SPOT
A SELECTION OF ARTICLES CONTRIBUTED TO 'ON THE SPOT' DEALING WITH TOPICS OF INTEREST TO AUSTRALIAN MIST OWNERS AND BREEDERS
SPOT
SNAKE BITE
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.
Bezique
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
improved.
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.
Onset
of
clinical signs is usually sudden with collapse or vomiting within
minutes
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.
dilated
pupils, slow or absent pupillary light reflexes, respiratory distress;
shallow or abdominal respiration, hindquarter weakness, pallor,
jaundice,
non-clotting blood. extended coagulation time, proteinuria, haematuria,
haematemesis, continued bleeding from fang marks or other wounds, and
flaccid
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.
Premedication
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.
Nursing
Care
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
SPOT OF
HEALTH
In response
to the Snake Section above, as included in Issue 49, Lesley Roberts
wrote:
I was
interested
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
roadworks
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.
I've
catproofed
the garden with wire mesh hooked/clipped to the top of the "asbestos"
fencing
so the cats can't get out, but unfortunately the baby snakes still
squeeze
through thin cracks in the "asbestos" - probably heading for water
after
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
making
special vibrating noises which help the eggs mature and hatch.
The
rather dubious words of the last snake catcher I spoke to were:
"There's
absolutely no way a snake will hang around in a dog's backgarden - too
much ground vibration!"
Bye for now,
Lesley
P.S.
Satu Gamelan sends his regards.
As I
knew
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.
Precautions
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.
When
exercising
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
where
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.
The 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
Description
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
Web Sites
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
Life Cycle
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
Action of venom
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
Clinical signs
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
Treatment
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
What 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.
Necrotic Arachnidism
This
condition
encompasses a broad spectrum of responses to spider bite, from very
mild
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
the
Americas,
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
1
Sutherland,S
K (1990) Antivenom use in Australia. Medical Journal of Australia
157: 734-739
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
From
'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.
How common is this
disease?
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’.
Fleas may cause cat
scratch
fever!
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.
Is there a vaccine or
treatment
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.
From On
the
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
ulcer?
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
diagnosed?
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
treated?
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.
Will
there
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.
PROMPT
TREATMENT
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.
UNDERSTANDING
THE VIRUS
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.
Carriers
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.
THE
VIRUS
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:
1. Rejection
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
2. The
Disease
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
3. Latency
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.
CREATING
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.
On
retesting,
the cat may be positive again, in which case you should consider
desexing
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.
VACCINATION
REGIMES
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.
BUT IS
IT
SO SIMPLE?
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.
NOW
THE
UPDATE
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.
Chlamydia
was only relatively recently discovered because it is a difficult
organism
to culture in laboratories, and difficult to see under the
microscope.
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.
Zithromax,
Azithromycin, Pfizer) is a new, safe antibiotic which is highly
effective
against Chlamydia. Vibravet takes four weeks to wipe out Chlamydia
while Zithromax does it in a single dose. Many veterinarians will not
have
heard of Zithromax, which may not have been promoted to them as an
animal
drug. However, it is very safe and it works well.
Dosage
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.
Summary
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.
Observations
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!.
While
obviously
this information will be of greatest interest to breeders, there is no
reason why pet owners shouldn't also benefit from it, specially if
their
cats are confined to indoors (so are less likely to reinfect themselves
through external contacts) and most particularly if any of their cats
have
chronically runny/weepy/dirty eyes. Any feed back would be most
welcome,
as I am sure we would all be interested in the outcome. This is
certainly
one to add to any revised edition of Breeding Cats..... a practical
guide
- both in general and under 'Fading Kitten Syndrome'.
Truda M
Straede