdoors, to also have them immunised - at least as kittens, and with their first annual revaccination.
The article also evaluates the frequency of adverse reactions to Leucogen vaccination. These included minor systemic reactions, transient fever, depression, lack of appetite, and of minor local reactions: pain, swelling, irritation and nodule formation. Combined these have been recorded in 19/100,000 doses in Australia. I am inclined to think that this is a great underestimate - reactions, particularly local swelling must be really common - but never reported. I would estimate that more than 50% of my kittens have had this reaction, and many have also had nodule formation, but the information has never been passed on to my vet. Other breeders have made much the same observation.
More severe reactions, such as an acute allergic reaction and suspected or confirmed fibrosarcoma, have been reported for 0.6 in 100,000 doses. I must say, that with the tendency of Australian Mist of some colours to be inclined to allergies, I have never had an acute allergic reaction to the vaccine. Nintu Jelly Bean, of late and loving memory did develop permanent lumps, but not only from Leucogen - he had a complete record of all his lifetime of vaccinations. None of these became cancerous. ....
In summary, I would still say steady as she goes - though perhaps a whip around adult cats every 3 years if you think that they might be exposed through their lifestyle (perhaps particularly popular Stud cats) would do no harm for those who wish to err on the side of caution.
Truda M Straede
From On the Spot 58 June 2002
Chlamydia is a relatively newly discovered bacteria, which causes serious problems in many species of animal as well as humans. In Australia, Chlamydia has found its way into koala populations where it is a major cause of reduced fertility and declining populations. In kangaroos it causes blindness resulting in unfortunate animals hopping into trees and other solid objects resulting in stress, difficulty feeding and ultimate death. In humans, Chlamydia is responsible for the sexually transmitted "NSU" - Non Specific Urethritis, which causes pain on urination and a penile discharge males and may cause scarring of the fallopian tubes and infertility in women who may have no symptoms until they try to become pregnant.
In many species, including felines and humans Chlamydia is a common cause of Respiratory Tract Infections (RTI), and Upper Respiratory Tract Infections (URTI). URTIs cause nasal congestion and discharge and in cats runny eyes. RTIs affect the lungs and may cause pneumonia.
was only relatively recently discovered because it is a difficult
to culture in laboratories, and difficult to see under the
It responds poorly to most common antibiotics.
Until recently the best medical treatment was a long course (4 weeks) of vibramycin, (VibraVet, doxycycline, Pfizer Animal Health) - a tetracyline based antibiotic.
In cats, Chlamydia is very common and a major health problem for breeders. It cause a flu like illness with sneezing, serous (clear) discharge from the nose and runny eyes. Some prominent Persian breeders feel that Chlamydia may be endemic in some catteries and is a contributing cause to the chronic runny eyes in their cats. I feel Chlamydia is also a common cause of pneumonia in young kittens. Many of us have had kittens who seems well until about two weeks then became ill, stopped feeding, developed a rattly chest and eventually died. This is probably Chlamydial pneumonia. It may well be one of the causes of Fading Kitten Syndrome which may affect kittens as young as 24 hours old.
Azithromycin, Pfizer) is a new, safe antibiotic which is highly
against Chlamydia. Vibravet takes four weeks to wipe out Chlamydia
while Zithromax does it in a single dose. Many veterinarians will not
heard of Zithromax, which may not have been promoted to them as an
drug. However, it is very safe and it works well.
The dose of Zithromax for cats is 20mg Zithromax per kg body weight.
It is available in a syrup, with 600mg Zithromax in 15mls. The dose for an average 3kg adult cat would be 3 times 20mg ie 60mg or 1.5mls of syrup.
It is also available in 250mg and 500mg tablets. The dose for an average 3kg cat would be 1/4 of a 250mg table or 1/8 of a 500mg tablet.
Use of Zithromax in Breeding Catteries
Entire Cattery Populations - If you have many problems with respiratory infections, runny eyes and noses and sneezing, do a culture for Chlamydia. If it is positive, I would advocate treating the whole cattery.New Cats - If you are buying a new breeder and you have little knowledge of the breeding cattery or cannot inspect it because it is interstate or distant, I would advocate treating the new breeder with a single dose of Zithromax before introducing the cat to your resident population.
Pregnant Queens - It would seem that Chlamydia can exist in cats in a dormant form, and that some resistance is given to kittens by maternal antibodies which fade out at about 2 weeks after birth, which is when many kittens will get sick, develop pneumonia and die. If you have any suspicion your pregnant queens have, have had, or have been exposed to Chlamydia (this probably includes most queens), I advocate giving a single dose of 20mg/kg of Zithromax on about the 58th day of pregnancy. At this stage there is no risk to the unborn kittens, who may otherwise contract Chlamydia from the queen during birth or soon after.
I feel that if this became standard cattery practice, kitten losses may well be significantly reduced.
Zithromax is a new and highly effective and safe single dose treatment for Chlamydia. Though not widely known by veterinarians it has wide applications in breeding catteries and may help cure many chronic health problems. If given to a pregnant queen on the 58th day, may well help prevent losses of newly born and young kittens. The dose is 20mg/kg bodyweight of cat.
Since writing this article I have received feedback from some catteries that a single dose quietens down the symptoms in badly affected cats, but may recur in a few weeks.
Zithromax remains at an effective concentration within the tissues for a week, thus giving a single dose is like giving a 7 day course of a shorter lived antibiotic. For severely affected cats, and cats that have been symptomatic for weeks or months, or catteries where virtually the whole population is symptomatic, I suggest repeating the 20mg/kg dose seven days after the initial dose. In these badly or chronically affected catteries, I must emphasise the treating of the whole cat population including domestic and household pets and any other animals that the cats may have come in contact with to eliminate non symptomatic carriers of Chlamydia. At the same time as treatment, nuke the cattery with bleach twice a week.
If the disease returns after this, consider whether there may be a human carrier, the owner perhaps or family or staff. Consult a doctor before treating humans! However, one dose is sufficient as prophylaxis in pregnant queens and Chlamydia affected cats if symptoms are mild and when given early in the course of the illness.
Comment from Richard Malik
This is one of several protocols that have appeared on cat lists on the internet for treating chlamydial infections with azithromycin. The published dose for this drug is 5mg/kg once a week for several weeks. It is interesting that 20mg/kg would appear to be well tolerated and possibly effective as a one-off treatment for Chlamydia in the cattery situation.
and Experiences with Zithromax in the Nintu Cattery
Having heard about Zithromax through the 'breeders' underground', I had tried it rather timidly - I have had tests for Chlamydia carried out on my cats from time to time, and though I had not had a positive result, I was still sure that the symptoms looked like it ..... And by the way, the suggested regimen using VibraVet is extremely conservative - I was instructed by a vet fresh from the UK where it had been a real well known problem in the cat population for a number of years was 6 weeks on the tablets, 6 weeks off, 6 weeks on. This is not only endlessly tedious for the cats, they do become a trifle resistant to medication after a couple of weeks, it is also easy to forget, and expensive. However, it did work!
I have now followed the instructions for dosing the whole cattery - though I wasn't quite up to doing the whole lot at once (expensive!! And all that extra cleaning - it takes 7 hours to do the lot just at the normal weekly thorough clean standard). I did about one third of the groups at one time, including in the first group the oldies that are allowed out during the day. I have some cats that always have dirty eyes (much like the Persians mentioned in the article), and some of these are very old. I repeated the dose for them. I could hardly believe how well they looked after treatment, though regrettably the effect wasn't permanent, as some of the dirty eyes are due in part to long term damage... However, this part of the treatment does seem to have contributed to an overall better looking lot of cats.
I am also trying dosing pregnant queens 7 days before the kittens are due. So far 3 queens have been dosed, but at the time of writing none of the litters had arrived, so I have yet to see how this part of the treatment works. I will certainly apply the treatment to any new members of the family (in fact I already have) as they join the cattery.
I was very interested in the implication that there may be an exchange of Chlamydia between cat and carer. For some time I have been fighting a recurrent urinary infection which had already started to ring warning bells to me - recurring every 3-4 weeks, and increasingly less responsive to antibiotic after antibiotic. Finally I expressed my thoughts to my new GP - could this be Chlamydia? Yes, it could, try a vibramycin (the Vibravet drug) antibiotic .... Well it worked, though that notoriously hard to detect Chlamydia didn't show up in Pathology, but I am trying the 6 week long course of vibramycin ..... maybe in the long term the cats and I will be sharing the packets of Zithromax!.
this information will be of greatest interest to breeders, there is no
reason why pet owners shouldn't also benefit from it, specially if
cats are confined to indoors (so are less likely to reinfect themselves
through external contacts) and most particularly if any of their cats
chronically runny/weepy/dirty eyes. Any feed back would be most
as I am sure we would all be interested in the outcome. This is
one to add to any revised edition of Breeding Cats..... a practical
- both in general and under 'Fading Kitten Syndrome'.
Truda M Straede
DNA TESTING On
the Spot SEPTEMBER 2011
DNA TESTING RESULTS.
As part of the GCCF requirements for registration of the Australian Mist, some DNA sampling was requested. I am of the personal opinion that this was really because no-one believed in gold and peach, and the fact that we had lots of cats with the light brown gene in the population!!
While some of the results were quite frankly a bit odd, the colour results thoroughly vindicated our recognition of gold and peach cats, all were shown to be homozygous for the light brown gene – so no mistaken identifications there!
Of course the spate of ‘Burmese’ coloured kittens produced over the previous months was also confirmed – many of the tested cats are heterozygous for the Agouti gene (Aa) so that when mated together a proportion of ‘plain’ non patterned Burmese lookalikes (aa) have appeared. These tests certainly provide a pointer for the breeders who desire to NOT produce ‘spotless’ mists, and will enable them to eliminate the gene through judicious progeny testing when a parent is a known carrier.
The tests were, however, much more wide ranging, and included blood typing. Perhaps not unexpectedly both group A/AB and b groups are present in the population, undoubtedly derived at least in part from Australian Domestics. While not unexpected, this is a factor which should be borne in mind if certain matings produce otherwise unexpected kitten losses in the days immediately after birth. bb kittens are unable to fend off antigens from the milk of a A/AB mother, resulting in their death. While it might be an excellent idea to try and remove b from the population, it is probably a counsel of excellence.
Testing for PKD (Polycystic Kidney disease), both known HCMs (Hypertrophic Cardiomyopathy), GM2(Gangliosidosis Burmese), the other 2 GM mutants and blindness MRA CEP290 were negative for the ten cats sampled.
One unwanted inheritance from the Abyssinian foundation stock, PK Deficiency showed up in one subject tested. The extract from the Feline Advisory Bureau included opposite indicates how this potential problem may be managed, without creating kittens exhibiting the problem, and in the longer term eliminating the defect from our population. In Victoria, we are under a legal obligation (POCTA) to not KNOWINGLY create kittens or puppies with heritable defects. While DNA testing is presently available in the US and UK, the test isn’t as yet available in Australia, though one laboratory is certainly intending to acquire the rights to the test.
Subsequent to these results arriving from the US, Val King had a further 6 cats tested, none were PK deficiency carriers, nor were any carriers of b blood group. I also had 4 cats tested for their blood groups – 2 of the 3 girls were carriers of b, the one male was not.
Extract from Feline Advisory Bureau Fact Sheet (2009)
Pyruvate kinase (PK) deficiency
Pyruvate kinase (PK) deficiency is an inherited disease occasionally encountered in Abyssinian and Somali cats, and also reported in the domestic shorthair cat. Pyruvate kinase is an enzyme found within red blood cells which enables them to produce energy to survive. If this enzyme is lacking, the lifespan of the red blood cells is significantly reduced, resulting in a reduction in the number of red blood cells in the circulation (anaemia).
What signs does it cause?
The main consequence of the disease is the development of anaemia. However, since the body can quickly manufacture new red blood cells, the anaemia is usually only intermittently detectable. Most of the time the anaemia is either only mild, or occurs gradually, enabling the cat to adapt to the anaemia and not show any obvious signs. Anaemia often results in only vague signs such as lethargy and lack of appetite. However, a rapid severe life-threatening anaemia can also develop. Although PK deficiency is hereditary, the anaemia is usually mild and clinical signs may not be obvious, and thus may not be noticed until the cat is quite old.
How is PK deficiency inherited?
The disease is inherited as an autosomal recessive trait (see box 1). This means that a cat can be carrying the defective gene (heterozygous) without having any symptoms of the disease at all. Affected cats (homozygous) arise when two carrier cats are mated with each other. Since carrier cats remain healthy, and the anaemia of affected cats may not be detected until they are a few years of age, the potential exists for carrier cats and affected cats to have had significant numbers of offspring before the disease is identified. However, the positive side of this is that it also means if carrier cats are identified they can still be used for breeding as long as we ensure that they are NOT mated with another carrier. Mating a carrier with a non-carrier will not produce any offspring that will suffer from PK deficiency, and 50 per cent of the offspring will be free of the defective gene. As long as the offspring are also tested, even carriers can be bred from again as long as it is ensured that they are only mated with a non-carrier cat. In this way, controlled breeding programmes can be implemented so that important lines can be retained within the gene pool.
Probably the most fascinating
result obtained was for Long Hair. Short is, of course the
wild type, and quite recently tests for the 4 isolated recessives which
underlie long hair have become available. One of the 10 US sampled cats
was homozygous for Mutant 4, and another was a carrier. Subsequent
tests revealed at least one other homozygous M4 cat – which also looks
shorthaired. There is certainly more to be learnt here!! Below is a
reprint of the article on the LH test written by Lesley Lyons and
posted on the UC Davis website. On careful reading perhaps as in
formative by what it fails to say, as what it actually says!
Long-Hair Test for Felines
Cat hair coat colors, patterns and texture are determined by the combined action of several genes. One gene – fibroblast growth factor5 (FGF5) – determines hair length. Short hair is a dominant trait determined by the wild-type form of FGF5. Long hair is a recessive trait. Four mutations in FGF5 have been identified that are associated with long hair in cats. Long-haired cats can carry two copies of the same mutation (homozygote recessive) or have two different mutations, one on each chromosome (compound heterozygote). Three of the mutations are fairly breed specific, while the fourth is present in all long-haired cat breeds and crossbreds, as follows:
Mutation 1 (M1): present in Ragdolls
Mutation 2 (M2): present in Norwegian Forest Cats
Mutation 3 (M3): present in Maine Coons and Ragdolls
Mutation 4 (M4): present in all breeds of long hair cats, including Ragdolls, Maine Coons, and Norwegian Forest Cats.
N/N: Cat has short hair. None of the 4 long hair mutations detected. Cat cannot produce long-haired kittens.
N/M1, N/M2, N/M3 or N/M4: Cat has short hair and carries one copy of a long hair mutation. Cat can produce short and long-haired kittens depending on genotype of the mate.
M1/M1, M2/M2, M3/M3 or M4/M4: Cat has long hair and will produce only long-haired kittens when bred to a long-haired mate.
M1/M2, M1/M3, M1/M4, M2/M3, M2/M4, M3/M4: Cat has long hair and carries two different long hair mutations (compound heterozygote). Cat will produce only long-haired kittens when bred to other long-haired cats.
Drogemuller C., S. Rufenacht, B. Wichert, T. Leeb. Mutations within the FGF5 gene are associated with hair length in cats. Animal Genetics 38(3):218-221 (2007).
Kehler J. S., V. A. David, A. A. Schaffer, K. Bajema, E. Eizirik, D. K. Ryugo, S. S. Hannah, S. J. O'Brien, M. Menotti-Raymond. Four independent mutations in the feline fibroblast growth factor 5 gene determine the long-haired phenotype in domestic cats. Journal of Heredity 98(6):555-566 (2007).
DNA UPDATE Mar 2013 On the Spot.
Episodic Hypokalaemic Polymyopathy
Familial Episodic Hypokalaemic polymyopathy is characterized by episodes of low serum potassium levels and high CPK (an enzyme that indicates muscle damage). Clinical signs include episodic general or localized skeletal muscle weakness. The symptoms are more obvious in the neck and limbs and as a result affected cats tend to have problems walking and holding their head correctly.
This is an autosomal recessive mutation, meaning that two copies of the mutant gene are required for the cat to be affected.
Cat Breeds at Risk of Burmese Hypokalaemia
Asian, Australian Mist, Bombay, Burmese, Burmilla, Cornish Rex, Devon Rex, Singapura, Sphynx, Tiffanie, Tonkinese
Interpretation of Results
Normal The cat does not have the known genetic mutation causing Burmese Hypokalaemia.
Carrier The cat has one copy of the Burmese Hypokalaemia mutation. The cat will not have Burmese Hypokalaemia, but may pass the mutation to their offspring.
Affected The cat has two copies of the Burmese Hypokalaemia mutation. The cat will have Hypokalaemia.
Blood Group DNA Testing
Recently, the DNA sequence that result in the specific feline blood groups was found, enabling DNA testing to identify a cat’s blood group.
A cat’s blood group is controlled by a gene called cytidine monophosphate-N-acetylneuramic acid hydroxylase (CMAH). This gene is responsible for the production of specific chemicals in the cats red blood cells.
The A allele encodes a fully functioning CMAH enzyme while the AB allele codes for a partially active enzyme and the b allele encodes an inactive enzyme.
Knowing a cat’s blood group can be important, particularly in preventing a condition known as neonatal isoerythrolysis. Neonatal isoerythrolysis can occur in kittens when a b type queen is bred to an A type male. Type A kittens will then absorb the A type antibodies found in the mothers colostrum when nursing, leading to a haemolytic crisis.
The detection of the mutation that causes the differences in the blood groups can be identified by DNA testing. The presence of the mutation has been designated as the b allele. Hence a cat that has inherited two copies of the b allele (ie bb) will have the b blood group. If, on the other hand a cat inherits either one copy, or no copies of the b allele will either be Type A or Type AB. It is important to note that this test cannot distinguish between Types A or AB.
A simple cheek swab will enable breeders to identify carriers of the b allele and plan breed programs accordingly.
Result Blood Type Interpretation
non-b / non-b Type A or Type AB
b / non-b Type A or Type AB (carrier of b)
b / b Type b
SOME THOUGHTS (AND ADVANCE?) ON
Streptococcus G On the Spot March/June 2014
Some of you may remember that in the 90’s Sue Rodger-Withers, Jeanette Perkins and I, in co-operation with our vets, and a friendly pathologist managed to nail down Streptococcus G as the cause of much perinatal death in kittens as well as early failure to thrive. We developed a treatment protocol centred around Clindamycin, which is specific to killing Strep G, to apply to our queens, with really amazing outcomes. It subsequently turned out that these perinatal deaths and failure to thrive had become a world-wide problem, right across pedigree breeds, and we, as a group became the recipients of much gratitude from breeders world-wide.
It is unfortunate that no-one has ever considered it worthwhile to establish the correctness of our hypothesis, and recommended treatment through rigorous scientific testing, but I do think that the widespread dissemination of our hypothesis, and treatment, via the Internet, has led to the successful use of our protocol all over the world, and the survival and thriving of many, many kittens. It is a pity that we couldn’t pull all this information together in some way to have the diagnosis and subsequent treatment enter veterinary medicine in the approved manner. Instead, it is generally a case of the breeder finding out about it for themselves, when desperately hunting for something which would help them to stop losing every litter …. And then being forced to go to their vets and to browbeat them until they prescribed the requisite course of capsules, or drops.
I, and more particularly Sue, (and Jennifer) still receive loads of emails about the problem, and recently I received the following from Marva Marrow who long ago prepared a very good summary on her website:
Thanks for getting in touch, Truda! I really do have to thank you and Sue for your extremely important part in this story!! About the boys. After many hundreds of litters and tons of feedback, I do think that this is an STD and that treating the boys gives them some measure of protection - and that they can spread the germs to the girls. Seems that G Strep is the most common cause of abortions in human females too and clindamycin is the drug of choice - one of those that have not been overused - this, according to a human obstetrician who is also a breeder.
The testing has been iffy here. The only time I actually saw a positive read was on the placenta of a stillborn (not mine), but never or almost never from swabs or the still born kitten itself. But anyway, overall this works, very thankfully. We don't in the US, and in Europe they don't, have that kind of coordination with the pathology. (I had described how to insure accurate pathology tests). Even though they will get samples quickly, they still don't get accurate results at all. The Long Lasting Penicillin is really just a secondary precaution, but the whole thing overall seems to do the trick. I still get at least a couple of emails every single week from all over the world about all of this.. anyway - thanks for writing and again, you and Sue were lifesavers at the time. I just wrote it all up and then refined over time, due to additional veterinarian and breeder feedback. For sure, all due to the power of the internet! And the first article I wrote was a LONG time ago!! Thanks again to you and to Sue from the bottom of my heart - and from the hearts of many breeders around the world.
Now I believe that I might have a new observation to add:
Some of you ( particularly Trish Beech) will remember the ‘Wonkies’ I had in a couple of litters in the 90’s.
These kittens appeared to lack co-ordination in their rear ends, and looked as though they had suffered some kind of neurological damage. My vet (Karen Hedberg) couldn’t shed any further light on their condition, and they lived out their lives (some quite long!) in this state.
These cases occurred just before/around about when I was suffering from all the perinatal problems which subsequently were corrected by the isolation and treatment of Streptococcus G.
Just recently I had a queen who produced a litter of 4 kittens – 2 large and healthy girls, and 2 weedy little boys. Mum had been treated with antirobe prior to birth – if she hadn’t been I’m sure the boys would have been born dead. The girls grew, the boys did not. I treated them with Antirobe and yoghurt, and they responded wonderfully. In due course, I stopped treating them. They always remained much smaller than the girls, but one seemed normal, the other a poor doer.
When they were 11 weeks old I had them castrated. Then I went off to hospital for my knee replacement. When I arrived home the girls were wonderful still, and the boys were staggering all over the place, eating poorly, and their coats looked open and starey. Initially I thought there had been a fall, but with 2 of them this seemed odd, some kind of neurological problem ….
Once I could get into my car to drive, I took them to my vet, and explained their whole history – the upshot was that we put them back onto Clindamycin, a long course, the prognosis being that we wouldn’t see much for some time, and it would take 3 weeks to resolve completely, and they might never return to normal ….
In less than 48 hours they had improved, eating wolfishly, playing vigorously and much less wobbly ….
Now after 10 days, I am entertaining the hope that they will return to normal, well and truly….
And of course, this was when I remembered those ‘wonkies’, well before we knew about Strep G – could they have been cured if only we had known? Have I uncovered one of the longer term sub lethal impacts of Strep G on developing kittens???
Truda Straede 12 May 2014
October 2016 These two are still resident here, they move in 2
dimensions only, cannot jump up, still wobble, and are very
sensitive to touch. But, they eat and keep themselves clean!!
ANOTHER OF THOSE THINGS THAT VETS PROBABLY DON’T WANT US TO KNOW ….. On the Spot March 2016
Duration of immunity for canine and feline vaccines: a review
Vet Microbiol. October 2006;117(1):75-9. 25 Refs
Ronald D Schultz, Ronald D Schultz
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA.Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin-Madison, 2015 Linden Drive, Madison, WI 53706, USA. firstname.lastname@example.org
(DURATION OF IMMUNITY)
In our studies aimed at assessing the minimum duration of vaccinal immunity (DOI), approximately 1000 dogs have been vaccinated with products from all the major US veterinary biological companies. The DOI for the various products is determined by antibody titres for all dogs and, by challenge studies in selected groups of dogs. Recently, all major companies that make canine vaccines for the U.S. market have completed their own studies; published data show a 3 years or longer minimum DOI for the canine core products, canine distemper virus (CDV), canine parvovirus type 2 (CPV-2), and canine adenovirus-2 (CAV-2).
Studies with feline core vaccines - feline parvovirus (FPV) (‘feline enteritis’), calicivirus (FCV) and herpes virus type I (FHV-1)(‘rhinotracheitis’) have shown a minimum DOI of greater than 3 years.
Based on these results, the current canine and feline guidelines (which recommend that the last dose of core vaccines be given to puppies and kittens > or =12 weeks of age or older, then revaccination again at 1 year, then not more often than every 3 years) should provide a level of protection equal to that achieved by annual revaccination.
In contrast, the non-core canine and feline vaccines, perhaps with the exception of feline leukaemia vaccines (Leucogen vaccine probably lasts at least as long as core vaccines) , provide immunity for < or =1 year. In general the effectiveness of the non-core products is less than the core products. Thus, when required, non-core vaccines should be administered yearly, or even more frequently.
The so called 3 year vaccines now available DON’T cover the ‘flu’s’ herpes and caliciviruses and one of my vets said, rather nastily ‘they never will’… obviously the vaccine manufacturers/vets can’t/don’t or won’t read …..
(Italicised notes are mine- Ed)
ANOTHER GENETIC NASTY FOUND IN AN AUSTRALIAN MIST
Progressive Retinal Atrophy was detected in a total DNA screen by an older breeder, and the information passed on to owners of breeding stock descended from the affected cat. Further screening of this progeny was carried out, with a mix of results. Breeding of new stock with an eye to eliminating the problem is now under way. Like many of the inherited problems which screening has revealed, this is a recessive gene, and allows the process of ‘breeding out’ to be carried on without creating any actually affected progeny.
Many thanks to the honest breeder who let us know… the problem you don’t know about takes the longest to solve!
When I read the information below (taken from Orivet genetic Pet Care website (http://www.animalsdna.com), it became immediately obvious that Australian Mist, being part Abyssinian, should have been listed amongst those breeds likely to be affected.
Progressive Retinal Atrophy (PRA) is an inherited, late-onset blindness found in Abyssinian, Somali and Ocicat breeds. The disease has also been observed in Siamese and related breeds and poses a significant health risk in these breeds. Other cat breeds at risk are Javanese/Balinese and Oriental Shorthair. Bengal cats, American wirehair, Tonkenese and American curls are at lower risk.
It is typically characterised by a progressive degeneration of photoreceptors in the eye. A mutation in a gene called CEP290 has been found to be associated with PRA in the above mentioned breeds.
It is normal for photoreceptors to develop after birth to about 8 weeks of age. However in kittens affected with PRA, the photoreceptors develop, but as the cat ages, the photoreceptors degenerate, leading initially to night blindness and progressing to total blindness at around 3-5 years of age.
PRA is inherited as an autosomal recessive disorder, meaning that two copies of the mutation are needed for the disease to occur. Carriers of only one copy of the mutation are not affected and will have normal vision.
A simple cheek swab will enable breeders to identify both carriers and affected animals and plan breed programs accordingly.
CEP290 Mutation Not Found / Carrier / Affected
NB: Other causes of PRA may exist which are not identified by this test.
Not found = The CEP290 mutation was not found.
Carrier = One copy of the CEP290 mutation was found. Such cats are carriers but
will not be affected and will have normal vision. Precautions should be taken in breeding programs.
Affected = Two copies of the CEP290 mutation were found and PRA is likely to
A Cure for
George by Sam Atherton-Ryan
through 100 odd channels one night I came across a science programme
discussing research into faeces and the bacteria in the gut and faeces.
programme was outlining the fact that
the lack of bacteria in the gut had been linked to a variety of
illnesses from diabetes to stroke. It was explaining that the next
stage of the
looking at treating a whole host of illnesses with bacteria
instead of drugs.
in 1921, Buster Lloyd Jones watched animals seeking out plant matter to
themselves, is this unknowingly what he was watching? The collection of
Prebiotic material? He later went on to become one of the most sought
vets of his time and to develop Denes Herbal remedies which are still
this day and his studies and observations help many animals even now.
to George and finding a lifelong cure for him my mind was still asking
questions - mainly if I stop feeding his good bacteria he starts to
Why? This takes me back to diet So I looked at his original food and
prescription Diets that he had trialled earlier on his road to recovery
what I found wasn't good, a lot more research and I realised that the
ingredients in the pet food was dire.
are obligate carnivores which simple means that they need meat to
there was no meat, just grains, cereals, fillers and waste products
chemicals to make it palatable. How on earth was this going to feed
him? So we
set about trialling grain free but in order for this to work all the
to have the grain free to make sure George didn't get his paws on any
others food. The results were amazing. Whilst doing this we found a
another cat Sui that had constant bouts of idiopathic cystitis,
This took us further, as the cats are obligate carnivores they need meat. So they all went on to a raw diet with immediate effect and OMG the difference was amazing. This was the final piece of the puzzle. They were all healthier, their coats glossy, no allergies, no more cystitis for Sui and what really struck me was that the queens some that would call every two weeks in a most unhealthy and unnatural way started to regulate their cycles and only call twice in a year. 
why is a
manufacturer of a prescription diet allowed to make a diet for dietary
inadequacies and allergies when all the ingredients that cause the
present in the food?
Are we as humans disregarding
the animal welfare laws. Two of
the five freedoms are ‘Freedom from hunger and thirst by providing
to fresh water and a diet to maintain health, and freedom to express
behaviour.’ Well diets provided by huge corporate companies, found in
supermarkets are not a diet to maintain
health because they are made from waste, and normal behaviour for a cat
hunt and eat prey!
diet chart ALWAYS specifies raw meat, including muscle, fat, bone and
odd chewy bits. Unfortunately some people really don’t believe that I
know better than the vets who throw up their hands and declare that you
NEVER feed a cat raw meat ‘because of all the parasites’ – ouch. They
on to recommend a worming schedule which reflects a naturally fed cat –
also do… I have had far too many pet owners ring me distressed about
problems and asking me for help (and often implying that it is my fault
creating a breed with allergy problems….) A little digging invariably
that they have strayed far from the whole raw food diet I originally
recommended, and on which their kitten was raised ….
 This is an
extremely interesting observation Sam, I
have never heard it before – but it
does make good sense. Ed