Bridlewood Veterinary Clinic

2013-10-18T04:00:00.000-07:00

Acupuncture for Mobility

Maestro's Mom has written a lovely Blog about his first Acupuncture Treatment and the results that he experienced together with pictures. If you have a furry friend that is afflicted with lameness, pain, arthritis or mobility problems and have been underwhelmed by routine standard treatment than you might find this article which reflects Maestro's response to his first acupuncture treatment.
With thanks to Maestro's Mom for taking time to write this blog.

Dr Mark Rubensohn
Bridlewood Veterinary Clinic

http://dogblog.musespeak.com/2013/10/maestros-first-canine-acupuncture-treatment.html

2013-10-01T08:16:00.000-07:00

Ear Crop Posting

I have found this very useful site to assist our ear crop clients to review how to post the ears of therir puppies.
I hope this will be helpful.

http://www.rockytopboxers.com/Earwraps.html

2013-06-08T15:04:00.000-07:00

Caution – Jerky Treats from China

In the light of increasing cases and information of illness in dogs that have been exposed to “Jerky Treats” manufactured in China, we would like to make sure that our clients are aware of this potential problem. We advise the use of pet foods and treats that are manufactured locally by recognized and trusted companies.

Signs to look out for that may be associated with jerky pet treats include decreased appetite and activity, vomiting, diarrhea and increased drinking and urinating. Laboratory findings may include signs of kidney problems including glucose and/or protein in the urine. Some of the reported cases may be the result of causes other than the consumption of jerky treats. This concern has not been definitively isolated to jerky treats so caution is indicated with all pet food products that originate from China. Currently the US FDA and numerous veterinary authorities are investigating this problem. Should you have a concern that your pet has become ill after exposure to imported treats, please notify your veterinarian immediately.

More information can be found at the following sites:

http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm295445.htm

http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm319463.htm

2013-06-01T21:55:00.002-07:00

Some Toxic Foods for Dogs

This is a portion of the full article which can be viewed by clicking on the title above.
Recognition is hereby given to the NCIB and the authors of this article.

Chocolate, caffeine and other methylxanthines

Chocolate is derived from the roasted seeds of Theobroma cacao and its toxic principles are the methylxanthines theobromine (3,7-dimethylxanthine) and caffeine (1,3,7-trimethylxanthine). Theobromine is also found in tea, cola beverages, and some other foods.

Chocolate toxicoses occur especially at holidays: Valentine's day, Easter, Halloween, and Christmas and may result in potentially life-threatening cardiac arrhythmias and CNS dysfunction (Stidworthy et al.,

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Destroy user interface control 1999).

Sources

Most poisonings from methylxanthines occur as a result of chocolate ingestion. Chocolate is toxic to all species, especially to smaller dogs, though a toxic dose will vary depending on factors like whether the dog ate the chocolate on an empty stomach, if the dog is particularly sensitive to chocolate, and the type of chocolate, since dark chocolate is more toxic, whereas milk chocolate less so, and white chocolate must be consumed in extremely large quantities to cause a serious problem. Contributing factors include indiscriminate eating habits and readily available sources of chocolate. Deaths have also been reported in livestock fed cocoa byproducts and in animals consuming mulch from cocoa-bean hulls. Cocoa bean hulls or waste used as bedding for animals has caused toxicosis primarily in horses. Third most prevalent poisoning from these agents is a result of caffeine tablets ingested by dogs or hype race horses (tablets often contain 100 mg each). Theophylline tablets or elixirs are also used as human or veterinary medication.

The methylxanthine content

The most important toxic component of chocolate – the methylxanthine alkaloid theobromine is present in variable concentrations dependent on the quality of the chocolate – the darker or richer in cocoa solids the more dangerous the preparation. Cocoa powder and cooking chocolate are the most toxic forms (Sutton,

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Destroy user interface control). Table 1 shows the total methylxanthine concentration in chocolate (www.merckvetmanual.com).

Table 1

The total methylxanthine concentration in chocolate (www.merckvetmanual.com).

The amount of theobromine found in chocolate is small enough that chocolate can be safely consumed by humans in large quantities, but animals that metabolize theobromine more slowly can easily consume enough chocolate to cause poisoning. Although the concentration of theobromine in chocolate is 3–10 times that of caffeine, both constituents contribute to the clinical syndrome seen in chocolate toxicosis.

Toxic doses

A 10-kilogram dog can be seriously affected if it eats a quarter of a 250 g packet of cocoa powder or half of a 250 g block of cooking chocolate. These forms of chocolate contain ten times more theobromine than milk chocolate. Thus, a chocolate mud cake could be a real health risk for a small dog. Even licking a substantial part of the chocolate icing from a cake can make a dog unwell. A dog needs to eat more than a 250 g block of milk chocolate to be affected. Obviously, the smaller the dog, the less it needs to eat. A typical 20 kg dog will normally experience intestinal distress after eating less than 240 g of dark chocolate, but will not necessarily experience bradycardia or tachyarrhythmia unless it eats at least a half a kilogram of milk chocolate. According to the Merck Veterinary Manual (

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Destroy user interface control 1998), approximately 1.3 g/kg b.wt. of baker's chocolate is sufficient to cause symptoms of toxicity, e.g. a typical 25 g baker's chocolate bar would be enough to bring out symptoms in a 20 kg dog.

The negative effects depend on the dosage, the size of the dog, and the type of chocolate. LD50 of methylxanthines in animals are summarised in Table 2 (www.actionagainstpoisoning.com).

Table 2

LD50 of methylxanthines in animals (www.actionagainstpoisoning.com).

Absorption, distribution, metabolism, excretion (ADME)

Theobromine and caffeine are readily absorbed from the GI tract and are widely distributed throughout the body. They are metabolized in the liver and undergo enterohepatic recycling and then excreted in the urine as both metabolites and unchanged parent compounds. Methylxanthines also readily pass in the milk of exposed lactating animals. Very little parent compound is passed in the feces. The half-lives of theobromine and caffeine in dogs are 17.5 h and 4.5 h, respectively.

Mechanism of action

Methylxanthines cause a competitive antagonism of cellular adenosine receptors. Inhibition of adenosine receptors causes CNS stimulation, constriction of some blood vessels, diuresis, and tachycardia. Methylxanthines also increase intracellular calcium levels by increasing cellular calcium entry and inhibiting intracellular sequestration of calcium by the sarcoplasmic reticulum of striated muscles. The net effect is increased strength and contractility of skeletal and cardiac muscle. Methylxanthines may also compete for benzodiazepine receptors within the CNS and inhibit phosphodiesterase, resulting in increased cyclic adenosine monophosphate (AMP) levels. They may also increase circulating levels of epinephrine and norepinephrine (www.merckvetmanual.com).

Clinical signs

Clinical signs of toxicosis usually occur within 6–12 h of ingestion, e.g. nausea, vomiting, diarrhoea, dyspnoe, thirst, and increased urination. These can progress to dehydration, restlessness, hyperactivity, cardiac arrhythmias, internal bleeding, heart attacks, tachypnea, ataxia, tremors, seizures, weakness, coma, cyanosis, hypertension, hyperthermia, and eventually death. The high fat content of chocolate products may trigger pancreatitis in susceptible animals. In general, mild signs (vomiting, diarrhoea, polydipsia) may be seen in dogs ingesting 20 mg/kg, cardiotoxic effects may be seen at 40–50 mg/kg, and seizures may occur at doses ≥60 mg/kg (www.merckvetmanual.com). A dog, which ingested a lethal quantity of garden mulch made from cacao bean shells, developed severe convulsions and died 17 h later. Analysis of the stomach content and the ingested cacao bean shells revealed the presence of lethal amounts of theobromine (Drolet et al.,

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Treatment

Once animals have stabilized, or in animals presenting before clinical signs have developed (e.g. within 1 h of ingestion), decontamination should be performed. Induction of emesis using apomorphine (0.08 mg/kg i.m. or s.c.) or hydrogen peroxide should be initiated; in animals that have been sedated due to seizures, gastric lavage may be considered. Activated charcoal (1–4 g/kg, p.o.) should be administered; because of the enterohepatic recirculation of methylxanthines, repeated doses should be administered every 3 h for up to 72 h in symptomatic animals (control vomiting with metoclopramide, 0.2–0.4 mg/kg, s.c. or i.m.). Erythromycin and corticosteroids should be avoided because they interfere with excretion of methylxanthines. For ventricular-origin tachyarrythmias lidocaine is applicated (1–2 mg/kg i.v. until effect, followed by 25–80 mg/kg/min infusion rate to effect to maintain). However, lidocaine cannot be used in cats. If lidocaine fails, metoprolol injection is preferred over propranolol, since metoprolol does not slow renal excretion of methylxanthines as propranolol can. Suggested starting dose for injectable form of either metoprolol or propranolol is 0.02–0.06 mg/kg slow i.v., which can be repeated and increased if needed. The rate of administration should not exceed 1 mg/2 min i.v. For bradycardia (less prevalent) atropine is used at 0.01–0.02 mg/kg i.m. or s.c. Artificial respiration is applicated if needed. To release seizures diazepam (0.5–2.0 mg/kg, slow i.v.) or barbiturates are applicated. Fluid diuresis may assist in stabilizing cardiovascular function and hasten urinary excretion of methylxanthines. Other treatment for symptomatic animals includes thermoregulation, correcting acid/base and electrolyte abnormalities, monitoring cardiac status via electrocardiography, and urinary catheter placement (methylxanthines and their metabolites can be reabsorbed across the bladder wall). Clinical signs may persist up to 72 h in severe cases.

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Grapes, raisins and sultanas

One of the more striking poisonings to have emerged as a potential concern over the last few years has been that of raisin poisoning in dogs. The ingested doses involved in these fatal cases ranged from 10 to 57 g of fruit per kg b. wt. There are now several reports that confirm that ingestion of these fruits can cause renal failure in dogs. Grapes contain an unknown toxin (Gwaltney-Brant et al.,

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Destroy user interface control; Campbell and Bates,

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Destroy user interface control; Mazzaferro et al.,

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Destroy user interface control 2004, Sutton and Campbell,

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Destroy user interface control 2006, Campbell,

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Destroy user interface control 2007).

Mechanism of action

The toxic mechanism remains to be elucidated, and the apparent lack of a reproducible dose response relationship has led some authors to suggest this may reflect either a component of the fruits that is present in varying quantities, or the existence of an extrinsic compound that may not always be present. Individual variations in response may also occur (McKnight,

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Destroy user interface control 2005).

Toxic doses

The general consensus at present is that potentially any dose should be considered a problem. Estimated amounts of grapes associated with renal injury in dogs are about 32 g/kg; amounts of raisins associated with signs range from 11–30 g/kg (www.merckvetmanual.com).

Clinical signs

Clinical effects usually become apparent within 6 h of ingestion, and always within 24 h. Early signs are vomiting (in almost all cases), diarrhoea within 6–12 h of ingestion, anorexia, abdominal pain, weakness, dehydration, tremors and lethargy. Ingesta may be present in the vomitus or faeces. Polydipsia may also be apparent. Oliguric or anuric renal failure develops within 24–72 h of exposure; once anuric renal failure develops, most dogs die or are euthanized. Urinalysis may reveal proteinuria, glucosuria, microscopic haematuria and, rarely, crystalluria. Urine and blood tests will provide definitive evidence for it. Transient elevations in serum glucose, calcium, phosphorus, liver and pancreatic enzymes develop in some dogs (Eubig et al.,

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Destroy user interface control 2005). It is generally agreed that prognosis in dogs with oliguria or anuria is poor.

Necropsy

In some of the cases with fatal outcomes proximal renal tubule necrosis and renal calcification was described (Morrow et al.,

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Destroy user interface control 2005).

Therapy

Ingestion of any quantity of grapes, raisins or sultanas by a dog should be considered treatable. Digestion of the fruits appears to be slow and decontamination several hours post-ingestion may be worthwhile as whole grapes and swollen raisins have been recovered after remaining in the stomach overnight. Gut decontamination should be considered by means of emesis or gastric lavage. Emesis can be induced with 3% hydrogen peroxide (2 ml/kg; no more than 45 ml), followed by activated charcoal. Activated charcoal may be of benefit, but care should be taken to ensure bowel sounds are regular before this is administered. If spontaneous vomiting is protracted it must be consider to use anti-emetics such as metoclopramide (0.5–1 mg p.o., s.c. or i.m. 6–8 h or 1–2 mg/kg per day by slow i.v. injection). Aggressive i.v. fluid therapy for at least 48 h for rehydration and support of renal function is important (Campbell,

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Destroy user interface control 2007). Renal function and electrolytes should be monitored for at least 72 h post-ingestion. Where necessary the use of furosemide (2 mg/kg i.v. initially followed by i.v. infusion of 5 mg/kg/h), dopamine (0.5–3 μg/kg/min, i.v.) or mannitol (0.25–0.5 g/kg i.v. over 5–10 min) may be considered to re-establish urine output in oliguric dogs (McKnight,

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Destroy user interface control 2005). However, the efficacy of these therapies remains unproven and that there is evidence that tubular necrosis or renal tubule obstruction may prevent urine flow. Anuric dogs are unlikely to survive unless peritoneal dialysis or hemodialysis is performed, and even then the prognosis is guarded.

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Onion toxicosis

The onion (Allium cepa) is one of the oldest crops. Its world production has increased by at least 25% over the past 10 years with current production being around 44 million tonnes making it the second most important horticultural crop after tomatoes. Because of its storage characteristics and durability for shipping, onion has always been traded more widely than most vegetables. Onion is versatile and is often used as an ingredient in many dishes and is accepted by almost all traditions and cultures. Onion consumption is increasing significantly and this is partly because of heavy promotion that links flavour and health. Onion is rich in two chemical groups that have perceived benefits to human health – flavonoids and alk(en)yl cysteine sulphoxides. Apart from its culinary uses – fresh, cooked or dehydrated – medicinal properties have been attributed to both since ancient times, prompting in recent years an accurate chemical analysis of the most characteristic active ingredients. Compounds from onion have a range of health benefits which include anticarcinogenic properties, antiplatelet, antithrombotic activity, antiasthmatic, antidiabetic, hypocholesterolaemic, fibrinolytic and various other biological actions, and antibiotic effects (Augusti,

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Destroy user interface control; Briggs et al.,

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Destroy user interface control; Griffiths et al.,

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Destroy user interface control; Slimestad et al.,

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Destroy user interface control). On the other hand, onion contains the toxic components which can damage red blood cells and cause haemolytic anaemia accompanied by the formation of Heinz bodies in erythrocytes of animals (Desnoyers,

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Destroy user interface control 2000), e.g. in cattle (Carbery,

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Destroy user interface control; Rae,

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Destroy user interface control; Van Der Kolk,

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Destroy user interface control), horses (Thorp and Harshfielf,

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Destroy user interface control 1939), dogs (Stallbaumer,

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Destroy user interface control; Harvey and Rackear,

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Destroy user interface control; Solter and Scott,

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Destroy user interface control 1987; Yamatoet al.,

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Destroy user interface control) and cats (Kobayashi,

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Destroy user interface control 1981).

Heinz body anaemia is an uncommon finding in dogs, and few other toxicants, e.g. methylene blue, acetaminophene, zinc, benzocaine, vitamin K, phenylhydrazine (Houston and Myers,

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Destroy user interface control) can induce it, so onion ingestion must always be suspected in such situations.

Mechanism of action

Various factors are implicated in the wide variation in species susceptibility, including differences in hemoglobin structure and protective enzyme systems. The mechanism of onion toxicity has been known for several decades, but recent studies have shown that more than one toxin is involved. The toxic components in all type of onions, garlic, leeks, shallots, and other plants of the Allium family, are sulfoxides and aliphatic sulfides, specifically allyl and propyl di-, tri-, and tetrasulfides. Onions contain also the relatively rare amino acids S-meth and S-prop (en)ylcysteine sufoxides (SMCO). It is widely agreed that n-propyl disulphide is the principal toxin that reduces the activity of glucose-6-phosphate dehydrogenase in red blood cells; thereby interfering with regeneration of reduced glutathione needed to prevent oxidative denaturation of haemoglobin (Thrall,

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Destroy user interface control 2004). Denaturated haemoglobin, when developed, precipitates on the surface of red blood cells (named Heinz bodies) and triggers intra- and extravascular haemolysis (Lincoln et al.,

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Destroy user interface control; Tang et al.,

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Destroy user interface control). The haemolytic effect of sodium n-propylthiosulphate, which had been isolated from boiled onions, was studied in dogs by Yamato et al. (

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Destroy user interface control). The oral administration of 500 mumol/kg b. wt. of the compound to dogs resulted in a haemolytic anaemia associated with an increase of Heinz body formation in erythrocytes, which was more severe in dogs with the hereditary condition which results in erythrocytes with high concentrations of reduced glutathione and potassium than in normal dogs. In the affected dogs there was a 10-fold increase in the concentration of oxidised glutathione in their erythrocytes 12 h after the administration of the compound, whereas in normal dogs there was almost no change.

Toxicity

Consumption of as little as 5 g/kg of onions in cats or 15 to 30 g/kg in dogs has resulted in clinically important hematologic changes (Cope,

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Destroy user interface control 2005). Onion toxicosis is consistently noted in animals that ingest more than 0.5% of their b. wt. in onions at one time. A relatively high dosage (600–800 g) in one meal or spread apart over a few days can damage red blood cells and cause haemolytic anaemia accompanied by the formation of Heinz bodies in erythrocytes.

All forms of onion can be a problem including: dehydrated, raw or cooked onions, table scraps containing cooked onions or garlic, left over pizzas, chinese dishes, any feeding stuff containing onions.

Humans are the most resistant species studied. On the other hand, there is some concern about the susceptibility of certain ethnic groups that have a genetic deficiency of glucose-6-phosphate dehydrogenase.

Although the dog appears to be one of the most susceptible species, there are very few reports in the scientific literature concerning accidental canine poisoning associated with onion ingestion. Cats are more susceptible than dogs. Since baby food is often used in sick cats that are not eating (to stimulate their appetite), there was concern that the onion powder would cause a Heinz body anemia in these cats (Robertson et al.,

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Destroy user interface control). Many baby food manufacturers add onions or onion powder to increase palatability. It is generally accepted that sheep, goats, rats and mice are more resistant to onion toxicosis than other domestic animals (Thrall,

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Destroy user interface control 2004; Aslani et al.,

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Destroy user interface control 2005). The safety of feeding culled onions to livestock depends upon species susceptibility and the toxic potential of the onions. Sheep can be maintained on diets of up to 50% onions with no clinical abnormalities or detrimental effects on growth. Even when onions are fed free choice, sheep have only transient hemoglobinuria and anemia, with few deaths even reported. In contrast, cattle should be fed onions with caution, due to the relative susceptibilty of their erythrocytes to oxidative damage. Daily feeding of onions could have a cumulative effect due to ongoing formation of Heinz bodies versus a single exposure with a wide gap until the next exposure, allowing the bone marrow time to regenerate the prematurely destroyed red cells.

Clinical signs

The first symptoms are usually of gastro-enteritis: vomiting, diarrhoea, abdominal pain, loss of appetite, depression and dehydration. It will take a few days for the dog to display the symptoms associated with the loss of red blood cells: pale mucous membranes, rapid respiratory rate, difficulty to breath, lethargy, dark coloured urine – reddish or brown, jaundice, weakness, rapid heart rate. Haematology may reveal neutrophilia, lymphopenia, Heinz-body anaemia and methaemoglobinaemia.

Therapy

There is not any antidote, however, supportive care may be helpful: hospitalisation, administration of intra-venous fluids, blood transfusions. Treatment is advocated of ingestion of any quantity. For recent ingestions gastric decontamination should be considered, and use of adsorbents, but thereafter management is largely supportive. It is important that the animals remain hydrated; antiemetics may be given to control persistent vomiting. Nonenzymatic reductants such as ascorbic acid may also be useful (in dog 30 mg/kg b. wt. i.v. each 6–8 h). Antioxidant prevention (by N-acetylcysteine, vitamin E, ascorbate) of Heinz body formation and oxidative injury in cats was recommended by Hill et al. (

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Destroy user interface control). In severely poisoned animals blood transfusions have been successfully employed.

Nevertheless, even taking into account that lethal effects are infrequent in dogs, avoiding exposure to any kind of A. cepa in this and other domestic animal species seems to be the best preventive health strategy.

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Garlic

Garlic (Allium sativum) is considered to be less toxic and safe for dogs than onion when used in moderation. Allicin and ajoene, pharmacologically active agents in garlic, are potent cardiac and smooth muscle relaxants, vasodilators, and hypotensive agents (Malik and Siddiqui,

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Destroy user interface control; Martin et al.,

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Destroy user interface control). Lee et al. (

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Destroy user interface control) studied wether dogs given garlic extract developed hemolytic anemia. Garlic extract was administered intragastrically (1.25 ml/kg of b.wt. (5 g of whole garlic/kg) once a day for 7 days). Compared with initial values, erythrocyte count, haematocrit and hemoglobin concentration decreased to a minimum value on days 9 to 11. Heinz body formation, an increase in erythrocyte-reduced glutathione concentration, and eccentrocytes were also detected, however, no dog developed hemolytic anemia. Eccentrocytosis appears to be a major diagnostic feature of garlic-induced hemolysis in dogs (Lee et al.,

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Garlic is toxic also for horses, at a daily dose of >0.2 g/kg causes Heinz body anemia in them (Pearsonet al.,

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Destroy user interface control).

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Avocado

Avocado fruit, pits, leaves and the actual plant are all potentially poisonous to dogs, along with other pets like cats, mice, rats, birds, rabbits, horses, cattle and goats, among others.

Persin is a fungicidal toxin found in both the fruit and leaves of the avocado tree (Persea americana). It has been isolated only recently and discovered to kill breast cancer cells. It has also been shown to enhance the effect of the breast cancer fighting drug Tamoxifen. This could potentially reduce the necessary dosage of current cancer drugs. Persin is however highly insoluble, and more research will be needed to put it into a soluble tablet form.

Feeding avocados to any non-human animal should be completely avoided. The lethal dose is not known; the effect is different depending upon the animal species. Avocados will trigger fluid accumulation in the lungs and chest, leading to difficulty breathing and death due to oxygen deprivation. Fluid accumulation can also occur in the heart, pancreas and abdomen (Buoro et al.,

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Destroy user interface control). High fat content of avocado can lead to pancreatitis.

Clinical signs

The symptoms include gastrointestinal irritation, vomiting, diarrhoea, respiratory distress, congestion, fluid accumulation around the tissues of the heart and even death. Birds seem to be particularly sensitive to this toxic compound and the symptoms are the increased heart rate, myocardial tissue damage, labored breathing, disordered plumage, unrest, weakness, and apathy. High doses cause acute respiratory syndrome (asphyxia), with death approximately 12 to 24 h after consumption. In lactating rabbits and mice non-infectious mastitis and agalactia after consumption of leaves or bark was observed. In rabbits cardial arrhythmia, submandibular edema and death after consumption of leaves occur. In cows, horses and goats mastitis after consumption of leaves or bark was observed.

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Macadamia nuts

Macadamia nuts originate from the trees Macadamia integrifolia in the continental USA andMacadamia tetraphylla in Hawaii and Australia. They are commonly present in cookies, so owners should be careful what they feed their dog. Macadamia nuts (both raw and roasted) as well as macadamia butter contain an unknown toxin that affects the muscles, digestive system and nervous system and can cause locomotory difficulties, weakness, dyspnoe, tremors and swollen limbs. Macadamia nuts and walnuts can also trigger pancreatitis and peanuts a deadly allergic reaction (Knottet al.,

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The mechanism of action

The mechanism of toxicity is unknown; but may involve a constituent of the nuts, processing contaminants or mycotoxins.

Toxicity

The toxic dose to dogs ranges from 2.4–62.4 g per kg b.wt. This is a very large range and can mean that some dogs will get ill with just a small amount of nuts ingested, while other dogs need to eat a lot of nuts to show signs (Hansen et al.,

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Destroy user interface control).

Clinical signs

Dogs are the only species in which signs have been reported (www.merckvetmanual.com). Within 12 h of ingestion, dogs develop weakness (more pronounced in hind limbs), depression, vomiting, abdominal pain, ataxia, muscle tremors, swollen and painful limbs, paralysis of the hindquarters, hyperthermia (with rectal temperatures up to 40.5 °C), an elevated heart rate, lameness, stiffness and recumbency. Tremors may be secondary to muscle weakness. Macadamia nuts may be identified in vomitus or feces. Mild transient elevations in serum triglycerides, lipases, and alkaline phosphatase were reported in some dogs experimentally dosed with macadamia nuts; these values quickly returned to baseline by 48 h after experimental dosing (Hansen et al.,

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Destroy user interface control). Signs generally resolve within 12–48 h (Hansen et al.,

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Destroy user interface control; Hansen,

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Destroy user interface control 2002). The onset of clinical signs was reported as <12 h in 79% of the cases. The duration of clinical signs for the majority of cases was <24 h. The amount of macadamia nuts ingested was estimated in 72% of the calls with a mean of 11.7 g/kg bw. All field and experimental dogs recovered uneventfully within 1 to 2 d whether treated by a veterinarian or not. No mortality has been reported.

Therapy

For asymptomatic dogs with recent ingestion of more than 1–2 g/kg, emesis should be induced; activated charcoal may be of benefit with large ingestions. Fortunately, most symptomatic dogs will recover without any specific treatment. Severely affected animals may be given supportive treatment such as fluids, analgesics or antipyretics (www.merckvetmanual.com). Use of mild laxatives may assist the passage of ingesta through the gastrointestinal tract. Luckily, the muscle weakness, while painful, seems to be of short duration and the patients do recover from the toxicity.

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Effects of xylitol ingestion

Xylitol, an artificial sweetener, is present in many products, such as candy, sugar-free chewing gums, toothpaste and baked goods. Ingestion of these foods by dogs results in a significant, and often sustained, insulin-mediated hypoglycemic crisis (Cope,

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Destroy user interface control). In both humans and dogs, the levels of blood sugar are controlled by the body's release of insulin from the pancreas. In human xylitol ingestion does not cause any significant changes in insulin levels or, therefore, blood glucose (Dunayer,

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Destroy user interface control). However, in dogs, xylitol is a strong promoter of insulin release, which results in a rapid decrease in blood glucose (hypoglycemia) (Asano et al.,

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Destroy user interface control; Dunayer,

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Destroy user interface control; Campbell and Bates,

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Destroy user interface control). A sudden drop in blood sugar then results in depression, ataxia, seizures and collapse (Thomas and Boag,

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Destroy user interface control). This compound can cause liver damage and death. This information was first published in July 2004.

Clinical signs

Clinical signs of xylitol toxicity can develop in as few as 30 min after ingestion and may include one or more of the following: vomiting, weakness, ataxia, depression, hypokalemia, seizures, coma, liver dysfunction and/or failure. Dunayer and Gwaltney-Brant (

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Destroy user interface control) observed in dogs lethargy and vomiting after ingestion of xylitol. In addition some dogs had widespread petechial, ecchymotic, or gastrointestinal tract hemorrhages, moderately to severely high serum activities of liver enzymes, hyperbilirubinemia, hypoglycemia, hyperphosphatemia, prolonged clotting times, and thrombocytopenia. Necropsy revealed severe hepatic necrosis, hepatocyte loss or atrophy with lobular collapse.

Treatment

The induction of vomiting is recommended if performed very soon after ingestion of the xylitol-containing product but before clinical signs develop. Frequent small meals or an oral sugar supplement may be used to manage dogs that have not yet shown clinical signs. Following the appearance of clinical signs intravenous dextrose can be used to control hypoglycemia. It may also be necessary to treat the patient for hypokalemia, if indicated. Treatment should be continued until the blood glucose levels return to normal levels.

Dunayer and Gwaltney-Brant (

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Destroy user interface control) recommended for treatment i.v. administration of fluids; plasma transfusions; and, if indicated, administration of dextrose. Cope (

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Destroy user interface control) revealed that binding of xylitol to activated charcoal is relatively low; however, activated charcoal administration may still be beneficial in some canine acute oral xylitol exposures.

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Alcohol toxicoses

Serious intoxications have occurred when dogs have been given alcohol to drink as a „joke“. Also, dogs seem to be attracted to alcoholic drinks, so drinks should not be left unattended. Dogs cannot tolerate alcohol, even in small amounts.

Ethanol is the alcohol in alcoholic beverages, perfumes and mouthwashes. Ethanol toxicosis in dogs occurred after ingestion of rotten apples (Kammerer et al.,

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Destroy user interface control), alcoholic beverages (van Wuijckhuise and Cremers,

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Destroy user interface control) or uncooked bread dough that contains Saccharomyces cerevisiae (brewer's and baker's yeast), which metabolizes carbohydrate substates to ethanol and carbon dioxide (Thrall et al.,

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Destroy user interface control; Suter,

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Destroy user interface control; Means,

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Destroy user interface control 2003). Ethanol toxicosis can also occur in dogs and cats after overdosage when ethanol is given intravenously as a compatitive substrate to treat ethylene glycol toxicosis (Thrallet al.,

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Destroy user interface control 1998).

Mechanism of action

The mechanism of action on the CNS is related in part to its interactions with biomembranes and its probable inhibition of gamma-amino butyric acid (GABA) receptors (Valentine,

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Destroy user interface control).

Clinical signs

Clinical signs include ataxia, lethargy, sedation, hypothermia, metabolic acidosis, vomiting, diarrhoea, poor breathing, liver failure, coma, and death. And the hops in beer are also potentially toxic to dogs and cause dyspnoe, increased heart rate, elevated temperature, seizures and death.

Therapy

Severe ethanol intoxication requires mechanical ventilation. Electrolyte and acid-base status should be also corrected (Richardson,

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Destroy user interface control 2006).

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Conclusion

There are also other human foods that may cause intoxications in pets, e.g. tomato, pottato, rhubarb, persimons, etc. The best advice must surely be to give animals foodstuffs and or treats specifically developed for their diets.

Anterior Cruciate Ligament Rupture

2012-11-24T08:00:00.000-08:00

Veterinary Partner.com is an excellent rescourse for veterinary information. It is free and written by well recognised authors. This is an article which I am posting here with thanks and acknowledgement to the authors of this article. This article discusses the causes, diagnosis and surgical options for treatment.The procedure that we typically perform in our hospital with a great deal of success is the extracapsular technique using a nylon or mersilene (soft flexible synthetic material) band.

Ruptured Anterior (Cranial) Cruciate Ligament

First, the Basics

The knee is a fairly complicated joint. It consists of the femur above, the tibia below, the kneecap (patella) in front, and the bean-like fabellae behind. Chunks of cartilage called the medial and lateral menisci fit between the femur and tibia like cushions. An assortment of ligaments holds everything together, allowing the knee to bend the way it should and keep it from bending the way it shouldn’t.

There are two cruciate ligaments that cross inside the knee joint: the anterior (or, more correctly in animals, cranial) cruciate and the posterior (in animals called the caudal) cruciate. They are named for the side of the knee (front or back) where their lower attachment is found. The anterior cruciate ligament prevents the tibia from slipping forward out from under the femur.

Finding the Rupture

The ruptured cruciate ligament is the most common knee injury of dogs; in fact, chances are that any dog with sudden rear leg lameness has a ruptured anterior cruciate ligament rather than something else. The history usually involves a rear leg suddenly so sore that the dog can hardly bear weight on it. If left alone, it will appear to improve over the course of a week or two but the knee will be notably swollen and arthritis will set in quickly. Dogs are often seen by the veterinarian in either the acute stage shortly after the injury or in the chronic stage weeks or months later.

The key to the diagnosis of the ruptured cruciate ligament is the demonstration of an abnormal knee motion called a drawer sign. It is not possible for a normal knee to show this sign.

The Drawer Sign

The veterinarian stabilizes the position of the femur with one hand and manipulates the tibia with the other hand. If the tibia moves forward (like a drawer being opened), the cruciate ligament is ruptured.

Another method is the tibial compression test where the veterinarian stabilizes the femur with one hand and flexes the ankle with the other hand. If the ligament is ruptured, again the tibia moves abnormally forward.

If the rupture occurred some time ago, there will be swelling on side of the knee joint that faces the other leg. This is called a medial buttress and is a sign that arthritis is well along.

It is not unusual for animals to be tense or frightened at the vet’s office. Tense muscles can temporarily stabilize the knee, preventing demonstration of the drawer sign during examination. Often sedation is needed to get a good evaluation of the knee. This is especially true with larger dogs. Eliciting a drawer sign can be difficult if the ligament is only partially ruptured so a second opinion may be a good idea if the initial examination is inconclusive.

Since arthritis can set in relatively quickly after a cruciate ligament rupture, radiographs to assess arthritis are helpful. Another reason for radiographs is that occasionally when the cruciate ligament tears, a piece of bone where the ligament attaches to the tibia breaks off as well. This will require surgical repair and the surgeon will need to know about it before beginning surgery. Arthritis present prior to surgery limits the extent of the recovery after surgery though surgery is still needed to slow or even curtail further arthritis development.

How Rupture Happens

Several clinical pictures are seen with ruptured cruciate ligaments. One is a young athletic dog playing roughly who takes a bad step and injures the knee. This is usually a sudden lameness in a young large-breed dog.

A recent study identified the following breeds as being particularly at risk for this phenomenon: Neapolitan mastiff, Newfoundland, Akita, St. Bernard, Rottweiler, Chesapeake Bay retriever, and American Staffordshire terrier.

On the other hand, an older large dog, especially if overweight, can have weakened ligaments and slowly stretch or partially tear them. The partial rupture may be detected or the problem may not become apparent until the ligament breaks completely. In this type of patient, stepping down off the bed or a small jump can be all it takes to break the ligament. The lameness may be acute but have features of more chronic joint disease or the lameness may simply be a more gradual/chronic problem.

Larger overweight dogs that rupture one cruciate ligament frequently rupture the other one within a year's time. An owner should be prepared for another surgery in this time frame.

What Happens if the Cruciate Rupture is Not Surgically Repaired

(almost) normal

damaged

Without an intact cruciate ligament, the knee is unstable. Wear between the bones and meniscal cartilage becomes abnormal and the joint begins to develop degenerative changes. Bone spurs called osteophytes develop resulting in chronic pain and loss of joint motion. This process can be arrested or slowed by surgery but cannot be reversed.

Osteophytes are evident as soon as 1 to 3 weeks after the rupture in some patients. This kind of joint disease is substantially more difficult for a large breed dog to bear, though all dogs will ultimately show degenerative changes. Typically, after several weeks from the time of the acute injury, the dog may appear to get better but is not likely to become permanently normal.
In one study, a group of dogs was studied for 6 months after cruciate rupture. At the end of 6 months, 85% of dogs less than 30 pounds of body weight had regained near normal or improved function while only 19% of dogs over 30 pounds had regained near normal function. Both groups of dogs required at least 4 months to show maximum improvement.

What Happens in Surgical Repair?

There are three different surgical repair techniques commonly used, and a fourth method that has fallen out of favor in recent years.

Extracapsular Repair

Lateral orthopedic wire is shown taking the place of the anterior cruciate ligament. Usually thick suture is used rather than wire but for illustrative purposes the wire shows where the suture would be placed around the knee.

This surgery is currently favored as it can be performed in a relatively shorter time than the other procedures and does not require specialized equipment. The knee joint is opened and inspected. The torn or partly torn cruciate ligament is removed. Any bone spurs of significant size are bitten away with an instrument called a rongeur. If the meniscus is torn, the damaged portion is removed. A large, strong suture is passed around the fabella behind the knee and through a hole drilled in the front of the tibia. This tightens the joint to prevent the drawer motion, effectively taking over the job of the cruciate ligament.

Typically, the dog may carry the leg up for a good 2 weeks after surgery but will increase knee use over the next 2 months, eventually returning to normal.
Typically, the dog will require 8 weeks of exercise restriction after surgery (no running, only outside on a leash, including the backyard).
The suture placed will break 2 to 12 months after surgery and the dog's own healed tissue will hold the knee.

Tibial Plateau Leveling Osteotomy (TPLO)

This procedure uses a fresh approach to the biomechanics of the knee joint and is meant to address the lack of success seen with the above technique long term in larger dogs. Unfortunately, the technique has not yielded clearly superior results and controversy continues. With this surgery, the tibia is cut and rotated in such a way that the natural weight-bearing of the dog actually stabilizes the knee joint. As before, the knee joint still must be opened and damaged meniscus removed. The cruciate ligament remnants may or may not be removed depending on the degree of damage.

This surgery is complex and involves specific training in this technique. Many radiographs are necessary to calculate the angle of the osteotomy (the cut in the tibia). This procedure typically costs substantially more than the extracapsular repair as it is more invasive to the joint.

Typically, most dogs are touching their toes to the ground by 10 days after surgery, although it can take up to 3 weeks.
As with other techniques, 8 to 12 weeks of exercise restriction are needed.
Full function is generally achieved 3 to 4 months after surgery and the dog may return to normal activity.

Tibial Tuberosity Advancement (TTA)

The TTA represents another take on how to use the biomechanics of the knee to create stabilization. The theory behind this procedure is that when the cruciate ligament is torn, the tibial plateau (the top of the tibia) and the patellar ligament should be repositioned at 90 degrees to one another to combat the shear force generated as the dog walks. To make this happen, the tibial tuberosity (front of the tibia where the patellar ligament attaches) is separated and anchored in its new position by a titanium or steel cage, “fork,” and plate. Bone grafts are used to assist healing. This procedure was developed in 2002 at the University of Zurich and since then over 20,000 patients worldwide have had this surgery. Some experts prefer it to the TPLO while others prefer the TPLO. Both procedures require specific equipment and expertise and, again, no procedure has demonstrated clear superiority; controversy continues.

Typically the leg is bandaged for a week after surgery.
The patient's activity must be restricted and confinement is a must with gradually increased activity over 3 to 4 months. Most dogs can return to normal activity by 4 months after surgery.

Intracapsular Repair (sometimes still called over the top method)We mention this procedure for its historical significance although it is not one of the "big three." This procedure has fallen out of favor lately as it has been unable to demonstrate results superior to those of the extracapsular technique described above, though apparently it is still a popular repair method in the U.K.

Intracapsular repair intuitively seems like it should do better as it uses living tissue (rather than an artificial material) to essentially make a new ligament. This takes more time surgically. As with the extracapsular repair, the knee joint is opened, fragments of the ligament are removed, as is damaged meniscus. After this a strip of connective tissue is dissected locally and passed through the middle of the joint exactly where the cruciate ligament used to be. The new ligament is attached at the opposite end to an implant or simply sewn into place.

Bandaging for a couple of weeks after surgery is commonly recommended.
Again, the dog may not bear weight for a good 2 weeks after surgery and will likely require 2 months to return to normal function.
Again, 8 to 12 weeks of exercise restriction will be necessary for healing.

General Rehabilitation after Surgery

Rehabilitation following the extracapsular repair method can begin as soon as the pet goes home. The area can be chilled with a padded ice pack for 10 minutes a couple times daily. (Do not try to make up for a skipped treatment by icing the area longer; prolonged cold exposure can cause injury.) Passive range of motion exercise where the knee is gently flexed and extended can also help. It is important not to induce pain when moving the limb. Let the patient guide you. Avoid twisting the leg. After the stitches or staples are out (or after the skin has healed in about 10 to 14 days), water treadmill exercise can be used if a facility is available. This requires strict observation and, if possible, the patient should wear a life jacket. Rehabilitation for patients with intracapsular repair is similar but slower in progression.

Rehabilitation after TPLO or TTA is gentler. Icing as above and rest are the main modes of therapy. After 3 to 4 weeks, an increase in light activity can be introduced. A water treadmill is helpful. No jumping, running or stair-climbing is allowed at first. Expect the osteotomy site to require a good 6 weeks to heal.

What if the Rupture Isn't Discovered for Years and Joint Disease is Already Advanced?

A dog with arthritis pain from an old cruciate rupture may still benefit from a TPLO surgery and possibly from the TTA. Ask your veterinarian if it may be worth having a surgery specialist take a look at the knee. Most cases must make do with medical management. Visit our section on arthritis treatment.

Meniscal Injury

We mentioned the menisci as part of the knee joint. The bones of all joints are capped with cartilage so as provide a slippery surface where the bones contact each other (if the bones contact each other without cartilage, they grind each other down). In addition to these cartilage caps, the stifle joint has two “blocks” of cartilage in-between the bones. These blocks are called the menisci and serve to distribute approximately 65% of the compressive load delivered to the knee. The only other joint with a meniscus is the jaw (tempero-mandibular joint).

When the crucial ligament ruptures, the medial (on the inner side of the knee) meniscus frequently tears and must either be removed, partly removed, or ideally repaired. This is generally done at the time of cruciate ligament surgery and we would be remiss not to mention it.

Pets with meniscal damage may have an audible clicking sound when they walk or when the knee is examined, but for a definitive diagnosis the menisci must actually be inspected during surgery. It is difficult to access the menisci and thus repairing a tear in the meniscus is problematic; furthermore, poor blood supply to the menisci also makes good healing less likely. For these reasons, removal of the damaged portion of the meniscus is the most common surgical choice. This leaves some meniscus behind to distribute the compression load on the knee but removes the painful, ineffective portion.

Areas of current research include techniques to improve blood supply to the healing meniscus so that repair can be more feasible. If meniscal damage has occurred in a cruciate rupture, arthritis is inevitable and surgery should be considered a palliative procedure.

Another Link for more Information

Watch the Vetstoria video explaining diagnosis of ruptured cruciate ligament.

http://www.veterinarypartner.com/Content.plx?P=A&S=0&C=0&A=1975

Alberta Spay Neuter Task Force

2012-11-10T07:13:00.000-08:00

The Alberta Spay Neuter Task Force (ASNTF) Team spayed, neutered, vaccinated, tattooed, and treated for parasites 187 dogs and cats. Our appreciation to the compassionate and caring medical team of 18 Veterinarians, 12 Animal Health Technicians and 4 veterinary students who provided great care for the animals that came to the clinic.

Thank-you so much to all of the awesome volunteers who assisted with our spay and neuter clinic for the Piikani First Nation, in Brocket, Alberta in October 2012!

Dr. Mark Rubensohn and Bridlewood Veterinary Clinic were pleased to once again be involved in this excellent program with the ASNTF.

For more information on this group and about there wonderful work visit the Alberta Spay Neuter Task Force Facebook page.

Caution – Jerky Treats from China

2012-11-03T08:00:00.000-07:00

Caution – Jerky Treats from China

In the light of increasing cases and information of illness in dogs that have been exposed to “Jerky Treats” manufactured in China, we would like to make sure that our clients are aware of this potential problem. We advise the use of pet foods and treats that are manufactured locally by recognized and trusted companies.

Signs to look out for that may be associated with jerky pet treats include decreased appetite and activity, vomiting, diarrhea and increased drinking and urinating. Laboratory findings may include signs of kidney problems including glucose and/or protein in the urine. Some of the reported cases may be the result of causes other than the consumption of jerky treats. This concern has not been definitively isolated to jerky treats so caution is indicated with all pet food products that originate from China. Currently the US FDA and numerous veterinary authorities are investigating this problem. Should you have a concern that your pet has become ill after exposure to imported treats, please notify your veterinarian immediately.

More information can be found at the following sites:

http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm295445.htm

http://www.fda.gov/AnimalVeterinary/SafetyHealth/ProductSafetyInformation/ucm319463.htm

2012-08-26T11:36:00.000-07:00

Beyond the reflection: the dangers of windows

by birdscalgary

Posted by Matthew Sim

As the fall migration starts to heat up and southbound warblers, vireos, flycatchers, sparrows and more pass through Calgary, birding can become quite exciting. While for us, this is a great time to be out and about, for the birds, it is dangerous; very dangerous. Migrating passerines (perching birds), for example, have to travel long distances all while on the lookout for predators such as hawks and cats, try to get food themselves and hope they don't get caught in an early cold-snap which could potentially kill them. And this is just the beginning, there are even more dangers; one of them which is the most lethal of them all.

According to Sibley Guides Bird Mortalities, window strikes (when a bird hits a window) kill between 97 and 976 million birds each year, more than any other cause of birddeaths. (http://www.sibleyguides.com/conservation/causes-of-bird-mortality/). I was in my neighbor's yard when I noticed one of these fatalities on his patio. While I had been there, a migrating Ovenbird had struck his window and had died. Though birds can crash into windows at any time of the year, window strikes tend to happen more frequently during migration as an influx of migrants come through unfamiliar territory, passing from tree to tree. As you can see in the photo below, it is quite easy for a birdto see its habitat reflected in a window and believe that it is simply another tree they are heading to; I'm sure most don't know what hit them.

If I were a bird, I would probably fly towards these trees too.

Many bird populations are declining already due to a number of reasons and we don't need to help them along with reflective windows when we could easily prevent window strikes occurring.

This Ovenbird had struck my neighbor's window while I was in his yard.

A closer look at the detail on the Ovenbird's feathers

Probably the worst part of all this is that window strikes are senseless; it's not like natural selection where it was meant to happen, window strikes are part of our devastating side effects on nature; however, they can also be easily prevented.

There are many ways to prevent birds from striking windows. If you are having birds fly from your feeders or bird baths into windows, you can either move these bird attracting features further away (25-30 feet) from the window or closer (1-3 feet) to the window so that if the birds do hit the window at just 1-3 feet they will not be going fast enough to do any harm to themselves.

Apparently, there is also a material called CollidEscape which can reduce reflectivity and transparency on the outside but still leave the windows transparent from the inside. You can check it out here.

Here are a few more options:

plant shade trees outside windows to break down reflections
install snap-on window dividers
put a hanging plant outside of the window

These are just a few of the ways you can avoid window strikes and help reduce the number of avian mortalities each year. Often, preventing window strikes can be as simple as closing the curtains or blinds when not using the windows. You can see even more solutions here.

If you have birds hitting your windows, there are many ways to stop it; help out bird populations!

I would like to thank Birds Calgary and Matt Sim for this insightful article which I have re-posted here in full.

Screw Tail of Bulldog

2012-04-30T21:53:00.002-07:00

We performed a very successful tail amputation on a bulldog with an Inverted Screw Tail this week. “Chase” has had his pinched in little tail since birth, but it has only started to present a problem for him in the past 6months or so. His tail was to tightly curled down that it could not be elevated at all and he has developed a severe case of under tail infection causing a great deal of discomfort. The area could not be accessed to bathe or clean in any way and no salves could be adequately applied. In an attempt to relieve his discomfort it was decided to anesthetize him and investigate further with a view to amputation of his tail tip. Even under general anesthetic the downward deviation of his tail was so severe that cleaning was impossible.

Surgery was performed and despite a great deal of anatomical challenge, the misshapen tail tip was amputated back to a point that would prevent further complications. Then the redundant folds of tail skin were resected to prevent any folds or wrinkles to interfere with normal stool passage, and to give a cosmetic ally balanced appearance. “Chase” has recovered well after his surgery, and we expect him to be completely resolved of rear end issues.

2011-12-19T21:17:00.000-08:00

To all of our Loyal Clients, Lovely Patients
and Regular Followers,

We wish you all Happy Holidays, Merry Christmas
and A Joyous New Year

The year is once again drawing to a close and the festive season is upon us. Again, in lieu of Christmas cards, we will be donating to our favorite animal and wildlife charities, listed below, with a view to helping these organizations continue with their fabulous work:

The Companion Animal Fund of the University of Calgary

The Companion Animal Fund of the University of Saskatchewan

Calgary Humane Society

Animal Cancer Therapy Subsidization Society (ACTSS)

Canadian Wildlife Federation

Canadian Parks and Wilderness Society (CPAWS)

During this holiday season while celebrating with our family, friends and pets, we would like to thank all of our wonderful clients and patients for all your support throughout the past year. Some of our most rewarding moments continue to come from the help we've been able to provide both to our patients and clients.

Throughout the year we've assisted in training a number of foreign graduate veterinarians, animal health technologists and veterinary receptionists. We’ve also been able to provide volunteer opportunities to high school students and have given presentations to children at local schools.

We have set up a veterinary blog at http://bridlewoodvc.blogspot.com/ and a presence on Facebook. We would be happy if you would visit us online, scan through some of our articles, and “Like” us on Facebook.

The doctors and staff of Bridlewood Veterinary Clinic would like to take this opportunity to wish all of our clients the very best of compliments of the season and a happy, healthy and wonderful New Year.

Clostridial Diarrhea and Colitis in Dogs

2011-12-11T22:13:00.000-08:00

Clostridium perfringens is a common cause of diarrhea in our canine patients. Clostridium is a soil dwelling bacterium which can be cultured from the feces of many normal dogs. Under certain circumstances it overgrows the normal colonic bacteria and forms spores which produce an endo-toxin. The toxin causes an inflammation of the colon resulting in diarrhea. This begins as a watery and mucus covered diarrhea progressing to include some blood and can become very serious. Some dogs will experience intermittent and recurrent bouts of diarrhea while being completely fine in between. On presentation to the clinic these dogs are often happy and healthy, excepting for the history of chronic watery persistent diarrhea and straining. Any age or breed of dog can be affected.

Diagnosis always begins with a clinical examination of the dog and rule out other causes of diarrhea. Fecal testing is performed to eliminate other causes of infectious and parasitic infestations. Microscopic examination will readily demonstrate a huge overgrowth of sporulating clostridial bacteria. Fecal samples can be submitted to a veterinary laboratory for PCR testing which can specifically identify the Clostridium perfringens toxin.

Treatment entails the use of an antibiotic. Generally we begin with metronidazole or amoxicillin. These antibiotics are typically used for a period of 7 to 10 days if it is a first occurrence. For recurrent cases we significantly extend the time for which we use the antibiotics.

Probiotics are used in an attempt to improve the intestinal and colonic flora. We now have specific dog products available to us and these have proved helpful. Dietary management is very useful adjuvant and we may recommend a specific gastrointestinal diet. Fortunately many commercial veterinary prescription diets are available to us. Occasionally we might also recommend the use of specific home prepared diets.

The majority of clostridial colitis patients responded quickly to the use of antibiotics and recurrences are infrequent. However, a number of dogs seem to be particularly susceptible to recurrence once the antibiotics are ceased. Typically the cause is an underlying immune incompetence or bowel sensitivity on the part of the dog, and ongoing medication is required. Fortunately even for patients requiring ongoing medication, we find the antibiotics are well tolerated and a return to full health occurs shortly after a return to antibiotic treatment.

Seeing Eye Dog

2011-11-23T19:26:00.000-08:00

This was forwarded to me and I like it so much that I have posted it here - Dr Mark Rubensohn.

A thousand words couldn't begin to tell the story in these pictures.

Lily is a Great Dane that has been

blind since a bizarre medical condition required that she have both eyes

removed. For the last 5 years, Madison, another Great Dane, has been

her sight. The two are, of course,

inseparable.

"People will forget what you said; People will forget what you did.
But people will never forget how you made them feel."

Dog Attacks

2011-08-05T10:46:00.000-07:00

The recent, very unfortunate event in Didsbury, Alberta, where two Akitas attacked and seriously injured two young people who were know to them as well as their dog, highlights the problem of dog attacks and what brings it about, once more.
There is no doubt that there are a number of facts leading to this particular attack:
1. The fact that there were new born (4 days old) puppies and that therefore the mother dog would have been increasingly protective
2. That the owner, who would have had the most control over the Akitas, was away. Also she would instill a sense of trust and calm into her dogs, which was not there due to her absence.
3. The couples beagle dog coming into the environment of the bitch with the new born puppies would almost surely have aggravated the protective instincts of the mother Akita
4. Dog aggression will be compounded by the flight and panic of the object of their attack. If the beagle and its owners were yelling in flight, then the aggression would have be aggravated.

What has made this incident even more sinister is that the couple and there beagle were well known to the Akita’s and that despite their attempts to escape they were persued by the Akitas until they could fight their way out of the garage.

The reality remains however, that despite the fact that we are talking about peoples pets, our “best friends”, and constant companions, animals that they love dearly, pets that are regarded as part of the family, that we experience aggression, biting, nipping and dominant behavior continuously from our dogs. As a veterinarian it is of great concern to me that so many of our dogs can not be controlled by their owners. That so many dogs are out of control and undisciplined, regardless of their size or breed. One need only tune into an episode of “Caesar Milan’s Dog Whisperer” on TV to see how dogs are ruling the behavior of their people, rather than the other way around.

The statistics of dog attacks show without exception that dogs that have been trained and are obedient have a statistically hugely lower incidence of attacks on people. This includes all breeds both large and small. In the UK Labradors have been one of the top listed breeds of dogs involved in attacks. Here in the US and Canada, German Shepherds were for a long time on top of the list but have now been replaced by the power breeds of Pit Bulls, Cane Corso’s and here we have a case of Akitas. The big difference with the power breeds of course is that they do more harm than the smaller breeds.

As a society we can do well to remember that the happiest dogs are those to which we assign jobs and work and from which we demand respect of our rules. No matter what the breed, all of our dogs have been bred to work and we need to not only allow them, but to teach them how to do this. All dogs should know how to sit on command. Also how to heel, lie down, stay, come and walk on a leash without pulling. No dogs should jump up on us without being invited to do so, or jump onto the furniture without invitation. Food should not be available all day, but should be given twice daily with the requirement that the dog sits obediently and only take the food on command. Praise and reward should be earned, and not unconditional. And the best “love” that you can give your dog is to give it adequate exercise and attention. If you need help in how to do this just tune in to an episode of “The Dog Whisperer” and if necessary enroll in training classes, which are available all over, and conveniently for us with the Calgary Humane Society. If you want to see a happy dog just attend a show of “Super Dogs” or go to any dog agility trial. All of this is available in Calgary. Empower your pet to attain it’s true potential with your help. That is what loving your pet is really about!

PS: After jotting down the above I requested feedback from three dog trainers with whom I work closely.
The following are their replies.

Janine:

I think there is a problem with the power breeds and biting it is quite inflammatory (and yes, they certainly happen but get spectacular press). This gives people the impression that their biting Dachshund or Cocker Spaniel isn't an issue as hospitalizations don't happen as often. A far bigger problem I feel is dogs in the home biting - usually the small breeds and although these don't make the headlines, yet they create an environment of owner terror and helplessness where the dogs rule the household.

Dave:

Well done Mark! I agree with your position and feel you have expressed it well. The Akita is breed that was bred to guard and this is an important fact that may help people understand why the dog might react in a certain way, even without the presence of new puppies, which as you mentioned would certainly escalate the situation. Often people tend to misread, or not pay attention, to what a dog is telling us through its body language.

It seems you are putting the responsibility on the owner and not the dogs, with which I agree with as well. It seems as though the dogs and those unfortunate people were placed in a horrible position by the owner. The situation was not the same as it was before the pups had arrived and they should have all thought about that before having the dogs with their puppies in the “passage way” to get into their home. Especially as you mentioned with another dog being present. So why should these dogs even be considered for being put down when they reacted with a normal animal behavior to protect their pack? The owner should be the one to suffer the cost to ensure the humans safely heal mentally and physically and the cost to rehabilitate the Akita's and place them in a proper environment with a human who knows how to handle a “power breed”.

I worked with an Akita who was on guard all the time and it only took 3 minutes for me to remove that with her. It took the owners a few months but they are now with a dog that has not attacked in over 8 months and has dog friends. Before the dog had attacked 3 dogs in 4 months. The dogs can be trained most of the time to be under control, but the owners have to want that for their pet, and to put in the required effort in.

Gail:

Great points Mark. I think that you've covered most of the basic issues with this horrible and tragic attack, especially in regards to why the Akitas were motivated to attack.

I'm a big believer in leadership as you know, and to me that is the foundation of proper and healthy dog ownership. I think that pet owners are often conflicted by this need to provide leadership and direction and for the usual reasons of needing the dog to meet their needs, be that as substitute children, security or friendship. I have often told my clients that they don't respect their dogs if they are unable or unwilling to treat their dogs as dogs and not as people.

I support your views of training and jobs one hundred percent. I would like to stress over and over, that dogs are dogs, and that they communicate with body language and voice tone. They have strong instinct, and that is what motivates their behavior. Therefore, in order to be good and responsible dog owners, we must learn to view life from the perspective of the dog and not dump our human thoughts and emotions on them. We've put them in a situation where for the most part, they are dependent on us to survive. Therefore, we need to provide them with their needs, not ours.

Marijuana Toxicity

2011-07-27T21:47:00.000-07:00

I came across this very interesting article in the "Veterinary Practise News" Journal and reproduce it here in it's entirety. I found it to be informative, comprehensive and in line with my experience with these cases which have been handled in a similar manner, usually while working at after hours emergency clinics.
Dr Mark Rubensohn

Treating Marijuana Toxicity
Posted: June 23, 2011, 3 p.m., EDT

By Patrick Mahaney, VMD
For Veterinary Practice News

When veterinarians think of regionally specific illness, toxicity caused by consumption of native plants and exposure to infectious organisms typically comes to mind.

In preparation for a move to Southern California, I studied the effects of sago palm ingestion and inhalation of Coccidioidomycosis with the anticipation of the conditions I would be diagnosing and treating in my clinical practice.

I did not anticipate that I would end up treating such a large number of dogs presenting with clinical signs consistent with marijuana (cannabis sativa) consumption. As the sale of medical marijuana is legal in many California cities, dispensaries provide human patients with smokable or edible products.

Unfortunately, humans can carelessly leave these products in locations accessible to their curious pets, leading to ingestion.

Clinical Signs

Although a pet could show signs of marijuana toxicity post-inhalation, the majority of cases I see are due to suspected or known oral ingestion. I have treated dogs almost exclusively, yet cats can be similarly affected. A 2002 study of 250 cases of marijuana exposure showed dogs to be the primary cannabis consumption culprits (96 percent). Cats followed in a distant second place (3 percent), and other species made up the smallest portion (1 percent).1

Mild cases present with lethargy, altered response to visual or verbal stimuli, injected (blood engorged) conjunctiva and behavior changes.

More severe cases display ataxia, hypothermia, hypotension, bradycardia, ptyalism, emesis, anorexia, urinary incontinence, diarrhea and dysphoria (vocalization). Coma and death are also possible in severe cases.

Clinical signs can occur within minutes to hours and can last for hours to days, in part due body fat storage of the active ingredients in marijuana.

A 2004 study of 213 dogs with oral marijuana exposure showed neurologic signs (lethargy, ataxia, dilated pupils, etc.) in 99 percent of patients. Gastrointestinal signs, such as vomiting, were seen in 30 percent of patients.2

Although marijuana can have an anti-nausea effect, the volume consumed in proportion to the patient’s body weight, other ingested ingredients, and the induced release of “feel-good” hormones like serotonin, can cause vomiting.

In a video available at VeterinaryPracticeNews.com/MarijuanaToxicity, an Italian greyhound that ingested marijuana overreacts to visual and audible cues, appears to have difficulty standing and walking, and ultimately ends up lowering itself to a sternal position on the ground in a staggered fashion.

Mechanism of Action

Marijuana contains delta-9-tetrahydrocannabinol (THC), which causes the release of the neurotransmitters acetylcholine, dopamine, norepinephrine and serotonin in the brain’s frontal cortex and cerebellum. The increased release of these neurotransmitters leads to the various clinical manifestations.

As the attending veterinarian, I consider the possibility of other factors contributing to the overall picture of health or illness. Did the pet consume only cannabis? Could prescription or over-the-counter human or veterinary medications, other recreational drugs or unknown intoxicating substances be involved?

Differential Diagnoses

Cannabis toxicity has a variety of differential diagnoses. Options include stimulants (ephedrine and ephedrine-like compounds, amphetamines, nicotine and methylxanthines found in chocolate), opioids, benzodiazepines, antidepressants, amitraz (such as that used in anti-parasitic collars), ivermectin (from heartworm preventives), bromethalin (rodenticides), ethylene glycol (antifreeze), and alcohol (ethanol from rotting fruit, bread dough, etc.).
The majority of cases I have treated presented with multiple clinical signs, leading to the top differential diagnosis of cannabis consumption. The diagnosis, however, may not necessarily be confirmed by the owner, who may be completely unaware that a pet was exposed to the drug.

Others are up front about their pets’ ingestion of cannabis. Most are somewhat reluctant to share the truth, but ultimately concede under gentle, direct questioning.

I always ask questions in a manner conveying my intention to help the pet and its treatment. In doing so, I create an environment where the owner can tell the truth, a realistic diagnosis can be achieved and I can expeditiously start the diagnostic and treatment process.
Besides the effects of THC, “edibles” can contain substances potentially adversely affecting a pet’s health. These include carbohydrates, fat, proteins, and other ingredients. Vomiting, diarrhea, anorexia, pancreatitis and other clinical signs can ensue and lead to further complications. The Italian greyhound in the video that ate the chocolate-, sugar- and butter-filled marijuana brownie created a rather unfavorable situation for itself after inquisitively snatching the goodie from the owner’s bag.

Treatment

Having treated innumerable cannabis toxicities, I feel comfortable that my patients will make a full recovery with the appropriate care. If other toxins are suspected or known, I start a case file with the National Animal Poison Control Center (use weblink aspca.org/pet-care/poi
son-control/).

I perform baseline blood diagnostics to evaluate organ function. Knowing the status of the liver, kidneys and other body systems helps to rule out other underlying metabolic derangement that could contribute to the presenting clinical signs. I also recommend abdominal radiographs to look for gastrointestinal foreign bodies or other abnormalities.
For exposures occurring less than two hours before presentation, emesis is induced to clear the stomach of the intoxicant.

Once vomiting is under control, administration of activated charcoal can reduce absorption of certain toxins and speeds their evacuation through the gastrointestinal tract.

Provided a pet is not vomiting or comatose, administration of activated charcoal is a component to treating many cases of toxic exposure because of its ability to reduce enterohepatic recirculation of a toxic substance. Enterohepatic recirculation occurs after a toxin enters the bloodstream through the digestive tract, gets processed by the liver, then is excreted back into the small intestine via bile from the gall bladder.

Patients showing more profound sedation, ataxia, hypothermia, vomiting or other clinical signs are hospitalized for supportive care. Intravenous fluids, thermoregulatory support and anti-nausea and antacid medications promote a more rapid recovery and positive outcome.
Marijuana toxicity patients are typically discharged upon resolution of clinical signs and once they can hold down water and food.

Prevention is Best

The best way to avoid illness secondary to toxic exposure to any substance, including marijuana, is through prevention. Owners must pet-proof their homes with the same effort and attention to detail as they would baby proof for a human child.

Pets are intrigued by all sorts of smells, sounds and appearances, often curiously using their nasal and oral openings to evaluate anything within reach.

Clients can help prevent a pet’s toxic exposure by not bringing specific substances into the home or at least storing foods, medications and other household products where the animals can’t get them.

Dr. Mahaney is a Southern California veterinarian offering integrative veterinary medicine on a house call and in-facility basis through his business, California Pet Acupuncture and Wellness (CPAW) Inc., including acupuncture, Chinese herbs, nutritional and environmental modification and emergency medicine.

FOOTNOTES

1. Janczyk P, Donaldson CW, Gualtney S: Two hundred and thirteen cases of marijuana toxicoses in dogs. Vet Hum Toxicol 2004 Vol 46 (1) pp. 19-21.
1. Shell, L: Marijuana Poisoning. Veterinary Information Network, 2006.

Chicken Jerky Treats

2011-06-04T23:28:00.000-07:00

IMPORTANT ALERT !!!!!! Chicken Jerky Treats manufactured in China have been implicated in causing disease in dogs in Ontario. Signs include decreased activity, vomiting and increased drinking and urinating. Blood tests may show increased kidney enzymes and increased blood glucose levels. Therefore at this stage we are recommending that all jerky type treats that come from stores be stopped till further information is available.

Fluoridation of Drinking Water

2011-05-23T11:03:00.000-07:00

It over the past 50 years one of the greatest public health advances and medical improvements that have been made in out society is the fluoridation of public drinking water. It has been a major factor responsible for the decline in tooth decay. Although other fluoride containing products are available, addition of fluoride to drinking water has proven to be the most cost-effective and efficient method of providing fluoride to all members within the community regardless of age, education, or level of income. The safety, efficiency and effectiveness of adding fluoride to water has been extensively and scientifically studied across numerous continents encompassing hundreds of cities and millions of people.

It has been shown that a community can expect to save $40 for every $1 invested to fluoridation of its public drinking water. In the review of numerous studies on the rate of tooth decay, it has been shown to be valuable not only for children but also for adults, with each new age group of older adults retaining more natural teeth than the generations before them. Safety has not been in question with the exception of abuse, generally in children who are swallowing toothpaste or over ingesting fluoride containing supplements, both generally occurring due to poor parental supervision. Dental staining or spotting has been reported where mild excess of fluoride has been ingested over time, with no damage to either the teeth or the subject.

Guidelines to the addition of fluoride have changed over the past 10 years due to the universal addition of fluoride to toothpastes. This has resulted in the increased exposure of individuals to fluoride. Thus Calgary City and Alberta Health Services as part of their ongoing review of the water fluoridation program reduced the level of fluoride to 0.7 mg/L (from the previous 1 mg/L) in 1998. (Fluoride naturally occurs in the Bow and Elbow Rivers, in concentrations varying throughout the year, between 0.1 and 0.4 mg/L).

As of May 2011, Calgary city Council has voted to remove the fluoridation of the city’s water due to pressure of self interest groups and against advice and recommendations of the region's chief medical officer of health, of Alberta health region, and they opted not to consult with the expert panel that was offered by the University of Calgary for free. Interestingly Major Nenshi was absent during this critical Council vote which impacts the health of all Calgarian's. Reasons for the vote to stop fluoridation included the cost to the city of $750,000 a year for implementation, plus additional costs to upgrade the fluoridation equipment. Other factors claimed included the rights of counsel to impose addition of fluoride to drinking water which might not be approved by 100% of the population.

References:

City of Calgary “Fluoride discontinued in Calgary’s drinking water”
Community Water Fluoridation and Dental Health in the U.S

http://www.healthyteeth.us/documents/FluoridationWilliamMaaspublicstatement.pdf

Recommended Sources for further information:

http://en.wikipedia.org/wiki/Water_fluoridation http://www.cdc.gov/fluoridation/index.htm

Free Nature Walks | Birds Calgary

2011-05-05T06:41:00.000-07:00

Free Nature Walks | Birds Calgary: "Sun May 8, 8am: Visit Frank Lake to look at the birds – and the insects that support them! Learn the reason for the varied birdlife – and the diverse aquatic invertebrates that the lake supports. Meet Anderson LRT Station, Macleod Tr., S of pedestrian overpass, or at 8:45am, at the gate to Frank Lake, S off Hwy 23, about 5 km E of High River. Bring lunch. Leaders, aquatic specialist, Danita Mazlankowski, 403-771-2461 and Greg Wagner, 403-601-3893."

Urine Grass Burn

2011-05-03T14:15:00.000-07:00

At this time of the year our grass is most susceptible to urine burn from our dogs. Also, unfortunately the bluegrass that is our most common lawn grass, is also the most susceptible to urine burn. The cause is the high nitrogen concentration of urine, due to it’s the ammonium content. Just as over fertilization will kill the grass, so does the urine. The only real cure is to liberally water the lawn where your pet is urinating. Once we get into the wetter and warmer time of the year, and we actually get into the growth phase of the grass, this is no longer such a problem. During the snow covered winter months the urine is often sufficiently diluted by the snow cover and so causes less damage. So if you are concerned about the spots of killed lawn, now is the time to start watering where your dog urinates.

Females dogs are more damaging to the lawn as they squat and localize their urine. Male dogs often urinate up against objects and so are urinating into the flower beds or have a disseminated stream.

For the most part many of the products that are recommended to prevent grass burn which are sold for dogs are poorly effective or potentially harmful. After many years of experience with a variety of products, we have yet to find anything that works any better than water, re-seeding and time.

Raw Food Diets

2011-04-29T22:02:00.001-07:00

We at Bridlewood Veterinary Clinic have used home prepared and raw food diets for many years (Dr Mark has fed his own and clients pets for over 20 years) with the greatest success. We have found our pets to not only love this diet, but to gain many benefits. It can be used for both weight loss and gain with good results. The pet’s coats are always shinier and softer, they display increased energy, this food is good for allergies, dogs at risk for gastric torsion, and stool volume is hugely decreased. Dental condition improves, especially where raw bones are used as part of the protocol.

In the past we have fed Mountain Dog Food which is mainly a chicken based diet. Currently we are using Farm Fresh Pet Foods which comes as either cooked or raw preparations. It is also available as a beef base with oatmeal which is our preference. However for dogs that have allergies there is a Bison and Berry formulation and there is also a grain free beef formulation, where this is a requirement.

Ranula (Sialocele) in a Cat

2011-04-18T15:28:00.000-07:00

This is a very uncommon condition to be found in a cat. In fact after 35 years in veterinary practice this is the first one that I have ever seen. This condition is more commonly seen in dogs, and even then we would not commonly see more than 1-2 in a year.

This is caused by the inflammation of the sublingual and sub-mandibular saliva glands. It is generally associated with trauma, but could also be associated with inflammation or infection. The condition causes a large swelling under the tongue. It is usually only on one side, however it could also be bilateral. This particular cat was presented with the typical very large swelling under the tongue, and inability to swallow due to the swelling and thus an inability to eat. The mouth was wet with excess saliva due to the inability to swallow. The cat had a fever, was lethargic and dehydrated. Antibiotics anti-inflammatories and pain medication was administered, but after 24 hours there was very little improvement. Therefore, after discussion with a medical and surgical specialists, we performed surgery on this patient. The large inflamed and edematous salivary ducts were resected on both sides below the tongue, using a method called marsupialization.

Within hours there was a huge improvement, the patient displayed a significant increase in it’s amount of comfort and was able to begin eating within 12 hours. Shortly thereafter it was in a sufficiently stable condition to be able to bedischarged, and on subsequent follow-up it has continued to do well, is able to eat well, and is returning to full and normal activity.

This was a rare and very interesting case particularly because it was in a cat, and we are all very gratified that the results which turned out so favorably.

Anal Sacculitis of dogs and cats

2011-04-16T15:28:00.000-07:00

One of the more common conditions that we see in our patients is problems to do with the anal glands. All canines and felines have these glands under the tail, and in the wild they would serve the purpose of territorial marking and individual identification. The purpose would be to let other animals that may inadvertently enter into their territory know that they do so at your own risk. In the case of our domestic pets, these glands are actually redundant. However they are prone to pathology which includes impaction, infection and abscess formation.

To put this into perspective, we would be expressing anal glands on a daily basis in our practice. We treat three to four infected or abscessed glands in a week, and are only required to surgically remove chronically infected glands three or four times in a year.

Anal glands become impacted when the secretion becomes thickened or the glandular ducts become narrowed. At this stage they can easily be manually expressed by external or internal rectal digital pressure. Our groomers would typically perform this procedure on most dogs that come into the grooming salon on a daily basis. In a lesser degree of cases we see glands that have become infected and the discharge becomes particularly fetid, yellowish and pussy looking. In this case we would be required to use antibiotics in addition to the manual expression of the glands. Occasionally, the first sign that we become aware of, is once the gland has already formed an abscess, or an anal gland abscess has already burst. In this case cleaning the affected area and antibiotics would be required.

In all cases of anal gland problems the signs would be similar in that it would be a dog that is scooting, licking or biting at its rear end, is experiencing discomfort, and occasionally owners will report difficulty with defecation. Some authors would suggest that this condition is more common in small dog breeds, however we have found it to be not uncommon in all breeds including and less frequently in cats.

In dogs where recurrence is frequent and discomfort is persistent the recommendation is to remove the glands surgically. This is relatively easily done, and we experience a very good prognosis for a full and complete recovery, and resolution of the problem.

As far as prevention of the condition, there is unfortunately very little that one can practically do. As previously mentioned routine expression during grooming is always recommended. Also, at the first signs of scooting or rear end discomfort it is recommended that your pet be checked by your veterinarian, and the anal glands expressed if that is the problem. Antibiotic treatment, where required, will sometimes reduce the rate of recurrence of this problem. Unfortunately dietary management and/or weight control or reduction is rarely of any benefit.

Coccidiomycosis in a Dog in Calgary

2011-04-04T13:16:00.000-07:00

Abstract:

A diagnosis of Coccidiomycosis has been made in a Greyhound in Calgary. This dog was introduced from Arizona. She was presented with a mild fever, unilateral hind leg lameness, and later with a suppurating peri-anal fistula. Swabs revealed fungal spherules, and fungal titres were positive for Coccidioides immitis. Treatment was started with ketoconazole at 5mg/kg bid and an immediate improvement was achieved. It is expected that this dog will receive medication for a minimum of one year, and possibly for life.

Case History:

A 2-year-old spayed female Greyhound “Cabby” was presented for a post adoption examination on March 9,2002. She was adopted via the Greyhound Rescue Society and had originated in Arizona.

On presentation “Cabby” was bright, alert, and responsive. The right submandibular lymph node was enlarged (¾” diameter), she had a right otitis externa and a nail bed infection (L/F D2). She was placed on antibiotics (Cephalexin 250 mg bid) for 2 weeks. She was then re-examined and the lymph node had reduced in size (½ “ diameter) and the nail bed infection and ear were healed.

On July 13, 2002, “Cabby” was presented with a fever (39.5 C) and limping on the left hind leg. Clinical examination was unremarkable and she was placed on Metacam (Meloxicam 0.1 mg/kg sid). On July 23, 2002, the limp had not improved (painful upon extension of the left hind and sensitive in the groin area), “Cabby” had developed a draining fistula at the site of the left anal gland. She was placed on antibiotics (Amoxicillin 500 mg bid for 1 week) for a suspected anal gland abscess, and appeared to improve after 3 days with decreased discharge and discomfort. On August 6, 2002, “Cabby” was checked again. The left hind lameness was worse, she was again febrile (40.5 C), with persistent peri-anal fistula drainage.

The fistula was probed to a depth of 3.5 cm. A swab from the fistula showed a pyo-granulomatous discharge containing spherules of Coccidiodes immitis. Hematology revealed a monocytosis of 1.730 10e9/L (0.000-0.980) as well as a basophilia of 0.111 10e9/L (0-0.100). Blood chemistry revealed severe hyperproteinemia of 86 g/l (54-71) due to an exaggerated hyperglobulinemia of 62 g/l (20-40). Radiographs showed granulomatous pelvic osteomyelitis. The systemic fungal panel was positive for antibodies to Coccidiodes (+1:16). As low grade infections with Ehrlichia canis is not uncommon in dogs of the southern USA, an E. canis titre was run and found to be negative.

After discussion with the owner, “Cabby” was started on ketoconozole at a dosage of 100mg every 12 hours (5mg/kg bd). She was also placed on a diet of canned puppy food (Medi-Cal Development) to augment her diet as ketoconozole can act as an appetite suppressant. “Cabby” responded well to treatment. Her fever reduced (39.2C); she is bright and eats well. The treatment will continue for a minimum of one year, after which her condition will be reassessed.

DISCUSSION: (Courtesy of Suzanne Stack, D.V.M.)

The desert southwest (Arizona, N. Mexico, S. California) is the hotbed for Coccidiomycosis (Coccidiodes immitis) in the U.S. “Cocci” or "Valley Fever" is a fungus that lives in the desert soil and forms spores when released into the air. Events such as the digging of building foundations and pools help to release the spores more quickly. Periods of rain, which cause fungal growth, are usually followed by more cases of Valley Fever being diagnosed. The spores are inhaled by man, dogs, and horses (cats seem to be resistant), causing the disease, VF. Any dog that breathes air in an endemic region can become infected. There is no vaccine or prevention in existence short of moving away from the area.

Greyhounds seem particularly susceptible to VF, perhaps due to their normally low white blood cell numbers. Natural immunity plays a part in which dogs contract VF (a new arrival to the area is more susceptible than a dog that grew up there). We see as many cases of VF in indoor dogs that are out only briefly to do their duty as in outdoor dogs that run around all day with their noses to the ground. Additionally, if one dog in a household gets VF, there is no increased risk to other dogs in that home.

Symptoms:

Valley Fever is a disease that can be obscure and may progress before the owner sees sufficient reason to visit a veterinarian. Some dogs display no specific signs, especially early on; they may not feel as well, eat inconsistently, or lose weight. Despite the name, half of Valley Fever dogs have normal temperatures at presentation. They may, however, run fluctuating fevers at home and have times of feeling well interspersed with times of lethargy.

These ADR ("Ain't Doin' Right") dogs inevitably go on to develop more specific signs if undiagnosed and untreated. The most common signs are poor appetite, weight loss, lameness, bone pain, spinal pain, and coughing. This is because in the early ("primary") form, the fungus infects the lungs, then moves on to infect the bones ("secondary" form). Lungs and bones account for most cases; other systems VF can affect are the central nervous system, eyes, and less commonly, the heart or skin.

With Greyhounds, we seldom see the coughing stage. In most cases, the Greyhound presents with bone involvement or nonspecific illness/weight loss. While other dogs tend to present with equal proportions of lung vs. bone form, Greyhounds run approximately 10% lung, 30% ADR, 60% bone, and the odd neurological case.

Of particular concern with Greyhounds is how much the VF bone lesions resemble bone cancer (osteosarcoma) on radiographs. Lesions can be either osteoproliferative or osteolytic. If your Greyhound is ever diagnosed by radiography with "bone cancer," be sure a Coccidiosis antibody titre is done. I strongly recommend a titre be done early on any Arizona Greyhound, sick for any reason. Catching the disease a few weeks early may save months or years of treatment down the road. Additionally, be sure to also check the Greyhound for Ehrlichia, as some Greyhounds have both diseases together.

Treatment:

Ketoconazole is the first line of treatment. It is used at a dose of 5 mg/kg every 12 hours with food. MINIMUM treatment time is one year, unless there is only lung involvement, in which case a minimum of 6 months. In reality, most Greyhounds are on anti-fungal medications for years. Treatment is continued until titers are negative and radiographs are clear (if bone involvement).

In the first 2-3 weeks of treatment, the Greyhound is usually anorexic, due both to the disease and to the ketoconazole. Ketoconazole is an appetite killer – it depresses steroids in the body which is why it can be used as a treatment for Cushing’s Disease (fun fact). We usually force-feed the dogs through the first few weeks. That way a full dose of medication can be administered, thereby keeping them from losing any more weight until they begin to improve. From there on it's usually smooth sailing. Relapses are rare in a dog that is on full dose medication; they are more common when medications are being discontinued. So, while the Greyhound may be on ketoconazole for years, he is not necessarily sick for years.

Ketoconazole is absorbed better with a fatty meal, so it helps to feed substantial amounts of canned dog food at least in the beginning of treatment. Once they are stable, I usually just feed mostly dry food and a few spoons of canned. If you don't get food into the dog, don't give the ketoconazole because he will likely vomit. That's why the force-feeding is so important.

Though ketoconazole is labeled as hepato-toxic, I cannot think of having to take a dog off it for that reason. If we have to try medications other than ketoconazole, it is usually because of appetite suppression. With the adoption dogs we muscle our way through the first few weeks with force-feeding until things start to improve.

If a dog vomits even when ketoconazole is given with food, you can try using itraconazole (Sporonox) at a dose of 2.5 mg/kg every 12 hours. Itraconazole does not generally have any advantages over ketoconazole except to reduce side-effects. The premium VF medication (if you can afford it) is fluconazole (Diflucan) at a dose of 2.5 mg/kg BID. With really sick dogs sometimes it is helpful to use it for the first month or two, then revert back to ketoconazole for the long haul. The main advantage is that most dogs tolerate fluconazole much better than the other two (however even fluconazole can be an appetite suppressant). Although it is the drug of choice for CNS involvement, we have treated cases successfully with ketoconazole and amphotericin B before fluconazole was available. Whether or not fluconazole actually shortens the treatment period is uncertain. Regardless of which medication you use, I think it's critical to keep calories in the dog. He can't win this battle if he is not eating and is losing weight.

Some veterinarians recommend MSM to help with VF, some add Program (kills VF skeletons as well as flea skeletons), but this makes treatment relatively expensive. The dosage is one white (409.8 mg) Program tablet daily. Others give a Vitamin C (500 mg) with the medication as antifungals work better in an acidic stomach.

Lastly, with really sick dogs, amphotericin B is an option. It is a potent drug with the possibility of serious side effects. (It is known for kidney damage but I had one Greyhound become icteric after just one treatment.) Interestingly enough, this Greyhound had to discontinue amphotericin B and go right onto ketoconazole while still icteric. He stayed on ketoconazole for 4 years with no liver problems. Therefore amphotericin B (“amphoterrible") is usually reserved for seriously sick dogs. The drug itself is very inexpensive, but it has to be given over a period of 12 hours, first with a liter of 0.9% saline to flush, followed by a liter of 5% dextrose. Before each treatment, a urinalysis and blood urea nitrogen should be run. Full treatment course is twice weekly for 2 months. I've used it on perhaps 20 dogs that failed to improve with ketoconazole treatment, and many of them survived because of it, including two Greyhounds. Some dogs will still need to be maintained on oral medication after finishing the amphotericin B. Veterinarians who have actually used it get a sense of risk vs. benefit. It certainly is a stronger and faster working drug for seriously ill patients.

Prognosis:

VF can relapse even if the titres are negative. Some veterinarians consider VF to only be in remission and not cured, until the dog has gone several years without a relapse. One of my first Greyhounds had a vertebral lesion and was on ketoconazole for 4 years. His titres finally became negative, but every time I tried to take him off ketoconazole, his neck would start hurting again in a month or two, so we continued medicating. He eventually died at the fair age of 7 from right-sided heart failure - somewhat unusual, but I didn't autopsy to find out if it was from VF (titres were negative at the time). I do know of another Greyhound that started out terribly sick who also died of right-sided heart failure 2 years into ketoconazole treatment. (He was doing well on his medication until his heart gave out).

The Greyhounds do seem to have a worse time with VF than other dogs. Weaning dogs off the medication seems preferable to stopping medication entirely and risking a relapse, which can sometimes get the better of them.

Approximately 1/3 of VF dogs will die, 1/3 are cured, and 1/3 are OK as long as medication is continued.

References:

1. Suzanne Stack, DVM, Ironwood Veterinary Clinic, Yuma, Arizona

2. Central Laboratory for Veterinarians, Calgary, AB

3. R.V. Morgan: Coccidiomycosis. pp. 1119-1121. Handbook of Small Animal Practice, 3^rd Edition, W.B. Saunders, Philadelphia, 1997

4. Ettinger SJ, Feldman EC: Coccidiomycosis. pp. 444-448. Textbook of Veterinary Internal Medicine, 4^th Edition, Volume 1, W.B. Saunders, Philadelphia, 1995

Chapter 71, Wolf, Troy: Deep Mycotic Diseases

Laboratory Results:

			Calgary-Central Lab for Vets
			Unit 19, 5080 12A Street SE
			Calgary, Alberta T2G 5K9
			(403) 214-1506
BRIDLEWOOD VET CLINIC			PATIENT: CABBY
1-403-201-6427			AGE: 2 Y	SEX: F
26-17107 JAMES MCKEVITT RD SW			SPECIES: CANINE			DRWN: 08/06/02 17:50
CALGARY, ALBERTA						RCVD: 08/06/02 17:50
T2Y 3Y4						PRNT: 08/07/02 10:43

* * COMPLETE REPORT * *	ATTENDING VET: RUBENSOHN

TEST NAME	NORMAL		OUT OF RANGE		UNITS		REFERENCE RANGE

General Panel	. . . . .
cbc with differential	. . . . .
White cell cnt	11.7				10.9/l		4.0 - 15.0
CD-NEUTR	8.91				10e9/L		2.80 - 10.56
CD-LYMPHS			0.937 L		10e9/L		.960 - 4.800
CD-MONOCYTES			1.730 H		10e9/L		0.000 - 0.980
CD-EOSINOPHILS	0.012				10e9/L		0 - 1.231
CD-BASOPHILS			0.111 H		10e9/L		0 - 0.100
MORPHOLOGY	T

	This is an automated differential, all absolute number are in SI units.
	Platelet numbers are adequate. Platelets clumped. Variability
	in platelet size apparent. Rbc morphology normal.

Red cell cnt			8.12 H		10.12/l		5.50 - 8.00
Hemoglobin	188				g/l		138 - 199
Hematocrit	0.545				l/l		0.390 - 0.560
Mean Corp Vol.	67				fl		63 - 77
Mean Corp Hemoglobin	23.1				pg		22.0 - 27.4
Mean Corp Hemoglobin Conc	345				g/l		326 - 374
RDW	16.6						10.0 - 19.0
Platelet cnt	INV				10.9/l		170 - 400
Mean Platelet Volume	INV				fl		7. - 14
Chemistry Screen	. . . . .
Glucose	4.2				mmol/l		3.0 - 6.6
Grey Glucose	4.0				mmol/l		3.0 - 6.1
Blood Urea Nitrogen	4.9				mmol/l		2.5 - 9.20
Creatinine	110				umol/l		68 - 141
Bun/Cr Ratio	11
Sodium	150				mmol/l		140 - 151
Potassium	4.7				mmol/l		4.0 - 5.4
Na/K Ratio	32
Calcium	2.37				mmol/l		2.24 - 2.83
Phosphorus	1.56				mmol/l		0.72 - 2.08
Total protein			86 H		g/l		54 - 71
Albumin			24 L		g/l		31 - 42
Globulin			62 VH		g/l		20 - 40
Albumin/Globulin Ratio			0.4 L				0.8 - 2.3
Bilirubin total	5				umol/l		0 - 7
Alkaline phosphatase	82				iu/l		04 - 113
Sgpt (alt)	35				iu/l		0 - 113
Gamma gt	9				iu/l		2.- 20
Chloride	118				mmol/l		108 - 118
Carbon Dioxide	20				mmol/l		15 - 26
Calculated Osmolality	296.8				mmol/kg		278 - 306
Anion Gap	17						10.- 22
Creatinine Phosphokinase	59				iu/l		00 - 314

Cytology	T
	THE ONE SMEAR FROM THE PERIANAL REGION REVEALED
	A HIGH NUCLEATED CELLULARITY WITH A PREDOMINANCE
	OF NEUTROPHILS AND MACROPHAGES A LOW NUMBER OF
	VARIABLE SIZED SPHERULES WITH THE RARE CLUMP AND
	INDIVIDUAL ENDOSPORES WERE NOTED. THESE STRUCTURES
	MOST CLOSELY RESEMBLE COCCIDIOMYCOSIS ORGANISMS
	SUGGEST SYSTEMIC FUNGAL PANEL SEROLOGY AND BIOPSY
	TO HELP CONFIRM THESE INITIAL FINDINGS RADIOLOGY
	IS RECOMMENDED ANY LAMENESS OR RESPIRATORY SIGNS?
	Dr. Norman Lowes

COMMENT	TO15
	STRESS LEUKON WITH MONOCYTOSIS INCREASED TISSUE
	DEMAND FOR PHAGOCYTOSIS SHIFT IN AG RATIO CHECK
	ELECTROPHORESIS IF NOT RESOLVING WITH SURGICAL
	INTERVENTION?
	Dr. Norman Lowes

	SYSTEMIC FUNGAL PANEL, SUSPECT COCCIDIOMYCOSIS

Systemic Fungal Panel	T	A		TITER
	BLASTOMYCES AB:		NEGATIVE
	COCCIDIOIDES AB:		POS 1 : 16
	HISTOPLASMA AB:		NEGATIVE
	APERGILLUS AB:		NEGATIVE
	CRYPTOCOCCUS AG:		NEGATIVE
COMMENT	TO15
	Dr. Lily Edwards

Ehrlichia canis	NEG
COMMENT	TO15
	Dr. Sally Lester

Corn’s in Greyhounds

2011-04-02T13:13:00.000-07:00

Absract:

"Corns" or "digital keratomas" are a frustrating and not uncommon problem of Greyhounds (racing or pet) causing significant lameness. They are circular, firm to hard, flat or slightly raised thickened plaques, ranging in color from black to whitish, extending up from the central surface of the pads, usually on the areas that bear the most weight. They may be secondary to either traumatic implantation of glass, sand or other foreign material or due to papillomavirus infection, or maybe both or idiopathic. No one knows for sure. The papillomavirus has been isolated in only a few cases by immunoflourescent assay. Radiographs have been taken to look for foreign bodies but these have rarely been found.

Unfortunately there is no current reliable good medical management for corns. Therefore treatments range from “shelling” or “hulling” out the corns using a dental elevators; deep surgical removal (with varied success and significant recurrences); laser surgery (also with significant recurrences); human corn and wart removers with salicylic acid (ineffective), anti-viral therapy using systemic alpha-interferon or topical Imiquamod (Aldara) or Docosonal (Abreva); surgical neurectomy of the nerves to the affected toes due to counteract intractable pain; and toe amputation.

Discussion:

Various theories have been advanced regarding the etiology of Greyhound corns. These include the lack of fat in the Greyhound pad associated with repeated trauma of racing and concussion, foreign bodies, chemical irritation associated with kennel disinfection, and viral infection. The response seen with Aldara or Abreva and Interferon would suggest a viral etiology. However it is strange that other breeds do not seem to be affected. It is also difficult to explain how one hound in a house can be infected while the others seem to remain free.

Diagnostic approaches have included:

1. biopsies that have come back as "hyperkeratosis and epidermal hyperplasia"

2. radiographs have been taken to look for foreign bodies but these have rarely been found

3. immuno-histochemistry in an attempt to demonstrate virus has been mostly unremarkable

Treatment approaches would seem to begin with a “shelling” or “hulling” procedure. One can “dig” these corns out using a dental root elevator. This can usually be done without any sedation, and provides instant relief. Some suggest softening the foot with soaks prior to “shelling” procedure. Some owners are able to performing this procedure on there own dogs. Unfortunately there is a high rate of recurrence of the corns ranging at about a + 60% rate within 1 to 6 months. Recently reports of using Abreva or Aldara cream in the hollowed out foot pad once daily for an indefinite period seem to have decreased the rate of recurrence, with some reports of resolution following repeated “shelling”. Use of Interferon with doses ranging from 1,000 units daily to 1 million units 3 times weekly have been recorded with some favorable results. Some reports indicate that after stopping Interferon treatment after 2 months of use led to a relapse, so medication was re-instituted. Interferon has been administered by injection and orally. The use of humane wart or corn remedies (salicylic acid) seems to have given no improved results.

Surgical options include deep full thickness elliptical incisions into the foot pad to remove the corn in total. The wound is sutured, and kept well padded to reduce additional trauma to the surgical site for at least 14 days. Antibiotics are used. However recurrences still occur. Laser surgical techniques have not improved this rate of recurrence. Amputation may have to be considered for stubborn cases, but because corns may occur on multiple toes one remains concerned to resort to this. Local neurectomy seems a viable option for stubborn cases where lameness due to pain is a concern.

Soft surfaces such as grass and carpet as well as using padded boots (TheraPaws) improve comfort for these dogs.

References:

Veterinary Information Network - Carol Foil, Malcolm Ness, Harry Newman, Wendy Lorch, Therry Olivry (NC State University), Sonya Bettanay, Kimberley Lower, Adi Nell
Carol Macherey
Dr Bill Freeman
Dr Alastair Smith – Sandown Veterinary Clinic- Sandown Greyhound Racetrack, Melbourne, Australia
Dr Suzzane Stack
Dr Gary Yocham

Cherry Eye and Kerato-Conjunctivitis Sicca

2011-04-01T10:38:00.000-07:00

Cherry eye is the common name for a condition that is caused when the gland of the third eyelid of the dog (otherwise known as the Hardarian or Nictitans gland), becomes inflamed, swells up and pops out in front of the eye. It becomes inflamed, swollen and irritated and can cover 1/3 of the whole eyeball of the dog. It can be expected that if the gland of one eye prolapses, that there is a high probability of the second eye also prolapsing within a few months.

Historically when dogs developed cherry eye, the gland would simply be removed. However, in the past decade, it has become the common and recommended practice to attempt to replace the gland by various methods. This is due to the problem of reduced tear production leading to a condition called “dry eye” or keratoconjunctivitis sicca (KCS). KCS is a serious condition causing significant discomfort to the dog and requiring ongoing daily medication to the eye for ever. Tear flow is measured by means of the Schirmer Tear Test and should be between 14 and 24 mm in a minute. Breeds particularly susceptible to KCS include many of the brachycephalic breeds, and include the following:

Miniature Schnauzer

Cocker Spaniel

English Bulldog

Beagle

Poodle

Pug

Pekenese

Shih Tzu

Lhasa Apso

Yorkshire terrier

West Highland Terrier

Boston Terrier

Currently the most commonly recommended surgical procedure for the replacement of “cherry eye” is called "the pocket technique”. In a retrospective study the following results were found:

If the gland was left out and untreated, 43% of the eyes developed KCS
if the gland was excised 48% of the eyes developed KCS
but if the gland was surgically replaced only 14% of the eyes developed KCS
using the unaffected eyes as controls, 5.5% of these eyes developed KCS.

There is significant feeling amongst breeders of Neapolitan Mastiffs, Presa Canario and Cane Corso's, (as well as other large breed affected dogs) that excision is a preferable technique to gland replacement. This belief is centered around the fact that the prolapsed gland is so large in these breeds as to cause significant problems in successfully replacing it, and thus repeated prolapse is unacceptably high. Also as these breeds are not high on the list of dogs experiencing KCS, thus the chances of developing this complication are significantly reduced. It is this authors experience that we have had no incidents of KCS in excised glands from these breeds, although it must be stated that this certainly is possible. Some surgeons may choose to cut away some of the gland prior to replacement, and so reduce the likelihood of repeated prolapse, but how that affects the incidence of KCS is uncertain.

Below is a YouTube video of a pocket technique replacement procedure:

http://www.youtube.com/watch?v=xrBSxppLrT4

References:

Dr Rhea Morgan, Diplomate ACVIM, ACVO
Dr Sherilyn Allen, DVM, Ironstone. USA
Schering Plough Animal Health

Dr Mark Rubensohn

Bridlewood Veterinary Clinic

Calgary, Alberta

Antibiotic Responsive Neuromuscular (Cerebral) Ataxia

2011-03-31T13:08:00.000-07:00

Abstract

Since 1994 numerous cases of neuromuscular ataxia have been observed and documented in various dog breeds across Canada and the USA. The incidence appears to be highest in the spring and summer and seems to be related to contact with cattle. The onset appears to be aggravated by inoculations or other stress inducing episodes e.g.: shipping, dog shows or illness. It occurs in any age with young dogs being more highly represented. Signs are varied and begin with inappetance, anorexia, weight loss, ocular discharge, poor thrift, diarrhea or vomiting, and progresses to compromised mobility. Sometimes skin disorders have been recorded. The condition progresses in a waxing and waning pattern. Most cases have responded to a variety of antibiotics and antimicrobials noted for the efficacy against protozoal conditions. Some dogs have required larger than normal dosage for longer periods of time to achieve results. Clindamycin has proven to be the most efficacious remedy used to date.

Laboratory testing has to date failed to reveal any etiological diagnosis except for one case of Neospora canninum.

If anyone can add any information or observations to the above scenario, kindly contact Dr. Mark Rubensohn at e-mail: bridle@telus.net

Attachments:

1. Observations from a dog breeder who has been involved with this problem

Attachment:

I grew up showing Scottish Terriers, my father raised them and I started showing when I was about 10 years old. The Scottish terrier is documented as having an ailment known as “Scottie Cramp”; it has been used as a catchall for any mobility problems afflicting the Scottie. About 10 years ago, I noticed some of these “Scottie Cramp” puppies had an ailment that caused the movement to deteriorate over time. The breed has recently had many dogs diagnosed with “Cerebral Abiotrophy”, which is being differentiated from Scottie Cramp.

I believe that while there certainly are some dogs with an inherited disorder which causes symptoms of Cerebral Ataxia, there are also some dogs with a parasite mitigated form of the disorder and that these dogs will respond to antibiotic therapy specific to protozoan parasites. All tests performed on these dogs have to date come back normal, including those for Neospora, which would suggest another parasite, as yet unnamed. I believe this parasite is causing ataxia symptoms in numerous breeds of dogs in addition to Scotties.

Scottie Cramp affected dogs are normal at rest and exhibit normal ability to walk until they are stressed. Common stimuli are exercise, hunting, fighting, or courtship. As the dog's level of stress increases, his gait begins to change. The forelegs move out to the side and forward rather than straight forward in a movement called winging. The spine in the lumbar area may arch and the rear legs begin to overflex. If the excitement or exercise continues, the dog begins to exhibit a "goose-stepping" gait. If the dog is running, he may somersault and fall. Severely affected dogs may find their ability to walk or run completely inhibited. This is not a seizure. There is no loss of consciousness. As soon as the stimulus abates, the symptoms disappear almost immediately.

The severity of symptoms in affected dogs varies widely as does the amount and type of stimulation necessary to elicit clinical signs. The symptoms appear to be caused by a buildup or depletion of some chemical compound in the dog's central nervous system, most probably serotonin.

I had some wonderful mentors in my youth, old terrier men who took me under their wing and taught me much about the breed and breeding, terriers and dogs in general. At that time, Scottie cramp was something that was talked about but was seldom seen. One or two in a lifetime was the norm, if you read the old books you will see reference to it with the same rider, that it is seldom seen. But, the Scottie cramp that is referred to is always the traditional form of Scottie cramp, usually becoming apparent at about 4-6 months and coming on after certain stimuli. It is never the type seen in young puppies often showing up a few days after inoculations and progressively deteriorating from then on. It is an episodal affliction that usually diminishes with maturity. It is not a constant ongoing affliction such as what we now see in Cerebral Abiotrophy. The old timers in the breed have been honest and thorough in their documentation and Cerebral Abiotrophy’s symptoms are not mentioned. I believe it is a relatively recent addition to the problems affecting the Scottish Terrier.

The first time that I noticed this problem was in the spring of 1994 at dog show that was held in the Alberta. This building had recently held a cattle show and it was inadequately cleaned between the two shows. Several dogs of various breeds and sizes that had been at the show became ill with some or all of the following symptoms; diarrhea, vomiting, inappetence, fever, anorexia, eye discharge. They all became noticeably unsteady in their movement. After a time, many dogs that had not been in attendance at the show also became ill in the same way. Some dogs made full recoveries, some had to be euthanized and some retained some residual movement problems. It progressed through the pet community through the summer and it came to be known as the “Wonky Flu”. The number of cases dropped off with winter and it ceased being a concern. Although, a few cases show up every spring and I have heard of it appearing in other communities, by veterinarians who are seeing a cluster of dogs with movement problems of no known cause.

A Southern Alberta breeder of Irish Wolfhounds had a litter born in 1996. When the puppies were about 8 weeks old, some of them started to show a deterioration of muscle tone and an unsteadiness of gait in the rear. After extensive testing it was determined that the puppies were infected with “Neospora”, a protozoan parasite. It was a mystery as to how they had come in contact with the parasite as it had only been seen in the Southern United States at that time and had only been diagnosed in dogs a few times. As it turned out, some 14 hours North in the Peace River district the cattle ranchers were dealing with an outbreak of Neospora in their cattle. Researchers in this area suspected a connection to the wild canine population. It was felt that Neospora had been in the canine population for a long time but had been unidentified and misdiagnosed as other conditions. The Irish Wolfhounds had been infected in their own backyard as they lived on acreage adjacent to a field that pastured cattle.

The puppies were treated with Clindamycin and the Neospora was stopped. Unfortunately, the damage that had been done was not reversible. While the puppies were able to make improvements from the point at which the parasite was stopped, they could not be returned to “normal”.

I became very interested in this parasite and learned as much as I could about it. One of the characteristics which impressed me was their ability to be passed from mother to offspring in utero. This gives it the potential to be mistaken for an inherited disorder. I also noted that the parasite will affect only some of the puppies, usually when the immune system is suppressed or stressed, i.e.; immediately after inoculations, after shipping to a new home, a dog show or after another illness.

June 1999, I had a litter of 6 Scottie puppies; all were thriving until given inoculations at seven weeks. Within 36 hours every puppy in the litter was showing some degree of rear movement disorder. This did not appear to be normal “Scottie cramp” but was more of an ataxia like syndrome. I was needless to say devastated. About one week later I decided to deworm and used a product called Drontal Plus manufactured by Bayer (ingredients: Praziquantel, Pyrantel and Febantel) at the suggested dosage.

Within 36 hours of deworming these puppies they had all returned to normal movement. This was almost a miraculous occurrence and I tried to analyze what had just occurred. I came to the conclusion, that either one of the drugs in Drontal plus had a neurological side effect or we had just killed a parasite. I called my vet, Dr. Gary Carter (Calgary, AB) and asked him if there were any known side effects of this nature to these drugs and told him what had occurred. He didn’t believe there were any side effects of this nature and felt it likely we had killed a parasite but decided to check with Bayer. The head research vet from Bayer contacted me and told me that all of the drugs used in Drontal plus have been well tested and have been in use for a long time and there were no known neurological side effects for any of them. He felt we had probably killed a parasite, probably protozoan. He told me that one of the drugs in Drontal was shown to have some effect on protozoa. (Note: Since that time both Praziquantel and Febantel have been shown to be effective against protozoa.) The puppies were also tested for exposure to Neospora and all tests proved negative. I dewormed the puppies with a second dosage 10 days later and kept the puppies for an extended period of time. The movement problems did not return. They were placed in homes and were followed and all remained healthy. *See attached document

Bayer was interested in following up with further studies and agreed to supply us with Drontal Plus to be used on puppies diagnosed with “Scottie cramp” ie: movement disorders. The Canadian Scottish Terrier club advertised on their web site that we were interested in Scotties with Scottie cramp for a study and offered any who were interested some Drontal Plus for their afflicted dogs.

We had a little interest and what we found was that some puppies if caught early, usually those that showed signs of ataxia/cramping at 6-10 weeks of age could improve. Dogs that had been afflicted for some time showed very little or no improvement. In a conversation with Bayer, it was suggested that we were probably dealing with more than one disorder and that the puppies that improved were probably afflicted with a protozoan parasite yet to be named.

Nothing further was done as there wasn’t enough interest to warrant it. Locally we did notice that dogs of many breeds would show early symptoms of movement disorders and/or topline issues that could be improved with certain antibiotics (Tetracycline, Metronidazole, Sulfamethoxizole & Trimethoprim, Clindamycin and Drontal Plus.) It was also found that bitches that had been experiencing fertility issues if given Tetracycline from the time estrus started until 2 weeks after the 1^st breeding were more likely to conceive and carry to term.

Two years ago, a dog imported from Brazil acquired the movement disorder six weeks after arriving here. We were able to completely return him to normal with the use of the antibiotic “Clindamycin”. This helped us to have a clear course of action for treatment and some of the individual dog studies follow:

Indy a wire haired fox terrier born April 1998, arrived in Alberta, Canada October 2002 from Brazil through the US. He had been shown throughout the US and South America. 6 weeks after arriving he became very unsteady on his feet and was progressively deteriorating. He reached a point of being too unstable to rise on his own or urinate without assistance. He was seen by Dr. Mark Rubensohn (Calgary, AB) who did blood and urine analysis both showed nothing abnormal. Stool samples were normal, temperature was normal. Clindamycin was prescribed on the possibility that Neospora tests would prove positive. The Blood test for Neo-spora and other possible causes also showed negative results. But, after beginning treatment with Clindamycin, 75mg BID, improvement was rapid with deterioration stopping after 36 hours and improvements evident from that point on. The dog had some residual muscle weakness that returned to normal within 2-3 months. 2 years have passed and there has been no reoccurrence. He is a healthy dog completely steady on his feet. *See attached document

Maggie has produced several puppies with problems she lives on a Dairy farm

The following are from Maggies 1^st litter of 4 puppies born 4/1/00

Lexi - female puppy with Scottie cramp or ataxia type symptoms at 3 months this puppy has done well according to our last contact with the owners. No treatment was given

Tiffy – Born 04/01/00 to Maggie

She has been generally healthy. Her topline has never seemed right. She has been somewhat itchy with no signs of rashes or sores. She has never produced a viable puppy. She has conceived twice, producing one puppy each time, neither lived. An autopsy was done on the first puppy; samples were saved as this puppy was not mobile in any way from birth. The second puppy was still born. She has been treated occasionally with Tetracycline *See attached document

The other two puppies appear to be normal.

The following are from Maggie’s 2^nd litter of 6 puppies born 11/20/03

Molly, female Scottish terrier puppy arrived in Alberta, Canada April 2004. At the age of six months she became unsteady on her feet and progressed rapidly with symptoms of extreme ataxia. She was seen by Dr. Mark Rubensohn and he observed her in several episodes of unsteadiness to the point of being unable to stand. Tests were done, temperature, blood and urine showed nothing abnormal, neospora tests were negative. Stool tests did show some Coccidia, she was put on TMS 120mg BID and showed immediate improvement, reverting to normal ambulation. Dr Mark Rubensohn witnessed the improvement to complete normalcy while on antibiotic treatment. When she completed the 14 day prescription she began to deteriorate immediately. Put back on TMS she required a larger dosage 240mg BID to obtain improvement and she remained on TMS for 30 days. Again she deteriorated almost immediately when taken off of the prescription.

She was put on Clindamycin 75 mg BID and immediately improved, she remained normal while on Clindamycin. She remained on Clindamycin for 6 weeks and still retains relatively normal ambulation with only some small residual effects from the times when she deteriorated between prescriptions. *See attached document

Zeplin – male Scottish Terrier presented at 3 ½ months with rear movement problems. X-rays, blood tests showed no indications of any problems. Communication with the owner broke down at this time, no further updates possible.

Toni – female Scottish Terrier given second Vaccination at 3mons - one week later movement problems were seen resembling Scotty cramp. But, unlike Scottie cramp, it progressively got worse, especially when excited. Her back became very roached. Some days she would not be able to walk without falling over. She also had a skin rash that could become very red and scabby but never itchy.

A hair analysis was sent away and we were given a summary of the treatment path.

*(See attached document)

June 4/04 - She was put on TMS 1 – 250 mg pill a day An immediate improvement was seen. But after 8 or 9 days movement problems reoccurred so we doubled her dose to 500mg once a day. She did well for a period 3 weeks and then relapsed to some extent.

July 1/04 – some movement abnormalities have returned intermittently. She was medicated for 10 days with Clindamycin 100mg BID, 10 days with Metronidazole 500mg once a day, 5 days with Drontal Plus 2 pills once a day then Tetracycline 250mg BID until Aug 16.

Aug. 16/04 - She developed a lump in the throat and had a significant relapse.

Aug. 18/04 - prescribed Clindamycin 100mg once a day. Stopped TMS treatment. Biopsy done on throat lump. Biopsy was sent to the Saskatoon Vet College, results were inconclusive.

Aug. 20/04 – significant improvements are apparent there is no hopping while walking, no stiff leggedness . she is feeling good but is not eating. Still hopping while running.

Aug. 22/04 – Increased dosage to 150 mg Clindamycin once a day. Still not eating.

Aug. 23/24 – added 240 mg TMS once a day. Eating small amounts. She is still hopping while running.

September 1/04 – Toni is doing very well. The lump in her throat is almost gone. She is more willing to eat. She is moving more freely with a stiff legged gait only when she breaks out into a run. Lively and very playful now. She is on 150mg of Clindamycin once a day and 240mg TMS TID

*(See attached document)

September 15/04 – Toni has returned to a near normal state. Her health, her skin, her movement all appear normal. She is running, playing, jumping on furniture, wrestling with other dogs. These are things she was never able to do before.

September 23/04 – started reducing TMS while maintaining Clindamycin.

Oct 7/04 – she has had a significant relapse, she is on 240mg TMS once a day, 150mg Clindamycin once a day.

Oct 11/04 – she was returned to higher dosages of 240mg TMS BID and 150 mg Clindamycin BID

Oct 23/04 – she has again returned to near normal movement and her overall health is improving.

Tululah – female Scottish Terrier - Phoned owners when problems arose with other puppies. The owners said she seemed fine but sometimes noticed that she had a stiffness in her rear leg. X-rays etc. were done with no abnormal findings.

The other two puppies appear normal

Additional dogs with problems include:

Aaron – male Scottish Terrier Born 6/10/02

July 05, 2004 - He seemed normal in every way until he went to a dog show in Winnipeg MB. A friend noticed strange rear leg movement and arching of back while he was being gaited in the ring. Another competitor described it as the worst case of Scotty cramp they had ever seen. He returned home on the 8^th and we notice progressively worsening rear movement and arching of his back, he also vomited on the Wednesday and Thursday.

July 8, 2004 – prescribed Clindamycin in the evening which we gave immediately, improvement was evident by noon the next day. A video was taken of him gaiting on Friday noon. Movement problems are still evident on the tape but significantly decreased from the day before.

Aug. 15^th Aaron is doing very well. He seems normal in every way.

Tory – Born 08/07/94

In the last few years it has been difficult for him to climb or descend stairs, he has been unable to lift his leg to urinate without falling over. His rear leg movement, leg muscles and back have been slowly but progressively deteriorating. Because of our success with the younger dogs we decided to start this dog on a treatment of Tetracycline 250 mg BID in the middle of July. We have noticed a significant improvement in his abilities in day to day activities

September 1/04 - Tory is doing very well. His topline is very different now. It has been six weeks since starting his treatment. He is very playful and is able to run more. He is now able to climb stairs, run and lift his leg to urinate.

A video was taken of his improvement. We are gradually taking him off of the Tetracycline.

September 30/04 - Tory has been off of Tetracycline 1 week and we have noticed regression, he is stumbling more and losing his topline.

October 7/04 – We have started Tory on 150mg Clindamycin once a day.

October 23/04 – He is on Clindamycin 150mg once a day. He is improving daily, he can run again and has reverted to near normal movement. His topline has improved and his overall health and attitude are good.

Because of Tory’s success we have started 2 other older dogs on treatment and will continue to monitor and videotape them. Their history follows:

Teddy a male Scottish terrier born July 1993 was a healthy puppy born in Alberta, Canada. At about 9 months of age his topline started to roach and his tail developed a distinctive curl. He slowly deteriorated and by 1 ½ years of age was clearly having unsteadiness on the rear. It has continued to deteriorate over the years in a pattern of holding steady and then having a period of deterioration usually accompanied by other health concerns such as ear infections or skin pyoderma.

August 23, 2004 - He has been started on a regimen of 75mg Clindamycin tablets BID. A video has been taken for comparison. Aug 29, I received a call from Teddy’s owner expressing amazement at the improvements she is seeing in his overall health. He has a higher energy level, he is sleeping and eating better, his skin condition is improved and he is more mobile. I will continue to monitor him and will video him again in a few weeks.

Sept 23, 2004 – Teddy has improved in several ways but most obvious is that he is no longer shaking and can stand and look about without problems. He is moving with more confidence but is still stepping very high behind.

Drum - a male Scottish terrier born May 1997 was a healthy puppy born in Alberta Canada. At about 8 months of age his topline started to roach and his tail developed a distinctive curl. He slowly deteriorated and by 1 year of age was clearly having unsteadiness on the rear. It has continued to deteriorate over the years in a pattern of holding steady and then having a period of deterioration. He was given Drontal Plus once per month and while on it he appeared to be able to maintain his condition with little deterioration. He was taken off the Drontal Plus approximately two years ago when because of current literature and studies, it was assumed that he had the inherited form of Cerebral Abiotrophy. He has deteriorated rapidly since that time. He currently has extreme muscle atrophy on the right rear leg and does not weight bear on it.

Aug 30, 2004.- He has been started on a prescription of Clindamycin

He has been videotaped and we will follow up with further video.

Sept 23, 2004 – Drum’s owner describes his improvements as miraculous. He is no longer shaking and has better head control. He is weight bearing on his right rear leg. He is moving with much more ease and confidence and is able to climb over door sills and back onto his favorite spot looking out of the window. These are things he has been unable to do in over 6 months.

*See attached document

Gracie is added to the video to demonstrate traditional Scotty Cramp

Additional note:

Both Cheryl Lang and I have each had a puppy born in the last 2 years who had to be euthanized because of paralysis from birth with no known cause.

This document accompanies a DVD. To navigate in the DVD, highlight a dog and press play and it will show you a clip from the date shown on the screen. There are multiple menu screens, if you look on the bottom right hand side you will see a multiple headed arrow, if you highlight it and press play it will take you to the next menu. If you highlight the single arrow head and press play it will play through from start to finish.