Saturday, November 16, 2013

Date with your dog: DIY xmas card

Little Santa and his big helper. Possibly looking beyond the camera at a tasty treat. (Photo by Jenny Parker).
So this year my effort wasn't 100 per cent DIY, but making a dog-themed xmas card is definitely an exciting way to spend some time with your dog (or dogs).

In this case we enlisted in a Shoot-ya-pooch photo shoot, as we have come to the conclusion that whilst I am an enthusiastic photographer, Phil seems to save his cutest poses for Jenny Parker.

The shoot was intense. The boys were very excited and kept changing position. They probably posed like this for a nanosecond.

But Jenny managed to turn this...
The making of...note the mayhem and awkwardness...
Into this...
Bosca looks like an innocent reindeer, while Phil looks like badass Santa from the 'hood. He is ruling that antique chair.
So I got onto snapfish and made them into cards. Imagine getting THIS in the mail!!!
You can upload any photo you want on the card.
Of course you don't need a professional photographer to make your own pet-themed xmas cards (but in this case it helped).

Have you ever featured a pet on an xmas or holiday card? If so, SAT would love to know! Send a photo and we will feature it through December.

In other news...

The Lort Smith Animal Hospital has teamed up with Dr Arthur House to provide a webinar on the medical and surgical management of burns in companion animals, to be held on November 21 at 7.30pm. For more information sign up here.

The second is an ad and whilst it pains me to post advertisements, this one is a Rube Goldberg Machinefor dogs and I think must be commended.

It’s very much in the tradition of OkGo, whose film clip to This Too Shall Pass (wise words to recite whilst you’re waiting for a dog to eliminate a foreign body from the distal colon) is awesome. 

(But as SAT readers know their best clip ever has to be their canine-filled video for White Knuckles – if you Google the making of videos you can lose a Saturday morning).

See. There I go.

SAT reader Merryn sent this very worthy compilation of cats stealing dogs’ beds. 

Oh and this one has done the rounds of the internet but cats with unusual markings is worth a second look. I am particularly enamoured with permanent top hat cat and moustache cat. 


Friday, November 15, 2013

Seizures in dogs and cats

A chihuahua is presented for investigation of seizures. (Note the painted nails are not related in anyway. This breed commonly suffers from hydrocephalus.
Veterinary neurologist Georgina Child presented a fantastic webinar on seizures this week. Seizure disorders are common in companion animals and may be acute (often secondary to a toxicity of some kind) or recurrent. Seizures are incredibly distressing to witness and if left untreated can increase in frequency.

We tend to think characterised seizures as generalised seizures (by far the most common and the classic tonic/clonic type seizure) or focal seizures (much harder to detect). Petit-mal or absent seizures aren’t properly recognised in dogs although they are a common seizure disorder in people.

Dr Child said that her job was easier thanks to smartphones as owners can now present her with footage of seizure events, making characterisation much easier. Differential diagnoses for seizures include syncope, movement disorders, narcolepsy and some compulsive behaviours.

“Anything that presents as a stereotypic set of events that comes out of a background of normality then finishes abruptly with the animal returning to normal has to be considered a possible seizure,” she said.

Causes of seizures are divided into two main categories:

Intracranial or extracranial. 
Extracranial causes include metabolic disease and toxins.
Intracranial causes include underlying structural abnormalities which may or may not be progressive, eg tumours, previous head injury, cerebrovascular accidents. There are also idiopathic seizures for which no underlying cause is found, though Dr Child said that many such dogs had inherited the seizure disorder.

Seizures always indicate a forebrain abnormality. Focal seizures occur due to a transient disturbance in a specific area of the brain rather than the whole forebrain. Contrary to popular belief, focal seizures may also be familial in origin.

The term epilepsy refers to a syndrome of recurrent seizures – it is not a disease per se. It is the most common cause of seizures in dogs under five years old.

Commonly affected breeds include border collies, Belgian shepherds, Siberian huskies, malamutes, retrievers and collies of all kinds. Dr Child’s own border collie Tilly has epilepsy, so as she said she lives the nightmare of her clients.

According to Dr Child, the chances of finding a metabolic abnormality in dogs with a seizure disorder is less than 1 in 50 for dogs without interictal signs, but they should be looked for as these can be treated.

All animals should undergo a full neurological examination once they have recovered from the postictal period – but in some cases this can last for a day or more.

In a dog under one year old with no obvious interictal neurological signs or metabolic abnormalities, Dr Child recommends liver function tests to rule out hepatic encephalopathy which may be secondary to a portosystemic shunt. MRI may be helpful in identifying intracranial causes such as hydrocephalus.

In dogs where seizures commence between 1 and 5 years of age, the most likely cause is idiopathic epilepsy.

Previously well controlled epileptics may develop an increased frequency of seizures. This can be due to emergence of a concurrent intracranial problem, e.g. brain tumour, or may be due to pharmacoresistance which develops in about 40% of dogs with time.

Hyperlipidaemia/hyperliperproteinaemia is an hereditary problem in mini schnauzers and can be associated with the development of seizures. Fasted triglyceride level should be performed.

Interestingly, Dr Child made the comment that cerebrovascular infarcts occur more commonly in animals than we have heretofore appreciated.

In dogs over 5 years old, it is vital to take a fasting blood glucose. But these animals have a 50% probability of having intracranial disease, specifically a brain tumour. Assessment for extracranial neoplasia is warranted e.g. thoracic radiographs, abdominal ultrasound.

Dr Child always recommends performing an MRI prior to CSF tap as CSF tap is more risky in animals with clinical signs suggestive of neurological disease. If imaging is suggestive of inflammation or an infectious process, a CSF tap may be indicated.

Dr Child always considers DNA-testing in breeds with known familial neurodegenerative disease, including Staffordshire terriers.

Cats are a bit different - epilepsy is less common than in dogs; infectious CNS disease and systemic hypertension are more common.

When should anticonvulsant treatment be instituted?

This is a subject that experts disagree on, but Dr Child’s recommends treatment when:
  • Progressive intracranial disease is present
  • If there is more than one seizure every 4-6 weeks
  • There are 2 or more seizures in a 24 hour period (cluster seizures)
  • Any history of status epilepticus (seizure >5 minutes – most last 60-90 seconds).


There is no guarantee that any medication will stop seizures completely.

She discussed her drug regimes and monitoring protocols at length.

Seizure control in emergencies


Animals may present as an emergency for treatment of seizures including status epilepticus or cluster seizures. 

Drug
Dose
Route
Comments
Diazepam
0.5-1mg/kg
Intravenous

Diazepam
2mg/kg
Per rectum
Can repeat at 5 and 20 mins – no more than 3 doses in 24 hours. Can be given intranasally.
Midazolam
0.06-0.3mg/kg
IV or IM
Useful if no IV access; preferred in cats
Levetiracetam
40-60mg/kg
Intravenous; can also give via any route
Then 20mg/kg every 8 hours
Phenobarbitone
2-10mg/kg (average 5mg/kg)
Slow IV, IM, PO
Continue for up to 6-12 hours. May take 30 mins to take effect.
Propofol
Bolus to effect then 0.05-0.1mg/kg/min to a max of 6mg/kg/hr
As constant rate infusion

Thiopentone/propofol + inhalation anaesthetic



CRI diazepam/midazolam added to CRI maintenance requirement



Pentobarbitone
To effect – much less than GA dose


In all continue phenobarbitone and/or levetiracetam at maintenance doses.
HALVE ALL DOSES FOR CATS AND ADMINISTER THIAMINE.

Thursday, November 14, 2013

Designing pet-friendly accommodation for the aged & are birds capable of altruistic behaviour & pet loss

Footprints and pawprints in the sand (even though it does appear that the person walking has two left feet!!!).
Getting old is inevitable, but getting old without the company of your companion animals - or having to part with them to move into a retirement village, aged care facility or nursing home - is downright awful.

The Pets and Aged Care Steering Group (chaired by the wonderful Jan Phillips and Di Johnstone) ran a fantastic workshop on designing pet-friendly aged care. You can download and read the papers by clicking here including the case for pet friendly planning of aged-care accommodation, design considerations and a veterinarian's perspective.

If you think you might ever need aged care (and I daresay that most of us will), you should be acting on this now to ensure that appropriate pet-friendly accommodation is available.

On another note, Alex the Parrot used to say "I love you". What did he mean? One theory is that he was simply seeking a reward and he realised that this combination of words led to exactly that being produced. I'm not so sure we can draw this conclusion.


Are magpies capable of altruistic behaviour?
SAT reader Ro sent this fascinating link discussing the explanation behind a scenario involving two magpies. If you take an anthropomorphic position you might just think that one of these magpies is helping the other seek treatment for an injury. But if you take a behaviourist approach it could be just a sophisticated way of seeking a food reward. My personal take is we don't know enough to conclude either way, but in this scenario the anthropomorphic stance works better. What do you think?

Finally, Do You Believe in Dog Blogger Mia Cobb wrote this beautiful post about the death of her dog Elke. Elke was rescued in a cruelty investigation by the RSPCA as a puppy. Though life started out rough, she was adopted by the Cobb Mob and shared her life with a loving family who wanted to give her positive experiences (Mia has provided some gorgeous photos). Mia discusses her own grief but also the human animal bond and grief in general, as well as sharing some resources for those who want to read further. 

Wednesday, November 13, 2013

Cane toads: a history, a gross case study, and first aid tips

Two cane toads. Image courtesy Mark Lewis, Radio Pictures, Mullumbimby.
Today’s post contains not only a fantastically gross case study of ingestion of a canine toad by an unwitting canine, some practical first-aid tips and some previously little known history about the introduction of cane toads into Australia, thanks to a dedicated scholar who unearthed some incredible documents.

Cane toads are one of the world’s most invasive species, and nowhere have they caused more of an ecological catastrophe than in Australia. Today, a toxic cane toad “slick” rims Northern Australia. When one counts the toll of native animals and pets affected by toads, usually fatally, one is tempted to wonder “who was the bonehead who deliberately introduced these things into the country?”

But according to Charles Darwin University’s Nigel Turvey, author of CaneToads: A tale of sugar, politics and flawed science, there’s no single individual or institution at which to squarely point the finger (and that’s not for want of trying – he admits that he spent five years trying to uncover the blame-worthiest target). In fact, what we should be doing is examining the history and asking how such an unfortunate sequence of events came about – because history loves repeating itself.


Dr Turvey brought a friend along to the launch – Michael, the grandson of Cyril Pemberton, the entomologist who brought cane toads into Hawai’i, from where they were shipped to Australia. When Michael was introduced to the room, there was an audible gasp. I am dead certain that the guy sitting across the aisle from me was thinking, “If only I could get hold of a time machine and bump off his grandpa…”, but I suspect he’d changed his mind by the conclusion of proceedings.

A baby cane toad.
The talks that followed were gripping. The folks that brought cane toads to our shores were far from boneheads. They were credible scientists, on top of their game. As Michael said, his grandfather was a studious, decent family guy who spent months researching any species in its environment before importing it, studying it further then releasing it as a means of biological control (in those days, that was considered an appropriate time frame for study).

The sugar cane industry was being punished by the impact of the scarab beetle, the larva or grubs of which knaw the roots of sugar cane and destroy it. It happened that cane toads had been used around the world as a form of biological pest control. In France in the 1800s they even had toad markets, at which people would drop in and pick up a few toads to control snails and slugs in their gardens. Imagine ducking out to the shops. "Honey, I'm just off to grab a few cane toads for the garden - need anything while I'm out?".

Toads on Tour at Sculptures by the Sea, by Hannah Kidd.
Fast forward to the 20th century, where scientists were debating the merits of the cane toad, Bufo marinus, as a means of controlling the scarab beetle. Remember, this is in the pre-pesticide era. Biological control was all the rage.
A scientist named Raquel Dexter collected 301 cane toads and dissected them, analysing their stomach contents. She found that they had eaten adult beetles, and presented a small paper in a stream at a conference that concluded (falsely) that cane toads control the grub.

No one challenged it. That paper, Dr Turvey argues, had disproportionate influence over members of the sugar industry and key scientists. The essence of the dumb idea was the assumption that earthbound toads would control soil-dwelling grubs by eating the airborne adults.

The truth is that cane toads didn’t spread around the world – they were PULLED. They were in hot demand because just about everyone thought they were awesome.

In Australia, the trigger was spring rains in Brisbane in 1932. It rained all weekend, and Bureau of Sugar Experiment Stations scientist Arthur Bell knew the bugs would pupate and growers would get on his back. The following day he went to his office and wrote a memo to his staff proposing introduction of the cane toad. One dissented, to which Bell responded with a copy of Dexter’s paper. The dissenter became a convert and personally escorted the first shipment to Australia.

On Monday, June 17, 1935, Bufo marinus docked in Sydney Harbour. They were released in Cairns on August 19.

Artist's impression: Hannah Kidd's sculpture indicating just how cane toads conquered Australia.
The only vocal opponent was the aptly named Walter Froggatt, the retired former Chief Entomologist of NSW.

In letters unearthed by Dr Turvey, Froggatt wrote that “all our small ground fauna will be at their mercy and become their prey.” History proved him correct, but at the time everyone pooh-poohed him as a pessimistic nay-sayer. The Prime Minister at the time, Joseph Lyons, personally signed off on the toad release.

The terrible truth is that the cane toad “was the product of a consensus of well-trained scientists in prestigious institutions, and the companies and funding organisations that supported them,” Dr Turvey said.

The thing is, it took much longer than months to work out that the introduction of cane toads was a mistake. Everyone was blinded by the expectation that these creatures would save the sugar industry.

And why not? Dr Turvey summarised this: cane toads came from a background where biological control had been successful; it replaced nasty pesticides like arsenic; was supported by a published, scientific paper; had international peer review; was endorsed by our peak scientific body (the then CSIR) and a consensus of scientists; championed by industry; promoted by the QLD Govt; subjected to quarantine and even endorsed by the PM.

The big question, of course, is whether we (scientists today) are qualitatively different? Shouldn’t we always be suspicious of a consensus of experts – given their diverse backgrounds and perspectives – and shouldn’t scientists always question the science?

It was 40 years before the first research (a 1975 survey) was published – and 70 years before the impact of cane toads began to be fully appreciated (well, I am not sure that appreciated is the right word there).

The big problem for Australia was that while toads had been introduced to other countries, those countries had predators that had evolved to cope with native toad poisonings. There were NO native toads in Australia. Subsequently we had a wave of native animal mortalities that had not been seen anywhere else.

The audacity: this cane toad posed for me.
According to Professor Shine, native mammal populations were already in decline before the advent of the cane toad – but for many species that was the final nail in the coffin.

Cane toads lay 30,000 eggs per clutch, but according to Professor Shine there is evidence that the ecosystem is fighting back.

“It’s not quite as doomy and gloomy as you might think,” he told the crowd. “We have to get used to toads being around but we can probably extinguish them in local areas if we need to.”

There is evidence that aversion training of quolls and even blue-tongue lizards can prevent fatalingestion of cane toads by these species.

He said that there is evidence that educating a single generation of a species was enough to pull them out of a toad-related extinction vortex, but added that no one had had much success in training snakes.

Cane toad ingestion: one dog’s lucky escape

[If you have a weak stomach, please don't scroll down - the next photo is pretty disgusting].

A couple of years ago now my colleague Dr Stephen Cutter treated a colourful case of cane toad ingestion in which the toad survived being swallowed by a dog and spending 40 minute’s in the animal’s stomach.

The top-end toad, which was expelled following a single dose of apomorphine, was shaken but remarkably unscathed. The dog survived too.

Toads produce bufotoxins which, when ingested, can lead to a range of disturbing clinical signs including hypersalivation, vomiting, restlessness, seizures and death. Often pets that have ingested cane toads are found dead, though low doses of the toxin aren’t usually fatal (some dogs will get away with mouthing a cane toad, and there are reports of some animals and a few stupid humans becoming addicted to the toxin, licking the backs of toads and acting “stoned”.

When Steve saw this particular dog, Bella, a female Staffordshire terrier cross, she had no clinical signs.

“Usually affected dogs are starting to twitch or seizure, but she was completely normal so we asked him if he was sure she swallowed a toad.”

Oh yes. He was sure. The owner had been dumping the contents of his freezer – an assortment of mince, pies and pasties – in his backyard when Bella hoed in. A toad jumped onto the pile when she took a gulp, in full view of the owner.

On induction of vomiting, Bella produced a bunch of semi-frozen meat, and a solitary toad.

Photo courtesy of Dr Stephen Cutter.
“We looked at this pile of vomit on the lawn and it started to move,” said Steve. “The toad got up and started to walk.”

As the toad emerged from the chunky pile in front of the stunned owner and hospital staff, Dr Cutter fulfilled a science-fiction fantasy, proclaiming “it’s alive!”

Bella, still a bit drowsy from her apomorphine injection, didn’t bother to chase her former tenant.

“Interestingly enough, when the toad came out it wasn’t upset,” Steve added. “When they’re pissed off you see toxin oozing from the glands.”

His hypothesis (which remains unconfirmed by double-blinded, placebo controlled studies) is that the party pies and pasties protected the toad from the harsh gastric acid in Bella’s stomach.

What do you do if your pet eats a cane toad?

You can read Dr Stephen Cutter's article about first aid for cane toad toxicity here.
  1. If the cane toad is in your pet’s mouth, remove it.
  2. Gently rinse the mouth out with a slow-hose or tap water, being careful to point the hose across (not towards the back of) the mouth – you don’t want to drown the animal.
  3. Use a damp cloth to wipe the mouth and gums as the toxin is very sticky.
  4. If your pet is exhibiting twitching, tremors or seizures, seek veterinary attention immediately.

Tuesday, November 12, 2013

The root of all evil, and why dental xrays are really very useful.

Phil's health issues all seem to surround his problem teeth. Here he is relaxing prior to his final (we hope) dental procedure.
SAT readers will be familiar with Phil’s colourful history of periodontal disease (if not, you might want to read about it here). As a rescue dog I can’t take credit for his oral care in the formative years (and I'm not sure I'd want to), but as a microdog he was already at risk of developing periodontal disease.

For some time he’s been cruising along with two teeth (his lower canines). But a few weeks ago he shook his head (as he is want to do sometimes) and in doing so threw himself about six inches (at 2kg there is not much weight to hold him down) – hitting my foot with the side of his face.

No, I didn’t kick him. It was one of those freak accidents. He yelped, I grabbed him and he seemed okay but wouldn’t let me examine his mouth. The next day the halitosis set in. I assumed he must have fractured his tooth or developed an abscess secondary to trauma. Trouble is, no one, and I mean NO ONE, could look in that mouth. 

I was prepared to refer him for root canal treatment to save his last two teeth, but when I anaesthetised him to examine his mouth properly it was bad news. His little gums peeled right away, exposing wells of pus. Dental radiographs revealed severe lysis and osteomyelitis of the jaw. Which looked like this.

Radiograph of Phil's mandibular canines. Those in the know will note the marked bone resorption, lysis and periapical abscesses (see the dark halos esp around the lower root in the pic). To those not in the know - essentially, there should be a lot more white (bone) in this x-ray. This kind of x-ray makes your heart sink.
There was no option but to extract those teeth – without fracturing the mandible. It was a delicate procedure, but with major assistance of my wonderful colleague May (in fact I mostly wrung my hands whilst May worked away patiently at those teeth) and the moral support of veterinary dentist Christine Hawke on the phone, the offending canines were gently coaxed from their attachments.

My focus was entirely on those mandibular canines, but whilst Phil was in recovery I checked out an image I'd taken of his maxilla (upper jaw). And there was a retained tooth root, mocking me. This xray also made my heart sink.

Can you spot the retained root? Clue: it is on his right hand side (the lower part of the photo) and looks curved. Once you see it you can't unsee it - it stands out like a neon sign, or, if you are into art/propaganda, it looks like this lady's fist. (If you can't see it, scroll down a bit - there's an arrow in the next pic).
You see, I had known it was there for some time. Phil has had an issue with recurrent unilateral (one-sided) nasal discharge which I'd done a full work up on, including CT, earlier this year. It started after an insect sting last year, and since then he was producing nasal discharge in spectacular volumes. I flushed his nares, hoping to dislodge a nasal foreign body such as a grass seed or leaf, to no avail. Radiographs at the time did not seem to reveal any lysis. 

Antibiotics resulted in limited improvement. Steroids did nothing. He would have periods without nasal discharge then shoot out mucus like a kid spraying silly string. On one memorable occasion he produced a mucus cord so long it circumnavigated his entire muzzle (and I had the camera handy).

Phil's legendary "monster booger". I make light of it now, but I was deeply concerned for his health.
Fearing a nasal mass of the sinister variety, I took him to CT and he had a nasal biopsy. 

Phil undergoes a CT scan (under general anaesthesia).

Phil's CT scan. I don't read these things for a living, but my initial clinical impression was "there's an alien in there".  (Seriously, it looks like it has really ornate eyebrows and might be smoking a hollow cigar).
At the time it was noted that there was a retained right maxillary incisor root, but the working diagnosis was non-neoplastic rhinitis (the biopsy confirmed "lymphocytic plasmacytic rhinitis", cause undetermined). I was relieved it wasn't cancer, but his ongoing signs caused both of us stress. 

So when I noted the marked asymmetry of the rostral maxilla on the recent xrays, I grew convinced that that little hook might well be the root of all evil. 

It wasn't clear cut and there was much debate. Some colleagues told me it was very likely to be the cause of his rhinitis, others said nope, it wasn't associated with a periapical abscess (you can trace the periodontal ligament). There was vigorous debate. But if you've ever had an ingrown toenail (I did once and I was grade 4 lame (I have a photo but some things aren't meant to be blogged)) you'll know that a tiny foreign body can cause disproportionate inflammation, irritation and pain. Its the "princess and the pea" all over again.

So, even though Phil is technically toothless, Dr Hawke and I went in to find that root (I know, when I read that I have flashbacks from "Inner Space" - it wasn't quite that exciting). And it was there waiting for us. There was a tiny fistula which accommodated the dental probe. This lead to a little stream of pus, in which was floating a tiny piece of bone that Dr Hawke deftly flicked out. We stared at it long and hard. Was this insignificant shard really the source of Phil's woes? 

The probe slides into a fistula adjacent to the maxillary incisor root.
On repeat radiographs it was evident that there was significant bony involvement. Flushing of the fistula proved that it communicated with his nasal cavity: saline went into the hole and came out of his right nostril - the hallmark of an oronasal fistula.
You can see the root (arrow) surrounded by a well of darkness (bone resorption/osteomyelitis). There are some artefacts on this image, but the important thing is the hook-shaped root.

See - its not there now!
I didn't want to recover Phil prematurely and leave any part of the offending root behind, so we took a repeat radiograph to confirm its absence.

Retained tooth root beside 5 cent piece for scale.
There you have it. Is this definitely the root of all evil? Time will tell. Naturally Phil is snorting a little bit and he produced another legendary "monster booger" tonight - but that's to be expected given the extensive curettage and lavage of the affected region. I expect the signs will resolve in coming weeks, but I will keep you posted (I can say as I type this he is dancing on the carpet having eaten three bowls of food).

How come it read like an incidental finding on the CT report? Maybe the lysis wasn't as bad at the time of CT? And as May said, this is a very small patient. Its so easy for a dog this size to develop a miniscule oronasal fistula. 

Why didn't I do dental radiographs earlier? Well, I was attached to the allergic rhinitis hypothesis and my mind had omitted the tooth root infection hypothesis when the CT came back. After all, the onset of clinical signs coincided with an insect sting, which in retrospect was a bum steer (maybe the associated inflammation upset an otherwise dormant root fragment?). The other thing was that the signs would subside and he would be sniffle free for extended periods of time. I wondered about intermittent exposure to some unknown allergen.

The CT didn't say the tooth root was NOT a problem. I was happy to be reassured by colleagues who said "no, that isn't it" as I wasn't keen to go digging. I am certain that serial radiographs would have indicated progression of osteomyelitis in the vicinity of the root. 

I am glad for Phil's sake that we got there in the end. It might be a tiny piece of bone, but it was very satisfying sealing it up in a jar where it can't cause any more discomfort. Hurrah!

[If you want to read more about how attachment to a diagnosis can affect medical judgement, I highly recommend Jerome Groopman's How Doctors Think].